The MIT Encyclopedia of Communication Disorders

The MIT Encyclopedia of Communication Disorders

Edited by Raymond D. Kent

A Bradford Book The MIT Press Cambridge, Massachusetts London, England

( 2004 Massachusetts Institute of Technology All rights reserved. No part of this book may be reproduced in any form by any electronic or mechanical means (including photocopying, recording, or information storage and retrieval) without permission in writing from the publisher. This book was set in Times New Roman on 3B2 by Asco Typesetters, Hong Kong, and was printed and bound in the United States of America. Library of Congress Cataloging-in-Publication Data The MIT encyclopedia of communication disorders / edited by Raymond D. Kent. p. cm. Includes bibliographical references and index. ISBN 0-262-11278-7 (cloth) 1. Communicative disorders—Encyclopedias. I. Kent, Raymond D. II. Massachusetts Institute of Technology. RC423.M56 2004 616.850 50 003—dc21 2003059941

Introduction ix Acknowledgments xi

Part I: Voice


Acoustic Assessment of Voice 3 Aerodynamic Assessment of Vocal Function 7 Alaryngeal Voice and Speech Rehabilitation 10 Anatomy of the Human Larynx 13 Assessment of Functional Impact of Voice Disorders 20 Electroglottographic Assessment of Voice 23 Functional Voice Disorders 27 Hypokinetic Laryngeal Movement Disorders 30 Infectious Diseases and Inflammatory Conditions of the Larynx 32 Instrumental Assessment of Children’s Voice 35 Laryngeal Movement Disorders: Treatment with Botulinum Toxin 38 Laryngeal Reinnervation Procedures 41 Laryngeal Trauma and Peripheral Structural Ablations 45 Psychogenic Voice Disorders: Direct Therapy 49 The Singing Voice 51 Vocal Hygiene 54 Vocal Production System: Evolution 56 Vocalization, Neural Mechanisms of 59 Voice Acoustics 63 Voice Disorders in Children 67 Voice Disorders of Aging 72 Voice Production: Physics and Physiology 75 Voice Quality, Perceptual Evaluation of 78 Voice Rehabilitation After Conservation Laryngectomy 80 Voice Therapy: Breathing Exercises 82 Voice Therapy: Holistic Techniques 85 Voice Therapy for Adults 88 Voice Therapy for Neurological Aging-Related Voice Disorders 91 Voice Therapy for Professional Voice Users 95

Part II: Speech


Apraxia of Speech: Nature and Phenomenology Apraxia of Speech: Treatment 104 Aprosodia 107 Augmentative and Alternative Communication Approaches in Adults 110 Augmentative and Alternative Communication Approaches in Children 112 Autism 115 Bilingualism, Speech Issues in 119 Developmental Apraxia of Speech 121 Dialect, Regional 124

Dysarthrias: Characteristics and Classification 126 Dysarthrias: Management 129 Dysphagia, Oral and Pharyngeal 132 Early Recurrent Otitis Media and Speech Development 135 Laryngectomy 137 Mental Retardation and Speech in Children 140 Motor Speech Involvement in Children 142 Mutism, Neurogenic 145 Orofacial Myofunctional Disorders in Children 147 Phonetic Transcription of Children’s Speech 150 Phonological Awareness Intervention for Children with Expressive Phonological Impairments 153 Phonological Errors, Residual 156 Phonology: Clinical Issues in Serving Speakers of African-American Vernacular English 158 Psychosocial Problems Associated with Communicative Disorders 161 Speech and Language Disorders in Children: ComputerBased Approaches 164 Speech and Language Issues in Children from AsianPacific Backgrounds 167 Speech Assessment, Instrumental 169 Speech Assessment in Children: Descriptive Linguistic Methods 174 Speech Development in Infants and Young Children with a Tracheostomy 176 Speech Disfluency and Stuttering in Children 180 Speech Disorders: Genetic Transmission 183 Speech Disorders in Adults, Psychogenic 186 Speech Disorders in Children: A Psycholinguistic Perspective 189 Speech Disorders in Children: Behavioral Approaches to Remediation 192 Speech Disorders in Children: Birth-Related Risk Factors 194 Speech Disorders in Children: Cross-Linguistic Data 196 Speech Disorders in Children: Descriptive Linguistic Approaches 198 Speech Disorders in Children: Motor Speech Disorders of Known Origin 200 Speech Disorders in Children: Speech-Language Approaches 204 Speech Disorders Secondary to Hearing Impairment Acquired in Adulthood 207 Speech Issues in Children from Latino Backgrounds 210 Speech Sampling, Articulation Tests, and Intelligibility in Children with Phonological Errors 213 Speech Sampling, Articulation Tests, and Intelligibility in Children with Residual Errors 215 Speech Sound Disorders in Children: Description and Classification 218



Stuttering 220 Transsexualism and Sex Reassignment: Speech Di¤erences 223 Ventilator-Supported Speech Production 226

Part III: Language 229
Agrammatism 231 Agraphia 233 Alexia 236 Alzheimer’s Disease 240 Aphasia, Global 243 Aphasia, Primary Progressive 245 Aphasia: The Classical Syndromes 249 Aphasia, Wernicke’s 252 Aphasia Treatment: Computer-Aided Rehabilitation 254 Aphasia Treatment: Pharmacological Approaches 257 Aphasia Treatment: Psychosocial Issues 260 Aphasic Syndromes: Connectionist Models 262 Aphasiology, Comparative 265 Argument Structure: Representation and Processing 269 Attention and Language 272 Auditory-Motor Interaction in Speech and Language 275 Augmentative and Alternative Communication: General Issues 277 Bilingualism and Language Impairment 279 Communication Disorders in Adults: Functional Approaches to Aphasia 283 Communication Disorders in Infants and Toddlers 285 Communication Skills of People with Down Syndrome 288 Dementia 291 Dialect Speakers 294 Dialect Versus Disorder 297 Discourse 300 Discourse Impairments 302 Functional Brain Imaging 305 Inclusion Models for Children with Developmental Disabilities 307 Language Development in Children with Focal Lesions 311 Language Disorders in Adults: Subcortical Involvement 314 Language Disorders in African-American Children 318 Language Disorders in Latino Children 321 Language Disorders in School-Age Children: Aspects of Assessment 324 Language Disorders in School-Age Children: Overview 326 Language Impairment and Reading Disability 329 Language Impairment in Children: Cross-Linguistic Studies 331 Language in Children Who Stutter 333 Language of the Deaf: Acquisition of English 336 Language of the Deaf: Sign Language 339

Lingustic Aspects of Child Language Impairment— Prosody 344 Melodic Intonation Therapy 347 Memory and Processing Capacity 349 Mental Retardation 352 Morphosyntax and Syntax 354 Otitis Media: E¤ects on Children’s Language 358 Perseveration 361 Phonological Analysis of Language Disorders in Aphasia 363 Phonology and Adult Aphasia 366 Poverty: E¤ects on Language 369 Pragmatics 372 Prelinguistic Communication Intervention for Children with Developmental Disabilities 375 Preschool Language Intervention 378 Prosodic Deficits 381 Reversibility/Mapping Disorders 383 Right Hemisphere Language and Communication Functions in Adults 386 Right Hemisphere Language Disorders 388 Segmentation of Spoken Language by Normal Adult Listeners 392 Semantics 395 Social Development and Language Impairment 398 Specific Language Impairment in Children 402 Syntactic Tree Pruning 405 Trace Deletion Hypothesis 407

Part IV: Hearing


Amplitude Compression in Hearing Aids 413 Assessment of and Intervention with Children Who Are Deaf or Hard of Hearing 421 Audition in Children, Development of 424 Auditory Brainstem Implant 427 Auditory Brainstem Response in Adults 429 Auditory Neuropathy in Children 433 Auditory Scene Analysis 437 Auditory Training 439 Classroom Acoustics 442 Clinical Decision Analysis 444 Cochlear Implants 447 Cochlear Implants in Adults: Candidacy 450 Cochlear Implants in Children 454 Dichotic Listening 458 Electrocochleography 461 Electronystagmography 467 Frequency Compression 471 Functional Hearing Loss in Children 475 Genetics and Craniofacial Anomalies 477 Hearing Aid Fitting: Evaluation of Outcomes 480 Hearing Aids: Prescriptive Fitting 482 Hearing Aids: Sound Quality 487 Hearing Loss and the Masking-Level Di¤erence 489 Hearing Loss and Teratogenic Drugs or Chemicals 493 Hearing Loss Screening: The School-Age Child 495 Hearing Protection Devices 497 Masking 500 Middle Ear Assessment in the Child 504



Noise-Induced Hearing Loss 508 Otoacoustic Emissions 511 Otoacoustic Emissions in Children 515 Ototoxic Medications 518 Pediatric Audiology: The Test Battery Approach Physiological Bases of Hearing 522 Pitch Perception 525 Presbyacusis 527 Pseudohypacusis 531 Pure-Tone Threshold Assessment 534 Speech Perception Indices 538 Speech Tracking 541


Speechreading Training and Visual Tracking 543 Suprathreshold Speech Recognition 548 Temporal Integration 550 Temporal Resolution 553 Tinnitus 556 Tympanometry 558 Vestibular Rehabilitation 563 Contributors 569 Name Index 577 Subject Index 603

The MIT Encyclopedia of Communication Disorders (MITECD) is a comprehensive volume that presents essential information on communication sciences and disorders. The pertinent disorders are those that a¤ect the production and comprehension of spoken language and include especially disorders of speech production and perception, language expression, language comprehension, voice, and hearing. Potential readers include clinical practitioners, students, and research specialists. Relatively few comprehensive books of similar design and purpose exist, so MITECD stands nearly alone as a resource for anyone interested in the broad field of communication disorders. MITECD is organized into the four broad categories of Voice, Speech, Language, and Hearing. These categories represent the spectrum of topics that usually fall under the rubric of communication disorders (also known as speech-language pathology and audiology, among other names). For example, roughly these same categories were used by the National Institute on Deafness and Other Communication Disorders (NIDCD) in preparing its national strategic research plans over the past decade. The Journal of Speech, Language, and Hearing Research, one of the most comprehensive and influential periodicals in the field, uses the editorial categories of speech, language, and hearing. Although voice could be subsumed under speech, the two fields are large enough individually and su‰ciently distinct that a separation is warranted. Voice is internationally recognized as a clinical and research specialty, and it is represented by journals dedicated to its domain (e.g., the Journal of Voice). The use of these four categories achieves a major categorization of knowledge but avoids a narrow fragmentation of the field at large. It is to be expected that the Encyclopedia would include cross-referencing within and across these four major categories. After all, they are integrated in the definitively human behavior of language, and disorders of communication frequently have wide-ranging e¤ects on communication in its essential social, educational, and vocational roles. In designing the content and structure of MITECD, it was decided that each of these major categories should be further subdivided into Basic Science, Disorders (nature and assessment), and Clinical Management (intervention issues). Although these categories are not always transparent in the entire collection of entries, they guided the delineation of chapters and the selection of contributors. These categories are defined as follows: Basic Science entries pertain to matters such as normal anatomy and physiology, physics, psychology and psychophysics, and linguistics. These topics are the foundation for clinical description and interpretation, covering basic principles and terminology pertaining to the communication sciences. Care was taken to avoid substantive overlap with previous MIT publications, especially the MIT Encyclopedia of the Cognitive Sciences (MITECS). The Disorders entries o¤er information on issues such as syndrome delineation, definition and characterization of specific disorders, and methods for the identification and assessment of disorders. As such, these chapters reflect contemporary nosology and nomenclature, as well as guidelines for clinical assessment and diagnosis. The Clinical Management entries discuss various interventions including behavioral, pharmacological, surgical, and prosthetic (mechanical and electronic). There is a general, but not necessarily one-to-one, correspondence between chapters in the Disorders and Clinical Management categories. For example, it is possible that several types of disorder are related to one general chapter on clinical management. It is certainly the case that di¤erent management strategies are preferred by di¤erent clinicians. The chapters avoid dogmatic statements regarding interventions of choice. Because the approach to communicative disorders can be quite di¤erent for children and adults, a further cross-cutting division was made such that for many topics



separate chapters for children and adults are included. Although some disorders that are first diagnosed in childhood may persist in some form throughout adulthood (e.g, stuttering, specific language impairment, and hearing loss may be lifelong conditions for some individuals), many disorders can have an onset either in childhood or in adulthood and the timing of onset can have implications for both assessment and intervention. For instance, when a child experiences a significant loss of hearing, the sensory deficit may greatly impair the learning of speech and language. But when a loss of the same degree has an onset in adulthood, the problem is not in acquiring speech and language, but rather in maintaining communication skills. Certainly, it is often true that an understanding of a given disorder has common features in both the developmental and acquired forms, but commonality cannot be assumed as a general condition. Many decisions were made during the preparation of this volume. Some were easy, but others were not. In the main, entries are uniform in length and number of references. However, in a few instances, two or more entries were combined into a single longer entry. Perhaps inevitably in a project with so many contributors, a small number of entries were dropped because of personal issues, such as illness, that interfered with timely preparation of an entry. Happily, contributors showed great enthusiasm for this project, and their entries reflect an assembled expertise that is high tribute to the science and clinical practice in communication disorders. Raymond D. Kent

MITECD began as a promising idea in a conversation with Amy Brand, a previous editor with MIT Press. The idea was further developed, refined, elaborated, and refined again in many ensuing e-mail communications, and I thank Amy for her constant support and assistance through the early phases of the project. When she left MIT Press, Tom Stone, Senior Editor of Cognitive Sciences, Linguistics, and Bradford Books, stepped in to provide timely advice and attention. I also thank Mary Avery, Acquisitions Assistant, for her help in keeping this project on track. I am indebted to all of them. Speech, voice, language, and hearing are vast domains individually, and several associated editors helped to select topics for inclusion in MITECD and to identify contributors with the necessary expertise. The associate editors and their fields of responsibility are as follows: Fred H. Bess, Ph.D., Hearing Disorders in Children Joseph R. Du¤y, Ph.D., Speech Disorders in Adults Steven D. Gray, M.D. (deceased), Voice Disorders in Children Robert E. Hillman, Ph.D., Voice Disorders in Adults Sandra Gordon-Salant, Ph.D., Hearing Disorders in Adults Mabel L. Rice, Ph.D., Language Disorders in Children Lawrence D. Shriberg, Ph.D., Speech Disorders in Children David A. Swinney, Ph.D., and Lewis P. Shapiro, Ph.D., Language Disorders in Adults The advice and cooperation of these individuals is gratefully acknowledged. Sadly, Dr. Steven D. Gray died within the past year. He was an extraordinary man, and although I knew him only briefly, I was deeply impressed by his passion for knowledge and life. He will be remembered as an excellent physician, creative scientist, and valued friend and colleague to many. Dr. Houri Vorperian greatly facilitated this project through her inspired planning of a computer-based system for contributor communications and record management. Sara Stuntebeck and Sara Brost worked skillfully and accurately on a variety of tasks that went into di¤erent phases of MITECD. They o¤ered vital help with communications, file management, proofreading, and the various and sundry tasks that stood between the initial conception of MITECD and the submission of a full manuscript. P. M. Gordon and Associates took on the formidable task of assembling 200 entries into a volume that looks and reads like an encyclopedia. I thank Denise Bracken for exacting attention to the editing craft, creative solutions to unexpected problems, and forbearance through it all. MITECD came to reality through the e¤orts of a large number of contributors— too many for me to acknowledge personally here. However, I draw the reader’s attention to the list of contributors included in this volume. I feel a sense of community with all of them, because they believed in the project and worked toward its completion by preparing entries of high quality. I salute them not only for their contributions to MITECD but also for their many career contributions that define them as experts in the field. I am honored by their participation and their patient cooperation with the editorial process. Raymond D. Kent


Part I: Voice .


1972). the deviations from periodicity may be either random or correlated. such as noise-to-harmonics ratio (NHR). 1987): an increase in any one of the underlying phenomena detected by a single measure will also a¤ect the other measures. it should be understood that perturbations and NHR-type measures will usually covary for many reasons. The interdependence between f0 and intensity is mapped in a voice range profile. At the physiological level. Awan. however. 1990). 1993). the primary level of concern is the signal. 2000). Table 1 categorizes measures (Buder. Furthermore. jitter. Multi-Dimensional Voice Program [MDVP]. The first two. however. levels spanning a client’s vocal range in both f0 and intensity. and in part because of long-term precedent for perturbation (Lieberman. the simplest ones being methodological (Hillenbrand. and NHR—can provide some very basic characterizations of vocal health. at the perceptual level. an abbreviated or focused profiling in which samples related to habitual f0 by a set number of semitones. These basic descriptors are not in any way comprehensive of the range of available measures or the available signal properties and dimensions. Interdependence of Basic Measures. which is an especially valuable assessment for the professional voice user (Coleman. or phonetogram. it is logical to conceive of voice measures in terms of the degree to which a given sample deviates from pure periodicity. some more modern algorithms process components through several types. and other measures of irregularity. these basic acoustic descriptors—f0 . and other software/hardware systems). Table 1.) Modern algorithmic approaches should be selected for (1) interpretability with respect to aerodynamic and physiological models of phonation and (2) the incorporation of multivariate measures to characterize vocal function. intensity. Although these categories are intended to be exhaustive and mutually exclusive. could be standardized to control for this dependence e‰ciently. 1961) and spectral noise measurements (Yanagihara. glottal morphology is multidimensional—superior-inferior asymmetry is a basic feature of the two-mass model (Ishizaka and Flanagan. many factors related to deviations from a pure f0 can contribute to pitch perception (Zwicker and Fastl. (For more detail on the measurement types. Note. These measures are widely used. Finally. and speech tasks designed to elicit variation (Titze. or related to habitual intensity by a set number of decibels. for example. have very clear perceptual correlates—pitch and loudness. Most voice quality algorithms are based on the prior identification of the periodic component in the signal (based on glottal pulses in the time domain or harmonic structure in the frequency domain). At the level of the signal. perhaps because of the time-consuming and strenuous nature of a full voice profile. 2000. At any or all of these levels. Ideally. Pabon. Finally. Absolute measures of vocal intensity are equally basic but require calibrations and associated instrumentation (Winholtz and Titze.g. 1990. The chief problem with nearly all acoustic assessments of voice is the determination of f0 . 1991). Periodicity as a Reference. 1995. that not all measures will be appropriate for all tasks. cycle-to-cycle perturbations of period ( jitter) and intensity (shimmer). it becomes questionable to characterize deviations with pure periodicity as a reference. perturbation statistics. shimmer. Because phonation is ideally a nearly periodic process. In acoustic assessment. and in many cases they are so extreme as to preclude identification of a regular period. The National Center for Voice and . respectively—and should be assessed for both stability and variability and compared to age and sex norms (Kent. 2000. running speech. in part because of the availability of electronic and microcomputer-based instruments (e. 1967). Independently.Acoustic Assessment of Voice Acoustic assessment of voice in clinical applications is dominated by measures of fundamental frequency ( f0 ). 1997). the dependence of perturbations and signal-to-noise ratios on both f0 and intensity is well known (Klingholz. and some anteriorposterior asymmetry is also inevitable—rendering it unlikely that a glottal pulse will be marked by a discrete or even a single instant of glottal closure. are usually valid only when extracted from sustained vowel phonations. However. see Buder. 2000) based on primary basic signal representations from which measures are derived. Outline of Traditional Acoustic Algorithm Types f0 statistics Short-term perturbations Long-term perturbations Amplitude statistics Short-term perturbations Long-term perturbations f0 /amplitude covariations Waveform perturbations Spectral measures Spectrographic measures Fourier and LPC spectra Long-term average spectra Cepstra Inverse filter measures Radiated signal Flow-mask signals Dynamic measures This dependence is not often assessed rigorously. The materials to be assessed should be obtained following standardized elicitation protocols that include sustained vowel phonations at habitual levels. 1994. Baken and Orliko¤. 2001). Kay Elemetrics Computerized Speech Laboratory [CSL] or Multispeech. There are many conceptual problems with this simplification.. Real-Time Pitch. these tasks are recorded over headset microphones with direct digital acquisition at very high sampling rates (at least 48 kHz). f0 and intensity. and Baken and Orliko¤.

initiating the algorithm within the subharmonic segment predisposes it to identify the lower fundamental. (Here the waveform-matching algorithm implemented in CSpeechSP [Milenkovic. 2001). although it can also be understood in this context as a subharmonic to the original fundamental.4 Part I: Voice Figure 1. In this sustained vowel phonation by a middle-aged woman with spasmodic dysphonia. This typology capitalizes on the categorical nature of dynamic states in nonlinear systems. limit cycles. As in most highly nonlinear dynamic systems. depending on where in the waveform the algorithm is applied. Speech issued a summary statement (Titze. Two f0 extractions are presented for this segment. %jitter. 1994. 1997] does identify either frequency.. . . deviations from periodicity can be categorized on the basis of bifurcations. . Approximately 900 ms of a sustained vowel phonation waveform (top panel) with two fundamental frequency analyses (bottom panel). one at the targeted level of approximately 250 Hz and another which the tracker finds one octave below this. and chaos can be observed in voice signals (Herzel et al. There is therefore some ambiguity as to which fundamental is valid during this episode. depending on the basic glottal pulse form under consideration. all the major categories.) The acoustic measures of the segments displayed in Figure 1 reveal the nontrivial di¤erences that result. Satalo¤ and Hawkshaw. including stable points. Figure 1 displays a common form for one such bifurcation and illustrates the importance of accounting for its presence in the application of perturbation measures. period-doubling/tripling/. a transition to subharmonics is clearly visible in segment b (similar patterns occur in individuals without dysphonias). inspection of the waveform and a perceived biphonia both justify this 125-Hz analysis as a new fundamental frequency. 1995) recommending a typology for categorizing deviations from periodicity in voices (see also Baken and Orliko¤. and an automatic analysis could plausibly identify either frequency. . or sudden qualitative changes in vibratory pattern from one of these states to another. When the pulses of segment a are considered. for further subtypes). %shimmer. and SNR results for selected segments were from the ‘‘newjit’’ routine of TF32 program (Milenkovic. 2001). 2000. Average f0 .

but the segment-bysegment validity of applying perturbation measures with a particular f0 as reference. The e¤ect of turbulence due to high airflow through the glottis is schematized by (d). which is positively correlated with overall harmonic energy).Acoustic Assessment of Voice 5 the perturbations around the base period associated with the high f0 are low and normative. perturbations around the longer periods of the lower f0 are still low ( jitter is improved. assessment by means of perturbation statistics with no consideration of their underlying sources is unwise. this low-frequency region is also positively correlated with open quotient and peak volume velocity measures of the glottal flow waveform). However. Alternatively. including the Liljencrants-Fant (LF) model of glottal flow and aperiodicity source models developed by Stevens. The LF model of glottal flow is shown at top left. Perceptual. the perturbation statistics are all increased by an order of magnitude. aerodynamic models Figure 2. Aerodynamic. See voice acoustics for other graphical and quantitative associations between glottal status and spectral characteristics. It is only by reference to a specific model that any assessment on acoustic grounds can be interpreted (though this does not preclude development of an independent model for a pathological phonatory mechanism). when all segments are considered together to include the perturbations around the high f0 tracked through segment b and into c. If. However. as guided by auditory experience and in conjunction with the ear and other instrumental assessments. careful acoustic analysis can be oriented to the identification of physiological status. acoustic voice assessment often serves to corroborate perceptual assessment. and Physiological Correlates of Acoustic Measures. In attempting to draw safe and reasonably direct inferences from acoustic signal. showing the rate of change in flow. In any case. However. In clinical settings. but again. . Regarding perceptual voice rat- ings. these points may not apply to acoustic analysis if (1) acoustic analysis is validated on its own success and not exclusively in relation to the problematic perceptual classifications. At right is a spectrum schematic showing four e¤ects. Gerratt and Kreiman (2000) have critiqued traditional assessments on several important methodological and theoretical points. jitter and shimmer are ascribed to ‘‘random’’ variations. At bottom left is the LF model of glottal flow derivative. and (c) pulse skewing (which is negatively correlated with low-frequency harmonic energy. Many important methodological and theoretical questions should be raised by such common scenarios in which we must consider not just voice typing. (b) dynamic leakage or non-zero return phase following the point of maximum excitation (which is negatively correlated with high-frequency harmonic energy). Gerratt and Kreiman also argue that clinical classification may not be derived along a continuum that is defined with reference to normal qualities. this argument may need to be reversed for the acoustic domain. in segment b. while shimmer and the signal-to-noise ratio show some degradation). the perturbations might be analyzed with respect to the subharmonic f0 . These e¤ects include three derived parameters of the LF model: (a) excitation strength (the maximum negative amplitude of the flow derivative. Spectral features associated with models of phonation. indicating the associated appearance of high-frequency aperiodic energy in the spectrum. as is often assumed. and (2) acoustic analysis is thoroughly grounded for interpretation in some clear aerodynamic or physiological model of phonation. then the correlated modulations of a strong subharmonic episode should be excluded.

Hanson. Speech Communication. or employ curve-fitting and statistical models to produce more robust measures (Alku. Spectral correlates of glottal voice source waveform characteristics. Journal of Voice. and Kreiman. Murphy. (1994).. Glottal to noise excitation ratio: A new measure for describing patholocial voices. (2000).. Kent. Michaelis. and Orliko¤. Cornell. Madison. may be an e¤ective alternative when guided by knowledge of glottal aerodynamics and acoustics (Hanson. 1233–1268. and Palmer. J. (2001). (1999). K. Bell System Technical Journal.). 597–603. J. 1064–1077. 51. P. TF32 [Computer software]. Journal of the Acoustical Society of America. and Saleh. 110. Berry. Fant. S. Interpretation of spectral features.. Journal of the Acoustical Society of America. Roy. J. R. (1999). Glottal characteristics of male speakers: Acoustic correlates and comparison with female data. E. 106. Acustica. E. H. M. 4. Callen. and ¨ Strube.. (2000).. J. Gramss. and Vilkman. 7. N. Strube. The voice diagnostic profile: A practical guide to the diagnosis of voice disorders.. H. In M. has been especially successful in combination with other measures (Frohlich et al. Sources of variation in phonetograms. Gerratt.. P. Journal of the Acoustical Society of America... Austin. Rather than attempting to eliminate the e¤ects of the vocal tract. Journal of Speech and Hearing Research. (1987). 1997.). R. Klingholz. 1989) and useful in refined e¤orts at inverse filtering (Frohlich. Hillman. MD: Aspen. such as the amplitudes of the first harmonics and at the formant frequencies. E. Hanson and Chuang. Lieberman. L. H. (2001). Journal of Speech and Hearing Research.g. M. R. Awan. 1997... 2000. 1628–1638. WI: University of Wisconsin–Madison. and Sundberg. and Milstein. Attempts to recover the glottal flow waveform. 1973) or a microphonetransduced acoustic recording (Davis. W. D. I. ¨ and Strube. Frohlich. H. P. (2000). 1999). 58. see also voice acoustics for other approaches relating glottal status to spectral measures. J. H. Journal of the Acoustical Society of America. Coleman. and Strube. Buder.. (1997). Ishizaka. D. F. Frohlich. Liljencrants. Reference manual for communicative sciences and disorders: Speech and language. Hanson. 103–116). Milenkovic. Figure 2 summarizes selected parameters ´ of the LF source model following Nı Chasaide and Gobl (1997) and the glottal turbulence source following Stevens (1998). (1990). Michaelis. M.. 1998. Language. A methodological study of perturbation and additive noise in synthetically generated voice signals. J. (2001). D. The use of acoustic ¨ techniques for voice will only improve with the inclusion of more knowledge-based measures in multivariate representations (Wolfe. San Diego. R. T. 119–244). Madison. Sophisticated spectral noise characterizations control for perturbations and modulations (Murphy. the glottal-to-noiseexcitation ratio (Michaelis. Qi..6 Part I: Voice quality measurement (pp. Voice quality measurement (pp. R. Strik. 101. SIII. Acoustic representation of speaking-voice quality. (1994). Analysis of vocal disorders with methods from nonlinear dynamics.. D. Perturbations in vocal pitch. Callen et al. (1989). Kent. 1999). 466–481. CA: Singular Publishing Group. and Strube. Michaelis. ´ 1997. H. and Kruse. F. and Vilkman. 1008–1019. 32. and Hearing Research.. Selec¨ tion and combination of acoustic features for the description of pathologic voices. 706–720. 83. Nı Chasaide and Gobl. 1975). B. Synthesis of voiced sounds from a two-mass model of the vocal cords. Liljencrants. via the types of features displayed in Figure 2. 22. 2000). Journal of Phonetics. Michaelis. 448–461. 28.. 2000). Journal of Voice. Gaithersburg. Acoustic analysis of voice quality: A tabulation of algorithms 1902–1990. J. H. either from a face mask-transduced flow recording (Rothenberg. A particularly valuable modern technique for detecting turbulence at the glottis. Perturbation-free measurement of the harmonics-to-noise ratio in voice signals using pitch synchronous harmonic analysis. 1998). Glottal characteristics of female speakers: Acoustic correlates. Frohlich. G. Frohlich. Other spectral-based measures implement similar model-based strategies by selecting spectral component ratios (e. P. 105. P. A four-parameter model of glottal flow. In M.. (2000). —Eugene H. (1997). as is a model with clear and meaningful parameters. 103. 1997). 1–14. 700–706. D.. (1998). Journal of the Acoustical Society of America. of glottal behavior present important links to the physiological domain. Milenkovic. SIM¨ simultaneous inverse filtering and matching of a glottal flow model for acoustic speech signals. F. 1999.. Journal of Speech. Journal of the Acoustical Society of America.. 335–342. (1961). Michaelis. 2001). and Tasko. J. and infer. Baken. N. 1985). Parabolic spectral parameter: A new method for quantification of the glottal flow. E. Davis. have ´ proved to be labor-intensive and prone to error (Nı Chasaide and Gobl. and Strube. H. 479–488. San Diego. CA: Singular Publishing Group. such as the Liljencrants-Fant (LF) model (Fant. it may be more fruitful to understand its in situ relationship with phonation. Wuyts et al. D. D. W. and Chuang. WI: University of Wisconsin–Madison. and Lin. Clinical measurement of speech and voice. S. 2000).. Titze. 67–79. Journal of the Acoustical Society of America. (1993). Speech Transmission Laboratory Quarterly Progress and Status Report. 33. Stevens. Theoretical and methodological development in the study of pathological voice quality. M... TX: Pro-Ed.. Herzel. (1985). M. (1997). Gramss.. Preliminary results using inverse filtering of speech for automatic evaluation of laryngeal pathology. ¨ Acoustic voice analysis by means of the hoarseness diagram. CSpeechSP [Computer software]. M. San Diego. R. The use of self-organizing maps for the classification of voice disorders.. the status of the glottis as a sound source. 556–565. S. (1972). Ball (Ed. 43. Schoentgen. (2000). 1994. Q. 1997). 37. and Lin. Buder References Alku. 2866–2881. J. Michaelis. The parameters of the LF model have proved to be meaningful in acoustic studies (Gau‰n & Sundberg. E. Hillenbrand. Journal of Speech and Hearing Research. (1997). the VTI and SPI parameters of MDVP).. M. D. B. J. Strik. and Flanagan. Ball (Ed. and Bucella. 1–13. (1975). Voice . Bensaid. 4. and Strube. 1991. H. S. 213–219. Deep familiarity with acoustic mechanisms is essential for such interpretations (Titze. 30. CA: Singular Publishing Group. Gau‰n.

1632–1645. The handbook of phonetic sciences (pp. Molenberghs.. 1967). and Hawkshaw.. B. 1971) or pneumotachograph (Isshiki. Qi. to a limited extent. 509–516. Objective acoustic voice-quality parameters in the computer phonetogram. S. S. Ladefoged..e. 105. M. (2000). 1987. Watson and Hixon.). and Mead. The basic assumption underlying the indirect approaches is that changes in lung volume are reflected in proportional changes in body torso size. (1973). Heidelberg. 2000) have helped motivate the development and application of indirect measurement approaches. as opposed to assessing air volume usage during phonatory tasks that involve only laryngeal production of voice (e. 796–809. Measurement of Airflow.. Wolfe. R. (1997). et al. R. and Gobl. 203–216. 1996. Laver (Ed. (1990). Journal of the Acoustical Society of America. Millet. Air volumes are measured in standard metric units (liters.. Hixon. and Hearing Research. I. Titze. The methods have been mostly used in research to investigate mechanisms that underlie normal and disordered voice and speech production. 1994) that unobtrusively monitor changes in the dimensions of the rib cage and abdomen (referred to collectively as the chest wall) that account for the majority of respiratory-related changes in torso dimension (Mead et al. 417–421. 1985.. More often used for speech breathing research are transducers (magnetometers: Hixon. (2000). R.. 1493–1508. Pabon. 10. Cambridge. San Diego. Voice source variation. 1959). 1997. Goldman. Wuyts.. Multivariate statistical analysis of flat vowel spectra with a view to characterizing dysphonic voices. Germany: Springer-Verlag. (1991). Hillman. One relatively cumbersome but time-honored approach has been to place subjects in a sealed chamber called a body plethysmograph to allow estimation of the air volume displaced by the body during respiration (Draper. 7 Aerodynamic Assessment of Vocal Function A number of methods have been used to quantitatively assess the air volumes. Hillman. Acoustic phonetics.. R. 2532–2535. . CA: Singular Publishing Group. I. Workshop on acoustic voice analysis: Summary statement. (1998). Measurement of Air Volumes. G. Both direct and indirect methods have been used to measure air volumes expended during phonation. There are also ongoing e¤orts to develop more accurate methods for noninvasively monitoring chest wall activity to capture finer details of how the three-dimensional geometry of the body is altered during respiration (see Cala et al. C. P. airflows. volume of air displaced per unit of time). and Mead. H. 1996). 34. Hoit and Hixon. and air pressures involved in voice production. I. These approaches have been primarily employed to study respiratory function during continuous speech and singing tasks that include both voiced and voiceless sound production. R. R. Y. A. V. (2001). Direct measurement of orally displaced air volumes during phonatory tasks can be accomplished.g. (1991). and Whitteridge. Hillman. J. M. and Hearing Research. Englewood Cli¤s. Iowa City. Journal of Voice. and on specifying the ranges of lung inflation levels across which such tasks are normally performed (cf. K. Cornell.. 1964).. Goldman. Principles of voice production. 43. and Fastl. 11. Rothenberg. L. M. C. Volume velocity airflow rates for voice production are typically reported in metric units of volume displaced (liters or cubic centimeters) per second. Journal of Speech and Hearing Research. 43. by means of a mouthpiece or face mask connected to a measurement device such as a spirometer (Beckett. The Dysphonia Severity Index: An objective measure of vocal quality based on a multiparameter approach. and Milstein. H. Heylen. Schoentgen. Bensaid. Journal of the Acoustical Society of America... W.).. E. Chaos in medicine: Source readings. L. (1997).. (Eds. 427–461). N. so that auditory feedback is reduced or distorted and simultaneous acoustic analysis is limited. and Zeitels. Conversion of a headmounted microphone signal into calibrated SPL units. (1999). Satalo¤. The estimation of signal-to-noise ratio in continuous speech for disordered voices. 5. F. and Palmer. 531–541. Stevens. In J. UK: Blackwell. J. Airflow associated with phonation is usually specified in terms of volume velocity (i. MA: MIT Press. IA: National Center for Voice and Speech. 1990). plus additional measurement-related restrictions (Hillman and Kobler.Aerodynamic Assessment of Vocal Function ´ Nı Chasaide. inductance plethysmographs: Sperry. Language. 2000). These limitations. and Perkell. M. which are inherent to the use of devices placed in or around the mouth to directly collect oral airflow. Zwicker. Oxford. F.. Psychoacoustics: Facts and models. De Bodt. (1967). Significance of harmonic changes and noise components in hoarseness. Yanagihara. which are su‰cient for assessing selected volumetric-based phonatory parameters. M. Journal of Voice. Journal of Speech and Hearing Research. The use of a mouthpiece essentially limits speech production to sustained vowels.. (1994). The clinical use of aerodynamic measures to assess patients with voice disorders has been increasing (Colton and Casper. and Bucella. 1973. N. Hoit et al... Journal of Speech. Titze. NJ: Prentice Hall. A new inverse-filtering technique for deriving the glottal air flow waveform during voicing.. Acoustic correlates of pathologic voice types. (1995). Respiratory research in human communication has focused primarily on the measurement of the air volumes that are typically expended during selected speech and singing tasks. and Titze. Winholtz. There are also concerns that face masks interfere with normal jaw movements and that the oral acoustic signal is degraded. cubic centimeters. T. Most speech breathing research has been carried out using indirect approaches for estimating lung volumes by means of monitoring changes in body dimensions. sustained vowels). milliliters) and lung inflation levels are usually specified in terms of a percentage of the vital capacity or total lung volume. C. 53. Journal of Speech. Remacle. 1973. Montgomery. Hillman and Kobler.. Language.

Estimates of average glottal airflow rates can be obtained from the oral airflow during vowel production because the vocal tract is relatively nonconstricted. average subglottal air pressure. Holmberg. intraoral air pressure. Instrumentation and resulting signals for simultaneous collection of oral airflow. Thus. and glottal waveform parameters. Hillman. in which the major resonances of the vocal tract are estimated and the oral airflow signal is processed (inverse filtered) to eliminate them (Rothenberg. There have also been e¤orts to obtain estimates of the actual airflow waveform that is generated as the glottis rapidly opens and closes during flow-induced vibration of the vocal folds (the glottal volume velocity waveform). This has typically been accomplished aerodynamically by processing the output of a fastresponding pneumotachograph (high-frequency response) using a technique called inverse filtering. Figure 1. and chest wall (rib cage and abdomen) dimensions during production of the syllable string /pi-pi-pi/. lung volume. There has also been somewhat limited use of hot wire anemometer devices (mounted in a mouthpiece) to estimate average glottal airflow during sustained vowel phonation (Woo. The glottal volume velocity waveform cannot be directly observed by measuring the oral airflow signal because the waveform is highly convoluted by the resonance activity (formants) of the vocal tract. 1987). Colton. and Shangold.8 Part I: Voice Estimates of average airflow rates can be obtained by simply dividing air volume estimates by the duration of the phonatory task. 1977. the acoustic signal. with no major sources of turbulent airflow between the glottis and the lips. . and Perkell. recovery of the glottal volume velocity waveform requires methods that eliminate or correct for the influences of the vocal tract. Average glottal airflow rates have usually been estimated during vowel phonation by using a mouthpiece or face mask to channel the oral air stream through a pneumotachograph (Isshiki. 1964). Signals shown in the bottom panel are processed and measured to provide estimates of average glottal airflow rate. 1988).

CA: Singular Publishing Group. R. This method works because the vocal folds are abducted during /p/ production. Clinical measurement of voice and speech. there are several sources in the literature that provide estimates of normative values for selected aerodynamic measures (Kent. indirect estimates of subglottal air pressure can be obtained by measuring intraoral air pressure during specially constrained utterances (Smitheran and Hixon. (1987). 1996). The deflated esophageal balloon is attached to a catheter that is typically inserted transnasally and then swallowed into the esophagus to be positioned at the midthoracic level. H. Journal of Speech and Hearing Research. A.. Hillman. T. M. 81. 1988). L. —Robert E. These methods cannot be tolerated by all subjects. (1996). 1). Direct measures of subglottal air pressure can be obtained by inserting a hypodermic needle into the subglottal airway through a puncture in the anterior neck at the cricothyroid space (Isshiki. Aliverti. Aerodynamic measures of voice production. The catheter is connected to a pressure transducer and the balloon is slightly inflated. See also voice production: physics and physiology. J. P. Kent and M. Current diagnostics and o‰ce practice: Use of objective measures of vocal function in the multidisciplinary management of voice disorders. .. This is usually done by sensing air pressure just behind the lips with a translabially placed catheter connected to a pressure transducer. Journal of Applied Physiology. Kenyon.. 1543– 1551. 36. and the heavy topical anesthetization of the larynx that is required can a¤ect normal function. As is the case for most measures of vocal function. (2000). 2680–2689. D. it is usually assumed that supraglottal pressure is essentially equal to atmospheric pressure and only subglottal pressure measurements are obtained. Beckett. 2.. or that relate aerodynamic parameters to simultaneously obtained acoustic measures. Understanding voice problems: A physiological perspective for diagnosis and treatment. Measurements of air pressures below (subglottal) and above (supraglottal) the vocal folds are of primary interest for characterizing the pressure di¤erential that must be achieved to initiate and maintain vocal fold vibration during normal exhalatory phonation. (1985). 172–175. The respirometer as a diagnostic and clinical tool in the speech clinic. thus allowing pressure to equilibrate throughout the airway.. Hillman. Methods for collecting such data have not been standardized. (1959). Cala. Kinematics of the chest wall during speech production: Volume displacements of the rib cage. 5.g.. Such derived measures usually take the form of ratios that relate aerodynamic parameters to each other. Holmberg. R. and Whitteridge. B.. Normative Data. 77. CA: Singular Publishing Group. J. and Casper. and Hixon. Colton and Casper. Ladefoged. Additional Derived Measures. Goldman. 1988). 78–115. M. Journal of Speech and Hearing Disorders. Journal of the Acoustical Society of America. and Zeitels. and (3) measures that interrelate glottal volume velocity waveform parameters (Holmberg. Under these conditions. E.. and Perkell. or to use an array of miniature transducers positioned directly above and below the glottis (Cranen and Boves. Baken. J. (1973). J. The handbook of voice quality measurement. J. Noninvasive. (1996). and Kobler. Draper. Hillman. Current Opinion in Otolaryngology–Head and Neck Surgery. abdomen. Montgomery. 1968). San Diego.. Pedotti. 16. 1996. there is not currently a set of normative data for aerodynamic measures that is universally accepted and applied in research and clinical work. 1980. and Boves. Air pressures associated with voice and speech production are usually specified in centimeters of water (cm H2 O). 1981). P. Hillman. There have been numerous attempts to extend the utility of aerodynamic measures by using them in the derivation of additional parameters aimed at better elucidating underlying mechanisms of vocal function. E. (1971). S. J. M. A. 351–366.Aerodynamic Assessment of Vocal Function 9 Measurement of Air Pressure. J. Journal of Speech and Hearing Research. Respiratory muscles in speech. (1996). Colton. Chest wall and lung volume estimation by optical reflectance motion analysis. San Diego. K. M.). S. (2) vocal e‰ciency (Schutte. Hixon. Age and speech breathing. 16–27. et al. G. Carnevali. making intraoral pressure equal to subglottal pressure (Fig. and lung. Ferrigno.. R.. 1994. This method is very accurate but also very invasive.. 1964). R. Cranen.. air pressure measurements related specifically to voice production are typically acquired during vowel phonation when there are no vocal tract constrictions of su‰cient magnitude to build up positive supraglottal pressures. L. Hillman References Baken. /pi-pi-pi-pi-pi/) at constant pitch and loudness. Indirect estimates of tracheal (subglottal) air pressure can be obtained via the placement of an elongated balloon-like device into the esophagus (Liberman. Ball (Eds. 1985). Baltimore: Williams and Wilkins. In practice. 30. It is also possible to insert a very thin catheter through the posterior cartilaginous glottis (between the arytenoids) to sense subglottal air pressure during phonation. Pressure measurements during speech production using semiconductor miniature pressure transducers: Impact on models for speech production. Common examples include (1) airway (glottal) resistance (see Smitheran and Hixon.. and study samples have generally not been of su‰cient size or appropriately stratified in terms of age and sex to ensure unbiased estimates of underlying aerodynamic phonatory parameters in the normal population. and Perkell. B. P. The needle is connected to a pressure transducer by tubing. M. (1997). However. 1981). 235–241. J. R.. and Mead. Both direct and indirect methods have been used to measure subglottal air pressures during phonation. C. In R. W. D. Journal of Speech and Hearing Research. Hoit. T... Accurate use of this invasive method also requires simultaneous monitoring of lung volume. These intraoral pressure measures are obtained as subjects produce strings of bilabial /p/ þ vowel syllables (e.

L.. the most significant communicative component to be addressed via voice and speech rehabilitation is the lost voice source. Hillman. (1985). the tracheal airway will remain separate from the oral cavity. and Shangold. R. the preferred term for this alaryngeal voicing source is the pharyngoesophageal (PE) segment.. 1989. Watson. and Perkell. P. pharynx. 1980). the larynx. J.. and Perkell. 1994). P. (1967). 511–529. but the intimate relationship between the pulmonary system and that of the structures of the upper airway.. Phonatory airflow analysis in patients with laryngeal disease. psychosocial. 20. Holmberg. W. when malignant lesions are su‰ciently large or when the location of the tumor threatens the lymphatic compartment of The two most prominent methods of intrinsic alaryngeal speech are esophageal speech (Diedrich. Methods of Postlaryngectomy Communication Following laryngectomy. or total laryngectomy. Kent. These categories are best described as intrinsic and extrinsic methods. J. social. that is. Watson. less aggressive approaches to medical intervention may be pursued. Direct comparison of subglottal and esophageal pressure during speech. 46. 33. extrinsic methods of alaryngeal speech rely on the use of an external sound source. D. (1990). J. Journal of Speech and Hearing Disorders. (1977). Regulatory mechanisms of vocal intensity variation. J.. (1980). San Diego. This may include radiation therapy or partial surgical resection. or the use of combined chemoradiation protocols (Hillman et al. involves resectioning the entire framework of the larynx. (1964). Journal of Medical SpeechLanguage Pathology. 549–555. height. Therefore. both rely on generation of an alaryngeal voice source by creating oscillation of tissues in the area of the lower pharynx and upper esophagus. J. 155–176. 7. P. J. Journal of Speech and Hearing Research. Intrinsic Methods of Alaryngeal Speech Alaryngeal Voice and Speech Rehabilitation Loss of the larynx due to disease or injury will result in numerous and significant changes that cross anatomical. Sperry. In some instances. This vibratory structure is somewhat variable in regard to width.. B. N. However. and Mead. J. 43. J. In contrast. Once the larynx is removed. or the electrolarynx. (1968). Mead. J. Grimgy. the trachea is brought forward to the anterior midline neck and sutured into place near the sternal notch. The distinction between these two methods is contingent on the manner in which the alaryngeal voice source is achieved. alternative physical-anatomical structures are used to generate sound.. Under these circumstances. if verbal communication is to be acquired and used postlaryngectomy. 104–122. Reference manual for communicative sciences and disorders. Although total laryngectomy may occur in some instances due to traumatic injury. (1987). S. 1994) and tracheoesophageal (TE) speech (Singer and Blom. the majority of cases worldwide are the result of cancer. 84. There are two general categories in which an alternative. Damste. Journal of Speech and Hearing Research. 1157–1164. Orliko¤ et al. Glottal airflow and transglottal air pressure measurements for male and female speakers in soft. E. 1998. Isshiki.. Intrinsic alaryngeal methods imply that the alaryngeal voice source is found within the system.. not only is the primary structure for voice generation lost. When the laryngectomy is completed. Doyle. One . Rothenberg. which seeks to conserve portions of the larynx. 2. an alternative method of creating an alaryngeal voice source must be achieved. The use of an inductance plethysmograph to assess respiratory function in a patient with nodules. normal. 17–29. Smitheran. and esophagus. ‘‘alaryngeal’’ sound source is required. P. R. Speech breathing in children and adolescents. Once the larynx is surgically removed from the top of the trachea. and consequently the vocal tract. Measurement of airflow in speech. Respiratory kinematics in classical (opera) singers.. 85(4). H. Science. Journal of Speech and Hearing Research. N. and loud voice [published erratum appears in Journal of the Acoustical Society of America. T. 137–145. T. 1966. or what is termed the artificial larynx. H. T. E. 1966. N. Schutte. 1383–1384. and Hixon. alaryngeal voice source may be achieved. Lieberman. (1994). E.. S. Groningen. J. 156. 1986). 1999). and Hixon. M. 51–69. E. physiological. hence.. R. The e‰ciency of voice production. psychological. A clinical method for estimating laryngeal airway resistance during vowel production. 1787]. Annals of Otology. Rhinology. Journal of Speech and Hearing Research. and Laryngology. Thus. Journal of the Acoustical Society of America. Approximately 75% of all laryngeal tumors arise from squamous epithelial tissue of the true vocal fold (Bailey. Colton. The Netherlands: Kemper. (1981). typically an electronic source.. J.10 Part I: Voice Hoit. Pulmonary ventilation measured from body surface movements. Hixon. Journal of the Acoustical Society of America. Woo.. 96.. (1994). J. 28. 138–146. CA: Singular Publishing Group. R. While these two intrinsic methods of alaryngeal speech are dissimilar in some respects. 1985). E¤ects of Total Laryngectomy The two most prominent e¤ects of total laryngectomy as a surgical procedure are change of the normal airway and loss of the normal voicing mechanism for verbal communication. total laryngectomy necessitates that the airway be permanently separated from the upper aerodynamic (oral and pharyngeal) pathway. Peterson.. total laryngectomy is often indicated for reasons of oncological safety (Doyle. D. R. is disrupted. and Morgan. Surgical removal of the larynx. some alternative method of providing a new. and location (Diedrich and Youngstrom. Hillman. and because of the location of many of these lesions. (1988). The fundamental di¤erences between intrinsic and extrinsic methods of alaryngeal speech are discussed below. and communication domains.

While the frequency of TE speech is still reduced from that of normal speech. which o¤ers several distinct advantages relative to esophageal speech. perceptual identification of b for p) are common. his or her ability to modify the physical (frequency. either by hand or via use of a complementary tracheostoma breathing valve. which ultimately alters the normal rhythm of speech. This results in a negative pressure in the esophagus relative to the normal atmospheric pressure within the oral cavity/vocal tract (Diedrich and Youngstrom. 1994). The design of the TE puncture voice prosthesis is such that when the tracheostoma is occluded. Diedrich. the tissue of this sphincter will oscillate. and as a result.g. intensity is reduced by about 10 dB SPL from that of the normal speaker (Weinberg. 1961). in TE speech the speaker is able to access and use pulmonary air as a driving source. For esophageal speech. intensity. The acquisition of esophageal speech is a complex process of skill building that must be achieved under the direction of an experienced instructor. (3) the ability to maintain adequate duration of voicing. either at the time of laryngectomy or as a second procedure at some point following laryngectomy. Clinical emphasis typically involves tasks that address four skills believed to be fundamental to functional esophageal speech (Berlin. Two methods of insu¿ation may be utilized. fundamental frequency is reduced by about one octave (Curry and Snidecor. TE speech is best described as a surgical-prosthetic method of voice restoration. This access permits a variety of frequency.. Limitations in application must be considered. stop consonants). Because the TE speaker has direct access to a pulmonary air source. 1963): (1) the ability to phonate reliably on demand. and Smith.Alaryngeal Voice and Speech Rehabilitation 11 muscle that comprises the PE segment is the cricopharyngeal muscle. 1966. These methods might be best described as being either direct or indirect approaches to insu¿ation. Because of this. intonation. Tracheoesophageal Speech. Speech intelligibility is also decreased due to limits in the aerodynamic and voicing characteristics of esophageal speech. Once insu¿ation occurs.. Thus. As it is not an abductory-adductory system. Though widely used. 1968). 1980). While a distinction between direct and indirect methods permits increased understanding of the physical requirements for esophageal voice production. Regardless of which method of insu¿ation is used. 1968. Air then moves passively across the PE segment in order to equalize pressures between the pharynx and esophagus. TE speech uses the same voicing source as traditional esophageal speech. 1984. This is achieved by the surgical creation of a controlled midline puncture in the trachea.e. 1980).. many esophageal speakers who exhibit high levels of proficiency will often utilize both methods for insu¿ation. Beyond the commonality in the use of the PE segment as a vicarious voicing source for both esophageal and TE methods of alaryngeal speech. juncture). the speaker must move air from the oral cavity across the tonically closed PE segment in order to insu¿ate the esophageal reservoir (located inferior to the PE segment). 1998). this air can be used to generate PE segment vibration in the same manner following other methods of air insu¿ation.. air is directed from the trachea through the prosthesis and into the esophageal reservoir. Doyle.. the speaker indirectly creates a negative pressure in the esophageal reservoir via rapid inhalation through the tracheostoma. the manner in which these methods are achieved does di¤er. air will move across the segment (inferiorly) into the esophagus. TE voice restoration is not problem-free. When pressure build-up is achieved in the oral cavity via compression maneuvers. and durational variables to be altered in a fashion di¤erent from that of the traditional esophageal speaker (Robbins et al. Such changes have a positive impact on auditory-perceptual judgments of this method of alaryngeal speech. esophageal speakers will exhibit limitations in the physical dimensions of speech. and durational) characteristics of the signal in response to changes in the aerodynamic driving source. and (4) the ability to sustain voicing while articulating. These foundation skills have been shown to reflect those progressive abilities that have historically defined speech skills of ‘‘superior’’ esophageal speakers (Wepman et al. 1953. for the indirect (inhalation) method of air insu¿ation. and the . the PE segment. Pauloski. stress. However. is enhanced considerably. the prosodic contour of esophageal speech and associated features is often perceived to be abnormal. Horii. This may be accomplished with nonspeech tasks (tongue maneuvers) or as a result of producing specific sounds (e. Esophageal speakers must frequently reinsu¿ate the esophageal reservoir to maintain voicing. the successful acquisition of esophageal speech may be limited. this air can then be forced back up across the PE segment. it is not uncommon to see esophageal speakers exhibit pauses at unusual points in an utterance. the TE method capitalizes on the individual’s access to pulmonary air for esophageal insu¿ation. In contrast to esophageal speech. and when the pressure becomes of su‰cient magnitude to overcome the muscular resistance of the PE segment. However. This is a direct consequence of the esophageal speaker’s inability to insu¿ate large or continuous volumes of air into the reservoir. and the durational characteristics of speech are also reduced. intensity. the intensity is greater. followed by insertion of a oneway TE puncture voice prosthesis (Singer and Blom. Regardless of which method of air insu¿ation is used. and complications may occur. along with associated changes in prosodic elements of the speech signal (i. (2) the ability to maintain a short latency between air insu¿ation and esophageal phonation. This esophageal sound source can then be manipulated in the upper regions of the vocal tract into the sounds of speech.g. Specifically. In contrast. voiced-for-voiceless perceptual errors (e. Snidecor. Similarly. Esophageal Speech. Direct methods require the individual speaker to actively manipulate air in the oral cavity to e¤ect a change in pressure. for many reasons.

Extrinsic methods of alaryngeal voice production are common. W.12 Part I: Voice durational capabilities meet or exceed those of normal speakers (Robbins et al. C. B. (1985). physiological. But an important caveat is necessary: Just because a method of alaryngeal speech has been acquired and it has been deemed ‘‘proficient’’ at the clinical level (e. the individual speaker’s needs. Journal of Speech and Hearing Disorders. All individuals who have undergone a laryngectomy will confront myriad restrictions in multiple domains.. 1985). 1984). Alaryngeal speech. Professionals who work with individuals who have undergone total laryngectomy must focus on identifying a method that meets each speaker’s particular needs. Some obstacles to learning esophageal speech. Although some pneumatic devices have been introduced. Clinical measurement of esophageal speech: I. Journal of Speech and Hearing Disorders. M. Laryngoscope.. P. Whether the electrolaryngeal tone is introduced into the oral cavity directly or through transmission via tissues of the neck. 303–317. results in good speech intelligibility) and is ‘‘functional’’ for basic communication purposes. pitch is near normal. 71. See also laryngectomy. 28. Damste. and speech rate and prosody is near normal. Doyle. In this way. Diedrich. Finally. Eadie References Bailey. Foundations of voice and speech rehabilitation following laryngeal cancer. P. a mechanical quality is common and it requires the use of one hand. CA: Singular Publishing Group. C. however.. for artificial larynx speech. pp. Advantages for esophageal speech include a nonmechanical and hands-free method of communication. (1963). Bailey and H. and Reed. Further.). it is only one dimension of the complex picture of a successful return to as normal a life as possible. Darley (Eds. 85–92). The electrolayrnx is generally easy to use. communicative. (1968). Speech can be acquired relatively quickly. loudness exceeds normal. they are not widely used today. Methodology and curves of skill acquisition. it may be acquired quickly by most people and may be used in conditions of background noise. Springfield. given the external nature of the alaryngeal voice source and the electronic character of sound production. P. (1961). and at least . For TE speech. and Youngstrom. Surgery of the larynx (pp. 53. J. 1994). —Philip C. F. or electrolarynx. San Diego. Berlin. 415–424. G. whether esophageal. TE. M. As a result. nothing prevents an individual from using multiple methods of alaryngeal speech. and Reed. Biller (Eds. although one or another may be preferred in a given communication context or environment..g. postlaryngectomy rehabilitation e¤orts that address these areas may increase the likelihood of a successful postlaryngectomy outcome. L. for artificial larynx speech. Rehabilitative Considerations All methods of alaryngeal speech. The reacquisition of verbal communication is without question a critical component of recovery and rehabilitation postlaryngectomy. loudness. disadvantages for esophageal speech include lowered pitch.e. San Diego: College-Hill Press. Curry.. (1994). C. one method can be used with a functional communicative outcome in most instances. The intelligibility of electrolaryngeal speech is relatively good. research into the influence of increased aerodynamic support in TE speakers relative to traditional esophageal speech on speech intelligibility has suggested that positive e¤ects may be observed (Doyle. Its major limitations have traditionally related to negative judgments of electrolaryngeal speech relative to the mechanical nature of many devices. Artificial Laryngeal Speech. (1986). Keith and F. C. L.. In contrast. and Snidecor. In B. J. it involves use and maintenance of a prosthetic device with associated costs. J. (1966). have distinct advantages and disadvantages. 400–407. this does not imply that ‘‘rehabilitation’’ has been successfully achieved. or electrolaryngeal. must be considered. Philadelphia: Saunders. no matter how proficient the speaker’s skills. Annals of the New York Academy of the Sciences. and the device o¤ers a reasonable method of functional communication to those who have undergone total laryngectomy (Doyle. These devices provide an external energy (voice) source that is introduced either directly into the oral cavity (intraoral) or by placing a device directly on the tissues of the neck (transcervical). including anatomical. J. Listeners’ perceptions of consonants produced by esophageal and tracheoesophageal talkers. IL: Charles C. voicedfor-voiceless errors) due to the fact that the electrolarynx is a continuous sound source (Weiss and Basili. Doyle and Tanya L. While ‘‘normal’’ speech cannot be restored with these methods. T. Physical measurement and pitch perception in esophageal speech. Laryngectomee rehabilitation (2nd ed. Thomas. the rapidity of speech reacquisition in addition to the relative increases in speech intelligibility and the changes in the overall physical character of TE speech o¤ers considerable advantages from the perspective of communication rehabilitation. In R. and social. 257–278). (1988). E.. Danhauer. I. A reduction in speech intelligibility is primarily observed for voiceless consonants (i. psychological. Although clinical intervention must focus on making any given alaryngeal method as proficient as possible. H. Clearly. 155. use of a given method may be enhanced so that the individual may achieve the best level of social reentry following laryngectomy. as well as the relative strengths and weaknesses of each method. 1988) despite continued voiced-for-voiceless perceptual errors. the speaker is able to modulate the electrolaryngeal source into speech. Glottic carcinoma.). L. C. and speech rate.. W. Diedrich. Current research is seeking to modify the nature of the electronic sound source produced. A. The most frequently used extrinsic method of producing alaryngeal speech uses an electronic artificial larynx. For TE speech. all methods are viable postlaryngectomy communication options. 42–51. Doyle. Danhauer. K. The mechanism of esophageal speech.

Current status of laryngectomee rehabilitation: I. C. G. 8. In E. B. Assessing vocal function after chemoradiation for advanced laryngeal carcinoma. Contemporary considerations in the treatment and rehabilitation of head and neck cancer: Voice. J. at the crossroads of the upper respiratory and upper digestive tracts. E. E.. deglution. Blom. 9. W. D. 27. A. 921–925. A. 8–14. Current Opinion in Otolaryngology and Head and Neck Surgery. 109–124. T. D. C. B.. The larynx is intimately involved in respiration. Cantu. 3. (1999). M. Essentials for alaryngeal speech: Psychology and physiology. 337–349). Speech and voice rehabilitation of patients treated for head and neck cancer. C. 111.. and Yoshida. Ryan. Pfister. Self-help for the laryngectomee (pp. M. and Shelton. San Antonio. Blom.. G. I. 202–210. J. D. Williams. Doyle. P. 67. speech. Singer. P. (1985). K.. S. Cantu. S. E. Pfister. A. and Basili. Darley (Eds. Journal of Speech and Hearing Research. Applications of the voice prosthesis during laryngectomy. Hamaker. et al. G. J. 2–27.. and Ward. C. P. L. and Smith. (1953). P. D. Singer. and Blom. and Keith. Hanson. Current status of laryngectomy rehabilitation: II. C. A comparative acoustic study of normal.. Rhinology. E. Primary voice restoration at laryngectomy.. Journal of Speech and Hearing Research. D. W. 417– 427. IL: Charles C. Reed.. Walsh. Gandour. 107. Batsakis. TX: Pro-Ed.. Singer. Wong..). Communicative Disorders. (1982).. Electroacoustic analysis and enhancement of alaryngeal speech (pp. (1967). (2003). (1998). 18. E. I.. Budnick.... J. W. Snidecor. E. Hayashi. D. Baltimore: Williams and Wilkins. and tracheoesophageal speech production. G. Y.. I. Rhinology. H. 89. San Diego. (1984). Rhinology. Sessions. A. Thomas. (1980). (1985). 247–251. and Singer. B. 13 Further Readings Andrews. Horii. G. B. H. and Weinberg. 91. (1991). Shipp. et al. Doyle. American Journal of Otolaryngology. et al. 97–103. Harrison. (1982). 46. Hengested. S. T. Long-time spectral and intensity characteristics of esophageal speech. E. Singer. Journal of Speech and Hearing Disorders. R.Anatomy of the Human Larynx Hillman. Pauloski.). MacGahan. and R. In A. R. CA: Singular Publishing Group. (1980). C. and Hayden. M. M. 31–33). 111. G. A. Cooper. I. I. and Zelefsky. Surgical-prosthetic techniques for alaryngeal speech. Weiss. P. G.).. R. it must be viewed primarily as a respiratory organ. Attitudes about laryngectomee rehabilitation should change. Annals of Otology. T. Gates. (2000). F. R. A.. and Weinberg. esophageal. Austin. I. 216–219. L. and Laryngology. Mickel. D. E. C. Functional outcomes following treatment for advanced laryngeal cancer. D. Journal of Speech and Hearing Disorders. Rosen. In R.). Tumors of the head and neck: Clinical and pathological considerations (2nd ed. through . (Eds. The objective measurement of progressive esophageal speech development. Robbins. Annals of Otology. 10. B. G. G.. M. Iverson-Thoburn. prevents food from becoming lodged in the trachea or bronchi (which would threaten life and interfere with breathing).. C. and Laryngology. S. and Watson. G.. M. 5. Journal of Speech and Hearing Research. D. Rhinology and Laryngology. Tracheoesophageal voice restoration following total laryngectomy (pp. Sekey (Ed. 123–141). E. Archives of Otolaryngology. R. Journal of the Acoustical Society of America. (1981). American Journal of Otolaryngology. M. Speech after laryngectomy: An overview and review of acoustic and temporal characteristics of esophageal speech. Weinberg. 67–77. Acoustic and aerodynamic characteristics of tracheoesophageal voice. Lauder (Ed. Current status of laryngectomee rehabilitation: IV. Murry. and Laryngology. Blom. Gates.. Journal of Speech and Hearing Research. R. (1982). Orliko¤. 120–126. Weinberg. Production of intonation and contrastive contrasts in electrolaryngeal speech. B. and Hong.. Journal of Clinical Oncology. C. D. W. E.. IL: Charles C. Laryngectomee rehabiliation (pp. E. The upper esophageal sphincter: Role in alaryngeal speech acquisition. Keith and F. 576–578.. (1982). 294–300. Thomas. Larynx preservation with combined chemotherapy and radiation therapy in advanced but respectable head and neck cancer... G. D. S. F. Scarpino. K. Blom. F.. Ryan. 2. Shanks. J. In this capacity it controls the flow of air into and out of the lower respiratory tract. W. J. C.. 28. 8. (1987). J. 1781– 1784.. J. Salmon. 49. Woodson. S. Laryngoscope.. G. Electrolaryngeal speech produced by laryngectomized subjects: Perceptual characteristics. T. Annals of Otology. J. In E. Gates. Speech rehabilitation of the laryngectomized. R. S118–S123.. G. Hamaker. Major complications following tracheoesophageal puncture for voice restoration.... W. (1982).. Anatomy of the Human Larynx The larynx is an organ that sits in the hypopharynx. M. (1988). 5–48). Wolf. duration. Vocal function following successful chemoradiation treatment for advanced laryngeal cancer: Preliminary results. J. 98. R. (1979). (1996). Springfield. 562–567.. San Diego.. Y. CA: College-Hill Press. and swallowing... Strong. and. L. An endoscopic technique for restoration of voice after laryngectomy.. and phonation. E. Frequency. and Hearne.... M. S. A. Fisher. Rickard. Singer. N. G.. Springfield.. J. Although it is the primary sound generator of the peripheral speech mechanism.. 85–99. B. 3. Kraus. J. I. (1996/1997). Ryan. Lawlis. Singer.. B. R. Archives of Otolaryngology–Head and Neck Surgery.. Junctural contrasts in esophageal and normal speech. C. TX: Lauder Enterprises. Journal of Medical SpeechLanguage Pathology. and Blom. Fisher. Wepman.. 850–859. Results of therapy. E. (1983). and Lauder. J. 605–612. 97. Supplement II. Tracheostoma valve for postlaryngectomy voice rehabilitation. (1985).. American Journal of Otolaryngology.. E. J. 122. M. Annals of Otology. 858–864. 529–533. 161–168. Monahan. 1–7. J. Alaryngeal speech utilization: A survey. (1998). and Hamaker. I. (1968). and perceptual measures in relation to judgment of alaryngeal speech acceptability. Using an artificial larynx. M.. C. (1986). Phonoscope. J. 3. Head and Neck Surgery.. J. R.. L.). Madasu. Causes of failure. (1984). (1989). J. Pfister. (1997). Haines.). D. M. 182–186. Di¤erences in speaking proficiencies in three laryngectomy groups. Archives of Otolaryngology. B. Hamaker (Eds.. C.

Regional Anatomical Relationships. Lass [Ed. The epiglottis is a flexible leaf-shaped cartilage whose deformability results from its elastic cartilage composition. and sound production. Such changes in tension are the principal method of changing the rate of vibration of the vocal folds. the larynx continues to function relatively flawlessly. Cartilaginous Skeleton. F. Muscle fibers originating from the cricoid cartilage form part of the muscular valve. In adults. which in turn are attached to the upper rim of the cricoid. The thyroid.14 Part I: Voice the cough reflex. These cartilages support the soft tissues of the laryngeal cavity. ensuring continuity of the airway from the larynx into the trachea (the origin of the lower respiratory tract). Muscle fibers of the inferior pharyngeal constrictor attach to the posterolateral aspect of the thyroid and cricoid cartilages. which influence its capacity as a sound source. 1974). Principles of experimental phonetics. cricoid and arytenoid cartilages are interconnected to each other by two movable joints. The lowermost portion of the pharynx. The esophagus lies inferior and posterior to the larynx. Since the vocal folds are attached anteriorly to the inside face of the thyroid cartilage and posteriorly to the arytenoid cartilages. This is a tribute to the elegance of its structure. the cricothyroid and cricoarytenoid joints. though intimately associated with the larynx. They are interconnected by the cricothyroid joints and surround the laryngeal cavity. J. of the tongue is interconnected with the epiglottis of the larynx by three fibroelastic bands. with concomitant changes in tension. Throughout life. During swallowing. and the vestibular folds. [1996]. one pair of arytenoids. The cricoarytenoid joint joins the arytenoid cartilages to the superolateral rim of the cricoid. (From Orliko¤. 1).. the epiglottis closes over the entrance into the laryngeal cavity. which provides them with form and rigidity. surrounds the posterior aspect of the larynx. all but one pair of the intrinsic laryngeal muscles. or pharyngeal portion. It lies in front of the vertebral column and between the hyoid bone above and the trachea below. St. The thyroid and cricoid cartilages are composed of hyaline cartilage. the junction of the laminae forms an acute angle. Louis: Mosby. The larynx is composed of five major cartilages: thyroid. The larynx is located in the midline of the neck. The hyoid bone. The larynx also plays a central role in the development of the intrathoracic and intra-abdominal pressures needed for lifting. The cricothyroid joint joins the thyroid and cricoid cartilages and allows the cricoid cartilage to rotate upward toward the cricoid (Stone and Nuttal. It is a muscular tube that interconnects the pharynx and the stomach. These pyramid-shaped cartilages serve as points of Figure 1. The cricoid cartilage is signet ring shaped and sits on top of the first ring of the trachea. Despite these naturally and slowly occurring structural changes. The hyoid bone is not part of the larynx but is attached to it by the thyrohyoid membrane. In N. The thyroid cartilage is composed of two quadrangular plates that are united at midline in an angle called the thyroid angle or laryngeal prominence. it lies between the third and sixth cervical vertebrae. and the epiglottis (Fig. which could obstruct the airway and interfere with breathing. assists in dislodging material from the lower airway. This sexual dimorphism emerges after puberty.]. C. while in the female it is obtuse. the glossoepiglottic folds. is not part of it.) attachment for the vocal folds. this rotation e¤ects lengthening and shortening of the vocal folds. The cartilaginous components of the larynx are joined by ligaments and membranes. Laryngeal cartilages shown separately (top) and articulated (bottom) at the laryngeal joints. which opens to allow food to pass from the pharynx into the esophagus. 1996). thus preventing food and liquids from passing into the laryngeal cavity. Structure and function of the larynx. R. elimination of bodily wastes. the larynx undergoes maturational and involutional (aging) changes (Kahane. and Kahane. The arytenoid cartilages are interconnected to the cricoid cartilage via the cricoarytenoid joint. the hypopharynx. In the male. thereby protecting this vital passageway for unencumbered movement of air into and out of the lower airway. Reproduced with permission. cricoid. The root. Rocking motions of the arytenoids on the upper rim of the cricoid cartilage allow . J.

L. J. and sphincteric closure. These fibroelastic tissues (quadrangular membrane and conus elasticus) restore the dimensions of the laryngeal cavity. The suprahyoid and infrahyoid muscles also stabilize the hyoid bone. They are essential components of the exquisitely sensitive protective reflex mechanism within the larynx that includes initiating coughing. which is located between the vocal processes and the bases of the arytenoid cartilages. L. which become altered through muscle activity.]. The extrinsic laryngeal muscles are attached at one end to the larynx and have one or more sites of attachment to a distant site (e. The laryngeal cavity. Anatomy and physiology of the organs of the peripheral speech mechanism. producing devoicing and pauses. Although these muscles do not attach to the larynx. Yoder [Eds. 2). The overall dimensions of the intracartilaginous glottis remain relatively stable except during strenuous sphincteric valving.g. Decker. vocalization. it also provides filtration and moisturization of flowing air. Stratified squamous epithelium covers surfaces subjected to contact. J. These receptors are innervated by sensory branches from the superior and recurrent laryngeal nerves. The epithelium and immediately underlying connective tissue form the muscosa. McReynolds. The walls of the laryngeal cavity are formed by fibroelastic tissues lined with epithelium. which is bordered by the soft tissues of the vocal folds. [1988]. Cranial nerves V and VII . Here the laryngeal cavity is continuous with the lumen of the trachea. L.) the arytenoids and the attached vocal folds to be drawn away (abducted) from midline and brought toward (adducted) midline. The upper portion is a somewhat expanded supraglottal cavity or vestibule whose walls are reinforced by the quadrangular membrane.Anatomy of the Human Larynx 15 Figure 2. it is the narrowest portion. the sternum or hyoid bone). they influence laryngeal position in the neck through their action on the hyoid bone. the posterior two-fifths of the rima glottidis. Toronto: B. Lass. 3). E. (From Kahane. and sphincteric closure. through which it communicates with the hypopharynx. throat clearing. The suprahyoid and infrahyoid muscles attach to the hyoid bone and are generally considered extrinsic laryngeal muscles (Fig. passive stretch from adjacent structures. It extends from the laryngeal inlet (laryngeal aditus). 1976). J. The epithelium that lines the laryngeal cavity exhibits regional specializations. which forms the interior of the larynx (Fig. The larynx is moved through displacement of the hyoid bone. Northern. and vibratory forces. and facilitating modes of vocal atttack. Laryngeal Cavity. and D. Reproduced with permission. the infraglottal or subglottal region. The laryngeal cartilages surround an irregularly shaped tube called the laryngeal cavity. The e¤ect of such movements is to change the size and shape of the glottis. The anterior two-thirds of the glottis is an area of dynamic change occasioned by the positioning and aerodynamic displacement of the vocal folds. The suprahyoid and infrahyoid muscles are innervated by a combination of cranial and spinal nerves. which is of importance in laryngeal articulation. C. is bounded by the conus elasticus. The laryngeal cavity is conventionally divided into three regions. and aeromechanical forces. The middle region. the space between the vocal folds. as they are necessary for developing the transglottal impedances to airflow that are needed to initiate vocal fold vibration. The area of primary laryngeal valving is the glottal region. pain. The rima glottidis consists of an intramembranous portion. The thyroid cartilage is connected to the hyoid bone by the hyothyroid membrane and ligaments. and direction and velocity of airflow (Wyke and Kirchner. allowing other muscles in the neck to act directly on the laryngeal cartilages. compressive. which is supplied by an array of sensory receptors sensitive to pressure. to the level of the inferior border of the cricoid cartilage. The importance of these actions has been emphasized by von Leden and Moore (1961). chemical. In N. and an intracartilaginous portion. and tactile stimuli. is bounded by the vocal folds. C.. and nonvibrating portions of the vocal folds. where the shape and size of the rima glottidis or glottis (space between the vocal folds) is modified during respiration. Typical respiratory epithelium (pseudostratified ciliated columnar epithelium with goblet cells) is plentiful in the laryngeal cavity and lines the supraglottis. ventricles. Handbook of speech-language pathology and audiology. Laryngeal Muscles. The lowest region. as viewed posteriorly. The larynx is acted upon by extrinsic and intrinsic laryngeal muscles (Tables 1 and 2). called the glottal region.

assists vocal fold adduction Same as transverse fibers Adduction. relaxer of vocal folds (depending on what parts of muscles are active) Innervation External branch of superior laryngeal nerve (cranial nerve X) Lateral cricoarytenoid Posterior cricoarytenoid Interarytenoid Transverse fibers Recurrent laryngeal nerve (cranial nerve X) Recurrent laryngeal nerve (cranial nerve X) Recurrent laryngeal nerve (cranial nerve X) Recurrent laryngeal nerve (cranial nerve X) Recurrent laryngeal nerve (cranial nerve X) Oblique fibers Thyroarytenoid Horizontally coursing fibers extending between the dorsolateral ridges of each arytenoid cartilage Obliquely coursing fibers from base of one arytenoid cartilage Deep surface of thyroid cartilage at midline Inserts onto apex of opposite arytenoid cartilage Fovea oblonga of arytenoid cartilage.16 Part I: Voice Table 1. closes rima glottidis Abducts vocal folds. pars obliqua fibers attach to anterior margin of inferior corner of thyroid cartilage Anterior aspect of muscular process of arytenoid cartilage Muscular process of arytenoid cartilage Dorsolateral ridge of opposite arytenoid cartilage Function Rotational approximation of the cricoid and thyroid cartilages. lengthens and tenses vocal folds Adducts vocal folds. Morphological Characteristics of the Suprahyoid and Infrahyoid Muscles Muscles Suprahyoid Muscles Anterior digastric Posterior digastric Stylohyoid Mylohyoid Origin Digastric fossa of mandible Mastoid notch of temporal bone Posterior border of styloid process Mylohyoid line of mandible Insertion Body of hyoid bone To hyoid bone via an intermediate tendon Body of hyoid Median raphe. stabilizes hyoid bone When larynx is stabilized. medial end of clavical From upper border of scapula (inferior belly) into tendon issuing superior belly Posterior surface of manubrium. muscularis fibers attach more laterally . opens rima glottidis Approximates bases of arytenoid cartilages. Morphological Characteristics of the Intrinsic Laryngeal Muscles Muscle Cricothyroid Origin Lateral surface of cricoid cartilage arch. lowers hyoid bone. fibers divide into upper portion (pars recta) and lower portion (pars obliqua) Upper border of arch of cricoid cartilage Cricoid lamina Insertion Pars recta fibers attach to anterior lateral half of inferior border of thyroid cartilage. larynx is raised Cervical nerve I carried via descendens hypoglossi Ansa cervicalis Cervical nerves I–III carried by the ansa cervicalis Ansa cervicalis Cervical nerve I. edge of first costal cartilage Oblique line of thyroid cartilage Medial portion of inferior surface of body of hyoid bone Inferior aspect of body of hyoid bone Oblique line of thyroid cartilage Lower border of body and greater wing of hyoid bone Sternothyroid Thyrohyoid Table 2. through descendens hypoglossi Infrahyoid Muscles Sternohyoid Omohyoid Deep surface of manubrium. when hyoid is fixed. vocalis fibers attach close to vocal process. tensor. extending from deep surface of mandible at midline to hyoid bone Anterior surface of body of hyoid bone Function Raises hyoid bone Raises and retracts hyoid bone Raises hyoid bone Raises hyoid bone Innervation Cranial nerve V Cranial nerve VII Cranial nerve VII Cranial nerve V Geniohyoid Inferior pair of genial tubercles of mandible Raises hyoid bone and draws it forward Depresses hyoid bone Depresses hyoid bone Lowers hyoid bone.

and the vibratory behavior of the vocal folds. (3) the muscle fibers are generally uniform in diameter across the various intrinsic muscles. the positioning of the folds relative to midline. Hirano (1974) showed that the vocal folds are composed of several layers of tissues. particularly with changes in fundamental frequency. The intermediate and deep layers of the lamina propria are called the transition. laryngeal muscles di¤er from the standard morphological reference for striated muscles. called the external frame function. (2) they are less regular in shape. Sensory fibers from these nerves supply the entire laryngeal cavity. In particular.. 1982) have enabled us to appreciate the unique properties of the intrinsic muscles. (2) changing the position of the laryngeal cartilages relative to each other. The vocal fold consists of one layer of epithelium. each with di¤erent physical properties and only 1. also known as Reinke’s space. and (5) laryngeal muscles have a greater investment of connective tissues. while the thyrohyoid raises it. These movements are essential for developing the agitation and patterning of air molecules in transglottal airflow during voice production. which is the most mobile portion of the vocal fold. The intrinsic muscles of the larynx (Fig. IL: Charles C Thomas. and Mason. and (4) modifying laryngeal airway resistance by changing the size or shape of the glottis. The designation of extrinsic laryngeal muscles adopted here is based on strict anatomical definition as well as on research data on the action of the extrinsic laryngeal muscles during speech and singing. H. 4) are a collection of small muscles whose points of attachment are all in the larynx (to the laryngeal cartilages). (3) transiently changing the dimensions and physical properties of the vocal folds (i. Rosenfield et al. tension. is important clinically because it is the principal site of swelling or edema formation in the vocal folds following vocal abuse or in laryngitis. the epithelium and superficial layer of the lamina propria form the cover. mass per unit area. Wavelike mucosal disturbances travel along the surface during sound production. The intrinsic laryngeal muscles are innervated by nerve fibers carried in the trunk of the vagus nerve. Among the most important functional or biomechanical outcomes of the actions of the intrinsic laryngeal muscles are (1) abduction and adduction of the vocal folds. The anatomical properties of the intrinsic laryngeal muscles are summarized in Table 2. (From Bateman.2 mm thick. 5). while all other intrinsic laryngeal muscles are innervated by the inferior (recurrent) laryngeal nerve..e. One of the most convincing studies in this area was done by Shipp (1975). owing to the tendency for fibers to intermingle in their longitudinal and transverse planes. It provides . The cricothyroid muscle is innervated by the superior laryngeal nerve. (4) individual muscle fibers tend not to be uniform in their directionality within a fascicle but exhibit greater variability in the course of muscle fibers. The superficial layer of the lamina propria is composed of sparse amounts of loosely interwoven collagenous and elastic fibers. in varying proportions. and the vocalis fibers of the thyroarytenoid muscle (Fig.) supply all of the suprahyoid muscles except the geniohyoid. 1963. The vocal ligament is formed from elastic and collagenous fibers in these layers. [1984]. Hirano (1974) found that functionally. length. These branches are usually referred to as the superior and inferior laryngeal nerves. who showed that the sternothyroid and thyrohyoid muscles systematically change the vertical position of the larynx in the neck. This area. in several ways: (1) they typically have a smaller mean diameter of muscle fibers. and elasticity). Based on examination of ultrahigh-speed films and biomechanical testing of the vocal folds.. Reproduced with permission. R. Hirano and Kakita (1985) nicely summarized these behaviors (Table 3). Shipp demonstrated that the sternothyroid lowers the larynx with decreasing pitch.Anatomy of the Human Larynx 17 Figure 3. the limb muscles. Vocal Folds. Sonninen suggested that the extrinsic laryngeal muscles are involved in producing fundamental frequency changes by exerting forces on the laryngeal skeleton that e¤ect length and tension changes in the vocal folds. compliance. not a single homogeneous band. Springfield. fibers that control fine movements for prolonged periods (type 1 fibers) and fibers that develop tension rapidly within a muscle (type 2 fibers). three layers of connective tissue (lamina propria). The muscles can be categorized according to their e¤ects on the shape of the rima glottidis. The vocal folds are multilayered vibrators. All of the infrahyoid muscles are innervated by spinal nerves from the upper (cervical) portion of the spinal cord. M. Histochemical studies of intrinsic laryngeal muscles (Matzelt and Vosteen. E. The suprahyoid and infrahyoid muscles have been implicated in fundamental frequency control under a construct proposed by Sonninen (1956). Applied anatomy and physiology of the speech and hearing mechanism. The extrinsic laryngeal muscles. The intrinsic laryngeal muscles contain.

Northern. Decker. Yoder [Eds.]. J. McReynolds. Toronto: B. L. posterior (B). The intrinsic laryngeal muscles as shown in lateral (A).) . J. C. [1988]. J. Anatomy and physiology of the organs of the peripheral speech mechanism. L. Reproduced with permission. (From Kahane.18 Part I: Voice Figure 4. In N. Handbook of speechlanguage pathology and audiology. and D. E. C. and superior (C) views. L. Lass.

(1961). [1975]. and Kakita. The role of the external laryngeal muscles in length-adjustment of the vocal cords in singing. 447–457. The transition is sti¤er than the cover but more pliant than the vocalis muscle fibers. 73. San Diego. 135–140. San Diego. Morphological structure of the vocal cord as a vibrator and its vartions. strong e¤ect. Figure 5. Kahane References Faaborg-Andersen. From Hirano. G. Scientific foundations of otolaryngology (pp. 181. Cover-body theory of vocal fold vibration. B. San Diego. O‰cial report: Phonosurgery. S. Vinson. M. italics indicate marked e¤ect. CA: College-Hill Press. (1985).. IA. Abbreviations: CT. M. See also voice production: physics and physiology. Harrison (Eds. M. Hirano. Elf. In R.. Miller. lateral cricoarytenoid muscle. B. and Sonninen. R. M. 26. Reproduced with permission. C. E. (1960). (1976). and Kakita. cricothyroid muscle. 89–93. Co. Basic and clinical investigations. Y. In R. Matzelt. Speech science: Recent advances. (1975). (1996). Archives of Otolaryngology (Stockholm).). —Joel C. B. (1974). and Kirchner. R. (From Hirano. (1956). B.. The function of the extrinsic laryngeal muscles at di¤erent pitch. D. and Moore. Archiv fur Ohren-Nasen. M. J. Organic voice disorders (pp. which form the body of the vocal folds. T. A.und Kehlkopfheil¨ kunde. Schematic of the layered structure of the vocal folds. A. D. 78. elastic fibers. 218–231. D. Archives of Otolaryngology. Journal of Speech and Hearing Research. Hirano. Wyke.. Life span changes in the larynx: An anatomical perspective.Anatomy of the Human Larynx Table 3. G. P. and M. Crary (Eds. CA: College-Hill Press. Acta Otolaryngologica. 546–574). Sessions. Shipp. H. Danolo¤ (Ed.). Sonninen. Reproduced with permission. 51. In W. (1985). K. Y. The leading edge of the vocal fold with its epithelium is at left. Archives of Otolaryngology. vocalis muscle fibers.. 89–111).. These muscle fibers are active in regulating fundamental frequency by influencing the tension in the vocal fold and the compliance and elasticity of the vibrating surface (cover). Relative movements of the thyroid and cricoid cartilages assisted by neural stimulation in dogs. VOC. Hinchcli¤e and D. and Nuttal.. CA: Singular Publishing Group. Electroenoptische und enzymatische Untersuchungen an menschlicher Kehlkopfmuskulatur.) resiliency and longitudinal stability to the vocal folds during voice production. 662– 666.. Supplement. Brown. B. Folia Phoniatrica. M. H. collaginous fibers. posterior cricoarytenoid muscle. Kahane. 541–550. In R. 108. Acta Otolaryngologica. K. L. 21. 118. Vertical laryngeal positioning during continuous and discrete vocal frequency change. 18. A. vocalis muscle. London: Heinemann. Otologia [Fukuoka]. Actions of Intrinsic Laryngeal Muscles on Vocal Fold Position and Shape Vocal Fold Parameter Position Level Length Thickness Edge Muscle (body) Mucosa (cover and transition) CT Paramedian Lower Elongate Thin Sharpen Sti¤en Sti¤en VOC Adduct Lower Shorten Thicken Round Sti¤en Slacken LCA Adduct Lower Elongate Thin Sharpen Sti¤en Sti¤en IA Adduct 0 (Shorten) (Thicken) 0 (Slacken) (Slacken) PCA Adduct Elevate Elongate Thin Round Sti¤en Sti¤en 19 Note: 0 indicates no e¤ect. R. H. Cover-body theory of vocal fold vibration.). and Vosteen. J. (1963). 89–94.). Danilo¤ (Ed. PCA. 1–46). P. interarytenoid muscle. normal type indicates consistent. and Patten.. Stone. LCA. parentheses indicate slight e¤ect. 239–440. Neurology of the larynx. . Morphologic and histochemical characteristics of laryngeal muscle. A.. (1974). von Leden. Rosenfield. 707–718. The mechanics of the cricoarytenoid joint. A. (1982). Speech science: Recent advances (pp.

Acta Otolaryngologica. and Murry. and Cortesina. Treatment usually relates to the physical well-being of a patient. Ludlow and M. E‰cacy. interest has increased in determining the functional impact of the voice disorder due to the Internet in using patient-based outcome measures to establish e‰cacy of treatments and the desire to match treatment needs with patient’s needs. and handicap (World Health Organization. talent. on the other hand. Otolaryngology Clinics of North America. 2000). Histological color atlas of the human larynx. The developments and improvements of software for assessing acoustic objective measures of voice and relating measures of abnormal voices to normal voices have gone on for a number of years. In C. CA: Singular Publishing Group. objective measures primarily assess specific treatments and do not encompass functional outcomes from the patient’s perspective. (1975). Lombard. Louis: Mosby. 59.20 Part I: Voice Further Readings Fink. none have been related to the patient’s perception of the severity of his or her problem. San Diego. L. and Kahane. due to a voice disorder has gone virtually undocumented until recently. Handicap is the impact of the impairment of the disability on the social. looks at whether or not a treatment can produce an expected result based on previous studies. and Murry et al. St. The developmental anatomy of the larynx. and it is this physical well-being that generally takes priority when attempting to assess the severity of the handicap. (1928). Structure and function of the larynx. However. Hirano. In C. Orliko¤. (1970). motor end-plates and proprioceptors. V. This latter issue is important in all diseases and disorders when life is not threatened since it is ultimately the patient’s perception of disease severity and his or her motivation to seek treatment that dictates the degree of treatment success. M. F. F. Fitch. 1853–1868).. 74. St. (1998) have all demonstrated that voice communication is an essential element in patients’ perception of their quality of life following treatment for head and neck cancer. Rossi. Kahane. MD: American Speech-Language-Hearing Assoc. 2000). Otolaryngology Head and Neck Surgery (pp. Hirano.. R. Hart (Eds.. Konig. The mechanism of the larynx. This may be considered treatment effectiveness. Morphological study of the laryngeal muscles in man: Insertions and courses of muscle fibers. Cummings. W. and D. Assessment of Functional Impact of Voice Disorders Introduction Voice disorders occur in approximately 6% of all adults and in as many as 12% of children.. The peripheral nervous system of the human larynx: I. (1981). but until recently.. little attention has been given to the e¤ects of a voice disorder on the daily needs of the patient. acoustic. 3. L. the disease. Interest in the issues relating to functional use of the voice stems from the development of instruments to measure all aspects of vocal function related to the patient. or physiological instruments. H. The restriction of work. Within the adult group.. Hast. 1997). B. W. and measure changes that occur as a result of treatment (Dejonckere. Assessment of the physiological consequences of voice disorders has evolved from a strong interest in the relationship of communication ability to global qualityof-life measurement.). H.). and time on diagnosing and measuring the severity of voice disorders with various perceptual. St. but rather addresses the value of a particular treatment for a particular individual. A few objective and subjective measures are correlated with the diagnosis of the voice disorder (Wolfe. M. 575–592. and Martin. J. C. The human larynx. The mucous membrane. A. (1998). not necessarily to the severity of the disease. While voice scientists and clinicians have focused most of their energy. These measures do not necessarily discriminate the severity of handicap as it relates to specific professions. G. Measurement of functional impact is somewhat di¤erent from assessment of disease status in that it does not directly address treatment e‰cacy. Negus. G. Functional histology of the larynx and vocal folds. Harker. (1993). New York: Raven Press. M. 1980). and von Leden. specific professions report the presence of a voice problem that interferes with their employment. A more comprehensive approach might seek to address the patient’s own impression of the severity of the disorder and how the disorder interferes with the individual’s professional and personal lifestyle. C. This article reviews the evolution of the assessment of functional impact of voice disorders and selected applications of those assessments. Schuller (Eds.). M. Lass (Ed. Structure of the vocal fold in normal and disease states anatomical and physical studies. and the treatment. Voice Disorders and Outcomes Research Assessment of functional impact on the voice is barely beyond the infancy stage. Rockville. . Principles of experimental phonetics. C. Krause. E. 2001). Over the past few years. or economic functioning of the individual. (1996). categorize acoustic/physiological profiles of the disease (Hartl et al. K. J. environmental. Louis: Mosby. (1961). (1965). disability. J. Hassan and Weymuller (1993). 1–14. In N. (1998). Accordingly. Archives of Otolaryngology. Functional impact relates to the degree of handicap or disability. 1998). Proceedings of the Conference on the Assessment of Vocal Pathology (ASHA Reports 11). As many as 50% of teachers and 33% of secretaries complain of voice problems that restrict their ability to work or to function in a normal social environment (Smith et al. Louis: Mosby. Objective test batteries are useful to quantify disease severity (Rosen. Frederickson. Picarillo (1994). O. Patient-based assessment of voice handicap has been lacking in the area of noncancerous voice disorders. Functional impact relates to the degree of impact a disorder has on an individual patient. J. J. List et al. 413–438. and Sato. or lifestyle. there are three levels of a disorder: impairment.

1998). bodily pain. or quality of voice) than the acoustic measures obtained in the voice laboratory. and functional aspects of voice disorders. mental health. the subscale of the SF-36 known as bodily pain may not be quite appropriate. Assessing Voice Handicap Currently there are no federal regulations defining voice handicap. Rather. However. The functional subscale includes statements that describe the impact of a person’s voice on his daily activities. The SF-36 has been used for a wide range of disease-specific topics once it was shown to be a valid measure of the degree of general health. The first usually encompasses social factors as well as physical factors that are related to the specific disorder.. social functioning. vitality. her satisfaction with treatment regardless of the disease state. or the cost of the treatment. functioning. Voice disorders are somewhat di¤erent than the treatment of a life threatening disease such as laryngeal cancer. The other is to compare his or her voice to normal voice measures. 1990. Outcome Measures: General Health Versus Specific Disease There are two primary ways to assess the handicap of a voice disorder. these measures do not provide insight as to the degree of handicap and disability that a specific patient is experiencing. recovery from disease. Jacobson and her colleagues proposed a measure of voice handicap known as the Voice Handicap Index (VHI) (Jacobson et al. Thus. These measures have been used to quantify functional outcome following various interventions in auditory function. 1990). as well as physiological measures objectively obtained provide some input as to the severity of the voice compared to normal. her ability to continue with her current employment versus opting for a change in employment. etc. acoustic perceptual judgments. namely emotional. The voice handicap will be reflected to the extent that the voice is usable in those situations.. a 30-item . an individual’s quality of life. namely hearing loss and dizziness (Newman et al. it does not presume to assess overall patient satisfaction with treatment. general health. The emotional subscale indicates the patient’s a¤ective responses to the voice disorder. Thus. The items in the physical subscale are statements that relate to either the patient’s perception of laryngeal discomfort or the voice output characteristics such as too low or too high a pitch. For example. The measurement of voice handicap must take into account issues such as ‘‘can the person teach in the classroom all day?’’ or ‘‘can a shop foreman talk loud enough to be heard over the noise of factory machines?’’ An outcome measure that takes into account the patient’s ability to speak in the classroom or a factory will undoubtedly provide a more accurate assessment of voice handicap (although not necessarily an accurate assessment of the disease.. and vocal e¤ectiveness. such as endurance. when considering certain voice disorders. In addition.Assessment of Functional Impact of Voice Disorders 21 Moreover. a 36-item short-form general health survey (McHorney et al. measures eight areas of health that are commonly a¤ected or changed by diseases and treatments: physical functioning. or voice therapy requires the patient’s full cooperation throughout the course of treatment. Assessment of voice handicap involves the patient’s ability to use his or her voice under normal circumstances of social and work-related speaking situations. The 36-item short form. Outcome of treatment for laryngeal cancer is typically measured using KaplanMyer curves (Adelstein et al. role Development of the Voice Handicap Index In 1997. unlike the handicap measures associated with hearing loss.. videostroboscopic visual perceptual findings. This patient selfassessment tool consists of ten items in each of three domains: emotional. that there are handicap/disability measures developed for other aspects of communication. physical.. physical. The challenge to develop a specific scale related to a specific organ function such as a scale for voice disorders presents problems unlike the development of the SF-36 or other general quality-of-life scales. there are certain parameters of voice disorders that cannot be easily measured in the voice laboratory. one of the di‰culties with using such a test for a specific disease is that one or more of the subscales may not be important or appropriate. 1994). and health transition. economic. otherwise known as SF-36. this assessment has been used to validate other assessments of quality of life and handicap that are disease specific. the degree to which swallowing status improves and voice communication returns to normal are measured by instruments that generally focus on quality of life (McHorney et al. One measure that has been used to look at the e¤ect of disease on life is the Medical Outcomes Study (MOS). The SF-36 is a pencil-andpaper test that has been used in numerous studies for assessing outcomes of treatment. 1993). functional. Voice handicap measures may measure an individual’s perceived level of general health. Moreover. acceptance of a new voice. It should be noted. From an original 85-item list. Jacobson et al. the SF36 is not a direct assessment of voice handicap but rather a general measure of well-being. 1993). The quality and accuracy of surgery or the level of voice therapy may not necessarily reflect the long-term outcome if the patient does not cooperate with the treatment procedure.. as already indicated. pharmacology. which is regulated by the Department of Labor. The task of measuring the severity of a voice disorder may be somewhat di‰cult because of the areas that are a¤ected. One is to look at the patient’s overall well-being. Treatment that involves surgery. however. patient-based measures of voice handicap provide significant information that cannot be obtained from biological and physiologic variables traditionally used in voice assessment models. while measures such a perceptual judgments of voice characteristics. because each scale has been determined to be a reliable and valid measure of health in and of itself. While this tool measures the disease-related status of the patient.

Subjects with benign vocal fold lesions demonstrated the lowest perception of handicap severity before and after treatment. Overall. Although the quality of voice may be mildly disordered. Other measures of voice outcome have been proposed and studied. reliable assessment of the patient’s perception of voice handicap. Activity limitation refers to constraints imposed on voice activities and participation restriction refers to a reduction or avoidance of voice activities. Overall reliability of the VOS was related to the subscales of the SF-36 for a group of patients with unilateral vocal fold paralysis. The results suggest that a 10-question VHI produces is highly correlated with the original VHI. 43. benign vocal fold lesions (polyps/cysts). A recent addition to functional assessment is the Voice Activity and Participation Profile (VAPP). or a combination of both. singers (Murry and Rosen. Murry and Rosen (2001) evaluated the VHI in three groups of speakers to determine the relative severity of voice disorders in patients with muscular tension dysphonia (MTD). 1998).to post-treatment.. there was a 50% or greater improvement in the mean VHI for the combined groups. The 10-item questionnaire provides a quick. Moreover. Glovsky. in 81% of the patients. On the contrary. the voice handicap may be significant. voice therapy. and was validated against the SF-36. Although lower VHI scores were found in singers than in nonsingers. where he ‘‘always’’ felt this to be the case. The Voice Handicap Index was designed to assess all types of voice disorders. The VHI significantly separated singers from nonsingers in terms of severity. the mean VHI score for the professional singers was significantly lower (31. The same investigators examined the application of the VHI to a specific group of patients with voice disorders. Figure 1. Murry and Rosen examined 73 professional and 33 nonprofessional singers and compared them with a control group of 369 nonsingers. there still remained a measure of handicap in all subjects. e¤ect on social comminication.2) than for the recreational singers. several questions were singled out as specifically sensitive to singers. These authors presented a measure of voice-related quality of life (VR-QOL). One of the additional uses of the VHI as suggested by Benninger and others is to assess measures after treatment (1998). is known as the Voice Outcome Survey (VOS). Additional work has been done by Hogikyan (1999). It can be seen that in general.2 for the 336 nonsingers. 2000). and Montgomery examined outcomes in patients with vocal fold paralysis (Hogikyan and Sethuraman. This 30-item questionnaire was then assessed for test-retest stability in total as well as the three subscales. The mean VHI score for the 106 singers was 34. A detailed analysis of patient data using this test has recently been published (Benninger et al.7. and e¤ect on emotion.0 vs. Hogikian (1999) and Glicklich (1999) have both demonstrated their assessment tools to have validity and reliability in assessing a patient’s perception of the severity of a voice problem. Although the VHI scores following treatment were significantly lower. Recently. The VAPP has been found to be a reliable and valid assessment tool for assessing self-perceived voice severity as it relates to activity and participation in vocal activities. even those encountered by tracheoesophageal speakers. Singers are unique in that they often complain of problems related only to their singing voice. However. The instrument. Their subjects consisted primarily of unilateral vocal fold paralysis patients and showed a significant change from pre. Figure 1 shows that subjects with vocal fold paralysis displayed the highest self-perception of handicap both before and after treatment. Recently. Gliklich. was finally obtained. others have proposed similar tests of handicap. Since the VHI has been published. the patients with vocal fold paralysis initially began with the highest pretreatment VHI and remained with the highest VHI after treatment. and vocal fold paralysis prior to and following treatments. Pre. this does not imply that the VHI is not a useful instrument for assessing voice problems in singers. indicating he ‘‘never’’ felt this about his voice problem to 4. The findings of this study should alert clinicians that the use of the VHI points to the specific needs as well as the seriousness of a singer’s handicap.22 Part I: Voice questionnaire using a five-point response scale from 0. either because of surgery. e¤ect on daily communication. which contains five questions. A shift in the total score of 18 points or greater is required in order to be certain that a change is due to intervention and not to unexplained variability. compared with a mean of 53. They also found that this self-administered 10-question patient assessment of severity was related to changes in treatment. Rosen and Murry (in press) presented reliability data on a revised 10-question VHI. e¤ect on the job. This 28-item tool examines five areas: selfperceived severity of the voice problem. 1999).and post-treatment voice handicap scores for selected populations. there was a perception of significantly reduced voice handicap. This tool assesses the e¤ects voice disorders have on limiting and participating in activities which require use of the voice (Ma and Yiu. 2001). .

292–299. Gardner. Journal of Voice.. and Yiu. 12. et al. A. Ma. For many years... P. Weinstein. and Rosen.. G. 564–569. the degree of handicap can be identified. G. 480–488. International Classification of Impairments. Electroglottographic Assessment of Voice A number of instruments can be used to help characterize the behavior of the glottis and vocal folds during phonation. VOS.. and Sherbourne. and Murry. R. Smith. F. 229–235. investigators have focused on acoustic and aerodynamic measures of voice production to assess change in voice following treatment. Hans. J. or disease type.). S. (1990). One glottographic method. C. both of which are highly valuable in the assessment of vocal function. M. E. C. R. sex. Kirchner. Earle. The Hague. Geneva: World Health Organization. and Weymuller. (in press). Folia Phoniatrica. Rosen References Adelstein. 44.. T. 14.. H. Jacobson. W. 13. J. 12. P. Neurology. 109. D.. M. Rhinology. N. G. Taylor. and Ho¤man. E. A. Glovsky. Occupational voice disorders: Care and cure (pp. E. S. McHorney. Objective voice analysis after autologous fat injection for unilateral vocal fold paralysis. (2001).. The development of the Henry Ford Hospital Headache Disability Inventory (HDI). Medical Care. et al. M. (1994). and VR-QOL have demonstrated that regardless of age. via ultrasonography (Baken and Orliko¤. 152–158. Acoustic.. and Martin. F. glottal area. (1980). and Newman.. M. Head and Neck Surgery. A. conditioned. 511–524.. glottal width. Annals of Otology Rhinology and Larynology. R. Fitch. Validation of an instrument to measure voice-related quality of life (VRQOL). 13. B. the Netherlands: Kugler Publications. . H. A.. Patients’ self-assessment of perceived severity also allows investigators to make valid comparisons of the impact of an intervention for patients who use their voices in di¤erent environments and the patients’ perception of the treatment from a functional perspective. and Robbins. (1993). Ear and Hearing.. Dejonckere. and Hearing Research. (1990). Measures such as the VHI. Journal of Voice. Otolaryngology–Head and Neck Surgery. J. Cancer. Acoustic measures of dysphonic severity across and within voice types. including the glottal open quotient and the maximum flow declination rate. (1998). Unfortunately. Journal of Voice. and Sethuraman.. Atiuja. The signals derived from these instruments are called glottographic waveforms or glottograms (Titze and Talkin. A. 540–550.. C. Assessment of quality of life in head and neck cancer patients. B. Jr. S. 837–842. 247–263. 1981). Acute and chronic changes in swallowing and quality of life following intraarterial chemoradiation for organ preservation in patients with advanced head and neck cancer. Lu. C. 31. J. 764–769.. and vocal fold movement. Aggarwal. V. via inverse filtering. 66. C. and Grywalski. D. 49. A. Madassu. et al. Vaissiere. Assessing outcomes for dysphonic patients. The Voice Handicap Index (VHI): Development and validation. A. 485–494.. —Thomas Murry and Clark A... Sharon. (1999). 823–828. 120. (2000). S.. M. Lombard. (1993). (2001). Glicklich.. Jacobson. Wolfe. D. Disabilities and Handicaps: A manual of classification relating to the consequences of disease (pp.. Among the more common glottograms are those that track change in glottal flow. P.. J.. G.Electroglottographic Assessment of Voice 23 Summary The study of functional voice assessment to identify the degree of handicap is novel for benign voice disorders.. Newman. 557–559. A. although extremely useful in understanding treatment e‰cacy. D. N. Journal of Voice. Rosen. C... via photoglottography. A performance status scale for head and neck patients. The hearing handicap inventory for adults: Psychometric adequacy and audiometric correlates. and Rosen. (2001). Annals of Otology. H. and analyzed. V. 44. and Hug. M. Otolaryngology Clinics of North America. E. Journal of Speech. T. Riquet. via kymography. J. W. Murry. Occupational voice disorders and the voice handicap index. (1998). G. Grywalski. and Laryngology. Head and Neck Surgery.. Psychometric and clinical tests of validity in measuring physical and medical health constructs. In P. Hartl. Perceptual and laboratory assessment of dysphonia.. 20. Voice activity and participation profile: Assessing the impact of voice disorders on daily activities. Language. E. Voice Handicap Index results in singers. Such signals can be used to obtain several di¤erent physiological measures. 31–37. Lemke. Journal of Voice. American Journal of Clinical Oncology. 25– 43). These measures. Johnson. Hassan. Picarillo. 12. Ritter-Sterr. World Health Organization. Journal of Voice. E.. J. D. T. M.. A. 33–34. B. C. Martin. (1998). The MOS 36-item short form health survey (SF-36): II. (2000). Ramadan... S. List. W. C. Dejonckere (Ed. A. (1999).. 440–447. treatment for these handicaps can also be assessed in terms of e¤ectiveness for the patient. Rosen. Outcome research and otolaryngology. C. (1998). 33.. S. C. E. 15. (2000). Furthermore. (1997). J. Validation of a voice outcome survey for unilateral vocal fold paralysis. have not shed significant light on patients’ perception of their disorder. Murry. (1998). the routine application of these techniques has been hampered by the cumbersome and timeconsuming way in which these signals must be acquired. M. C. aerodynamic and videostroboscopic features of bilateral vocal fold lesions. 430–433. S.. Murry. M. L. Hogikyan.. 111. Ware. 2000). and Murry.. The VHI 10: An outcome measure following voice disorder treatment. 110. 11... Long-term results after chemoradiotherapy of locally confined squamous cell head and neck cancer. K. 540–550. T. 370–377. Jacobson. T. Montgomery.. and Lansky.. (1994). 113– 128). Otolaryngology–Head and Neck Surgery. Assessment of voice based on a patient’s perceived severity and the need to recover vocal function may be the most appropriate manner to assess severity of voice handicap. Benninger. T. Frequency of voice problems among teachers and other occupations. L..

the pattern of vocal fold vibration can be characterized quite well (Fig. The result is a waveform—sometimes designated Lx—that varies chiefly as a function of vocal fold contact area (Gilbert. medial compression. which contemporary theory suggests is a critical element in the assessment of voice production. whereas air is a particularly poor conductor. The contact pattern will vary as a consequence of several factors. the vocal folds engage in a quite complex undulatory movement during phonation. The glottal region. In short. In fact. high-frequency current is then passed between these electrodes. has emerged as the most commonly used technique. Instead of a simple mediolateral oscillation. Figure 1. . (2) it is easy to acquire. Because of their electrolyte content. First proposed by Fabre in 1957 as a means to assess laryngeal physiology. especially in the face of pathology. Electrical impedance is thus highest when the current path must completely bypass an open glottis and progressively decreases as greater contact between the vocal folds is achieved. At the top is shown a schematic representation of a single cycle of vocal fold vibration viewed coronally (left) and superiorly (right) (after Hirano. Given the complexity of the ‘‘rolling and peeling’’ motion of the glottal margins and the myriad possibilities for abnormality of tissue structure or biomechanics. including bilateral vocal fold mass and tension. and the anatomy and orientation of the medial surfaces. Potter. The clinical challenge. the clinical value of EGG rests in documenting the vibratory consequence of pathology rather than in diagnosing the pathology itself. however. EGG has a worldwide reputation as a useful tool to supplement the evaluation and treatment of vocal pathology. requiring no probe placement within the vocal tract. and (3) it o¤ers unique information about the mucoundulatory behavior of the vocal folds. Below it is a normal electroglottogram depicting relative vocal fold contact area. laryngeal height variation induced by respiration and articulation. Interest in EGG increased in the 1970s as the importance of mucosal wave dynamics for vocal fold vibration was confirmed. however. such that their inferior margins approximate before the more superior margins make contact. Because EGG tracks e¤ective medial contact area. is that a valid and reliable EGG assessment demands a firm understanding of normal vocal fold vibratory behavior along with recognition of the specific capabilities and limitations of the technique. An imperceptible low-amplitude. and accelerated greatly in the 1980s with the advent of personal computers and commercially available EGGs that were technologically superior to previous instruments. approximating the level of the vocal folds. the clinical potential of EGG was recognized by the mid-1960s. Because increasing and decreasing vocal fold contact has a relatively small e¤ect on the overall impedance. most of the changes in transcervical impedance are due to strap muscle activity. decreasing e¤ective voltage. forming the basis of the EGG signal. Electroglottography (known as electrolaryngography in the United Kingdom) is a plethysmographic technique that entails fixing a pair of surface electrodes to each side of the neck at the thyroid lamina. however. Today. In this way. the electroglottogram is both high-pass filtered to remove the far slower nonphonatory impedance changes and amplified to boost the laryngeal contribution to the signal. it is not surprising that e¤orts to formulate simple rules relating abnormal details to specific pathologies have not met with notable success. and Hoodin. the voltage across the neck is modulated by the contact of the vocal folds. the current path is forced to circumvent the glottal air space. the contact area function is far from perfectly understood. is quite small compared with the total region through which the current is flowing. When the vocal folds separate. The contact phases of the vibratory cycle are shown beneath the electroglottogram. Despite these e¤orts. The numbered points on the trace correspond approximately to the points of the cycle depicted above. Contact between the vocal folds a¤ords a conduit through which current can take a more direct route across the neck. Considerable research has been devoted to establishing the important features of the EGG and how they relate to specific aspects of vocal fold status and behavior.24 Part I: Voice electroglottography (EGG). tissue and body fluids are relatively good conductors of electricity. 1981). 1984). 1). alone or in conjunction with other speech signals. for several reasons: (1) it is noninvasive. and pulsatile blood volume changes.

Electroglottographic Assessment of Voice


Using multiple glottographic techniques, Baer, Lofqvist, and McGarr (1983) demonstrated that, for ¨ normal modal-register phonation, the ‘‘depth of closure’’ was very shallow just before glottal opening and quite deep soon after closure was initiated. Most important, they showed that the instant at which the glottis first appears occurs sometime before all contact is lost, and that the instant of glottal closure occurs sometime after the vocal folds first make contact. Thus, although the EGG is sensitive to the depth of contact, it cannot be used to determine the width, area, or shape of the glottis. For this reason, EGG is not a valid technique for the measurement of glottal open time or, therefore, the open quotient. Likewise, since EGG does not specify which parts of the vocal folds are in contact, it cannot be used to measure glottal closed time, nor can it, without additional evidence, be used to determine whether maximal vocal fold contact indeed represents complete obliteration of the glottal space. Identifying the exact moment when (and if ) all medial contact is lost has also proved particularly problematic. Once the vocal folds do lose contact, however, it can no longer be assumed that the EGG signal conveys any information whatsoever about laryngeal behavior. During such intervals, the signal may vary solely as a function of the instrument’s automatic gain control and filtering (Rothenberg, 1981). Although the EGG provides useful information only about those parts of the vibratory cycle during which there is some vocal fold contact, these characteristics may provide important clinical insight, especially when paired with videostroboscopy and other data traces. EGG, with its ability to demonstrate contact change in both the horizontal and vertical planes, can quite e¤ectively document the normal voice registers (Fig. 2) as well as abnormal and unstable modes of vibration (Fig. 3). However, to qualitatively assess EGG wave characteristics and to derive useful indices of vocal fold contact behavior, it may be best to view the EGG in terms of a vibratory cycle composed of a contact phase and a minimal-contact phase (see Fig. 1). The contact phase includes intervals of increasing and decreasing contact, whereas the peak represents maximal vocal fold contact and, presumably, maximal glottal closure. The minimalcontact phase is that portion of the EGG wave during which the vocal folds are probably not in contact. Much clinical misinterpretation can be avoided if no attempt is made to equate the vibratory contact phase with the glottal closed phase or the minimal-contact phase with the glottal open phase. For the typical modal-register EGG, the contact phase is asymmetrical; that is, the increase in contact takes less time than the interval of decreasing contact. The degree of contact asymmetry is thought to vary not only as a consequence of vocal fold tension but also as a function of vertical mucosal convergence and dynamics (i.e., phasing; Titze, 1990). A dimensionless ratio, the contact index (CI), can be used to assess contact symmetry (Orliko¤, 1991). Defined as the di¤erence between the increasing and decreasing contact durations divided by the duration of the contact phase, CI will vary be-

Figure 2. Typical electroglottograms obtained from a normal man prolonging phonation in the low-frequency pulse, moderate-frequency modal, and high-frequency falsetto voice registers.

tween À1 for a contact phase maximally skewed to the left and þ1 for a contact phase maximally skewed to the right. For normal modal-register phonation, CI varies between À0.6 and À0.4 for both men and women, but, as can be seen in Figure 2, it is markedly di¤erent for other voice registers. Pulse-register EGGs typically have CIs in the vicinity of À0.8, whereas in falsetto it would not be uncommon to have a CI that approximates zero, indicating a symmetrical or nearly symmetrical contact phase. Another EGG measure that is gaining some currency in the clinical literature is the contact quotient (CQ). Defined as the duration of the contact phase relative to the period of the entire vibratory cycle, there is evidence from both in vivo testing and mathematical modeling to suggest that CQ varies with the degree of medial compression of the vocal folds (see Fig. 3) along a hypoadducted ‘‘loose’’ (or ‘‘breathy’’) to a hyperadducted ‘‘tight’’ (or ‘‘pressed’’) phonatory continuum (Rothenberg and Mahshie, 1988; Titze, 1990). Under typical vocal circumstances, CQ is within the range of 40%– 60%, and despite the propensity for a posterior glottal


Part I: Voice

intonation, voicing, and fluency characteristics. In fact, EGG has, for many, become the preferred means by which to measure vocal fundamental frequency and jitter. In summary, EGG provides an innocuous, straightforward, and convenient way to assess vocal fold vibration through its ability to track the relative area of contact. Although it does not supply valid information about the opening and closing of the glottis, the technique a¤ords a unique perspective on vocal fold behavior. When conservatively interpreted, and when combined with other tools of laryngeal evaluation, EGG can substantially further the clinician’s understanding of the malfunctioning larynx and play an e¤ective role in therapeutics as well. See also acoustic assessment of voice. —Robert F. Orliko¤

Baer, T., Lofqvist, A., and McGarr, N. S. (1983). Laryngeal ¨ vibrations: A comparison between high-speed filming and glottographic techniques. Journal of the Acoustical Society of America, 73, 1304–1308. Baken, R. J., and Orliko¤, R. F. (2000). Laryngeal function. In Clinical measurement of speech and voice (2nd ed., pp. 394– 451). San Diego, CA: Singular Publishing Group. ´ ´´ ´ Fabre, P. (1957). Un procede electrique percutane d’inscription de l’accolement glottique au cours de la phonation: Glot´ tographie de haute frequence. Premiers resultats. Bulletin de ´ ´ l’Academie Nationale de Medecine, 141, 66–69. Gilbert, H. R., Potter, C. R., and Hoodin, R. (1984). Laryngograph as a measure of vocal fold contact area. Journal of Speech and Hearing Research, 27, 178–182. Hirano, M. (1981). Clinical examination of voice. New York: Springer-Verlag. Kakita, Y. (1988). Simultaneous observation of the vibratory pattern, sound pressure, and airflow signals using a physical model of the vocal folds. In O. Fujimura (Ed.), Vocal physiology: Voice production, mechanisms, and functions (pp. 207–218). New York: Raven Press. Orliko¤, R. F. (1991). Assessment of the dynamics of vocal fold contact from the electroglottogram: Data from normal male subjects. Journal of Speech and Hearing Research, 34, 1066–1072. Orliko¤, R. F. (1995). Vocal stability and vocal tract configuration: An acoustic and electroglottographic investigation. Journal of Voice, 9, 173–181. Rothenberg, M. (1981). Some relations between glottal air flow and vocal fold contact area. ASHA Reports, 11, 88–96. Rothenberg, M., and Mahshie, J. J. (1988). Monitoring vocal fold abduction through vocal fold contact area. Journal of Speech and Hearing Research, 31, 338–351. Titze, I. R. (1990). Interpretation of the electroglottographic signal. Journal of Voice, 4, 1–9. Titze, I. R., and Talkin, D. (1981). Simulation and interpretation of glottographic waveforms. ASHA Reports, 11, 48–55.

Figure 3. Electroglottograms representing di¤erent abnormal modes of vocal fold vibration.

chink in women, there does not seem to be a significant sex e¤ect. This is probably due to the fact that EGG (and thus the CQ) is insensitive to glottal gaps that are not time varying. Unlike men, however, women tend to show an increase in CQ with vocal F0. It has been conjectured that this may be the result of greater medial compression employed by women at higher F0s that serves to diminish the posterior glottal gap. Nonetheless, a strong relationship between CQ and vocal intensity has been documented in both men and women, consistent with the known relationship between vocal power and the adductory presetting of the vocal folds. Because vocal intensity is also related to the rate of vocal fold contact (Kakita, 1988), there have been some preliminary attempts to derive useful EGG measures of the contact rise time. Because EGG is relatively una¤ected by vocal tract resonance and turbulence noise (Orliko¤, 1995), it allows evaluation of vocal fold behavior under conditions not well-suited to other voice assessment techniques. For this reason, and because the EGG waveshape is a relatively simple one, the EGG has found some success both as a trigger signal for laryngeal videostroboscopy and as a means to define and describe phonatory onset, o¤set,

Further Readings
Abberton, E., and Fourcin, A. J. (1972). Laryngographic analysis and intonation. British Journal of Disorders of Communication, 7, 24–29. Baken, R. J. (1992). Electroglottography. Journal of Voice, 6, 98–110.

Functional Voice Disorders Carlson, E. (1993). Accent method plus direct visual feedback of electroglottographic signals. In J. C. Stemple (Ed.), Voice therapy: Clinical studies (pp. 57–71). St. Louis: Mosby– Year Book. Carlson, E. (1995). Electrolaryngography in the assessment and treatment of incomplete mutation (puberphonia) in adults. European Journal of Disorders of Communication, 30, 140–148. Childers, D. G., Hicks, D. M., Moore, G. P., and Alsaka, Y. A. (1986). A model of vocal fold vibratory motion, contact area, and the electroglottogram. Journal of the Acoustical Society of America, 80, 1309–1320. Childers, D. G., Hicks, D. M., Moore, G. P., Eskenazi, L., and Lalwani, A. L. (1990). Electroglottography and vocal fold physiology. Journal of Speech and Hearing Research, 33, 245–254. Childers, D. G., and Krishnamurthy, A. K. (1985). A critical review of electroglottography. CRC Critical Review of Biomedical Engineering, 12, 131–161. Colton, R. H., and Conture, E. G. (1990). Problems and pitfalls of electroglottography. Journal of Voice, 4, 10–24. Cranen, B. (1991). Simultaneous modelling of EGG, PGG, and glottal flow. In J. Gau‰n and B. Hammarberg (Eds.), Vocal fold physiology: Acoustic, perceptual, and physiological aspects of voice mechanisms (pp. 57–64). San Diego, CA: Singular Publishing Group. Croatto, L., and Ferrero, F. E. (1979). L’esame elettroglottografico appliato ad alcuni casi di disodia. Acta Phoniatrica Latina, 2, 213–224. Fourcin, A. J. (1981). Laryngographic assessment of phonatory function. ASHA Reports, 11, 116–127. Gleeson, M. J., and Fourcin, A. J. (1983). Clinical analysis of laryngeal trauma secondary to intubation. Journal of the Royal Society of Medicine, 76, 928–932. ´ ´les, J. L., and del Canizo Alvarez, C. (1988). Gomez Gonza ˜ ´ ´ Nuevas tecnicas de exploracion funcional larıngea: La ´ ´ electroglotografıa. Anales Oto-Rino-Otolarıngologica IberoAmericana, 15, 239–362. Hacki, T. (1989). Klassifizierung von Glottisdysfunktionen mit Hilfe der Elecktroglottographie. Folia Phoniatrica, 41, 43–48. ˚ Hertegard, S., and Gau‰n, J. (1995). Glottal area and vibratory patterns studied with simultaneous stroboscopy, flow glottography, and electroglottography. Journal of Speech and Hearing Research, 38, 85–100. Kitzing, P. (1990). Clinical applications of electroglottography. Journal of Voice, 4, 238–249. Kitzing, P. (2000). Electroglottography. In A. Ferlito (Ed.), Diseases of the larynx (pp. 127–138). New York: Oxford University Press. Motta, G., Cesari, U., Iengo, M., and Motta, G., Jr. (1990). Clinical application of electroglottography. Folia Phoniatrica, 42, 111–117. Neil, W. F., Wechsler, E., and Robinson, J. M. (1977). Electrolaryngography in laryngeal disorders. Clinical Otolaryngology, 2, 33–40. Nieto Altazarra, A., and Echarri San Martin, R. (1996). Elec´ ´ troglotografıa. In R. Garcıa-Tapia Urrutia and I. Cobeta ´ Marco (Eds.), Diagnostico y tratamiento de los transtornos de la voz (pp. 163–169). Madrid, Spain: Editorial Garsi. Orliko¤, R. F. (1998). Scrambled EGG: The uses and abuses of electroglottography. Phonoscope, 1, 37–53. Roubeau, C., Chevrie-Muller, C., and Arabia-Guidet, C. (1987). Electroglottographic study of the changes of voice registers. Folia Phoniatrica, 39, 280–289. Wechsler, E. (1977). A laryngographic study of voice disorders. British Journal of Disorders of Communication, 12, 9–22.


Functional Voice Disorders
The human voice is acutely responsive to changes in emotional state, and the larynx plays a prominent role as an instrument for the expression of intense emotions such as fear, anger, grief, and joy. Consequently, many regard the voice as a sensitive barometer of emotions and the larynx as the control valve that regulates the release of these emotions (Aronson, 1990). Furthermore, the voice is one of the most individual and characteristic expressions of a person—a ‘‘mirror of personality.’’ Thus, when the voice becomes disordered, it is not uncommon for clinicians to suggest personality traits, psychological factors, or emotional or inhibitory processes as primary causal mechanisms. This is especially true in the case of functional dysphonia or aphonia, in which no visible structural or neurological laryngeal pathology exists to explain the partial or complete loss of voice. Functional dysphonia, which may account for more than 10% of cases referred to multidisciplinary voice clinics, occurs predominantly in women, commonly follows upper respiratory infection symptoms, and varies in its response to treatment (Bridger and Epstein, 1983; Schalen and Andersson, 1992). The term functional implies a voice disturbance of physiological function rather than anatomical structure. In clinical circles, functional is usually contrasted with organic and often carries the added meaning of psychogenic. Stress, emotion, and psychological conflict are frequently presumed to cause or exacerbate functional symptoms. Some confusion surrounds the diagnostic category of functional dysphonia because it includes an array of medically unexplained voice disorders: psychogenic, conversion, hysterical, tension-fatigue syndrome, hyperkinetic, muscle misuse, and muscle tension dysphonia. Although each diagnostic label implies some degree of etiologic heterogeneity, whether these disorders are qualitatively di¤erent and etiologically distinct remains unclear. When applied clinically, these various labels frequently reflect clinician supposition, bias, or preference. Voice disorder taxonomies have yet to be adequately operationalized; consequently, diagnostic categories often lack clear thresholds or discrete boundaries to determine patient inclusion or exclusion. To improve precision, some clinicians prefer the term psychogenic voice disorder, to put the emphasis on the psychological origins of the disorder. According to Aronson (1990), a psychogenic voice disorder is synonymous with a functional one but o¤ers the clinician the advantage of stating confidently, after an exploration of its causes, that the voice disorder is a manifestation of one or more forms of psychological disequilibrium. At the purely phenomenological level there may be little di¤erence between functional and psychogenic voice disorders. Therefore, in this discussion, the terms functional and psychogenic will be used synonymously, which reflects current trends in the clinical literature (nosological imprecision notwithstanding).


Part I: Voice

In clinical practice, ‘‘psychogenic voice disorder’’ should not be a default diagnosis for a voice problem of undetermined cause. Rather, at least three criteria should be met before such a diagnosis is o¤ered: symptom psychogenicity, symptom incongruity, and symptom reversibility (Sapir, 1995). Symptom psychogenicity refers to the finding that the voice disorder is logically linked in time of onset, course, and severity to an identifiable psychological antecedent, such as a stressful life event or interpersonal conflict. Such information is acquired through a complete case history and psychosocial interview. Symptom incongruity refers to the observation that the vocal symptoms are physiologically incompatible with existing or suspected disease, are internally inconsistent, and are incongruent with other speech and language characteristics. An often cited example of symptom incongruity is complete aphonia (whispered speech) in a patient who has a normal throat clear, cough, laugh, or hum, whereby the presence of such normal nonspeech vocalization is at odds with assumptions regarding neural integrity and function of the laryngeal system. Finally, symptom reversibility refers to complete, sustained amelioration of the voice disorder with short-term voice therapy (usually one or two sessions) or through psychological abreaction. Furthermore, maintaining the voice improvement requires no compensatory e¤ort on the part of the patient. In general, psychogenic dysphonia may be suspected when strong evidence exists for symptom incongruity and symptom psychogenicity, but it is confirmed only when there is unmistakable evidence of symptom reversibility. A wide array of psychopathological processes contributing to voice symptom formation in functional dysphonia have been proposed. These mechanisms include, but are not limited to, conversion reaction, hysteria, hypochondriasis, anxiety, depression and various personality dispositions or emotional stresses or conflicts that induce laryngeal musculoskeletal tension. Roy and Bless (2000) provide a more complete exploration of the putative psychological and personality processes involved in functional dysphonia, as well as related research. The dominant psychological explanation for dysphonia unaccounted for by pathological findings is the concept of conversion disorder. According to the DSM-IV, conversion disorder involves unexplained symptoms or deficits a¤ecting voluntary motor or sensory function that suggest a neurological or other general medical condition (American Psychiatric Association, 1994). The conversion symptom represents an unconscious simulation of illness that ostensibly prevents conscious awareness of emotional conflict or stress, thereby displacing the mental conflict and reducing anxiety. When the laryngeal system is involved, the condition is referred to as conversion dysphonia or aphonia. In aphonia, patients lose their voice suddenly and completely and articulate in a whisper. The whisper may be pure, harsh, or sharp, with occasional high-pitched squeaklike traces of phonation. In dysphonia, phonation is preserved but disturbed in quality, pitch, or loudness. Myriad dysphonia types are encountered, including hoarseness (with or

without strain), breathiness, and high-pitched falsetto, as well as voice and pitch breaks that vary in consistency and severity. In conversion voice disorders, psychological factors are judged to be associated with the voice symptoms because conflicts or other stressors precede the onset or exacerbation of the dysphonia. In short, patients convert intrapsychic distress into a voice symptom. The voice loss, whether partial or complete, is also often interpreted to have symbolic meaning. Primary or secondary gains are thought to play an important role in maintaining and reinforcing the conversion disorder. Primary gain refers to anxiety alleviation accomplished by preventing the psychological conflict from entering conscious awareness. Secondary gain refers to the avoidance of an undesirable activity or responsibility and the extra attention or support conferred on the patient. Butcher and colleagues (Butcher et al., 1987; Butcher, Elias, and Raven, 1993; Butcher, 1995) have argued that there is little research evidence that conversion disorder is the most common cause of functional voice loss. Butcher advised that the conversion label should be reserved for cases of aphonia in which lack of concern and motivation to improve the voice coexists with clear evidence of a temporally linked psychosocial stressor. In the place of conversion, Butcher (1995) o¤ered two alternative models to account for psychogenic voice loss. Both models minimized the role of primary and secondary gain in maintaining the voice disorder. The first was a slightly reformulated psychoanalytic model that stated, ‘‘if predisposed by social and cultural bias as well as early learning experiences, and then exposed to interpersonal di‰culties that stimulate internal conflict, particularly in situations involving conflict over selfexpression or voicing feelings, intrapsychic conflict or stress becomes channeled into musculoskeletal tension, which physically inhibits voice production’’ (p. 472). The second model, based on cognitive-behavioral principles, stated that ‘‘life stresses and interpersonal problems in an individual predisposed to having di‰culties expressing feelings or views would produce involuntary anxiety symptoms and musculoskeletal tension, which would center on and inhibit voice production’’ (p. 473). Both models clearly emphasized the inhibitory e¤ects of excess laryngeal muscle tension on voice production, although through slightly di¤erent causal mechanisms. Recently, Roy and Bless (2000) proposed a theory that links personality to the development of functional dysphonia. The ‘‘trait theory of functional dysphonia’’ shares Butcher’s (1995) theme of inhibitory laryngeal behavior but attributes this muscularly inhibited voice production to specific personality types. In brief, the authors speculate that the combination of personality traits such as introversion and neuroticism (trait anxiety) and constraint leads to predictable and conditioned laryngeal inhibitory responses to certain environmental signals or cues. For instance, when undesirable punishing or frustrating outcomes have been paired with previous attempts to speak out, this can lead to muscularly inhibited voice. The authors contend that this conflict

Functional Voice Disorders


between laryngeal inhibition and activation (with origins in personality and nervous system functioning) results in elevated laryngeal tension states and can give rise to incomplete or disordered vocalization in a structurally and neurologically intact larynx. As is apparent from the foregoing discussion, the exquisite sensitivity and prolonged hypercontraction of the intrinsic and extrinsic laryngeal muscles in response to stress, anxiety, depression, and inhibited emotional expression is frequently cited as the common denominator underlying the majority of functional voice problems. Nichol, Morrison, and Rammage (1993) proposed that excess muscle tension arises from overactivity of autonomic and voluntary nervous systems in individuals who are unduly aroused and anxious. They added that such overactivity leads to hypertonicity of the intrinsic and extrinsic laryngeal muscles, resulting in muscle tension dysphonias sometimes associated with adjustment or anxiety disorders, or with certain personality trait disturbances. Finally, some researchers have noted that their ‘‘psychogenic dysphonia and aphonia’’ patients had an abnormally high number of reported allergy, asthma, or upper respiratory infection symptoms, suggesting a link between psychological factors and respiratory and phonatory disorders (Milutinovic, 1991; Schalen and Andersson, 1992). They have speculated that organic changes in the larynx, pharynx, and nose facilitate the appearance of a functional voice problem; that is, these changes direct the somatization of psychodynamic conflict. Likewise, Rammage, Nichol, and Morrison (1987) proposed that a relatively minor organic change such as edema, infection, or reflux laryngitis may trigger functional misuse, particularly if the individual is exceedingly anxious about his or her voice or health. In a similar vein, the same authors felt that anticipation of poor voice production in hypochondriacal, dependent, or obsessive-compulsive individuals leads to excessive vigilance over sensations arising from the throat (larynx) and respiratory system that may lead to altered voice production. Research evidence to support the various psychological mechanisms o¤ered to explain functional voice problems has seldom been provided. A complete review of the relevant findings and interpretations is provided in Roy et al. (1997). The empirical literature evaluating the functional dysphonia–psychology relationship is characterized by divergent results regarding the frequency and degree of specific personality traits (Aronson, Peterson, and Litin, 1966; Kinzl, Biebl, and Rauchegger, 1988; Gerritsma, 1991; Roy, Bless, and Heisey, 2000a, 2000b), conversion reaction (House and Andrews, 1987; Roy et al., 1997), and psychopathological symptoms such as depression and anxiety (Aronson, Peterson, and Litin, 1966; Pfau, 1975; House and Andrews, 1987; Gerritsma, 1991; Roy et al., 1997; White, Deary, and Wilson, 1997; Roy, Bless, and Heisey, 2000a, 2000b). Despite methodological di¤erences, these studies have identified a general trend toward elevated levels of (1) state and trait anxiety, (2) depression, (3) somatic preoccupation or

complaints, and (4) introversion in the functional dysphonia population. Patients have been described as inhibited, stress reactive, socially anxious, nonassertive, and with a tendency toward restraint (Friedl, Friedrich, and Egger, 1990; Gerritsma, 1991; Roy, Bless, and Heisey, 2000a, 2000b). In conclusion, the larynx can be a site of neuromuscular tension arising from stress, emotional inhibition, fear or threat, communication breakdown, and certain personality types. This tension can produce severely disordered voice in the context of a structurally normal larynx. Although the precise mechanisms underlying and maintaining psychogenic voice problems remain unclear, the voice disorder is a powerful reminder of the intimate relationship between mind and body. See also psychogenic voice disorders: direct therapy. —Nelson Roy

American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders—Fourth edition. Washington, DC: American Psychiatric Press. Aronson, A. E. (1990). Clinical voice disorders: An interdisciplinary approach (3rd ed.). New York: Thieme. Aronson, A. E., Peterson, H. W., and Litin, E. M. (1966). Psychiatric symptomatology in functional dysphonia and aphonia. Journal of Speech and Hearing Disorders, 31, 115– 127. Bridger, M. M., and Epstein, R. (1983). Functional voice disorders: A review of 109 patients. Journal of Laryngology and Otology, 97, 1145–1148. Butcher, P. (1995). Psychological processes in psychogenic voice disorder. European Journal of Disorders of Communication, 30, 467–474. Butcher, P., Elias, A., Raven, R. (1993). Psychogenic voice disorders and cognitive behaviour therapy. San Diego, CA: Singular Publishing Group. Butcher, P., Elias, A., Raven, R., Yeatman, J., and Littlejohns, D. (1987). Psychogenic voice disorder unresponsive to speech therapy: Psychological characteristics and cognitivebehaviour therapy. British Journal of Disorders of Communication, 22, 81–92. Friedl, W., Friedrich, G., and Egger, J. (1990). Personality and coping with stress in patients su¤ering from functional dysphonia. Folia Phoniatrica, 42, 144–149. Gerritsma, E. J. (1991). An investigation into some personality characteristics of patients with psychogenic aphonia and dysphonia. Folia Phoniatrica, 43, 13–20. House, A. O., and Andrews, H. B. (1987). The psychiatric and social characteristics of patients with functional dysphonia. Journal of Psychosomatic Research, 3, 483–490. Kinzl, J., Biebl, W., and Rauchegger, H. (1988). Functional aphonia: Psychosomatic aspects of diagnosis and therapy. Folia Phoniatrica, 40, 131–137. Milutinovic, Z. (1991). Inflammatory changes as a risk factor in the development of phononeurosis. Folia Phoniatrica, 43, 177–180. Nichol, H., Morrison, M. D., and Rammage, L. A. (1993). Interdisciplinary approach to functional voice disorders: The psychiatrist’s role. Otolaryngology–Head and Neck Surgury, 108, 643–647.


Part I: Voice

Pfau, E. M. (1975). Psychologische Untersuchungsergegnisse fur Atiologie der psychogenen Dysphonien. Folia Phonia¨ ¨ trica, 25, 298–306. Rammage, L. A., Nichol, H., and Morrison, M. D. (1987). The psychopathology of voice disorders. Human Communications Canada, 11, 21–25. Roy, N., and Bless, D. M. (2000). Toward a theory of the dispositional bases of functional dysphonia and vocal nodules: Exploring the role of personality and emotional adjustment. In R. D. Kent and M. J. Ball (Eds.), Voice quality measurement (pp. 461–480). San Diego, CA: Singular Publishing Group. Roy, N., Bless, D. M., and Heisey, D. (2000a). Personality and voice disorders: A superfactor trait analysis. Journal of Speech, Language and Hearing Research, 43, 749–768. Roy, N., Bless, D. M., and Heisey, D. (2000b). Personality and voice disorders: A multitrait-multidisorder analysis. Journal of Voice, 14, 521–548. Roy, N., McGrory, J. J., Tasko, S. M., Bless, D. M., Heisey, D., and Ford, C. N. (1997). Psychological correlates of functional dysphonia: An evaluation using the Minnesota Multiphasic Personality Inventory. Journal of Voice, 11, 443–451. Sapir, S. (1995). Psychogenic spasmodic dysphonia: A case study with expert opinions. Journal of Voice, 9, 270–281. Schalen, L., and Andersson, K. (1992). Di¤erential diagnosis and treatment of psychogenic voice disorder. Clinical Otolaryngology, 17, 225–230. White, A., Deary, I. J., and Wilson, J. A. (1997). Psychiatric disturbance and personality traits in dysphonic patients. European Journal of Disorders of Communication, 32, 121–128.

Hypokinetic Laryngeal Movement Disorders
Hypokinetic laryngeal movement disorders are observed most often in individuals diagnosed with the neurological disorder, parkinsonism. Parkinsonism has the following features: bradykinesia, postural instability, rigidity, resting tremor, and freezing (motor blocks) (Fahn, 1986). For the diagnosis to be made, at least two of these five features should be present, and one of the two features should be either tremor or rigidity. Parkinsonism as a syndrome can be classified as idiopathic Parkinson’s disease (PD) (i.e., symptoms of unknown cause); secondary (or symptomatic) PD, caused by a known and identifiable cause; or parkinsonism-plus syndromes, in which symptoms of parkinsonism are caused by a known gene defect or have a distinctive pathology. The specific diagnosis depends on findings in the clinical history, the neurological examination, and laboratory tests. No single feature is completely reliable for di¤erentiating among the di¤erent causes of parkinsonism. Idiopathic PD is the most common type of parkinsonism encountered by the neurologist. Pathologically, idiopathic PD a¤ects many structures in the central nervous system (CNS), with preferential involvement of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Lewy bodies, eosinophilic intracytoplasmatic inclusions, can be found in these neurons (Galvin, Lee, and Trojanowski, 2001). Alpha-synuclein is the primary component of Lewy body fibrils (Galvin, Lee, and Trojanowski, 2001). However, only about 75% of patients with the clinical diagnosis of idiopathic PD are found at autopsy to have the pathological CNS changes characteristic of PD (Hughes et al., 1992). Many patients and their families consider the reduced ability to communicate one of the most di‰cult aspects of PD. Hypokinetic dysarthria, characterized by a soft voice, monotone, a breathy, hoarse voice quality, and imprecise articulation (Darley, Aronson, and Brown, 1975; Logemann et al., 1978), and reduced facial expression (masked facies) contribute to limitations in communication in the vast majority of individuals with idiopathic PD (Pitcairn et al., 1990). During the course of the disease, approximately 45%–89% of patients will report speech problems (Logemann and Fisher, 1981; Sapir et al., 2002). Repetitive speech phenomena (Benke et al., 2000), voice tremor, and hyperkinetic dysarthria may also be encountered in individuals with idiopathic PD. When hyperkinetic dysarthria is reported in idiopathic PD, it is most frequently seen together with other motor complications (e.g., dyskinesia) of prolonged levodopa therapy (Critchley, 1981). Logemann et al. (1978) suggested that the clusters of speech symptoms they observed in 200 individuals with PD represented a progression in dysfunction, beginning with disordered phonation in recently diagnosed patients and extending to include disordered articulation and other aspects of speech in more advanced cases. Recent findings by Sapir et al. (2002) are consistent with this

Further Readings
Deary, I. J., Scott, S., Wilson, I. M., White, A., MacKenzie, K., and Wilson, J. A. (1998). Personality and psychological distress in dysphonia. British Journal of Health Psychology, 2, 333–341. Friedl, W., Friedrich, G., Egger, J., and Fitzek, I. (1993). Psychogenic aspects of functional dysphonia. Folia Phoniatrica, 45, 10–13. Green, G. (1988). The inter-relationship between vocal and psychological characteristics: A literature review. Australian Journal of Human Communication Disorders, 16, 31–43. Gunther, V., Mayr-Graft, A., Miller, C., and Kinzl, H. (1996). A comparative study of psychological aspects of recurring and non-recurring functional aphonias. European Archives of Otorhinolaryngology, 253, 240–244. House, A. O., and Andrews, H. B. (1988). Life events and difficulties preceding the onset of functional dysphonia. Journal of Psychosomatic Research, 32, 311–319. Koufman, J. A., and Blalock, P. D. (1982). Classification and approach to patients with functional voice disorders. Annals of Otology, Rhinology, and Laryngology, 91, 372–377. Morrison, M. D., and Rammage, L. (1993). Muscle misuse voice disorders: Description and classification. Acta Otolaryngologica (Stockholm), 113, 428–434. Moses, P. J. (1954). The voice of neurosis. New York: Grune and Stratton. Pennebaker, J. W., and Watson, D. (1991). The psychology of somatic symptoms. In L. J. Kirmayer and J. M. Robbins (Eds.), Current concepts of somatization. Washington, DC: American Psychiatric Press. Roy, N., and Bless, D. M. (2000). Personality traits and psychological factors in voice pathology: A foundation for future research. Journal of Speech, Language, and Hearing Research, 43, 737–748.

Hypokinetic Laryngeal Movement Disorders


suggestion. Sapir et al. (2002) observed voice disorders in individuals with recent onset of PD and low Unified Parkinson Disease Rating Scale (UPDRS) scores; in individuals with longer duration of disease and higher UPDRS scores, they observed a significantly higher incidence of abnormal articulation and fluency, in addition to the disordered voice. Hypokinetic dysarthria of parkinsonism is considered to be a part of basal ganglia damage (Darley, Aronson, and Brown, 1975). However, there are no studies on pathological changes in the hypokinetic dysarthria of idiopathic PD. A significant correlation between neuronal loss and gliosis in SNpc and substantia nigra pars reticulata (SNpr) and severity of hypokinetic dysarthria was found in patients with Parkinson-plus syndromes (Kluin et al., 2001). Speech and voice characteristics may di¤er between idiopathic PD and Parkinson-plus syndromes (e.g., Shy-Drager syndrome, progressive supranuclear palsy, multisystem atrophy). In addition to the classic hypokinetic symptoms, these patients may have more slurring, a strained, strangled voice, pallilalia, and hypernasality (Countryman, Ramig, and Pawlas, 1994) and their symptoms may progress more rapidly. Certain aspects of hypokinetic dysarthria in idiopathic PD have been studied extensively. Hypophonia (reduced loudness, monotone, a breathy, hoarse quality) may be observed in as many as 89% of individuals with idiopathic PD (Logemann et al., 1978). Fox and Ramig (1997) reported that sound pressure levels in individuals with idiopathic PD were significantly lower (2–4 dB [30 cm]) across a variety of speech tasks than in an ageand sex-matched control group. Lack of vocal fold closure, including bowing of the vocal cords and anterior and posterior chinks (Hanson, Gerratt, and Ward, 1984; Smith et al., 1995), has been implicated as a cause of this hypophonia. Perez et al. (1996) used videostroboscopic observations to study vocal fold vibration in individuals with idiopathic PD. They reported abnormal phase closure and symmetry and tremor (both at rest and during phonation) in nearly 50% of patients. Whereas reduced loudness and disordered voice quality in idiopathic PD have been associated with glottal incompetence (lack of vocal fold closure—e.g., bowing; Hanson, Gerratt, and Ward, 1984; Smith et al., 1995; Perez et al., 1996), the specific origin of this glottal incompetence has not been clearly defined. Rigidity or fatigue secondary to rigidity, paralysis, reduced thyroarytenoid longitudinal tension secondary to cricothyroid rigidity (Aronson, 1990), and misperception of voice loudness (Ho, Bradshaw, and Iansek 2000; Sapir et al., 2002) are among the explanations. It has been suggested that glottal incompetence (e.g., vocal fold bowing) might be due to loss of muscle or connective tissue volume, either throughout the entire vocal fold or localized near the free margin of the vocal fold. Recent physiological studies of laryngeal function in idiopathic PD have shown a reduced amplitude of electromyographic activity in the thyroarytenoid muscle accompanying glottal incompetence when compared with both aged-matched and younger controls (Baker et al., 1998). These findings and the observation of

reduced and variable single motor unit activity in the thyroarytenoid muscle of individuals with idiopathic PD (Luschei et al., 1999) are consistent with a number of hypotheses, the most plausible of which is reduced central drive to laryngeal motor neuron pools. Although the origin of the hypophonia in PD is currently undefined, Ramig and colleagues (e.g., Fox et al., 2002) have hypothesized that there are at least three features underlying the voice disorder in individuals with PD: (1) an overall neural amplitude scaledown (Penny and Young, 1983) to the laryngeal mechanism (reduced amplitude of neural drive to the muscles of the larynx); (2) problems in sensory perception of e¤ort (Berardelli et al., 1986), which prevents the individual with idiopathic PD from accurately monitoring his or her vocal output; which results in (3) the individual’s di‰culty in independently generating (through internal cueing or scaling) adequate vocal e¤ort (Hallet and Khoshbin, 1980) to produce normal loudness. Reduced neural drive, problems in sensory perception of e¤ort, and problems scaling adequate vocal output e¤ort may be significant factors underlying the voice problems in individuals with PD. —Lorraine Olson Ramig, Mitchell F. Brin, Miodrag Velickovic, and Cynthia Fox

Aronson, A. E. (1990). Clinical voice disorders. New York: Thieme-Stratton. Baker, K. K., Ramig, L. O., Luschei, E. S., and Smith, M. E. (1998). Thyroarytenoid muscle activity associated with hypophonia in Parkinson disease and aging. Neurology, 51, 1592–1598. Benke, T., Hohenstein, C., Poewe, W., and Butterworth, B. (2000). Repetitive speech phenomena in Parkinson’s disease. Journal of Neurology, Neurosurgery, and Psychiatry, 69, 319–324. Berardelli, A., Dick, J. P., Rothwell, J. C., Day, B. L., and Marsden, C. D. (1986). Scaling of the size of the first agonist EMG burst during rapid wrist movements in patients with Parkinson’s disease. Journal of Neurology, Neurosurgery, and Psychiatry, 49, 1273–1279. Countryman, S., Ramig, L. O., and Pawlas, A. A. (1994). Speech and voice deficits in Parkinsonian Plus syndromes: Can they be treated? Journal of Medical Speech-Language Pathology, 2, 211–225. Critchley, E. M. (1981). Speech disorders of Parkinsonism: A review. Journal of Neurology, Neurosurgery, and Psychiatry, 44, 751–758. Darley, F. L., Aronson, A. E., and Brown, J. B. (1975). Motor speech disorders. Philadelphia: Saunders. Fahn, S. (1986). Parkinson’s disease and other basal ganglion disorders. In A. K. Asbury, G. M. McKhann, and W. I. McDonald (Eds.), Diseases of the nervous system: Clinical neurobiology. Philadelphia: Ardmore. Fox, C., Morrison, C. E., Ramig, L. O., and Sapir, S. (2002). Current perspectives on the Lee Silverman voice treatment (LSVT) for individuals with idiopathic Parkinson’s disease. American Journal of Speech-Language Pathology, 11, 111– 123. Fox, C., and Ramig, L. (1997). Vocal sound pressure level and self-perception of speech and voice in men and women with


Part I: Voice Conner, N. P., Abbs, J. H., Cole, K. J., and Gracco, V. L. (1989). Parkinsonian deficits in serial multiarticulate movements for speech. Brain, 112, 997–1009. Contreras-Vidal, J., and Stelmach, G. (1995). A neural model of basal ganglia-thalamocortical relations in normal and parkinsonian movement. Biological Cybernetics, 73, 467– 476. DeLong, M. R. (1990). Primate models of movement disorders of basal ganglia origin. Trends in Neuroscience, 13, 281– 285. Forrest, K., Weismer, G., and Turner, G. (1989). Kinematic, acoustic and perceptual analysis of connected speech produced by Parkinsonian and normal geriatric adults. Journal of the Acoustical Society of America, 85, 2608–2622. Jobst, E. E., Melnick, M. E., Byl, N. N., Dowling, G. A., and Amino¤, M. J. (1997). Sensory perception in Parkinson disease. Archives of Neurology, 54, 450–454. Jurgens, U., and von Cramon, D. (1982). On the role of the anterior cingulated cortex in phonation: A case report. Brain and Language, 15, 234–248. Larson, C. (1985). The midbrain periaqueductal fray: A brainstem structure involved in vocalization. Journal of Speech and Hearing Research, 28, 241–249. Ludlow, C. L., and Bassich, C. J. (1984). Relationships between perceptual ratings and acoustic measures of hypokinetic speech. In M. R. McNeil, J. C. Rosenbek, and A. E. Aronson (Eds.), Dysarthria of speech: Physiology-acousticslinguistics-management. San Diego, CA: College-Hill Press. Netsell, R., Daniel, B., and Celesia, G. G. (1975). Acceleration and weakness in parkinsonian dysarthria. Journal of Speech and Hearing Disorders, 40, 170–178. Sarno, M. T. (1968). Speech impairment in Parkinson’s disease. Journal of Speech and Hearing Disorders, 49, 269–275. Schneider, J. S., Diamond, S. G., and Markham, C. H. (1986). Deficits in orofacial sensorimotor function in Parkinson’s disease. Annals of Neurology, 19, 275–282. Solomon, N. P., Hixon, T. J. (1993). Speech breathing in Parkinson’s disease. Journal of Speech and Hearing Research, 36, 294–310. Stewart, C., Winfield, L., Hunt, A., et al. (1995). Speech dysfunction in early Parkinson’s disease. Movement Disorders, 10, 562–565.

idiopathic Parkinson disease. American Journal of SpeechLanguage Pathology, 6, 85–94. Galvin, J. E., Lee, V. M., and Trojanowski, J. Q. (2001). Synucleinopathies: Clinical and pathological implications. Archives of Neurology, 58, 186–190. Hallet, M., and Khoshbin, S. (1980). A physiological mechanism of bradykinesia. Brain, 103, 301–314. Hanson, D., Gerratt, B., and Ward, P. (1984). Cinegraphic observations of laryngeal function in Parkinson’s disease. Laryngoscope, 94, 348–353. Ho, A. K., Bradshaw, J. L., and Iansek, T. (2000). Volume perception in parkinsonian speech. Movement Disorders, 15, 1125–1131. Hughes, A. J., Daniel, S. E., Kilford, L., and Lees, A. J. (1992). Accuracy of clinical diagnosis of idiopathic Parkinson’s disease: A clinico-pathological study of 100 cases. Journal of Neurology, Neurosurgery, and Psychiatry, 55, 181–184. Kluin, K. J., Gilman, S., Foster, N. L., Sima, A., D’Amato, C., Bruch, L., et al. (2001). Neuropathological correlates of dysarthria in progressive supranuclear palsy. Archives of Neurology, 58, 265–269. Logemann, J. A., and Fisher, H. B. (1981). Vocal tract control in Parkinson’s disease: Phonetic feature analysis of misarticulations. Journal of Speech and Hearing Disorders, 46, 348–352. Logemann, J. A., Fisher, H. B., Boshes, B., and Blonsky, E. (1978). Frequency and concurrence of vocal tract dysfunctions in the speech of a large sample of Parkinson’s patients. Journal of Speech and Hearing Disorders, 43, 47–57. Luschei, E. S., Ramig, L. O., Baker, K. L., and Smith, M. E. (1999). Discharge characteristics of laryngeal single motor units during phonation in young and older adults and in persons with Parkinson disease. Journal of Neurophysiology, 81, 2131–2139. Penny, J. B., and Young, A. B. (1983). Speculations on the functional anatomy of basal ganglia disorders. Annual Review of Neurosciences, 6, 73–94. Perez, K., Ramig, L. O., Smith, M., and Dromey, C. (1996). The Parkinson larynx: Tremor and videostroboscopic findings. Journal of Voice, 10, 354–361. Pitcairn, T., Clemie, S., Gray, J., and Pentland, B. (1990). Non-verbal cues in the self-presentation of parkinsonian patients. British Journal of Clinical Psychology, 29, 177– 184. Sapir, S., Pawlas, A. A., Ramig, L. O., Countryman, S., et al. (2002). Speech and voice abnormalities in Parkinson disease: Relation to severity of motor impairment, duration of disease, medication, depression, gender, and age. Journal of Medical Speech-Language Pathology, 9, 213–226. Smith, M. E., Ramig, L. O., Dromey, C., et al. (1995). Intensive voice treatment in Parkinson disease: Laryngostroboscopic findings. Journal of Voice, 9, 453–459.

Infectious Diseases and Inflammatory Conditions of the Larynx
Infectious and inflammatory conditions of the larynx can a¤ect the voice, swallowing, and breathing to varying extents. Changes can be acute or chronic and can occur in isolation or as part of systemic processes. The conditions described in this article are grouped by etiology.

Further Readings
Ackerman, H., and Ziegler, W. (1991). Articulatory deficits in Parkinsonian dysarthria. Journal of Neurology, Neurosurgery, and Psychiatry, 54, 1093–1098. Brown, R. G., and Marsden, C. D. (1988). An investigation of the phenomenon of ‘‘set’’ in Parkinson’s disease. Movement Disorders, 3, 152–161. Caliguri, M. P. (1989). Short-term fluctuations in orofacial motor control in Parkinson’s disease. In K. M. Yorkson and D. R. Beukelman (Eds.), Recent advances in clinical dysarthria. Boston: College-Hill Press.

Infectious Diseases
Viral Laryngotracheitis. Viral laryngotracheitis is the most common infectious laryngeal disease. It is typically associated with upper respiratory infection, for example, by rhinoviruses and adenoviruses. Dysphonia is usually self-limiting but may create major problems for a professional voice user. The larger diameter upper airway in

Infectious Diseases and Inflammatory Conditions of the Larynx


adults makes airway obstruction much less likely than in children. In a typical clinical scenario, a performer with mild upper respiratory symptoms has to carry on performing but complains of reduced vocal pitch and increased effort on singing high notes. Mild vocal fold edema and erythema may occur but can be normal for this patient group. Thickened, erythematous tracheal mucosa visible between the vocal folds supports the diagnosis. Hydration and rest may be su‰cient treatment. However, if the performer decides to proceed with the show, high-dose steroids can reduce inflammation, and antibiotics may prevent opportunistic bacterial infection. Cough suppressants, expectorants, and steam inhalations may also be useful. Careful vocal warmup should be undertaken before performing, and ‘‘rescue’’ must be balanced against the risk of vocal injury. Other Viral Infections. Herpes simplex and herpes zoster infection have been reported in association with vocal fold paralysis (Flowers and Kernodle, 1990; Nishizaki et al., 1997). Laryngeal vesicles, ulceration, or plaques may lead to suspicion of the diagnosis, and antiviral therapy should be instituted early. New laryngeal muscle weakness may also occur in post-polio syndrome (Robinson, Hillel, and Waugh, 1998). Viral infection has also been implicated in the pathogenesis of certain laryngeal tumors. The most established association is between human papillomavirus (HPV) and laryngeal papillomatosis (Levi et al., 1989). HPV, Epstein-Barr virus, and even herpes simplex virus have been implicated in the development of laryngeal malignancy (Ferlito et al., 1997; Garcia-Milian et al., 1998; Pou et al., 2000). Bacterial Laryngitis. Bacterial laryngitis is most commonly due to Hemophilus influenzae, Staphylococcus aureus, Streptococcus pneumoniae, and beta-hemolytic streptococcus. Pain and fever may be severe, with airway and swallowing di‰culties generally overshadowing voice loss. Typically the supraglottis is involved, with the aryepiglottic folds appearing boggy and edematous, often more so than the epiglottis. Unlike in children, laryngoscopy is usually safe in adults and is the best means of diagnosis. Possible underlying causes such as a laryngeal foreign body should be considered. Treatment includes intravenous antibiotics, hydration, humidification, and corticosteroids. Close observation is essential in case airway support is needed. Rarely, infected mucous retention cysts and epiglottic abscesses occur (Stack and Ridley, 1995). Tracheostomy and drainage may be required. Mycobacterial Infections. Laryngeal tuberculosis is rare in industrialized countries but must be considered in the di¤erential diagnosis of laryngeal disease, especially in patients with AIDS or other immune deficiencies (Singh et al., 1996). Tuberculosis can infect the larynx primarily, by direct spread from the lungs, or by hematogenous or lymphatic dissemination (Ramandan, Tarayi, and Baroudy, 1993). Most patients have hoarse-

ness and odynophagia, typically out of proportion to the size of the lesion. However, these symptoms are not universally present. The vocal folds are most commonly a¤ected, although all areas of the larynx can be involved. Laryngeal tuberculosis is often di‰cult to distinguish from carcinoma on laryngoscopy. Chest radiography and the purified protein derivative (PPD) test help establish the diagnosis, although biopsy and histological confirmation may be required. Patients are treated with antituberculous chemotherapy. The laryngeal symptoms usually respond within 2 weeks. Leprosy is rare in developing countries. Laryngeal infection by Mycobacterium leprae can cause nodules, ulceration, and fibrosis. Lesions are often painless but may progress over the years to laryngeal stenosis. Treatment is with antileprosy chemotherapy (Soni, 1992). Other Bacterial Infections. Laryngeal actinomycosis can occur in immunocompromised patients and following laryngeal radiotherapy (Nelson and Tybor, 1992). Biopsy may be required to distinguish it from radionecrosis or tumor. Treatment requires prolonged antibiotic therapy. Scleroma is a chronic granulomatous disease due to Klebsiella scleromatis. Primary involvement is in the nose, but the larynx can also be a¤ected. Subglottic stenosis is the main concern (Amoils and Shindo, 1996). Fungal Laryngitis. Fungal laryngitis is rare and typically occurs in immunocompromised individuals. Fungi include yeasts and molds. Yeast infections are more frequent in the larynx, with Candida albicans most commonly identified (Vrabec, 1993). Predisposing factors in nonimmunocompromised patients include antibiotic and inhaled steroid use, and foreign bodies such as silicone voice prostheses. The degree of hoarseness in laryngeal candidiasis may not reflect the extent of infection. Pain and associated swallowing di‰culty may be present. Typically, thick white exudates are seen, and oropharyngeal involvement can coexist. Biopsy may show epithelial hyperplasia with a pseudocarcinomatous appearance. Potential complications include scarring, airway obstruction, and systemic dissemination. In mild localized disease, topical nystatin or clotrimazole are usually e¤ective. Discontinuing antibiotics or inhaled steroids should be considered. More severe cases may require oral antifungal azoles such as ketoconazole, fluconazole, or itraconazole. Intravenous amphotericin is e‰cacious but has potentially severe side e¤ects. It is usually used for invasive or systemic disease. Less common fungal diseases include blastomycosis, histoplasmosis, and coccidiomycosis. Infection may be confused with laryngeal carcinoma, and special histological stains are usually required for diagnosis. Longterm treatment with amphotericin B may be necessary. Syphilis. Syphilis is caused by the spirochete Treponema pallidum. Laryngeal involvement is rare but may occur in later stages of the disease. Secondary syphilis


Part I: Voice

may present with laryngeal papules, ulcers and edema that mimic carcinoma, or tuberculous laryngitis. Tertiary syphilis may cause gummas, leading to scarring and stenosis (Lacy, Alderson, and Parker, 1994). Serologic tests are diagnostic. Active disease is treated with penicillin.

50% of cases. Dapsone, corticosteroids, and immunosuppressive drugs have been used to control the disease. Repeated attacks of laryngeal chondritis can cause subglottic scarring, necessitating permanent tracheostomy (Spraggs, Tostevin, and Howard, 1997). Cicatricial Pemphigoid. This chronic subepithelial bullous disease predominantly involves the mucous membranes. Acute laryngeal lesions are painful, and examination shows mucosal erosion and ulceration. Later, scarring and stenosis may occur, with supraglottic involvement (Hanson, Olsen, and Rogers, 1988). Treatment includes dapsone, systemic or intralesional steroids, and cyclophosphamide. Scarring may require laser excision and sometimes tracheostomy. Amyloidosis. Amyloidosis is characterized by deposition of acellular proteinaceous material (amyloid) in tissues (Lewis et al., 1992). It can occur primarily or secondary to other diseases such as multiple myeloma or tuberculosis. Deposits may be localized or generalized. Laryngeal involvement is usually due to primary localized disease. Submucosal deposits may a¤ect any part of the larynx but most commonly occur in the ventricular folds. Treatment is by conservative laser excision. Recurrences are frequent. Sarcoidosis. Sarcoidosis is a multiorgan granulomatous disease of unknown etiology. About 6% of cases involve the larynx, producing dysphonia and airway obstruction. Pale, di¤use swelling of the epiglottis and aryepiglottic folds is characteristic (Benjamin, Dalton, and Croxson, 1995). Systemic or intralesional steroids, antilepromatous therapy, and laser debulking are all possible treatments. Wegener’s Granulomatosis. Wegener’s granulomatosis is an idiopathic syndrome characterized by vasculitis and necrotizing granulomas of the respiratory tract and kidneys. The larynx is involved in 8% of cases (Waxman and Bose, 1986). Ulcerative lesions and subglottic stenosis may occur, causing hoarseness and dyspnea. Treatment includes corticosteroids and cyclophosphamide. Laser resection or open surgery is sometimes necessary for airway maintenance. —David P. Lau and Murray D. Morrison

Inflammatory Processes
Chronic Laryngitis. Chronic laryngeal inflammation can result from smoking, gastroesophageal reflux (GER), voice abuse, or allergy. Patients often complain of hoarseness, sore throat, a globus sensation, and throat clearing. The vocal folds are usually thickened, dull, and erythematous. Posterior laryngeal involvement usually suggests GER. Besides direct chemical irritation, GER can promote laryngeal muscle misuse, which contributes to wear-and-tear injury (Gill and Morrison, 1998). Although seasonal allergies may cause vocal fold edema and hoarseness (Jackson-Menaldi, Dzul, and Holland, 1999), it is surprising that allergy-induced chronic laryngitis is not more common. Even patients with significant nasal allergies or asthma have a low incidence of voice problems. The severity of other allergic accompaniments helps the clinician identify patients with dysphonia of allergic cause. Treatment of chronic laryngitis includes voice rest and elimination of irritants. Dietary modifications and postural measures such as elevating the head of the bed can reduce GER. Proton pump inhibitors can be e¤ective for persistent laryngeal symptoms (Hanson, Kamel, and Kahrilas, 1995). Traumatic and Iatrogenic Causes. Inflammatory polyps, polypoid degeneration, and contact granuloma can arise from vocal trauma. Smoking contributes to polypoid degeneration, and intubation injury can cause contact granulomas. GER may promote inflammation in all these conditions. Granulomas can also form many years after Teflon injection for glottic insu‰ciency. Rheumatoid Arthritis and Systemic Lupus Erythematosus. Laryngeal involvement occurs in almost a third of patients with rheumatoid arthritis (Lofgren and Montgomery, 1962). Patients present with a variety of symptoms. In the acute phase the larynx may be tender and inflamed. In the chronic phase the laryngeal mucosa may appear normal, but cricoarytenoid joint ankylosis may be present. Submucosal rheumatoid nodules or ‘‘bamboo nodes’’ can form in the membranous vocal folds. If the mucosal wave is severely damped, microlaryngeal excision can improve the voice. Corticosteroids can be injected intracordally following excision. Other autoimmune diseases such as systemic lupus erythematosus can cause similar laryngeal pathology (Woo, Mendelsohn, and Humphrey, 1995). Relapsing Polychondritis. Relapsing polychondritis is an autoimmune disease causing inflammation of cartilaginous structures. The pinna is most commonly affected, although laryngeal involvement occurs in around

Amoils, C., and Shindo, M. (1996). Laryngotracheal manifestations of rhinoscleroma. Annals of Otology, Rhinology, and Laryngology, 105, 336–340. Benjamin, B., Dalton, C., and Croxson, G. (1995). Laryngoscopic diagnosis of laryngeal sarcoid. Annals of Otology, Rhinology, and Laryngology, 104, 529–531. Ferlito, A., Weiss, L., Rinaldo, A., et al. (1997). Clinicopathologic consultation: Lymphoepithelial carcinoma of the larynx, hypopharynx and trachea. Annals of Otology, Rhinology, and Laryngology, 106, 437–444. Flowers, R., and Kernodle, D. (1990). Vagal mononeuritis caused by herpes simplex virus: Association with unilateral vocal cord paralysis. American Journal of Medicine, 88, 686–688.

Instrumental Assessment of Children’s Voice Garcia-Milian, R., Hernandez, H., Panade, L., et al. (1998). Detection and typing of human papillomavirus DNA in benign and malignant tumours of laryngeal epithelium. Acta Oto-Laryngologica, 118, 754–758. Gill, C., and Morrison, M. (1998). Esophagolaryngeal reflux in a porcine animal model. Journal of Otolaryngology, 27, 76– 80. Hanson, D., Kamel, P., and Kahrilas, P. (1995). Outcomes of antireflux therapy for the treatment of chronic laryngitis. Annals of Otology, Rhinology, and Laryngology, 104, 550– 555. Hanson, R., Olsen, K., and Rogers, R. (1988). Upper aerodigestive tract manifestations of cicatricial pemphigoid. Annals of Otology, Rhinology, and Laryngology, 97, 493–499. Jackson-Menaldi, C., Dzul, A., and Holland, R. (1999). Allergies and vocal fold edema: A preliminary report. Journal of Voice, 13, 113–122. Lacy, P., Alderson, D., and Parker, A. (1994). Late congenital syphilis of the larynx and pharynx presenting at endotracheal intubation. Journal of Laryngology and Otology, 108, 688–689. Levi, J., Delcelo, R., Alberti, V., Torloni, H., and Villa, L. (1989). Human papillomavirus DNA in respiratory papillomatosis detected by in situ hybridization and polymerase chain reaction. American Journal of Pathology, 135, 1179– 1184. Lewis, J., Olsen, K., Kurtin, P., and Kyle, R. (1992). Laryngeal amyloidosis: A clinicopathologic and immunohistochemical review. Otolaryngology–Head and Neck Surgery, 106, 372– 377. Lofgren, R., and Montgomery, W. (1962). Incidence of laryngeal involvement in rheumatoid arthritis. New England Journal of Medicine, 267, 193. Nelson, E., and Tybor, A. (1992). Actinomycosis of the larynx. Ear, Nose, and Throat Journal, 71, 356–358. Nishizaki, K., Onada, K., Akagi, H., Yuen, K., Ogawa, T., and Masuda, Y. (1997). Laryngeal zoster with unilateral laryngeal paralysis. ORL: Journal for Oto-rhino-laryngology and Its Related Specialties, 59, 235–237. Pou, A., Vrabec, J., Jordan, J., Wilson, D., Wang, S., and Payne, D. (2000). Prevalence of herpes simplex virus in malignant laryngeal lesions. Laryngoscope, 110, 194–197. Ramandan, H., Tarayi, A., and Baroudy, F. (1993). Laryngeal tuberculosis: Presentation of 16 cases and review of the literature. Journal of Otolaryngology, 22, 39–41. Robinson, L., Hillel, A., and Waugh, P. (1998). New laryngeal muscle weakness in post-polio syndrome. Laryngoscope, 108, 732–734. Singh, B., Balwally, A., Nash, M., Har-El, G., and Lucente, F. (1996). Laryngeal tuberculosis in HIV-infected patients: A di‰cult diagnosis. Laryngoscope, 106, 1238–1240. Soni, N. (1992). Leprosy of the larynx. Journal of Laryngology and Otology, 106, 518–520. Spraggs, P., Tostevin, P., and Howard, D. (1997). Management of laryngotracheobronchial sequelae and complications of relapsing polychondritis. Laryngoscope, 107, 936– 941. Stack, B., and Ridley, M. (1995). Epiglottic abscess. Head and Neck, 17, 263–265. Vrabec, D. (1993). Fungal infections of the larynx. Otolaryngologic Clinics of North America, 26, 1091–1114. Waxman, J., and Bose, W. (1986). Laryngeal manifestations of Wegener’s granulomatosis: Case reports and review of the literature. Journal of Rheumatology, 13, 408–411. Woo, P., Mendelsohn, J., and Humphrey, D. (1995). Rheumatoid nodules of the larynx. Otolaryngology–Head and Neck Surgery, 113, 147–150.


Further Readings
Badaracco, G., Venuti, A., Morello, R., Muller, A., and Marcante, M. (2000). Human papillomavirus in head and neck carcinomas: Prevalence, physical status and relationship with clinical/pathological parameters. Anticancer Research, 20, 1305. Cleary, K., and Batsakis, J. (1995). Mycobacterial disease of the head and neck: Current perspective. Annals of Otology, Rhinology, and Laryngology, 104, 830–833. Herridge, M., Pearson, F., and Downey, G. (1996). Subglottic stenosis complicating Wegener’s granulomatosis: Surgical repair as a viable treatment option. Journal of Thoracic and Cardiovascular Surgery, 111, 961–966. Jones, K. (1998). Infections and manifestations of systemic disease in the larynx. In C. W. Cummings, J. M. Fredrickson, L. A. Harker, C. J. Krause, D. E. Schuller, and M. A. Richardson (Eds.), Otolaryngology—head and neck surgery (3rd ed., pp. 1979–1988). St Louis: Mosby. Langford, C., and Van Waes, C. (1997). Upper airway obstruction in the rheumatic diseases. Rheumatic Diseases Clinics of North America, 23, 345–363. Morrison, M., Rammage, L., Nichol, H., Pullan, B., May, P., and Salkeld, L. (2001). Management of the voice and its disorders (2nd ed.). San Diego, CA: Singular Publishing Group. Raymond, A., Sneige, N., and Batsakis, J. (1992). Amyloidosis in the upper aerodigestive tracts. Annals of Otology, Rhinology, and Laryngology, 101, 794–796. Richter, B., Fradis, M., Kohler, G., and Ridder, G. (2001). Epiglottic tuberculosis: Di¤erential diagnosis and treatment. Case report and review of the literature. Annals of Otology, Rhinology, and Laryngology, 110, 197–201. Ridder, G., Strohhacker, H., Lohle, E., Golz, A., and Fradis, M. (2000). Laryngeal sarcoidosis: Treatment with the antileprosy drug clofazimine. Annals of Otology, Rhinology, and Laryngology, 109, 1146–1149. Satalo¤, R. (1997). Common infections and inflammations and other conditions. In R. T. Satalo¤ (Ed.), Professional voice: The science and art of clinical care (2nd ed., pp. 429–436). San Diego, CA: Singular Publishing Group. Tami, T., Ferlito, A., Rinaldo, A., Lee, K., and Singh, B. (1999). Laryngeal pathology in the acquired immunodeficiency syndrome: Diagnostic and therapeutic dilemmas. Annals of Otology, Rhinology, and Laryngology, 108, 214– 220. Thompson, L. (2001). Pathology of the larynx, hypopharynx and tarachea. In Y. Fu, B. M. Wenig, E. Abemayor, and B. L. Wenig (Eds.), Head and neck pathology with clinical correlations (pp. 369–454). New York: Churchill Livingstone. Vrabec, J., Molina, C., and West, B. (2000). Herpes simplex viral laryngitis. Annals of Otology, Rhinology, and Laryngology, 109, 611–614.

Instrumental Assessment of Children’s Voice
Disorders of voice may a¤ect up to 5% of children, and instrumental procedures such as acoustics, aerodynamics, or electroglottography (EGG) may complement auditory-perceptual and imaging procedures by providing objective measures that help in determining the nature and severity of laryngeal pathology. The use of


Part I: Voice

these procedures should take into account the developmental features of the larynx and special problems associated with a pediatric population. An important starting point is the developmental anatomy and physiology of the larynx. This background is essential in understanding children’s vocal function as determined by instrumental assessments. The larynx of the infant and young child di¤ers considerably in its anatomy and physiology from the adult larynx (see anatomy of the human larynx). The vocal folds in an infant are about 3–5 mm long, and the composition of the folds is uniform. That is, the infant’s vocal folds are not only very short compared with those of the adult, but they lack the lamination seen in the adult folds. The lamination has been central to modern theories of phonation, and its absence in infants and marginal development in young children presents interesting challenges to theories of phonation applied to a pediatric population. An early stage of development of the lamina propria begins between 1 and 4 years, with the appearance of the vocal ligament (intermediate and deep layers of the lamina propria). During this same interval, the length of the vocal fold increases (reaching about 7.5 mm by age 5) and the entire laryngeal framework increases in size. The di¤erentiation of the superficial layer of the lamina propria apparently is not complete until at least the age of 12 years. Studies on the time of first appearance of sexual dimorphism in laryngeal size are conflicting, ranging from 3 years to no sex di¤erences in laryngeal size observable during early childhood. Sexual dimorphism of vocal fold length has been reported to appear at about age 6–7 years. These reported anatomical di¤erences do not appear to contribute to significant di¤erences in vocal fundamental frequency ( f0 ) between males and females until puberty, at which time laryngeal growth is remarkable, especially in boys. For example, in boys, the anteroposterior dimension of the thyroid cartilage increases threefold, along with increases in vocal fold length. Acoustic Studies of Children’s Voice. Mean f0 has been one of the most thoroughly studied aspects of the pediatric voice. For infants’ nondistress utterances, such as cooing and babbling, mean f0 falls in the range of 300– 600 Hz and appears to be stable until about 9 months, when it begins to decline until adulthood (Kent and Read, 2002). A relatively sharp decline occurs between the ages of 12 months and 3 years, so that by the age of 3 years, the mean f0 in both males and females is about 250 Hz. Mean f0 is stable or gradually falling between 6 and 11 years, and the value of 250 Hz may be taken as a reasonable estimate of f0 in both boys and girls. Some studies report no significant change in f0 during this developmental period, but Glaze et al. (1988) reported that f0 decreased with increasing age, height, and weight for boys and girls ages 5–11 years, and Ferrand and Bloom (1996) observed a decrease in the mean, maximum, and range of f0 in boys, but not in girls, at about 7–8 years of age.

Sex di¤erences in f0 emerge especially strongly during adolescence. The overall f0 decline from infancy to adulthood is about one octave for girls and two octaves for boys. There is some question as to when the sex di¤erence emerges. Lee et al. (1999) observed that f0 di¤erences between male and female children were statistically significant beginning at about age 12 years, but Glaze et al. (1988) observed di¤erences between boys and girls for the age period 5–11 years. Further, Hacki and Heitmuller (1999) reported a lowering of both the habitual pitch and the entire speaking pitch range between the ages of 7 and 8 years for girls and between the ages of 8 and 9 years for boys. Sex di¤erences emerge strongly with the onset of mutation. Hacki and Heitmuller (1999) concluded that the beginning of the mutation occurs at age 10–11 years. Mean f0 change is pronounced in males between the ages of about 12 and 15 years. For example, Lee et al. (1999) reported a 78% decrease in f0 for males between these ages. No significant change was observed after the age of 15 years, which indicates that the voice change is e¤ectively complete by that age (Hollien, Green, and Massey, 1994; Kent and Vorperian, 1995). Other acoustic aspects of children’s voices have not been extensively studied. In apparently the only largescale study of its kind, Campisi et al. (2002) provided normative data for children for the parameters of the Multi-Dimensional Voice Program (MDVP). On the majority of parameters (excluding, of course, f0 ), the mean values for children were fairly consistent with those for adults, which simplifies the clinical application of MDVP. However, this conclusion does not apply to the pubescent period, during which variability in amplitude and fundamental frequency increases in both girls and boys, but markedly so in the latter (Boltezar, Burger, and Zargi, 1997). It should also be noted voice training can a¤ect the degree of aperiodicity in children’s voices (Dejonckere et al., 1996) (see acoustic assessment of voice). Aerodynamic Studies of Children’s Voice. There are only limited data describing developmental patterns in voice aerodynamics. Table 1 shows normative data for flow, pressure, and laryngeal airway resistance from three sources (Netsell et al., 1994; Keilman and Bader, 1995; Zajac, 1995, 1998). All of the data were collected during the production of /pi/ syllable trains, following the procedure first described by Smitheran and Hixon (1981). Flow appears to increase with age, ranging from 75–79 mL/s in children aged 3–5 years to 127–188 mL/s in adults. Pressure decreases slightly with age, ranging from 8.4 cm H2 O in children ages 3–5 years to 5.3–6.0 cm H2 O in adults. Laryngeal airway pressure decreases with age, ranging from 111–119 cm H2 O/L/s in children aged 3–6 years to 34–43 cm H2 O/L/s in adults. This decrease in laryngeal airway pressure occurs as a function of the rate of flow increase exceeding the rate of pressure decrease across the age range. Netsell et al. (1994) explained the developmental changes in flow, pressure, and laryngeal airway pressure

156–160. 79 girls and 85 boys. S. International Journal of Pediatric Otorhinolaryngology. Journal of Voice. P. LAR ¼ laryngeal airway resistance. I. one study provides normative data on a sample of 164 children. C.. J. (1999). open quotient—54.. K.. Green.. Hacki. closing quotient. J.3) 6.2) 6. Nuss. open quotient. Bloemenkamp. Archives of Otolaryngology–Head and Neck Surgery. Wieneke. with standard deviations in parentheses Reference N N K N N Z K N N K K N N Age (yr) 3–5 3–5 4–7 6–9 6–9 7–11 8–12 9–12 9–12 13–15 4–15 Adult Adult Sex F M F&M F M F&M F&M F M F&M F&M F M N 10 10 10 9 10 10 10 100 10 10 Flow (mL/s) 79 (16) 75 (20) 86 (19) 101 (42) 123 (30) 121 (21) 115 (42) 50–150 127 (29) 188 (51) Pressure (cm H2 O) 8. E.29) 7. Therefore. T.3 (24. This stability is remarkable in view of the major changes that are observed in laryngeal anatomy and physiology.1).82 (62. with and without education in singing. 2646–2654. and Massey. Acoustic characteristics of children’s voice. Burger.81 (2. closing quotient—14.. Z. and Bloom.2) 7. Nuss. Journal of the Acoustical Society of America. 1105–1108.4) 59 (7) 77 (23) 87. (1996). The means and standard deviations (in parentheses) for these measures were as follows: jitter—0. 35. as secondary to an increasing airway size and decreasing dependence on expiratory muscle forces alone for speech breathing with age. All data were collected using the methodology described by Smitheran and Hixon (1981).. R.. P. C. and opening quotient. L. Archives of Otolaryngology–Head and Neck Surgery.4 (1. these procedures may play a valuable role in the objective assessment of voice in children. Although EGG data on children’s voice are not abundant.9 (1. except for f0 and the aerodynamic measures. Development of the child’s voice: Premutation. (1994). Values shown are means. Milenkovic. 2. —Ray D. and Sadeghi.95) 43 (10) 34 (9) F ¼ female. See also voice disorders in children.4 (1. Aerodynamic normative data from three sources: N (Netsell et al. children are able to maintain normal voice quality in the face of considerable alteration in the apparatus of voice production. R. 107–115. 1994). H. Glaze. D. H. F0 -perturbation and f0 -loudness dynamics in voices of normal children.8). International Journal of Pediatric Otorhinolaryngology.. 10. 1975) (see electroglottographic assessment of voice). H. (1997). Apparently. L. Cheyne et al. Gender di¤erences in children’s intonational patterns. 125. H.4 (2. M ¼ male.Instrumental Assessment of Children’s Voice Table 1.. and opening quotient—31.0) 11. Kent and Nathan V.4 (1. The maintenance of rather stable values across a substantial period of childhood (from about 5 to 12 years) for many acoustic and EGG parameters holds a distinct advantage for clinical application.. and Heitmuller. mutation. . reported no significant e¤ect of age on the EGG measures of jitter. Computerassisted voice analysis: Establishing a pediatric database. 185– 190. and Z (Zajac. Dejonckere. T.. J. Tewfik. M. No consistent di¤erences in aerodynamic parameters were observed between female and male children. Ferrand. These values are reasonably similar to values reported for adults. 284– 291.. (1996). H. High standard deviations reflect considerable variation between children of similar ages (see aerodynamic assessment of voice). R.1% (4. 312–319. however.. Welham References Boltezar. although caution should be observed because of di¤erences in procedures across studies (Takahashi and Koike. One of the most striking features of the instrumental studies of children’s voice is that. 49(Suppl.5) 8. and Hillman. (1999). the values obtained from instrumental procedures change relatively little from childhood to adulthood. ages 3–16 years (Cheyne. Bless.61). Campisi. Schloss.07) 5. H.26) 7. D.. and the suitability of published normative data is open to question. International Journal of Pediatric Otorhinolaryngology... 49(Suppl. N. 1995).46 (2. P. (2002). Electroglottography in the pediatric population. Hollien. E. Electroglottographic Studies of Children’s Voice.3). 1999). 1998). 1). With the mutation. stability is challenged. and Lebacq. (1988). L. S311–S314. 130. S141–S144. R. 96. Instability of voice in adolescence: Pathologic condition or normal developmental variation? Journal of Pediatrics. 1). Longitudinal research on adolescent voice change in males. E. (1999). R..0 (1.3) 8. 128. D. It is also clear that instrumental procedures can be used successfully with children as young as 3 years of age. A. and Zargi...1% (3.1 (1. P. and Hillman. M.8% (3.4) 37 LAR (cm H2 O/L/s) 111 (26) 119 (20) 89 (25) 97 (39) 95.3 (1. G. K (Keilman & Bader. N ¼ number of participants. M.4) 7. Cheyne. 1995. and Susser. Pelland-Blais. Dejonckere.97 (2. Manoukian.3 (2. Journal of Voice.3) 5.. R. Voice problems in children: Pathogenesis and diagnosis. T.76% (0.

t. This therapy is e¤ective in least 90% of ADSD patients. and Schulte.. The posterior cricoarytenoid muscle is often involved in ABSD. Ford. Anatomic development of the craniofacial-oral-laryngeal systems: A review. 2001). 1992). 138–146. and Smith. and Emami. do not involve intermittent spasmodic changes in the voice. 1998). When acetylcholine release is blocked. Morrison. in ABSD. The toxin is injected into muscle. D. Other idiopathic voice disorders. Journal of Voice. 1988. Rather. The e¤ect is reversible: within a few weeks new nerve endings sprout.. producing voice breaks in vowels or breathy intervals in the abductor type. and Bless. which form the basis for diagnosis. a vesicle-docking protein essential for acetylcholine release into the neuromuscular junction (Aoki. Abnormalities in laryngeal adductor responses to sensory stimulation are found in both ADSD and ABSD (Deleyiannis et al. and Read. A. Development of aerodynamic aspects in children’s voice. Potamianos. 123–131. such as muscular tension dysphonia. Peters. D. 338. di¤uses.. two-thirds of ABSD patients obtain some degree of benefit from posterior cricoarytenoid . (2002). All of these conditions are idiopathic and all have distinctive symptoms. as has been demonstrated in a small randomized controlled trial (Truong et al. Muscular tension dysphonia may be confused with spasmodic dysphonia when ADSD patients develop increased muscle tension in an e¤ort to overcome vocal instability. however.. D. 138–144. and Vorperian. J. and Narayanan. with adductory movements of the vocal folds during inspiration that remit during sleep (Marion et al. 2001). E¤ects of a pressure target on laryngeal airway resistance in children. A 5-Hz tremor can be heard on prolonged vowels. (1998). (1995). Lotz. 1455–1468. BTX-A is less e¤ective in ABSD. (1975). H. voice breaks during vowels are associated with involuntary spasmodic muscle bursts in the thyroarytenoid and other adductor laryngeal muscles. owing to intensity and frequency modulation. CA: Singular/Thompson Learning. 1999). and is endocytosed into nerve endings. Takahashi.. 2000). 1991). (1995). Intermittent voice breaks are specific to the spasmodic dysphonias. which are perceived as breathy breaks. R. h). Smitheran. Brin. These nerve endings are later replaced by restitution of the original end-plates (de Paiva et al. Reductions in spasmodic muscle bursts relate to voice improvement (Bielamowicz and Ludlow. Vocal tremor is present in at least one-third of patients with ADSD or ABSD and can also occur in isolation. A variety of muscles may be involved in voice tremor (Koda and Ludlow. Kent.. 183–190. 1992). Developmental patterns of laryngeal and respiratory function for speech production. and paradoxical breathing dystonia. When voice breaks are absent. (1999). 105. 31. 1996). either prolonged glottal stops and intermittent intervals of a strained or strangled voice quality during vowels in ADSD or prolonged voiceless consonants (p. It di¤ers from vocal fold dysfunction. Y. 1999). and Stewart. Paradoxical breathing dystonia is rare. Zajac. Journal of the Acoustical Society of America. ‘‘spastic’’ dysphonia was renamed ‘‘spasmodic’’ dysphonia to denote the intermittent aspect of the voice breaks and was classified as a task-specific focal laryngeal dystonia (Blitzer and Brin. 1991) and in multiple case series (Ludlow et al.38 Part I: Voice Keilman. 31. tremor. W. and Hixon.).. Ludlow. although not in all patients (Cyrus et al. 3. L. 1999).. S. 1994). Blitzer and Brin. Acta Otolaryngolica Supplement (Stockholm). breathy breaks are due to prolonged vocal fold opening during voiceless consonants. Netsell. D. Zajac. Voice tremor occurs more often in women. R.. R. 46. In adductor spasmodic dysphonia (ADSD). In the 1980s. Some patients with voice tremor may also develop muscular tension dysphonia in an e¤ort to overcome vocal instability. A clinical method for estimating laryngeal airway resistance during vowel production. 212–213. H. Rammage. indicating a reduction in the normal central suppression of laryngeal sensorimotor responses in these disorders. BTX-A injection. either small bilateral injections or a unilateral injection produces a partial chemodenervation of the thyroarytenoid muscle for up to 4 months. (1995). When only ABSD patients with cricothyroid muscle spasms are injected in that muscle. International Journal of Pediatric Otorhinolaryngology. In ADSD. J. K. Some perceptual dimensions and acoustical correlates of pathological voices. Kent. The acoustic analysis of speech (2nd ed. 145–190. Cleft Palate–Craniofacial Journal. and Koike.. although bursts can also occur in the cricothyroid muscle in some persons (Nash and Ludlow. C. Tremor can a¤ect either or both the adductor or abductor muscles... and Bader. Lee.. The toxin cleaves SNAP 25.. 1996). San Diego. Such persons may respond to manual laryngeal manipulation (Roy. C. 1991. consistent abnormal hypertense laryngeal postures are maintained during voice production. J. f. Journal of Communication Disorders.. which is usually intermittent and often coincides with irritants a¤ecting the upper airway (Christopher et al. k. In the abductor type of spasmodic dysphonia (ABSD). J. Acoustics of children’s speech: Developmental changes of temporal and spectral parameters.. 1983. sometimes with an associated head tremor. E. Laryngeal Movement Disorders: Treatment with Botulinum Toxin The laryngeal dystonias include spasmodic dysphonia. muscle activation is normal in both adductor and abductor laryngeal muscles (Van Pelt. 1991). 1–24. T. S. ADSD a¤ects 85% of patients with spasmodic dysphonia. resulting in symptoms of both disorders. K. Journal of Medical Speech-Language Pathology. 32. Similarly. (1981). which may provide synaptic transmission and some reduction in muscle weakness. Journal of Speech and Hearing Disorders. A. the muscle fibers become temporarily denervated. Laryngeal airway resistance in children with cleft palate and adequate velopharyngeal function. 8. Botulinum toxin type A (BTX-A) is e¤ective in treating a myriad of hyperkinetic disorders by partially denervating the muscle. the other 15% have ABSD. Blitzer... s. (1994). significant improvements occur in 60% of cases (Ludlow et al.

Assessment of posterior cricoarytenoid botulinum toxin injections in patients with abductor spasmodic dysphonia. S. Laryngeal dystonia: A series with botulinum toxin therapy. K. Pharmacology and immunology of botulinum toxin serotypes. mucosal mechanoreceptor feedback will also change with reductions in adductory force between the vocal folds following BTX-A injection. Rhew. Such reductions in muscle activity and spasms may be the result of reductions in muscle spindle and mechanoreceptor feedback. Blitzer. reaching normal loudness levels as late as 3–4 weeks after injection. which reduces the force that can be exerted by a muscle following injection. Rhinology. by sipping through a straw. 163–167. voice breaks are significantly reduced. F.. for treating tremor than it is in ADSD (Warrick et al. —Christy L. maintain benefit for more than a year following injection.. Aviv. S. When speech symptoms were measured in blinded fashion before and after teatment. The breathiness resolves somewhat later. J. 406–412. F. when the patient’s voice is close to normal volume. Stewart. 2000). lasting from 3 to 5 months in ADSD but from 1 to 3 months in other disorders such as ABSD and tremor. C. K. however.. R. then. Because improvements in voice volume seem independent of recovery of swallowing. BTX-A administered as either unilateral or bilateral injections into the thyroarytenoid muscle has been used successfully to treat paradoxical breathing dystonia (Marion et al. whether the injection was unilateral or bilateral. during the period when axonal sprouting may occur (de Paiva et al. Eckert. 2001) than in ADSD (Ludlow et al. (1991). 1435–1441. J. Central control changes also appear to occur... 100.. In ADSD. L. 306. R. and Laryngology. resulting in lower motor neuron pool activity for all the laryngeal muscles. Blager.. 85–89. Laryngoscope. When objective measures were used (Warrick et al. however. Wood... C. 1999). while the side e¤ects of progressive breathiness and swallowing di‰culties increase over the 3–5 days after injection. A. K. 194– 203. 3–10.. usually occurring over a period of about 2 months during endplate reinnervation. Brin. 1994). The mechanisms responsible for benefit from BTXA in laryngeal dystonia likely di¤er with the di¤erent pathophysiologies: although BTX-A is beneficial in many hyperkinetic disorders. Annals of Otology... and Souhrada.. Raney. Most people report that benefits become apparent the second day. L. 1994). L. and Ludlow. Rhinology.. Some individuals. (1992). Bielamowicz. B. spasmodic bursts were significantly reduced on both sides of the larynx. BTX-A is much less e¤ective. L. 1998). R. although larger doses are sometimes more e¤ective.. 1999). BTX-A injection was beneficial in 50% of patients with voice tremors.Laryngeal Movement Disorders: Treatment with Botulinum Toxin 39 injections (Blitzer et al. possibly as patients learn to compensate. To maintain symptom control. (2001).. Di‰culty swallowing liquids may occur and occasionally results in aspiration. although voice loudness is not yet reduced. in persons with ADSD following BTX-A injection. and speech is more fluent. in addition to e¤erent denervation by BTX-A.. most patients return for injection about 3 months before the full return of symptoms. Christopher. The return of symptoms in ADSD is gradual. M. Perhaps changes in sensory feedback account for the longer period of benefit in ADSD than in other laryngeal movement disorders. F. the forcefulness of vocal fold hyperadduction is reduced and patients are less able to produce voice breaks even if muscle spasms continue to occur. Abductor laryngeal dystonia: A series treated with botulinum toxin.. although the duration of side e¤ects is similar in all disorders. When thyroarytenoid muscle injections were unilateral. di¤erent mechanisms may underlie recovery of these functions. Laryngoscope.. New England Journal of Medicine. 1988). Annals of Otology. Either unilateral or bilateral thyroarytenoid injections can be used. and it is rarely helpful in patients with abductor tremor.... F.. 1988). 1566–1570. The physiological e¤ects of BTX-A may be greater on the fusimotor system than on muscle fiber innervation (On et al. In all cases BTX-A causes partial denervation. Bielamowicz. C.. 1). Evans. Ludlow References Aoki. A. and Fahn. and Brin. Voice loudness and breaks gradually diminish as BTX-A di¤uses through the muscle. and Ludlow. (1983). Blitzer. 102. Botulinum toxin management of spasmodic dysphonia (laryngeal dystonia): A 12-year experience in more than 900 patients. C. Annals of Otology. C. (2001). M. it is more e¤ective in some than in others. E. (1998). 248(Suppl. B. 110. The di‰culties with swallowing gradually subside between the first and second weeks after an injection (Ludlow. S. 1992. Future approaches to altering sensory feedback may also have a role in the treatment of laryngeal dystonia. and Stewart. Grillone et al. 108. The benefit is greatest between 1 and 3 months after injection. (2000). Vocal-cord dysfunction presenting as asthma. A few persons report a sense of reduction in laryngeal tension within 8 hours following injection. Cyrus. This benefit period di¤ers among the disorders. however. Squire. E¤ects of botulinum toxin on pathophysiology in spasmodic dysphonia. Brin. Journal of Neurology. 109. A. (2001). BTX-A was less e¤ective in ABSD (Bielamowicz et al. 2000). Although only one portion of the human thyroarytenoid muscle may contain muscle spindles (Sanders et al. Rhinology. J. S. returning 2 or more years later for reinjection.. and Ludlow. with reduced hoarseness (Ludlow et al. Bielamowicz. 1992). S. C. A. and Laryngology. causing progressive denervation. Adductor muscle activity abnormalities in .. Bidus. C. Changes in laryngeal function following BTX-A injection in persons with ADSD are similar. and Laryngology. 2000).... and there were also reductions in overall levels of muscle tone (measured in microvolts) and maximum activity levels (Bielamowicz and Ludlow. R. Patients with adductor tremor confined to the vocal folds often receive some benefit from thyroarytenoid muscle BTX-A injections. and Nash. Blitzer. F. M. Patients are advised to ingest liquids slowly and in small volumes.. F.

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Botulinum toxin for essential tremor of the voice with multiple anatomical sites of tremor: A crossover design study of unilateral versus bilateral injection.. The irritable larynx syndrome. J. 113. Jankovic. P. 2262–2266. (1989). Moskowitz.. F. 37.. J. Y. Identification of symptoms for spasmodic dysphonia and vocal tremor: A comparison of expert and nonexpert judges.. Grillone. G. R.. C. Annals of Otology. Producing speech: Contemporary issues for Katherine Sa¤ord Harris (pp. 104. L. and Linden.. P. Bielamowicz. Laryngeal botulinum toxin injections for disabling stuttering in adults. Murry.. Otolaryngology–Head and Neck Surgery. Aronson. 264. and Fink. E.. C. Pakiam. J. and Ludlow. 38. M.. P. E. L. and Laryngology. and Ludlow. C.. T. Neurology. (1992). 237–252.. et al... 1–13. C. Annals of Otology. J. 24. 672–675. E¤ects of botulinum toxin injections on speech in adductor spasmodic dysphonia. Laryngoscope. A. 616–623. Neurosurgery. Pathophysiology of the spasmodic dysphonias. D. L. Rhinology. 38. Rhew.. 572– 577. Characteristics of late responses to superior laryngeal nerve stimulation in humans. and Ludlow. Ludlow. J. Brin. et al. A. M. and Jankovic. Koda. C. D.. Aoki. Baer. Ludlow. Laryngoscope. Annals of Otology. Task-specific focal tremor and dystonia: Categorization of occupational movement disorders. (1994). J. Han. Chest. Lancet. A. M. F. F. and Biller. 14. C. Sedory. E. Further Readings Barkmeier. Kirazli. 94. L.. R.. M. Botulinum toxin injection for adductor spasmodic dysphonia. 34. American Journal of Physical Medicine and Rehabilitation. Rhinology.. E... Agostino. M. and Smith. 33–42. M. On. and Hallett. (1991). Laryngoscope. Fiedler. Yamashita. 522–527.. (1991). In F. (1988). Klap. Mechanisms of action of phenol block and botulinus toxin type A in relieving spasticity: Electrophysiologic investigation and follow-up. J. Annals of Otology.....

. Stager. and modification of pathological innervation (Crumley. 271–276. S. All of the intralaryngeal muscles are innervated by the RLN. and Brin. D. (1997). F. 481–490). 1997.. Laryngoscope. J. In J. T. A¤erent fibers emanate from intramucosal and intramuscular receptors and travel along pathways that include the SLN (supraglottic larynx) and the RLN (subglottic larynx). The motor innervation of the larynx is somewhat more complicated.Laryngeal Reinnervation Procedures Sapienza. Hallett (Eds. These duties are physiologically opposite. L.. The nerve in question is identified through a transcervical approach. 1). Surely this is associated with advances in surgical optics as well as microsurgical instrumentation and technique. and its design is still being elucidated. E. A.. E. C. The larynx is further exposed after splitting the strap muscles in the midline. Sedory-Holzer. 2). Journal of Voice. 11. The internal (sensory) branch pierces the thyrohyoid membrane and terminates in the supraglottic submucosal receptors. Tureen. Stylized left lateral view of the left SLN. F.. Donovan. Howard. S. C.. who described reanastomosis of a severed RLN. 8–11. This nerve approaches the larynx from below in the tracheoesophageal groove. 41 Laryngeal Reinnervation Procedures The human larynx is a neuromuscularly complex organ responsible for three primary and often opposing functions: respiration. Branching of the SLN occurs proximally as it exits the carotid sheath. 1999). M. Indications for laryngeal reinnervation include functional reanimation of the paralyzed larynx. 95–103. Berke et al. Sensation to the supraglottic mucosal is supplied via the internal branch of the SLN. Weissler. T. but it was not until the last 30 years that reinnervation techniques were refined and became performed with relative frequency.. 250. 106. V. Adductor spasmodic dysphonia: Standard evaluation of symptoms and severity.. Speech functions are fine-tuned permutations of laryngeal opening and closure against pulmonary airflow. Autonomic fibers also innervate the larynx. 502–520. and Ludlow. Zwirner. Journal of Voice.. P.. New York: Marcel Dekker. B. S. M. Measurement of laryngeal resistance in the evaluation of botulinum toxin injection for treatment of focal laryngeal dystonia. and Martinkosky. (2000). Innervation of this organ is complex. and Murry. Anatomy and Technique of Reinnervation. (1994). L. Allen. Murry. Diamond. J. Usually a horizontal skin incision is placed into a neck skin crease at about the level of the cricoid cartilage. restoration of laryngeal sensation. The most primitive responsibilities include functioning as a conduit to bring air to the lungs and protecting the respiratory tract during swallowing. 86–92. Reinnervation of the larynx was first reported 1909 by Horsley. Aviv et al. C. Responses of stutterers and vocal tremor patients to treatment with botulinum toxin. and Woodson. E. This structure is easily identified as it pierces the thyrohyoid membrane on either side (Fig. E. The technique of reinnervation is similar for both sensory and motor systems. The anterior division supplies all of the laryngeal adductors except the cricothyroid muscle. L. 14. Figure 1. Stewart. Walton.). G. C. E¤erent fibers to the larynx from the brainstem motor nuclei travel by way of the vagus nerve to the superior laryngeal nerve (SLN) and the recurrent laryngeal nerves (RLNs). the larynx must form a wide caliber during respiration but also be capable of forming a tight sphincter during swallowing. Subplatysmal flaps are elevated and retracted.. K. prevention of denervation atrophy... Laryngoscope. and Ludlow.. M. swallowing. but these are poorly understood (see also anatomy of the human larynx). C. The external (motor) branch terminates in the cricothyroid muscle. Reports of laryngeal reinnervation spotted the literature over the next several decades. Adductor spasmodic dysphonia and muscular tension dysphonia: Acoustic analysis of sustained phonation and reading. L. The nerve enters the larynx from deep to the cricothyroid joint and immediately splits into an anterior and a posterior division (Fig.. (1996).. Blitzer. and speech. (1993). the posterior division supplies the only abductor of the . Therapy with botulinum toxin (pp. (1994). 104. A comparison of bilateral and unilateral botulinum toxin treatments for spasmodic dysphonia. European Archives of Otorhinolaryngology. F. Jankovic and M. P. 1991. S.. The swallowing side e¤ects of botulinum toxin type A injection in spasmodic dysphonia. Witsell.

and sometimes on the basis of laryngeal electromyography or radiographic imaging. The ansa cervicalis is a good example of an acceptable motor donor nerve (Crumley. The RLN divides into an anterior and a posterior division just deep to the cricothyroid joint. or neoplastic invasion of the recurrent nerve. The new motor or sensory nerve is brought into the field under zero tension and then anastomosed with several epineural sutures of fine microsurgical material (9-0 or 10-0 nylon or silk). but the condition may be due to inflammatory neuropathy. relatively few reports have demonstrated true volitional movement. The anterior division gives o¤ branches at the interarytenoid (IA) and lateral cricoarytenoid (LCA) muscles and then terminates in the midportion of the thyroarytenoid (TA) muscle. similar to an external approach to the arytenoid. 1984. 1991. Although many patients are successfully treated with various static procedures. Prior to the microsurgical age. 1983. with neurontization of the motor end-plates or the sensory receptors. This is important to avoid crushing trauma to the nerve stump. Over the past 20 years there has been increased interest in physiological restoration. the inferior cornu of the thyroid cartilage protects the RLN’s posterior division and the IA branch during further dissection. The anastomosis must be tensionfree. Selection of the appropriate donor nerve is discussed subsequently. A series of patients with unilateral vocal cord paralysis were treated with anastomosis of the distal RLN trunk to the ansa cervicalis. while the other muscles all receive unilateral innervation. The external branch of the SLN innervates the only external adductor of the larynx—the cricothyroid muscle. and McMicken. The anterior division further arborizes to innervate each of the intrinsic adductors in a well-defined order: the interarytenoid followed by the lateral cricoarytenoid. 1991. the adductor branches of the RLN can only be successfully approached after opening . The etiology is commonly idiopathic. If preserved during an anterior approach. theoretically. The diagnosis is made on the basis of history and physical examination including laryngoscopic findings. The branches to the TA and LCA are easily seen through a large inferiorly based cartilage window reminiscent of those done for thyroplasty. the best results would restore the organ to its preexisting physiological state. the thyroid cartilage. With modern techniques. Paralysis of the larynx is described as unilateral or bilateral. Once the cartilage is opened the anterior branch can be seen coursing obliquely toward the terminus in the midportion of the thyroarytenoid muscle. The donor nerve is still connected to its proximal (motor) or distal (sensory) cell bodies. The posterior division travels to the posterior cricoarytenoid (PCA) muscle. it is severed sharply with a single cut of a sharp instrument. Stylized left lateral view of the left RLN. a concept championed by Crumley (Crumley. A large inferiorly based window is made in the thyroid lamina and centered over the inferior tubercle. 1988). the posterior cricoarytenoid muscle. Sensory reinnervation is less clear. This nerve normally supplies motor neurons to the strap muscles (extrinsic accessory muscles of larynx. Identification and dissection of the fine distal nerve branches is usually carried out under louposcopic or microscopic magnification using precision instruments. 1999). Reinnervation for Laryngeal Paralysis. one can argue that. iatrogenic trauma. The posterior division is approached by rotation of the larynx. Crumley. The patient seeks care for dysphonia and aspiration or cough during swallowing. Izdebski. Although the SLN and the main trunk of the RLN can be approached without opening the larynx. end-to-end nerve-nerve anastomosis with epineural suture fixation is a superior and far more reliable technique of reinnervation. Once the damaged nerve is identified. The interarytenoid muscle is thought to receive bilateral innervation.42 Part I: Voice Figure 2.. Although physiological reinnervation is the goal. The unilaterally paralyzed larynx is more common and is characterized by a lateralized vocal cord that prevents complete glottic closure during laryngeal tasks. Berke et al. Over the next 3–9 months healing occurs. most reinnervation procedures of the larynx were carried out with nervemuscle pedicle implantation into the a¤ected muscle. The branching pattern is quite consistent from patient to patient. and lastly the thyroarytenoid muscles. one can hope to prevent muscle atrophy and help restore muscle bulk. Typically.

These patients are troubled by a fixed small airway and often find themselves tracheotomy dependent. Chhetri et al. arytenoidectomy. A laryngeal denervation and reinnervation procedure has been designed to provide a permanent alternative to Botox treatment (Berke et al. Transplantation of a physiologically functional larynx is the sought-after grail of reinnervation. Voicing issues are usually considered secondary to the airway concerns. 1997). one may see mass movement of the face with volitional movement because all the braches are essentially acting as one. 1999). however. These ‘‘bad’’ nerve stumps are then sutured outside the larynx to avoid spontaneous reinnervation. For a fully functional larynx. Animal experiments with this technique have demonstrated volitional and reflexive movement of the reinnervated vocal cord. Proponents of other techniques have argued that the ansa cervicalis may not have enough axons to properly regenerate the RLN. Chhetri et al. 1999). The majority of patients with bilateral vocal cord paralysis undergo a static procedure such as cordotomy. He suggests that the hypoglossal nerve would be more appropriate because of increased axon bulk and little donor morbidity. 1986. 1999). Fortunately. Berke . Although his results were supportive of his hypothesis. Spasmodic dysphonia is an idiopathic focal dystonia of the larynx. 1999). The size match to the RLN is excellent when using either the whole nerve bundle for main trunk anastomosis or an easily identifiable fascicle for connection to the anterior branch. Others have suggested use of the SLN as a motor source for the posterior cricoarytenoid muscle (Maniglia et al. In the facial nerve.. 1978). or tracheotomy to improve their airway. for example... Nasri et al. European groups have studied phrenic nerve to posterior branch of the RLN transfers (van Lith-Bijl et al. but volitional movement typically is not restored. 1997. The a¤ected vocal cord has good bulk. Lee. it has been shown that one of its nerve roots can be sacrificed without paralysis of the diaphragm.Laryngeal Reinnervation Procedures 43 the larynx). In the 1970s. eight nerves would be anastomosed—bilateral anterior and posterior branches of the RLN and bilateral external and internal branches of the SLN. Evaluation of these patients.. and Dahm. characterized by intermittent and paroxysmal spasms of the vocal cords during connected speech. Hemilaryngeal reinnervation with the ansa cervicalis has been shown to improve voicing in those patients undergoing the procedure (Crumley and Izdebski. and Dahm. The technique of microneural. success has been reliably achieved in the canine model (Berke et al. The RLN contains both abductor and adductor (as well as a small amount of sensory and autonomic) fibers. The phrenic nerve innervates the diaphragm and normally fires with inspiration. 1999). Unfortunately. More recently.. one may hypothesize that mass firing of all fibers cancels the firings of individual fibers out and thus produces a static vocal cord. With this concept in mind. Berke. the e¤ect of Botox is temporary. the distalmost branches of the laryngeal adductors are severed from their muscle insertion. Therapy is directed at restoring airway caliber while avoiding aspiration. microvascular. A fascicle of the ansa cervicalis is then suture-anastomosed to the distal thyroarytenoid branch for reinnervation. The mainstay of treatment for this disorder is botulinum toxin (Botox) injections into the a¤ected laryngeal adductor muscles. whose function is to elevate and lower the larynx during swallowing. many have had trouble repeating them. and mucosal anastomosis has been well worked out in the animal model. anastomosis of the greater auricular nerve to the internal branch of the SLN has been successfully used to restore sensation to the larynx (Aviv et al. Sensory Palsy. thus preventing atrophy and theoretically protecting that muscle by occupying the motor end-plates with neurons una¤ected by the dystonia. With reinnervation. Tucker advocated reinnervation of the posterior cricoarytenoid with a nerve muscle pedicle of the sternohyoid muscle and ansa cervicalis (Tucker. 1993) and partially achieved in one human (Strome et al. with about 95% of patients achieving freedom from further therapy. Clinically. Although most practitioners currently treat with static techniques. Recent work has highlighted the importance of laryngeal sensation.. Laryngeal Transplantation. 1999). Lee. it was shown that patients with stroke and dysphagia have a high incidence of laryngosensory deficit. when the ansa cervicalis is sacrificed. After development of an air-pulse quantification system to measure sensation. 1998). Most techniques of reinnervation for bilateral vocal cord paralysis still have not enjoyed the success of unilateral reinnervation and are only performed by a few practitioners. 1992.. 1994. Paniello has proposed that the ansa cervicalis is not the best donor nerve to the larynx (Paniello. does not demonstrate restoration of normal muscular physiology. some have recommended combining reinnervation with another static procedure to augment results (combination with arytenoid adduction) or to avoid the potential for synkinesis by performing the anastomosis of the donor nerve to the anterior branch of the recurrent nerve (Green et al. Studies performed in the laboratory demonstrated that reanastomosis of the internal branch of the SLN restored protective laryngeal reflexes (Blumin. Blumin and Gerald S. Reinnervation maintains tone of the thyroarytenoid. Synkinesis refers to mass firing of a motor nerve that can occur after reinnervation. Current research has been aimed at preventing transplant rejection. To date. or that synkinesis has occurred (Paniello.. Neurological bilateral vocal cord paralysis is often post-traumatic or iatrogenic. The majority of patients have the adductor variety.. In this procedure. Modification of Dystonia. 1989).. and repeated injections are needed indefinitely. —Joel H. This approach has had great success. the patient does not have noticeable disability. physiological restoration would be preferred. 2001). and Blackwell.

D. 110. Laryngeal abductor reinnervation with a phrenic nerve transfer after a 9-month delay. L. Chhetri. Kawamura. G. 99. Crumley. Groenhout. M. Recovery of laryngeal sensation after superior laryngeal nerve anastomosis. T. R. Zhou. and Berke. H. R.. T. L. Hicks. K. Gerratt. Rhinology.. (1997). and Laryngology. L. K. Peterson. B.. M. Ford. F. R. Crumley. J. R. 111. (2000). P. 598–604. (1991).. T. Hanson. M. 88. (1993). and Sercarz. Jacobs. and Biller. Annals of Otology. C. 104. Marie.. Wu. R.. Hypoglossal nerve transfer for laryngeal reinnervation: A preliminary study. histochemistry. Tucker... and Sercarz. J.. 251–256. E. 365–371. D. H. (1991). Annals of Otology. and Blackwell. F. H. Sercarz.. Update: Ansa cervicalis to recurrent laryngeal nerve anastomosis for unilateral laryngeal paralysis.. (1984). G. Voice quality following laryngeal reinnervation by ansa hypoglossi transfer. M. 517–529. Gerratt. (1999)... D. 103. F. and Laryngology. J. Green. S. K.. (1999). M. (1991). 109. R.. Rhinology. Osso¤.. Archives of Otolaryngology–Head and Neck Surgery. and Andrieu-Guitrancourt. (1999). European Archives of Otorhinolaryngology. and McMicken. Annals of Otology. and Coltrera. (1998). Transactions of the Southern Surgical Gynecology Association. Berke. Sanders.... 516–521. B. 611–616. and retrograde labeling in a canine model. 101. E. Clinical Anatomy. Rhinology.. Groenhout. M. Laryngeal transplantation and 40month follow-up. J. J. D.. Annals of Otology. Crumley.. Selective laryngeal reinnervation with separate phrenic and ansa cervicalis nerve transfers. 98. Paniello. L. Rhinology. 96... M. and Laryngology. J. Wenokur. Y. Burkey. 907–909. J. Paniello. 109. L. (1997).. A. E. Archives of Otolaryngology–Head and Neck Surgery. and Mahieu. Blitzer. S. Konings. Annals of Otology. Graves. 1676–1679... Berke. 466–474. 532–542. Manek.. Kreyer. 124.. Ye. 87–92. Annals of Otology. R. (2001). R. 857–864. S. 797–806. R. West. and Sercarz. Physiologic motion after vocal cord reinnervation: A preliminary study.. Crumley. Gould. (1997). Rhinology. Orthotopic laryngeal transplantation: Is it time? Laryngoscope. (1989). Selective laryngeal adductor denervation-reinnervation: A new surgical treatment for adductor spasmodic dysphonia. B. Y. Archives of Otolaryngology–Head and Neck Surgery.. P. Rhinology. Horsley.. Cervical anatomy of phrenic nerve roots in the rabbit. C.. L. Gerratt. 93.. N. W.. Maniglia. Crumley. Annals of Otology. M. Andrews. 79– 82. P. 1187–1193. S. and Berke. Laryngoscope.. 123. Netterville. R. Laryngoscope. 117. W. References Aviv. (1978).. G. J. 106.. Rhinology.44 Part I: Voice van Lith-Bijl. Izdebski... Sercarz. Long-term preservation of voice improvement following surgical medialization and reinnervation for unilateral vocal fold paralysis. J.. and Laryngology. (1996).. N. H. Rhinology. 116. Physiologic motion after laryngeal nerve reinnervation: A new method. (1999). Annals of Otology. P. R.. and Lee. P. Otolaryngology–Head and Neck Surgery. 1113–1117. S. Tadie. Phrenic nerve graft for bilateral vocal cord paralysis. K. R. W. (1989). Laryngoscope. M. Lee. I.. B.. 1928–1936.. and Laryngology.. B. L. (1992). Annals of Otology.. (1983). M. H. B.. 102. Laryngoscope. S. 22. J.. 108. W. A.. J. and Mahieu. J. Katirji. Cuan. A. A. J.. 13. Crumley. Ye. M. P. N. B. (1998).. C. Blumin. G. S. Otolaryngology–Head and Neck Surgery. 239–244.. Laryngoscope. Evaluation and treatment of the unilateral paralyzed vocal fold. J. 1522– 1527.. Archives of Otolaryngology–Head and Neck Surgery.. L. 108. 515–520. L. R. L. Mohr. Nasri. R. Block. H. D. 406–411.. D. B. M. Z. H. J. G.. et al. Kreiman. Stein. and Dahm. 227–231. Sloan... and Laryngology. 393–398. S... Verneil.. H. K. 113. Braun. 497–508. and Rosenbaum. 384–387. (1990).. J. M. L. P. A. F. Crumley. C. C. Ye. H. (1998). Strome.. Nerve transfer versus Teflon injection for vocal cord paralysis: A comparison.. Dodds. 108. S. Tucker. (1988). J. M. M. Laryngoscope. R. K. Otolaryngology–Head and Neck Surgery. and Wen. Crumley. Nasri... M. Kreiman. R. Laryngoscope. A. Laryngeal reinnervation with the hypoglossal nerve: I. et al. Dehesdin. 167–174. Li. K.. R. E.. and Mahieu. J. I. A. electromyography. S. Stolk. Berke. Muscle transfer for laryngeal paralysis: Restoration of inspiratory vocal cord abduction by phrenicomohyoid transfer. H.. and Laryngology. R. D. Nguyen. M.. (1986).. C. 109. 154–160. G. J. Graves. Rhinology. S. C. L. (1994). Tonnaer. J. 123. L. Combined arytenoid adduction and laryngeal reinnervation in the treatment of vocal fold paralysis. M. (1999). 255. Weed. C. S. Sorensen. R. and Laryngology. Osso¤.. D. 93. . and Berke. Restoration of laryngopharyngeal sensation by neural anastomosis. L. Tonnaer. Reinnervation of the allograft larynx in the rat laryngeal transplant model. (2000). Blackwell. Newer technique of laryngeal reinnervation: Superior laryngeal nerve (motor branch) as a driver of the posterior cricoarytenoid muscle. Laryngeal synkinesis following reinnervation in the rat: Neuroanatomic and physiologic study using retrograde fluorescent tracers and electromyography. Laryngeal synkinesis revisited. C. Reinnervation of the canine posterior cricoarytenoid muscle with sympathetic preganglionic neurons.. G. S.. E. (1909). J. Ye. 889–898. 1637–1641... Izdebski. G. 13.. Konings. D. 14–22. Downs. Objective measures of laryngeal function after reinnervation of the anterior and posterior recurrent laryngeal nerve branches. Lerosey. S. (2001). L. Zheng. Flint. J. Anastomosis between the external branch of the superior laryngeal nerve and the recurrent laryngeal nerve.. R. R. Journal of Voice. E¤ects of arytenoid adduction on laryngeal function following ansa cervicalis nerve transfer for vocal fold paralysis in an in vivo canine model. Laryngoscope. 351–356. 161–167.. Laryngoscope. et al... 100. (1994). Crumley. 3443. Laryngoscope. J. D. Lorenz. J.. and Laryngology. and Close. Annals of Otology. B. Esclamado. 425–428. 108. Update: laryngeal reinnervation for unilateral vocal cord paralysis with the ansa cervicalis. J. Chongkolwatana. Suture of the recurrent laryngeal nerve with report of a case. Reinnervation aspects of laryngeal transplantation. Rhinology. Laryngoscope. A. A. 1200–1204. Y. R. (1995). S. (1999)... Natividad. H. Physiology. Thomson.. R. Human laryngeal reinnervation: Long term experience with the nerve muscle pedicle technique.. D. A. N. van Lith-Bijl. Further Readings Benninger. T. Selective reinnervation of vocal cord adductors in unilateral vocal cord paralysis. M. 98. and Pomaroli. M. and Laryngology.. A. K.. Laryngeal synkinesis: Its significance to the laryngologist. Berke. G. New England Journal of Medicine. van Lith-Bijl. R. Jackson. Stolk. J. 98. R.

alveolus. In cases of blunt trauma to the larynx. and this treatment may have negative consequences on vocal and speech functions. Thus. Li. and auditory-perceptual components is essential. 119.. articulatory. and the like. Y. The treatment itself has clear potential to a¤ect speech production. the severity of impairment.. floor of the mouth. Blunt laryngeal trauma is most commonly reported in persons less than 30 years old. In some instances. and potentially deglutition and swallowing. additional surgical treatment may be warranted.g. S. deglutition. Z.Laryngeal Trauma and Peripheral Structural Ablations Zheng. Head and neck squamous cell carcinoma may occur in the epithelial tissue of the mouth. Because of the possibility of disease spread. when necessary. Estimates in the literature indicate that acute laryngeal trauma accounts for 1 in 15. medical intervention is first directed at determining airway patency and. Traumatic injury and surgical treatment for disease also may a¤ect isolated structures of the peripheral speech mechanism. When injuries are severe.. and swallowing may exist. lacerations of soft tissues. tongue. Speech management initially focuses on identifying which subsystems are impaired. the literature in this area is sparse. dysphagia. assessment methods typically employed with the dysarthrias may be most appropriate (e. Chen.. the primary presenting symptoms are hoarseness. and velum.g. Trauma to the mandible also can directly impact verbal communication. they may invade adjacent tissue.000 to 1 in 42. (1998). which may result in penetrating injuries not only of the larynx but also of other critical structures in the neck. which frequently requires more extensive . Injuries may involve fractures of laryngeal cartilages. Zhou. 1992). As tumors increase in size. radiation therapy is commonly used to eliminate occult disease. although when they do occur. and monitoring patient progress. changes in speech. Otolaryngology–Head and Neck Surgery. The majority of head and neck cancers involve squamous epithelial tissue. developing management strategies. in addressing any type of traumatic injury to the peripheral structures of the speech mechanism. or larynx. causes include motor vehicle collisions. nasal cavity. Tumors of the head and neck account for approximately 5% of all malignancies in men and 2% of all malignancies in women (Franceschi et al. maintaining an adequate airway through emergency airway management (Schaefer. These tumors have the potential to be invasive. Peripheral Structural Changes Resulting from Surgical Ablation In contrast to peripheral structural changes due to traumatic injury. the airway is of primary concern. However. therefore. no matter how minor. 1991). but changes in speech may be variable and ultimately depend on the structures treated. Laryngeal trauma is truly an emergency medical condition. structural changes due to surgical ablation for oral cancer also result in alterations in functions necessary for speech or swallowing. such injuries or their medical treatment may have a significant impact on speech. pain. holds real potential to a¤ect breathing. the literature on the dysarthrias often provides a useful framework for establishing clinical goals and evaluating treatment e¤ectiveness. Laryngeal Trauma Trauma to the larynx is a relatively rare clinical entity. S.. When airway compromise is observed. and the consequent reduction in speech intelligibility and communicative proficiency. and Cuan. A large number of such traumatic injuries are the result of accidental blunt trauma to the neck.000 emergency room visits. athletic injuries. or resonance system consequent to traumatic injury or the treatment of disease can significantly alter the functions of both voice and speech. pharynx.. acoustic. articulatory. or may have more widespread influences on entire speech subsystems (e. such as shooting or stabbing. Dworkin. In other instances these changes may result in dramatic alteration of one or more anatomical structures necessary for normal voice and speech production. and swelling of the tissues of the neck (cervical emphysema). Another portion of these injuries are the result of violence. velopharyngeal) and the related structures necessary for competent and e¤ective verbal communication. or combined types of injury. in addition to other oral functions. An experimental comparison of di¤erent kinds of laryngeal muscle reinnervation. whereas vocal disturbances are possible. 540–547. Although the clinical literature is meager in relation to injuries of the lip. subsequent changes to the larynx and oral peripheral system may be relatively minor and without substantial consequence to the individual. 45 Laryngeal Trauma and Peripheral Structural Ablations Alterations of the vibratory. and radical dissection of regional lymphatics is often required. Because of variability in the extent of traumatic injuries. and information on speech outcomes following injuries of this type is frequently anecdotal.. 1979). partial or complete dislocations. Information from each of these areas is valuable in identifying the problem. emergency tracheotomy is common. H. Unfortunately. A comprehensive evaluation that involves aerodynamic. the potential for spread of disease is substantial. In this regard. Speech Considerations. changes to the voice are of secondary importance. dyspnea (shortness of breath). Because laryngeal trauma. Malignant Conditions A¤ecting Peripheral Structures of the Speech System. 2000). the point-place system may provide essential information on the extent and degree of impairment of speech subsystems (Netsell and Daniel. hard palate. Injuries to the intrinsic structures of the oral cavity are also rare. falls.

Slowing the speech rate may help to augment articulatory precision in the presence of such defects following surgical treatment. others report pain. The destructive nature of a malignant tumor may cause adjacent muscular structures of the tongue or floor of mouth to become fixed. respiration. the potential for metastatic spread of disease is substantial. cell type. Healing and other e¤ects of treatment also need to be addressed during this period. Surgery for traumatic injury or tumors that invade the mandible. surgery may be necessary to debride infected tissue or to remove damaged bone. changes to the lip and alveolus may certainly limit the production of specific speech sounds. Although defects of the alveolus may be augmented quite well prosthetically. if the lesion is extensive and destructive. Palliative care focuses on pain control and maintaining some level of nutrition. function. In other situations.. Johnson. with a resulting decrease in salivary flow leading to a dry mouth (xerostomia). but regional spread of cancer to the mandible from other oral structures is not uncommon.. often with profound influences on oral communication. The literature in this area is scant to nonexistent. among others. while at the same time creating significant cosmetic deformities. which in turn improves vascularity. The primary deficit observed is velopharyngeal incompetence due to structural defects that eliminate the ability to e¤ectively seal the oral cavity from the nasal cavity (Brown et al. Once primary medical treatment (surgery. with distant spread. Defects in the alveolar ridge or lip may have variable e¤ects on speech and general oral function. or di‰culty breathing. when larger resections are performed on the tongue (partial or total glossectomy) or floor of the mouth.g. which is likely to result in loss of sensation (paresthesia). In both circumstances. However. Current treatment protocols for tumors involving structures of the peripheral speech mechanism include surgery. When considerable portions of both the hard and the soft palate are removed.g. drink. may be altered by surgical ablation of these structures.. Because surgical extirpation of maxillary tumors may involve extensive resection. di‰culty swallowing (dysphagia). Defects of the Tongue.g. Radiation delivered to the head and neck a¤ects both abnormal and normal tissues. during which the postsurgical anatomy changes and the prosthesis is changed in tandem. labiodental sounds). Surgical reduction of the gum ridge (alveolus) as well as the hard and soft palates may occur. Osteoradionecrosis may be decreased if the radiation exposure is limited to less than 60 cGy (Thorn et al. thus reducing tissue damage and related osteoradionecrotic changes following extractions (Marx. with a subsequent need for grafting. and floor of the mouth is frequently more radical than surgery for injuries or tumors of the maxilla. sounds that rely on pressure build-up (e. Isolated mandibular tumors are rare. This therapy facilitates oxygen uptake in blood and related tissues. Large resections and reconstructions also increase the potential for speech disruption because of limited mobility of the reconstructed areas (e. disease stage. Each treatment modality is associated with some additional morbidity that can significantly a¤ect structure. radiotherapy. radiotherapy) has been completed. which usually cause significant discomfort to the individual. stop-plosive sounds). 2000). and attain some level of functional speech. the integrity of the oral valve for articulatory shaping and the subsequent demands of the resonance system are substantially a¤ected. tongue. or pain. or chemotherapy. reconstruction with one of a variety of flap procedures is necessary. or sounds that require a fixed position for continuous generation or oral airway turbulence (e. Lip.g. the tumor may encroach on the nerve supply. Salivary glands may be damaged. the goals of rehabilitation are to maintain or restore anatomical structure and physiological function. In some cases. and Kline. Alveolus. however. Hyperbaric oxygen therapy is sometimes used to reduce the degree of osteoradionecrosis (Marx. and other factors. and subsequent treatment is contraindicated.. For example. swallowing. Extended lesions involving the mandible often require surgical resection. radiotherapy is commonly associated with a range of side e¤ects. 2000).46 Part I: Voice treatment because of the threat of distant spread of disease. resections are often substan- . Focal excisions may not result in any significant level of noticeable change in deglutition. more significant surgical resections of the hard and soft palate frequently have a dramatic influence on speech production. alone or in combination. The choice of modality usually depends on tumor location.. tissue changes. and quality of life. Floor of Mouth. However.. Rehabilitation involves a multidisciplinary team and occurs over several months. Because cancer has invaded bone. paralysis. lingual-alveolar sounds). which may result in dental caries following radiation treatment. Such procedures vary in the extent of resection and may be performed transorally or transfacially. 1985). cosmesis. Defects of the Maxilla and Velum. or infection. Surgery is the preferred method for treating cancer of the maxilla. The goals of rehabilitation include reducing the surgical defect through prosthetic management so that the individual can eat. these types of problems can be addressed using methods commonly employed for articulation therapy. Osteoradionecrosis may result in the exposure of bone. a significant reduction in the essential struc- tures for speech may exist post-treatment. 1983b). and human dignity. or speech. Similarly. portions of the tongue). 1983a. This decrease in saliva may then challenge normal oral hygiene and health. anterior sounds in which the lip is an active articulator (e. Surgery carries a clear potential for anatomical and physiological changes that may directly alter speech and swallowing. and Mandible. Some individuals are asymptomatic at the time of diagnosis. palliative care may be initiated instead. The mandible and tongue are movable structures that are intricately involved in swallowing and speech production. In many instances.

the devices must be created so that they do not impede normal breathing. The initial obturator is maintained for 1–2 weeks. Gillis and Leonard. The surgical obturator allows careful packing of the wound site. As each component of the system is assessed. Prosthetic rehabilitation for jaw defects resulting from injury or malignancy is essential (Adisman. treatment may disrupt neural processes. amplitude. Surgical treatment of maxillary tumors can result in a variety of problems postsurgically. This is typically a multistage process. Leonard and Gillis. Total or partial removal of the tongue (glossectomy) or resection of the anterior maxilla or mandible results in significant speech impairment. Reduction of surgically induced velopharyngeal incompetence is essential to enhancing residual speech capabilities. with the first obturator being placed in situ at the time of surgery. 1993. For soft palate defects.g. 1999. and spectral moments. 1989). attempts to facilitate this ability may be achieved by constructing a ‘‘palatal drop’’ prosthesis. 1990). speech assessment must evaluate the motor capacity as well as the capacity of the sensory system. subsequently requiring reconstruction with donor bone or plate reconstruction methods. These devices serve both speech and swallowing by helping to reduce velopharyngeal defects. Sills.. certain factors may alter the course of rehabilitation. prosthetist. 1977. The individual may then have greater ability to make the necessary oral contacts to improve articulatory precision and speech intelligibility (e. Leeper and . this obturator will be maintained permanently (Desjardins. Prosthetic adaptations of this type may also benefit eating and swallowing. as this creates problems in fitting and retention of the prosthesis. leakage of food or drink into the nasal cavity significantly disrupts eating and drinking. Tobey and Lincks. and Charles. changes in the mobility of the mandible pose a risk for changes in the overall acoustic structure of speech due to changes in oral resonance. Speech Assessment Systematic assessment of the peripheral speech mechanism includes formal evaluation of all subsystems— respiratory. In addition to the obvious defects in the structural integrity of the peripheral oral mechanism. is of clinical value (Gillis and Leonard. Although some minor adjustments to the definitive prosthesis are not uncommon. this area is not well documented in the clinical literature. Fabrication of a prosthesis is more di‰cult when teeth are absent. 1983). Again. In order for speech improvement to occur. As such. Early oral rehabilitation is essential. 1989). Leeper and Gratton. laryngeal. When reductions in the ability of the tongue to approximate superior structures of the oral cavity exist after treatment. particularly following larger resections of the maxilla. 1982. 1982. mandibular reconstructions may permit the individual to manipulate the mandible with relative e‰ciency for speech and swallowing movements. Acoustic considerations relative to speech intelligibility should also be addressed in this population using tools developed for the dysarthrias (Kent et al. Acoustic analysis. The results of peripheral structural ablations of the oral speech system are best addressed using the methods recommended for treatment of the dysarthrias (e. such surgical defects reduce articulatory precision and change the acoustic structure of speech because of changes in the volume of the vocal tract as well as resultant hypernasality and nasal emission (abnormal and perhaps excessive flow of air through the nasal cavity). Because respiration is paramount. Such a prosthesis is useful in patients who have healed after undergoing a maxillectomy or maxillary-mandibular resection.. Additionally. 1989). the surgical defect must be augmented with a prosthesis.. and radiologist. head and neck surgeon. and swallowing without a nasogastric tube. However. Together. prosthodontist. intraoral prostheses for those with surgical defects of peripheral oral structures seek to maintain the oral and nasal cavities as separate entities and to reduce velopharyngeal orifice area. 1999). auditory-perceptual evaluations of speech or voice parameters. changes in symmetry may emerge that may influence chewing and swallowing. its relative contributions to the overall speech deficits observed can be better defined for purposes of treatment monitoring.. which may result in secondary problems. keeps food and other debris from entering the wound. Aramany et al. 1978. drinking.. Anderson et al. Prosthetic Management of Surgical Defects. Kent et al. This may be compounded by di‰culties in chewing food or by dysphagia. Prosthetic Management. 1992). For example. early prostheses can be modified throughout the course of treatment to facilitate swallowing and speech. When the jaw is disrupted. To optimize the care of each patient. including both a¤erent and e¤erent components of the system. Most individuals use the interim device until complete healing has occurred and related treatments are completed. at which time an interim device is fabricated. and measures of speech intelligibility (Leeper. the expertise of multiple professionals. usually anywhere from 3 to 6 months after surgery. However. speech-language pathologist. In general.g. which elicit information on the aeromechanical relationship to oral port size and tongue–hard palate valving (Warren and DuBois.. However. for reasons that go beyond speech concerns. velopharyngeal. and allows immediate oral communication (Doyle. so that nutritional problems must always be considered. including evaluation of formant frequency. At this time a final or definitive obturator is fabricated. and articulatory. Oral Articulatory Evaluation. which supplements lingual inability by bringing the new hard palate inferior in the oral cavity. these types of changes to the peripheral oral structures will almost certainly result in decreased speech intelligibility and communication. permits eating. 1982.Laryngeal Trauma and Peripheral Structural Ablations 47 tial. is necessary. 1964). Subsystem evaluation may entail instrumentally based assessments (speech aerodynamics and acoustics). including a dentist.

Shockley. Netsell. F. A. Beery. Use of Netsell and Daniel’s (1979) physiological model allows the clinician to identify the relative contribution of each speech subsystem and to target appropriate therapy techniques in an e¤ort to optimize the system... Desjardins... Journal of Laryngology and Otology. Prosthodontic management of maxillofacial and palatal defects. J. Early rehabilitative management of the maxillectomy patient.. Archives of Otolaryngology–Head and Neck Surgery. External laryngeal trauma analysis of 392 patients. Louis: Mosby. (1999). P. Curtis. Osteoradionecrosis of the mandible: A review. and Lincks. 110–118.. J. Severe laryngeal injury cased by blunt trauma to the neck: A case report. R. and Ayslan. J. Baltimore: Williams and Wilkins. P. Journal of Oral and Maxillofacial Surgery. L. Austin.. Tobey.. and Sills.. Zlotolow. Leeper. McNally. Prosthetic management of the head and neck cancer patient. and . Q.. (1979). 107.. 1. and Tibrewala. (1993). 2. (1989). Dysarthria in adults: Physiologic approach to rehabilitation. In J. 23. G. American Journal of Otolaryngology. R. 920–923. Cleft Palate Journal. Journal of SpeechLanguage Pathology and Audiology. W... Journal of Prosthetic Dentistry.. and Bastholt. J. Gillis. J. 808–814. 39. M. Golz. E. E. 62. Huryn. Batsakis. R... Flax-Goldenberg. R. (1992). G. In K. J. Sills.. Oral prosthetic rehabilitation of individuals with head and neck cancer: A review of current practice. R. D.. S. D. Journal of the American Dental Association. W. 1991). and Rutledge. 41. Leeper. Prevention of osteoradionecrosis: A randomized prospective clinical trial of hyperbaric oxygen vs. R. 485–496. N. Bidoli. A modified classification for the maxillectomy defect. Batsakis (Ed.. (1979). (1999). Specht.. 52–71. (1983a). S. 877–880. 125.. J. R. G. 41. 36. 48. and Gratton. S. Oral cavity reconstruction: An objective assessment of function... V. (1999). D. Prosthetic treatment for speech and swallowing in patients with total glossectomy. (1983). P. S. Journal of Prosthetic Dentistry. Franceschi. 13. Louis: Ishiyaki EuroAmerica. A. 96. 109–116. Kent. San Diego. M. 38. D. Osteoradionecrosis: A new concept of its pathophysiology. Hassan. Maxillofacial rehabilitation: Prosthodontic and surgical considerations. and Daniel..). S. Dental Clinics of North America. S. R. Laryngotracheal trauma. 660–665. J. 351–357... Marx. 34. 23. D. Such evaluations aid in fine-tuning prosthetic management. J. J. A. 50. and Sutherland. —Philip C. 111. J. A. G.. Gratton. Goldenberg. and Charles. (1982). A. Warren. Foundations of voice and speech rehabilitation following laryngeal cancer (pp. P. Head and Neck. Archives of Physical Medicine and Rehabilitation. E. 111. J. Prosthesis serviceability for acquired jaw defects. E. Jewett. A. Assessment of quality of life in head and neck cancer patients.. R. Toward phonetic intelligibility testing in dysarthria. S. L.. D. V. Journal of Speech and Hearing Disorders. P. Shah. G. and Leonard. T. (1993). Schaefer. R. 78–81. Thorn. Kornblith. B. J. (1990). and Marunick. Canadian Journal of Oncology. Prosthodontic rehabilitation for glossectomy patients. 1999). S.). Dworkin. C. (1985).. T. S. (1978). direct speech treatment goals may include improving the control of the respiratory support system for speech. Leeper.. A. and related tasks that seek to improve intelligibility. and Boyle. (1996). Head and Neck.. E. 283–288. E. Downs. 118. F. 117–133. 449–455. 47. Tumours of the head and neck: Clinical and pathological considerations (2nd ed. Haribhakti. 311–318. J.. Hansen. 15. P. and Rosenbek.. C. 482–499.. 145). R. H. Acoustic analyses of speech changes after maxillectomy and prosthodontic management. (1983b). Kavarana. Anderson. Journal of Oral and Maxillofacial Surgery. Gooen. Squamous cell carcinomas of the oral cavity and the oropharynx. H. I. W.. R. A new concept in the treatment of osteoradionecrosis. G. Motor speech disorders: A treatment guide. Comparison of cancers of the oral cavity and pharynx worldwide: Etiological clues. 15. A pressure-flow technique for measuring velopharyngeal orifice area during spontaneous speech.. 22. B. Doyle. penicillin. modulating vocal intensity to improve oral resonance. E. Strong. P. Awde.. 424–435. 60. Cleft palate: Interdisciplinary issues and treatment (p. (1994).. Journal of Speech and Hearing Disorders.48 Part I: Voice Leonard. Spiro. A. R. N. The physiologic approach also permits continuous evaluation of each component in a comparative manner for prosthesis-in and prosthesis-out conditions. A. N. improving intelligibility through overarticulation. J. 97–122). and DuBois. H. Marx. (1993). S. and Kline. A. A. (2000). P. Herrero. (1997). Jurkovich. (1982). C. Z. (1989). Lerner. 1088–1093. I. S. Osteoradionecrosis of the jaws: Clinical characteristics and relation to the field of irradiation. Cherian. 54. Doyle.. Further Readings Balogh. T. CA: Singular Publishing Group. 119–124. W. 25–29. Moller and C. Johnson. (1986). (2000). and Weymuller. S. and Joachims. (1983). M. R. Beumer. (1992). Rogers. Treatment goals may best be achieved by using the methods previously described for the dysarthrias (Dworkin. and Luterman. Doyle References Adisman. 106–115.. 17–26. Head and Neck. Journal of Speech-Language Pathology and Audiology. (1993). J. B. 265–284. B. D. Brown... The acute management of external laryngeal trauma. Kent. (1964). E. N. 82. T. 598–604. Weismer. D. J. N. (1991). H.. M. Laryngoscope. E. Once obturation occurs. R. Journal of Prosthetic Dentistry. 58. Archives of Otolaryngology–Head and Neck Surgery. J. Journal of Oral and Maxillofacial Surgery. TX: Pro-Ed. Gussack. P.. A. (2000).. H. R. Journal of Laryngology and Otology. R. 49–54.. External laryngeal trauma: Analysis of 30 cases. increasing the accuracy of specific sound production (or potentially the directed compensation of sound substitutions). Desjardins. E¤ects of a prosthetic tongue on vowel intelligibility and food management in a patient with total glossectomy. St. Postlaryngectomy speech rehabilitation: Contemporary concerns in clinical care. D. 1174–1176. J. Journal of Prosthetic Dentistry. and Munoz. Obturator design for acquired maxillary defects. Aramany. and Gillis. Marx. J. Oral Oncology.). C. determining and maintaining the optimal speech rate. M. A. (1977).. D. 502–508. St. and Raman.. Journal of Prosthetic Dentistry. H. Starr (Eds.. R.

Oral and Maxillofacial Surgery Clinics of North America. Baker. progressive relaxation. B. and emotional inhibition (Case. 323–334. Comparison of maxillectomy patients with immediate versus delayed obturator prosthesis placement. 9. E. Postglossectomy deglutitory and articulatory rehabilitation with palatal augmentation prosthesis. 1998. S. E. P.. B. and Iko. 4. Cleft Palate Journal. and Sullivan. Longitudinal assessments of quality of life in laryngeal cancer patients. 1999... (1989). K. Dysphagia. M. J. Obturator prostheses after cancer surgery: An approach to speech outcome assessment. R. and Docherty. Head and Neck. A. Gunther et al. A.. and he or she is reassured regarding the absence of any structural laryngeal pathology.. J. T. J. Bowman. Mahanna. 18. It is asserted that the larynx. Journal of Otolaryngology. 1996). Wedel. Milutinovic. A. K. A. Yontchev. Horsley. 279–285. Journal of Speech and Hearing Research. and relieve pain and discomfort associated with muscle spasms. Beukelman.. R. (1979). J.. 310–316. (1998). and Krugler. Once the larynx is ‘‘released’’ and range of motion is normalized. 49 Psychogenic Voice Disorders: Direct Therapy Psychogenic voice disorder refers to a voice disorder that is a manifestation of some confirmed psychological disequilibrium (Aronson. 308–312. L.. Because excess or dysregulated laryngeal muscle tension is frequently o¤ered as the proximal cause of the psychogenic voice disorder. M. whispered speech) or partial voice loss (dysphonia). 1997. Logemann. Davis. 2000). 4. is vulnerable to excess or poorly regulated musculoskeletal tension arising from stress.. promote local circulation with removal of metabolic wastes. Carlsson. Sandor. 1996. Warren. P. (1987). Colangelo. the precise mechanisms underlying such psychologically based disorders have not been fully elucidated (see functional voice disorders for a review). In its purest form. 36. B. (1989). Rademaker. Heiser. Marshall. Speech and velopharyngeal function. 1990).. G. 1993.. O. A... R. E¤ects of intraoral prosthetics on swallowing in patients with oral cancer. 1992. Roy et al... and Close. 2000). (1994). with associated pain and discomfort when the circumlaryngeal region is palpated.. 118–120. Matz. Masticatory function in patients with congenital and acquired maxillofacial defects. F. and Ow. R. List. Lapointe. R. systematic kneading of the extralaryngeal region is believed to stretch muscle tissue and fascia. Gaebler. PERCI: A method for rating palatal e‰ciency. J. 267–276. Head and Neck. Before symptomatic therapy is begun. 18. visual and electromyographic biofeedback. and Jacob... the clinical voice literature is replete with evidence that symptomatic voice therapy for psychogenic disorders can often result in rapid and dramatic voice improvement (Koufman and Blalock. D. S. L. G. J. Circumlaryngeal massage is one such treatment approach. Andersson and Schalen. A.. Pauloksi. 388–393. McConnel. 1982. Pauloski. Acute management of laryngeal trauma. B. (1993). 1990. Hurst. Lampe. Roy and Leeper. Robbins. the psychogenic voice disorder is not associated with structural laryngeal changes or frank central or peripheral nervous system pathology. and Logemann. situational conflicts.. C. H. The following discussion considers voice therapy techniques aimed at directly alleviating vocal symptoms without specific attention to the putative psychological dysfunction underlying the disorder. 113. Aronson (1990) and Roy and Bless (1998) have described manual techniques to determine the presence and degree of laryngeal musculoskeletal tension. Roy and Bless (1998) also recently described a number of manual laryngeal reposturing techniques that can stimulate improved voice . 147–165. Journal of Prosthetic Dentistry. (1996). Carding and Horsley. conflict. M.. Logemann.e. The management of acute laryngeal trauma. H. 303–308. Skillfully applied. Stemple. 16. and circumlaryngeal massage aimed at reducing or rebalancing such tension (Boone and McFarlane.. et al. G. P... (1997). The confident clinician provides brief information regarding the therapy plan and the likelihood of a positive outcome. Speech and swallowing function after anterior tongue and floor of mouth resection with distal flap reconstruction. many voice therapies including yawn-sigh resonant voice therapy. 1214–1218. D. Prolonged hypercontraction of laryngeal muscles is often associated with elevation of the larynx and hyoid bone. Journal of Prosthetic Dentistry.. Carding. The hypothesized physical e¤ect of such massage is reduced laryngeal height and sti¤ness and increased mobility. Leeper. A. Such dysregulated laryngeal muscle tension can interfere with normal voice and give rise to complete aphonia (i. the discussion typically includes some explanation of the untoward e¤ects of excess or dysregulated muscle tension on voice production and its probable link to stress. 448–452. J. chewing therapy. Quality of life of maxillectomy patients using an obturator prosthesis. and Laryngology.. 79.. K. Myers. and Carmichael. Journal of Trauma. M. 98–104. fear. Schaefer.. Ritter-Sterr. Although numerous theories have been o¤ered to explain psychogenic voice loss. Light. 98. W. J. C. and Taylor. J. (1996). 1–10. the laryngological findings are reviewed with the patient.Psychogenic Voice Disorders: Direct Therapy Holland. (1987).. Journal of Prosthetic Dentistry. by virtue of its neural connections to emotional centers within the brain. Kahrilas. 72.. An explanation of the problem is then provided by the clinician.. G. (1997). A. Cardinale. In a similar vein. A. (1996). Rhinology. proportional improvement in voice is said to follow. Functional assessment testing for maxillofacial prosthetics. Improvement in voice and reductions in pain and laryngeal height suggest a relief of tension (Roy and Ferguson. or other psychological precursors that were identified during the interview. D. J. Despite considerable controversy surrounding causal mechanisms. as well as methods to relieve such tension during the diagnostic assessment and management session. Aronson. While the specific approach and emphasis vary among clinicians. M. 77. H. C. Archives of Otolaryngology–Head and Neck Surgery. C. 1990. B... Annals of Otology.. 25. C. M. 2001). A. relax tense muscles. S.

Aphonia and extreme tension. and patient motivation and tolerance. 1988). The rate of improvement during therapy for psychogenic voice disorders varies. Second. sigh. only the symptom of psychological disturbance has been removed. Digital cues can then be faded and the patient taught to rely on sensory feedback (auditory. and review possible causes of the problem and the prognosis for maintaining normal voice. Once this brief but relatively normal voice is reliably achieved. Once the larynx is correctly positioned. listening for any brief moments of clearer voice. cough. . Although signs of improvement should typically be observed within the first session. Of the few investigations that exist. not much is known about whether one therapy approach for psychogenic voice disorder is superior to another. For instance. Kinzl. 1962. and the clinician provides immediate feedback regarding the positive change. if the underlying psychological triggers are no longer active. the nature of psychological dysfunction needs to be better understood. These brief moments of voice improvement associated with laryngeal reposturing maneuvers are immediately identified for the patient and reinforced. discuss the patient’s feelings about the improved voice. 1995. During this process. 1993. Horsley. Finally. 1998. yet display normal voicing for vegetative or nonspeech acts. however. Ramig and Verdolini. 1996). the results regarding the durability of voice improvement following direct therapy are mixed (Gunther et al. it is shaped and extended into sustained vowels. Case. and Rammage. it would be logical to expect that such persistent factors would increase the probability of future recurrences (Nichol. When improved voice is elicited. emotional. Any partial relapses or return of abnormal voice during the therapy process can be dealt with by reassurance. Biebl. Andersson and Schalen. direct symptomatic therapy for psychogenic voice disorders can produce rapid changes. 1994). As a caveat. if significant secondary gain is present. Andersson and Schalen. the restored voice is usually maintained without compensatory e¤ort and may improve further during conversation. the better the prognosis. and proprioceptive) to maintain improved laryngeal positioning and muscle balance. Certainly. the patient needs to be an active participant and is encouraged to continually selfmonitor the type and manner of voice produced. 1998). gargle. it may be more di‰cult to eliminate the abnormal symptoms. 1997. Therefore. post-treatment referral to a psychiatrist or psychologist may be necessary to achieve more enduring improvements in the patient’s emotional adjustment and voice function (Butcher. If months or years have elapsed. to mention only a few. intensive treatment session or several sessions. It should be acknowledged that following direct voice therapy. If the situational. the foregoing observations have rarely been studied in any objective manner. some aphonic and severely dysphonic patients may be able to clear the throat. may be easier to modify than intermittent or mild dysphonia. 1993. kinesthetic. yet others report more frequent posttreatment recurrences. Other patients will appear to experience sudden return of voice without necessarily transitioning through phases of decreasing severity (Aronson. Morrison. words. and then conversation about any topic and with anyone in the clinical setting. and oral reading. some patients may need an extended. Colton and Casper. clinician experience and confidence in administering the approach. Certain patients with psychogenic dysphonia and aphonia appear to have lost kinesthetic awareness and volitional control over voice production for speech and communication purposes. 1997). recovery of normal voice can occur rapidly. Du¤y. 1996. however. 1996. Because there are few studies directly comparing the e¤ectiveness of specific therapy techniques. laugh. then. therefore they are best regarded as clinical impressions rather than factual statements. 1999). not the disturbance itself (Brodnitz. the time between the onset of voice problem and the initiation of therapy may be important.. then normal voice should be established quickly and improvement should be sustained (Aronson. and Raven. 1983. and Rauchegger. the clinician should debrief the patient regarding the cause of the voice improvement. Roy et al.. Finally. the more extreme the voice symptoms. it is instantly reinforced. this may interfere with progress and contribute to a poorer treatment outcome. When this phase of intervention is successful. Therefore. according to some authorities. verbal reinstruction. in some cases. 1990). or manual cueing. grunt. In symptomatic therapy. Third. 1998. Elias. and Docherty. depending on several variables. These e¤orts follow a trial-and-error pattern and require the seasoned clinician to be constantly vigilant. simple phrases. First. the patient is then engaged in casual conversation that begins with basic biographical information and proceeds to brief narratives. Such preserved voicing for nonspeech purposes represents a clue to the capacity for normal phonation. The goal of these voice maneuvers is to elicit even a brief trace of clearer voice so that it may be shaped toward normal quality or extended to longer utterances. The anecdotal clinical literature suggests that the prognosis for sustained removal of abnormal symptoms in psychogenic aphonia or dysphonia may depend on several factors.. the better the prognosis for improvement. The long-term e¤ectiveness of direct voice therapy for psychogenic voice disorders also has not been rigorously evaluated (Pannbacker.50 Part I: Voice and briefly interrupt patterns of muscle misuse. The sooner voice therapy is initiated following the onset of the voice problem. or produce a high-pitched squeak with normal or nearnormal voice quality. Roy et al. hum. including the therapy techniques selected. Most clinicians report that relapse is infrequent and isolated. or personality features that contributed to the development of the psychogenic voice disorder remain unchanged following behavioral treatment. Carding. Fex et al. 1990.. in some cases voice therapy can be a frustrating and protracted experience for both clinician and patient (Bridger and Epstein. If established. the patient is asked to produce such vocal behaviors. Patients may progress gradually through various stages of dysphonia on their way to normal voice recovery. 1998).

K. P. and Blalock. E. Fex.. McGrory. and Schalen. N. A. N. The voice source is a complex tone composed of a series of harmonic partials of amplitudes decreasing by about 12 dB per octave as measured in flow units. (1997). N. A. 240–244. 81–92. S101–S116. 22. and management. M. Stemple. Baltimore: Williams and Wilkins. and Epstein. C. D. Ramig. Biebl. (1990).. F0. length and sti¤ness of the vocal folds. C. 40. Case. Du¤y. A comparative study of psychological aspects of recurring and non-recurring functional aphonias. and Ferguson. H. D.. D. (1999). such that higher pitches .. P. (1994). which occur in the absence of structural laryngeal pathology. C. Journal of Voice. Manual circumlaryngeal therapy for functional dysphonia: An evaluation of short. An evaluation study of voice therapy in non-organic dysphonia. (1993). Functional voice disorders: A review of 109 patients. A study of the e¤ectiveness of voice therapy in the treatment of 45 patients with nonorganic dysphonia. and Littlejohns. K. Breathing. the two lowest formant frequencies determine vowel quality. N. TX: Pro-Ed. and Kinzl. H.. See also functional voice disorders.. Bless. Tasko. direct symptomatic therapy for psychogenic voice disorders can produce rapid and remarkable restoration of normal voice. L. Springfield. S. 225–230. Current Opinion in Otolaryngology and Head and Neck Surgery.. (1998). O. These voice disorders. Roy. Acoustic analysis of functional dysphonia: Before and after voice therapy (Accent Method).. (1992). 169–175. J. D. D. San Diego. Gunther. (1982). and Laryngology. Roy. —Nelson Roy References Andersson. Voice treatment techniques: A review and recommendations for outcome studies. Boone. D.. J. (1992). The voice source is mainly controlled by three physiological factors. Carding. I.. Functional aphonia: Psychosomatic aspects of diagnosis and therapy. New York: Thieme.. 11. (1998). 453–481).. Bless. L.. S. Raven. Voice and speech disorders: Medical aspects (pp.. Elias. L.. and Ford. J.. 12. A.. Psychogenic voice disorder unresponsive to speech therapy: Psychological characteristics and cognitivebehaviour therapy. 151–155.. Brodnitz.. (1997). Etiology and treatment of psychogenic voice disorder: Results of a follow-up study of thirty patients. 96–106. 253. P. and the degree of glottal adduction. (2001). M. R. Clinical voice disorders: An interdisciplinary approach (3rd ed. D. and Hearing Research. M. M. N.. Aronson. Schalen. European Journal of Disorders of Communication. Fex. Carding. 6.... Shiromoto. Heisey. (1996). Yeatman. H. respectively. Journal of Voice. J. Journal of Voice. San Diego. Roy. Folia Phoniatrica. Treatment e‰cacy: Voice disorders. J. 163– 167.). 17.The Singing Voice 51 In summary.. Journal of Laryngology and Otology. D. 321–331. J. S. and Bless. 137–158. Motor speech disorders: Substrates. and Docherty. R. and McFarlane. (1996). (1990). (2000).. 242–249. Boston: Allyn and Bacon. Rhinology. 1145–1148. Journal of Voice.). while the higher formant frequencies belong to the personal voice characteristics. L. 9. It is also varied with F0. Interdisciplinary approach to functional voice disorders: The psychiatrist’s role. Horsley. and Casper. Folia Phoniatrica. A. 131–137. 49–64. Pannbacker. S. Journal of Speech. (1998). (1987). H. 91. Kinzl. (1962). A.. 7. (1993). E¤ects of the manual laryngeal musculoskeletal tension reduction technique as a treatment for functional voice disorders: Perceptual and acoustic measures. Psychological correlates of functional dysphonia: An evaluation using the Minnesota Multiphasic Personality Inventory. W. N. and Andersson. and Verdolini. and Rammage. Language.. V. F. 7. M. J. Manual circumlaryngeal techniques in the assessment and treatment of voice disorders. K. Subglottal pressure determines vocal loudness and is therefore used for expressive purposes in singing. A. 11. These frequencies are determined by the vocal tract shape. and Rauchegger. British Journal of Disorders of Communication. R. (1998). Di¤erential diagnosis and treatment of psychogenic voice disorder. often represent some of the most severely disturbed voices encountered by voice pathologists. 108. Understanding voice problems: A physiological perspective for diagnosis and treatment. J. A.). Functional disorders of the voice. R. The Singing Voice The functioning of the voice organ in singing is similar to that in speech. Austin. Elias. C. I. Morrison. IL: Charles C Thomas. Journal of Voice. Clinical management of voice disorders (3rd ed. 8. and Leeper. M. Colton. 27. subglottal pressure. The voice and voice therapy (6th ed. R. Journal of Voice. (2000).). Louis: Mosby. M. Nichol.. In an experienced clinician’s hands. European Archives of Otorhinolaryngology. Roy. 42. F. Results of vocal therapy for phononeurosis: Behavior approach. Voice therapy: Clinical studies (2nd ed. Annals of Otology. St.. Thus. Bridger. Butcher. M.. F.. and Raven. CA: Singular Publishing Group.and long-term treatment outcomes. Levin (Ed. 643–647. 72–104. N. (1996). Z. CA: Singular Publishing Group. and Ford..). psychogenic voice disorders are powerful examples of the intimate connection between mind and body. Otolaryngology–Head and Neck Surgery.. These control parameters determine vocal loudness. O. Roy. and mode of phonation. P. Clinical Otolaryngology. the origin of the sound is the voice source—the pulsating airflow through the glottis..). For most vowel sounds. A. 372–377. G. (1988). 443–451. Heisey. P. (1993). Much remains to be learned regarding the underlying bases of these disorders and the long-term e¤ect of direct therapeutic interventions. D. J. 173–177. R. Butcher. Mayr-Graft. Miller. 13. 97.. M. Classification and approach to patients with functional voice disorders. (1995). American Journal of Speech-Language Pathology. Milutinovic. Formant frequency changes following manual circumlaryngeal therapy for functional dysphonia: Evidence of laryngeal lowering? Journal of Medical Speech-Language Pathology.. di¤erential diagnosis. and Hirano. M.. It propagates through the vocal tract and is thereby filtered in a manner determined by its resonance or formant frequencies. and Horsley. K. Koufman. Psychogenic voice disorders and cognitive behaviour therapy. 41(Suppl. (1983). In N. L.

varies with lung volume. The pitch perceived from a vibrato tone corresponds to its average F0. This phonation mode is often referred to as breathy. adapting it to both loudness and pitch. classically trained singers use an average lung volume range that is more than twice as large and occasionally may vary from 100% to 0% of the total vital capacity in long phrases. Because much higher lung volumes are used in singing than in speech.5 or 2 kPa. The slope of the source spectrum is determined mainly by the negative peak of the di¤erentiated flow waveform. The airflow waveform of the voice source is characterized by quasi-triangular pulses. no more than about 15%–20% of the total lung capacity is used. airflow escapes the glottis during the quasi-closed phase. loud tones. At low lung volumes. Subglottal pressure is determined by active forces produced by the breathing muscles and passive forces produced by gravity and the elasticity of the breathing apparatus. In addition. A main characteristic of classical singing is the vibrato. Thus. 1). subglottal pressures in singing are varied over a larger range than in speech. It corresponds to a quasi-periodic modulation of F0 (Fig. Instead. The modulation frequency. and vibrato extent tends to increase by about 15 cent per decade. The opposite extreme— that is. As the elasticity forces change from exhalatory at high lung volumes to inhalatory at low lung volumes. produced when the folds close the glottis more or less completely (Fig. The amplitude gain of higher partials is greater than that of lower partials. if the sound level of a vowel sound is increased by 10 dB. the partials near 3 kHz typically increase by about 17 dB. however. Thus. This type of phonation has been called flow phonation or resonant voice. singers’ vibrato rates tend to decrease by about one-half hertz per decade of years. The vibrato is generated by a rhythmical pulsation of the cricothyroid muscles. In classical singing.52 Part I: Voice are sung with higher subglottal pressures than lower pitches. where the categories are scale tones or the intervals between them. This steepness is linearly related to the subglottal pressure in such a way that a doubling of subglottal pressure causes an SPL increase of about 10 dB. lung volumes above FRC are preferred. In speech. This generates a source spectrum with strong high partials and a strong fundamental. This is in sharp contrast to speech. a firmer adduction produces a smaller air volume in a pulse. As a consequence. such that a continuous variation in F0 is heard as a continuous variation of pitch. inhalations are started from FRC. which reduces the amplitude of the fundamental. This generates noise and produces a strong fundamental. on the other hand. Figure 1. In tidal breathing. while in loud speech subglottal pressure may be raised to 1. It represents the main excitation of the vocal tract. . or F0 Á 2 1=6 . Voice Source. Whereas in conversational speech. frequently referred to as the maximum flow declination rate. Thus. where subglottal pressure is much more constant. for a given subglottal pressure. mostly between 5 and 7 Hz. At high lung volumes. is generally referred to as the vibrato rate and is rather constant for a singer. The acoustic significance of the waveform is straightforward. Singers therefore need to develop a virtuosic control of the breathing apparatus. generated by the lungs and the rib cage. singers may use pressures as high as 4 or 6 kPa for loud tones sung at high pitches. Curiously enough. on the other hand. The peak-to-peak modulation range is varied between nil and less than two semitones. and so raise F0. Typical flow glottogram showing transglottal airflow versus time. One possibility is that it emanates from a cocontraction of the cricothyroid and vocalis muscles. This phonation mode is generally referred to as hyperfunctional or pressed. In both speech and singing. the habitual use of too faint adduction—is called hypofunctional and prevents the vocal folds from closing the glottis also during the vibratory cycle. elasticity contributes an inhalatory force. As a result. elasticity produces an exhalatory force that may amount to 3 kPa or more. pitch is perceived categorically. Elasticity. these muscles cause a stretching of the vocal folds. 2). When contracting. This lung volume is called the functional residual capacity (FRC). pressed phonation is occasionally used for high. Thus. With increasing age. The air volume contained in a flow pulse is decisive to the amplitude of the source spectrum fundamental and is strongly influenced by the overall glottal adduction force. singers need to vary subglottal pressure constantly. An exaggerated glottal adduction thus attenuates the fundamental. apparently for expressive purposes. they reach an equilibrium at a certain lung volume. it tends to increase somewhat toward the end of tones. and followed by horizontal portions near or at zero airflow. pressed phonation is typically avoided. In nonclassical singing. In music. pitch is perceived in a continuous fashion. produced when the vocal folds open the glottis. singers seem to strive to reduce glottal adduction to the minimum that will still result in glottal closure during the closed phase. singers need to deal with much greater exhalatory elasticity forces. The neural origin of this pulsation is not understood.

which contribute significantly to the characteristic voice qualities of these classifications. and no singer’s formant is produced. As F2 of the vowel [i] is mainly dependent on the pharynx length. more speechlike formant frequencies are used. Typical ranges for basses. The formant frequencies in classical singing di¤er between voice classifications. If this resonance is appropriately tuned. 3). The singer’s formant spectrum peak is particularly prominent in bass and baritone singers. Lowering the larynx lengthens the pharynx cavity. such that individual singers’ voices are di‰cult to discern. each of which corresponds to a scale tone.5 and 3 kHz. The center frequency of the singer’s formant varies between voice classifications. a marked spectrum envelope peak between approximately 2.6. it will provide a formant cluster. such that the vowel quality approaches that of the vowel [y]. Figure 2. respectively. sopranos do not seem to produce a singer’s formant. Resonance. and the center frequency of a scale tone is 2 1=12 higher than its lower neighbor. The width of each scale tone is approximately 6% wide. apparently depending on the musical context. whose voices are supposed to blend. it tends to be about 2.The Singing Voice 53 Figure 3. Example of vibrato. These di¤erences probably reflect di¤erences in vocal tract length. basses have lower formant frequencies than baritones. The approximate pitch range of a singer is about two octaves. it can be regarded as a manifestation of vocal economy.5 kHz followed by a descent of about 9 dB per octave toward higher frequencies (Fig. These formant frequency deviations are related to the singer’s formant. probably reflect di¤erences in vocal tract length. F4. Spectra of the vowel [u] as spoken and sung by a classically trained baritone singer. The demands for pitch accuracy are quite high in singing. it will be lowered by a lowering of the larynx. This corresponds to less than one-tenth of a typical vibrato extent. Its resonance frequency can be somewhere between 2. baritones. Thus. If the area ratio between the larynx tube opening and the pharynx approximates 1 : 6 or less. and F5. 2. who have lower formant frequencies than tenors. The target F0 generally agrees with equal-tempered tuning. 4). the larynx tube acts as a separate resonator in the sense that its resonance frequency is rather insensitive to the crosssectional area in the remaining parts of the vocal tract. These di¤erences. where the soloist is provided with a sound amplification system that takes care of audibility problems. so that the singer’s formant makes the singer’s voice easier to perceive. where the interval between adjacent scale tones corresponds to the F0 ratio of 1 : 2 1=12 . It is produced by a clustering of F3. that appears in all voiced sounds produced by classically trained male singers and altos (Fig. In nonclassical singing. A common method to achieve a wide pharynx seems to be to lower the larynx. the sound level of an orchestra is comparatively low in the frequency region of the singer’s formant. the target F0 for a scale tone may deviate from its value in equal-tempered tuning by about a tenth of a semitone interval. the second formant of the vowel [i] is generally considerably lower in classical singing than in speech. For example. This clustering seems to be achieved by combining a narrow opening of the larynx tube with a wide pharynx.4. Also. As the singer’s formant is produced mainly by vocal tract resonance. baritones. Therefore. Thus. However. the F0 continuum is divided logarithmically into a series of bins. . tenors. In tenors and altos it is less prominent and in sopranos it is generally not observable.07 of a semitone interval. It does not appear in nonclassical singing.5 and 3 kHz. and tenors. The formant frequencies also deviate from those typically found in speech. which is typically observed in classically trained singers.8 kHz for basses. The singer’s formant seems to serve the purpose of enhancing the voice when accompanied by a loud orchestra. and 2. The long-term-average spectrum of a symphonic orchestra typically shows a peak near 0. or 0. Experts generally find that a tone is out of tune when it deviates from the target F0 by more than about 7 cent. On average. it is absent or much less prominent among choral singers.

In reality. implicated various vocal abuses as the primary causes of voice disorders. Singers. more implied and deduced than specific. In 1911. Most isolated vowel sounds can be correctly identified up to an F0 of about 500 Hz. they often need medical attention. Yet vowel identification is surprisingly successful also at high F0. Principles of voice production. and resort to a widening of the jaw opening when the e¤ect of this neutralization of the articulation fails to produce further increase of F1. Health Risks.54 Part I: Voice References Sundberg. The thin solid curve shows a rough approximation of a corresponding analysis of neutral speech at conversational loudness. we can take vocal hygiene to mean the science of vocal health and the proper care of the vocal mechanism. The 29th edition of Dorland’s Medical Dictionary defines it as ‘‘the science of health and its preservation. Above this frequency. Thus. Luchsinger and Arnold (1965) stressed the need for attention to the physiological norm as the primary postulate of vocal hygiene and preventive laryngeal medicine. For other vowels. Instead. DeKalb. Because F1 and F2 are decisive to the perception of vowels. Also relevant would be their use of high subglottal pressures. Vocal hygiene. Another classic text was Diseases and Injuries of the Larynx. hormones. this is achieved by widening the jaw opening. Concern was raised about the e¤ects of tobacco. (1987). singers seem first to reduce the tongue constriction of the vocal tract. Long-term-average spectrum of an orchestra with and without a tenor soloist (heavy solid and dashed curves). An inappropriate vocal technique. Because singers are extremely dependent on the perfect functioning of their voices. and surgical treatment is mostly considered inappropriate. identification deteriorates quickly and remains low for most vowels at F0 higher than 700 Hz. NJ: Prentice Hall. the wider the jaw opening. faulty habits. text intelligibility can be greatly improved by consonants. F3–F5 (175– 698 Hz). See also voice acoustics. A frequent origin of their voice disorders is a cold. also tends to cause voice disorders. Subsequently.’’ Thus. Persons who are educated about the structure and function of the phonatory mechanism are better able to grasp the need for care to restore it to health and to maintain its health. Although there are commonalities among vocal hygiene programs regardless of the pathophysiology of the voice disorder. Such nodules generally disappear after voice rest. (1994). In it the author. vocal hygiene is but one spoke in a total therapy program that also includes directed instruction in voice production techniques. This implies that F0 is often higher than the typical value of F1 in some vowels. until quite recently. they increase F1 so that it is always higher than F0. loud and excessive talking. —Johan Sundberg . The ideas about vocal hygiene expressed in this book were similar to those expressed in the current literature. the higher the pitch. focuses on changing an individual’s vocal behavior. sometimes associated with a habitually exaggerated glottal adduction or with singing in a too high pitch range. IL: Northern Illinois University Press. Titze. In some instances. these authors discussed the importance of this type of attention not only for teachers and voice professionals. I. J. alcohol. but also for children in the classroom. described many magical prescriptions used by famous singers to care for their voices. seem to avoid the situation in which F0 is higher than F1. In addition to the nature of the voice disorder. and cited rest and refraint from the behavior as the appropriate treatment. however. altos. however. and C4–C6 (262–1047 Hz). For the vowel [a]. The authors. which typically causes dryness of the glottal mucosa. G2–G4 (98–392 Hz). Englewood Cli¤s. The science of the singing voice. the substantial departures from the typical formant frequency values in speech a¤ect vowel identification. a German work by Barth included a chapter with detailed discussion of vocal hygiene. however. Remarkably. on the other hand. Patient education and vocal hygiene are both integral to voice therapy. Vocal Hygiene Vocal hygiene has been part of the voice treatment literature continuously since the publication of Mackenzie’s The Hygiene of Vocal Organs. in 1886. and sopranos are E2–E4 (82–330 Hz). which in some cases may lead to developing vocal nodules. the goal of patient education is understanding. and diet on the voice. factors Figure 4. virtually all voice texts have addressed the issue of vocal hygiene. More frequently. the science on which these ideas are based was. Despite long-held beliefs about the value of certain activities most frequently discussed as constituting vocal hygiene. that pathophysiology should dictate some specific di¤erences in the vocal hygiene approach. C3–C5 (131–523 Hz). a noted otolaryngologist. respectively. published in 1942. This disturbs the normal function of the vocal folds. a therapy program may be based completely on vocal hygiene. Both the general public and professionals in numerous disciplines commonly use the term hygiene. Jackson and Jackson.

radiation therapy. Environmental hydration facilitates the vocal fold vibratory behavior. Treatment may include dietary changes. Although this is clearly a medical treatment. fried foods. avoiding frequent throat clearing and other phonotraumatic behaviors. and Hanson (2000) noted the presence of mucous glands in the tissue of the vestibular folds and observed that these glands distribute a very important layer of lubricating mucus to the surface of the vocal folds. Jiang. These e¤ects may explain vocal fold injuries. as such. It is now common practice for patients scheduled for any laryngeal surgery to be placed on a preoperative course of antireflux medication that will be continued through the postoperative healing stage. the less air pressure is required and the greater is the ease of pho- nating. must also inform specific aspects of the vocal hygiene program. Rehydration by dripping saline onto the folds restored the oscillations. mainly because of the increased water content in this mucous layer and in the superficial epithelium. and excessive food intake have all been implicated in exacerbating the symptoms of laryngopharyngeal reflux. demonstrating the need for hydration and surface moisture for lower PTP. chronic throat clearing. . Both PTP and self-perceived vocal e¤ort were lower after hydration. which increases the secretions in and around the larynx and lowers the viscosity of those secretions. by which the hydration of vocal fold mucosa and the viscosity of the vocal folds are directly involved in the e¤ort required to initiate and maintain phonation. Other major components of vocal hygiene programs are reducing vocal intensity by eliminating shouting or speaking above high ambient noise levels. vocal nodules. Ca¤eine. pre or post). there appear to be a number of mechanisms. rapid removal of significant amounts of body water increased PTP and was associated with symptoms of mild vocal dysfunction in some patients. tobacco. lifestyle modifications. Viscosity is increased by hydration and decreased by drying—hence the importance of vocal fold hydration to ease of phonation. it appears that the body has robust cellular and neurophysiological mechanims to conserve the necessary hydration of airway tissues. External or superficial hydration may occur as a by-product of drinking large amounts of water. vocal hygiene programs that address healthy diet and lifestyle and that include reflux precautions appear to be well-founded. 2001). and Hanson (1999) showed that vocal fold oscillations cease in a matter of minutes in fresh excised canine larynges deprived of humidified air. This lends support to the widespread belief that loud and excessive voice use. and whether the vocal hygiene training stands alone or is but one aspect of a more extensive therapy process. 1994). the lower the phonation threshold pressure. It also supports the view that teachers and others in vocally demanding professions are prone to vibration overdose. and. Thus. including chronic or intermittent dysphonia. such as the most e¤ective method of hydration. Moreover. phonation threshold pressure. In a study of patients undergoing dialysis. and indeed other forms of harsh vocal productions. Reflux. (1990. not yet fully understood. tissue injury will probably ensue. Clearly. should be a focus of all vocal hygiene programs. Restoration of the body fluid reversed this trend (Fisher et al. 1991). Gastric acid and gastric pepsin. This was explored further in phonation by Jiang and Titze (1994). both gastroesophageal and laryngopharyngeal. the stage is set for cyclic tissue injury. Hydration and environmental humidification are particularly important to the health of the voice. issues of collision and the impact forces associated with increased loudness and phonotraumatic vocalization are appropriately addressed in vocal hygiene programs and in directed therapy approaches. have been found in refluxed material. Verdolini et al. Many questions remain in this area. viscosity is a measure of the resistance to deformation of the vocal fold tissue. The complexity of vocal physiology suggests a direct connection between viscosity and hydration. and the reduction in mucus production in aging. and the e¤ects of collision and shearing forces. Laryngopharyngeal reflux has been implicated in a long list of laryngeal conditions. alcohol. (PTP is the minimum subglottal pressure required to initiate and maintain vocal fold vibration. and malignant tissue changes. 1994) studied PTP in normal speakers subjected to hydrating and dehydrating conditions. and medication. a¤ects the health of the larynx and pharynx. The greater the viscosity of vocal fold tissue..Vocal Hygiene 55 such as timing of the program relative to surgery (i.) For example. Thus. can cause vocal fold pathology. the speech-language pathologist should provide information and supportive guidance through vocal hygiene instruction to ensure that patients follow the prescribed protocol. Both environmental humidity and surface hydration are important physiological factors in determining the energy needed to sustain phonation.. vocal fatigue. In one light. Titze (1994) theorized that if a vibrational dose reaches and exceeds a threshold level in a predisposed individual. Ng. Thus.e. The viscosity of secretions is thickened with ingestion of foods or medications with a drying or diuretic e¤ect. reflux laryngitis. Surgery is usually a treatment of last resort. Steam inhalation and environmental humidification further hydrate the surface of the vocal folds. and eventual voice or tissue change. with inadequate recovery time. Lin. A number of authors have studied the e¤ects of hydration and dehydration of vocal fold mucosa and viscosity of the folds on phonation threshold pressure (PTP). repair. and mucolytic agents may decrease the viscosity of the vocal folds. the latter implicated in the delayed healing of submucosal laryngeal injury (Koufman. The force of collision (or impact) of the vocal folds has been described by Titze (1994) as proportional to vibrational amplitude and vibrational frequency. Jiang. particularly with long-term vocal use that involves increased impact stress on the tissues during collision and shearing stresses (Jiang and Titze. who showed that intraglottal contact increases with increased vocal fold adduction. the higher the PTP that is required and the greater is the internal friction or shearing force in the vocal fold. inadequate fluid intake. Thus.

Pathologie und Hygiene der Menschlichen Stimme und Sprache. experienced significant improvement.. (1965). K. J.56 Part I: Voice pepsin in the development of laryngeal injury. which then deflates. Although the vocal hygiene group showed changes in the desired direction on all dependent measures. Chan. 51–59. L. (1942). 37. Jiang.. 8. (2001). London: Macmillan. D. An unanswered question is whether a vocal hygiene therapy program alone is adequate treatment for vocal problems. This allows frogs to produce multiple calls from the same volume References Barth. Titze. Casper Vocal Production System: Evolution The human vocal production system is similar in broad outline to that of other terrestrial vertebrates. Titze. birds. Otolaryngologic Clinics of North America. 101(Suppl. H. S. Englewood Cli¤s. E. Chan (1994) reported that a group of non-voice-disordered kindergarten teachers did show positive behavioral changes following a program of vocal education and hygiene. Jiang.. (1994). returning the air to the lungs. Gray. All tetrapods (nonfish vertebrates: amphibians. J. Phonatory e¤ects of body fluid removal.. and Stemple.. Simon. J. reptiles. This bears out the received wisdom that it is easier to take a pill—or wear an amplification device—than to change habits. 1985). Journal of Speech.. Journal of Voice. J. Voice-speechlanguage. The underlying rationale for vocal hygiene is su‰ciently compelling that a vocal hygiene program should continue to be a component of a broad-based voice therapy intervention. (2) a larynx that acts primarily as a quick-closing gate to protect the lungs. the study results suggest that the benefits of amplification may have exceeded those of vocal hygiene instruction. Measurement of vocal fold intraglottal pressure and impact stress. J.. M. or ‘‘buccal pumping. The lungs and attendant respiratory musculature provide the air stream powering phonation. (1886). A. 53). C. New York: Macmillan. J. In primitive air-breathing vertebrates. 13. and Hearing Research. and Jackson.. Journal of Voice. 286–296. The hygiene of vocal organs. 1993). CA: Wadsworth.. Phonation is typically powered by passive deflation of the elastic lungs. N. 132–144. K. Principles of voice production. It should be noted that the vocal hygiene program used in this study. N. (2001). (1911). Corbin-Lewis... Roy et al. C. 8. M. the lungs were inflated by rhythmic compression of the oral cavity. A. Sobecks. M. The functioning of the basic tetrapod vocal production system can be understood within the theoretical framework of the myoelastic-aerodynamic and source/filter theories familiar to speech scientists. D. Changes in phonation threshold pressure with induced conditions of hydration. Journal of Speech. 44. V. Luchsinger. Language. and Hanson. Ligon. 142–151. the amplification group reported higher levels of extraclinical compliance with the program than the vocal hygiene group. Dove. The otolaryngologic manifestations of gastroesophageal reflux disease: A clinical investigation of 225 patients using ambulatory 24 hr pH monitoring and an experimental investigation of the role of acid and . might more appropriately be described as a patient education program. and Hearing Research. D. The e¤ects of rehydration on phonation in excised canine larynges. Diseases and injuries of the larynx... Although study results are mixed. Mackenzie. An evaluation of the e¤ects of two treatment approaches for teachers with voice disorders: A prospective randomized clinical trial. Dependence of phonatory e¤ort on hydration level. Leipzig: Thieme. Journal of Voice. S. (1994). and often secondarily to produce sound. Titze. Most pairwise contrasts directly comparing the e¤ects of the two approaches failed to reach significance. being purely didactic and requiring no activity on the part of the participants. birds. 1–78. Jiang.. (1990).’’ and this system is still used by lungfish and amphibians (Brainerd and Ditelberg. Inspiration by active expansion of the thorax evolved later.. C. and Titze.. K. Ng. Fisher. Lin. and Arnold. Koufman. and Rose. Tanner. D. (1999). 354–367. Journal of Voice. E.. D. in the ancestor of reptiles. This was powered originally by the intercostal muscles (as in lizards or crocodilians) and later (in mammals only) by a muscular diaphragm (Liem. R. there is insu‰cient evidence to suggest that vocal hygiene instruction be abandoned. D. E. W. Einfuhrung in die Physiologie. Toledo. Roy et al. J. Verdolini. Journal of Speech. (2001). and Hanson. 44. L. and mammals) inherit from a common ancestor three key components: (1) a respiratory system with lungs. —Janina K.. Roy. however. Belmont. R. air expired from the lungs during phonation is captured in an elastic air sac. 44. Language. R. Of note.. K. Language. Vocal fold physiology.. Teachers who received a directed voice therapy program (Vocal Function Exercises). Voice amplification versus vocal hygiene instruction for teachers with voice disorders: A treatment outcome study. et al. a wide variety of interesting modifications of the vocal production system are known. or in some cases by active compression of the hypaxial musculature. and mammals. and Hearing Research. V.. Jackson. J. (2000). (1994). 286–296. Despite this shared plan. (1991). Laryngoscope. W. 4. (2001) found no significant improvement in a group of teachers with voice disorders after a course of didactic training in vocal hygiene. R. I. Verdolini-Marsten. Roy... In another study. (1994). NJ: Prentice Hall. Language. Gray. I.. and Fennell. 1. Weinrich. I. Does the voice improve with vocal hygiene education? A study of some instrumental voice measures in a group of kindergarten teachers. I. Dove.. (2002) examined the outcome of voice amplification versus vocal hygiene instruction in a group of voicedisordered teachers. 279–291. K. and Druker. Journal of Speech. and (3) a supralaryngeal vocal tract which filters this sound before emitting it into the environment. R. and Hearing Research. 699–718. In many frogs. 1001–1007. G. S. H.

and freed from the necessity of tracheal protection. the vocal cords. 1960). the evolution of the human speech apparatus involved several important changes. However. Vibration at a particular frequency does not typically require neural activity at that frequency. relatively normal phonation can be obtained by blowing moist air through an excised larynx. Although the larynx in these species can support a wide variety of vocalizations. and mammals. in which the larynx of males expands to fill the entire thoracic cavity. Sounds created by the larynx must pass through the air contained in the pharyngeal. in howler monkeys (genus Alouatta) the larynx and hyoid have grown to fill the space between mandible and sternum. However. Together with demonstrations of formant perception by nonhuman animals (Sommers et al. For example. This structure primitively includes a pair of barlike cartilages that can be separated (for breathing) or pushed together (to seal the airway) (Negus. while such aperiodic vocalizations are rare in nonpathological human voices. The inflated sac also increases the e‰ciency with which sound is radiated into the environment (Gans. which were subsequently lost in human evolution. a similar change occurs in human males at puberty: the larynx descends slightly to give men a longer vocal tract and lower formants than same-sized women (Fitch and Giedd. The most extreme example of laryngeal hypertrophy is seen in the hammerhead bat Hypsignathus monstrosus. larynx. and Herzel. to shape): they act as filters to shape the spectrum of the vocal output. the significance of their loss in human evolution is unknown. phonation in nonhumans appears to follow the principles of the myoelastic-aerodynamic theory of human phonation. formant frequencies provide a possible indicator of body size not as easily ‘‘faked’’ as the laryngeal cue of fundamental frequency. which virtually all tetrapods can produce. Fig. air sacs are occasionally observed in humans in pathological situations. this air has mass and elasticity and vibrates preferentially at certain resonant frequencies. and Peters. they can be important in animal vocal repertoires (Fitch. Human speech is thus produced by the same conservative vocal production system of lungs. and trachea down into the abdomen (Schneider. Kuhn. 1994). which are found in most frogs. Rice. During phonation. the movements of the vocal folds can be periodic and stable (leading to tonal sounds) or highly aperiodic or even chaotic (e. in screams). and some intriguing morphological adaptations have arisen to elongate the vocal tract (presumably resulting from selection to sound larger. All great apes posses large balloon-like sacs that open into the larynx directly above the glottis (Negus. 1949. the size of the larynx is not tightly constrained by body size. Elongations of the nasal vocal tract are seen in the long nose of male proboscis monkeys or the impressive nasal crests of hadrosaur dinosaurs (Weishampel. cat purring relies on an active tensing of the vocal fold musculature at the 20–30 Hz fundamental frequency of the purr (Frazer Sissom. In birds. the avian syrinx is a remarkably diverse structure underlying the great variety of bird sounds (King. it is possible to break the anatomical link between vocal tract length and body size. The airflow from the lungs sets the vocal folds (or syringeal membranes) into vibration. a laryngocele is a congenital or acquired air sac that is attached to the larynx through the laryngeal ventricle at precisely the same location as in the great apes (Stell and Maran. 2001). 1999). Thus. However. Schon ¨ Ybarra. Expiration through the partially closed larynx creates a turbulent hiss—perhaps the most primitive vocalization. 1991). However. giving these small monkeys remarkably impressive and low-pitched voices (Kelemen and Sade. 1981). Fitch and Kelley. vocal reptiles (geckos. Like any column of air. its primary function as a protective gateway appears to have constrained laryngeal anatomy. 1995). and Keleman. 2000b). 1992. this is seen in extreme form in the red deer Cervus elaphus. Again. Parsimony suggests that the common ancestor of apes and humans also had such air sacs. Neubauer. 2000). with long folds producing lower frequencies. Although our knowledge of animal phonation is still limited. 2002). Vocal tract resonances are termed formants (from the Latin formare. Because all tetrapods have a vocal tract.Vocal Production System: Evolution 57 of air. and the rate of vibration is passively determined by the size and tension of these tissues. a novel phonatory structure called the syrinx evolved at the base of the trachea. Because the vocal tract in mammals rests within the confines of the head. A similar though less impressive increase in larynx dimensions is observed in human males and is partially responsible for the voice change at puberty (Titze. 1997). However. and vocal tract shared by all tetrapods.g. and nasal cavities. oral. 1975). pushing the heart. more sophisticated vocalizations became possible after the innovation of elastic membranes within the larynx. Dedicated to vocal production. 1949). 1A. probably in response to selection for low-pitched voices (Fig. Formant frequencies are determined by the length and shape of the vocal tract. One was the loss of laryngeal air sacs. 1973). B). 1C–E ). Because the length of the vocal folds determines the lowest frequency at which they could vibrate (Titze. 1989). 1989). The lungs are protected by a larynx in all tetrapods.. crocodilians). and skull size and body size are tightly linked (Fitch. 1967). lungs. 1973). one might expect that a low fundamental would provide a reliable indication of large body size. . which retract the larynx to the sternum during territorial roaring (Fitch and Reby. this suggests that formants may have provided a cue to size in primitive vertebrates (Fitch. Thus. Large animals have long vocal tracts and low formants. Vocal tract elongation can also be achieved by lowering the larynx. Because the function of air sacs in ape vocalizations is not understood. collectively termed the supralaryngeal vocal tract or simply vocal tract. all have formants. However. a huge larynx has independently evolved in many mammal species.. and rodents and bats can produce ultrasonic vocalizations at 40 kHz and higher (Suthers and Fattu.

In particular. T. Journal of the Acoustical Society of America. Hammerheaded bat. W. Also. —W. and Giedd. 559–574. P. Of course. Fitch. The now extinct duckbilled dinosaur Parasaurolophus had a hugely elongated nasal cavity (shown in gray) that filled the bony crest adorning the skull. Klatt. 1969). J.. 1949). 49. 1213–1222. Neubauer. the descended larynx is clearly an important component of human spoken language (Lieberman.. 163–183. and Herzel. Ethology. 1984). W. J. T. all mammals can produce a diversity of sounds. which together with the enlarged hyoid fills the space beneath the mandible (larynx and hyoid shown in gray). 102. A. which they lower to the sternum when roaring. L. H. and Wilson. recent fossils suggest that an expansion of the thoracic intervertebral canal occurred during the evolution of Homo some time after the earliest Homo erectus (MacLarnon and Hewitt. Calls out of chaos: The adaptive significance of nonlinear phenomena in . 1999). W. Grus americana. the ‘‘point vowels’’ /i. W. Phonetica. T. Hypsignathus monstrosus. 1511–1522. a. 1984). Fitch. Fitch. 106. which could have served a simpler speech system. speech typical of modern humans appears to require a descended larynx. T. Howler monkeys Alouatta spp. W. Morphology and development of the human vocal tract: A study using magnetic resonance imaging. Fitch. Given the existence of these vowels in virtually all languages (Maddieson. S. (2000a). resulting in an extremely elongated vocal tract (shown in gray). lessening the gap between humans and other animals.. W. Skull dimensions in relation to body size in nonhuman mammals: The causal bases for acoustic allometry. The phonetic potential of nonhuman vocal tracts: Comparative cineradiographic observations of vocalizing animals. Finally. (2000). (1997). 2000a). 40–58. 103. Fitch. Tecumseh Fitch References Brainerd. and Kelley. Fitch. D. Zoology. Journal of the Acoustical Society of America. have the largest relative larynx size among primates. B. Humans— Homo sapiens—have a descended larynx. Perception of vocal tract resonances by whooping cranes. 2001). A second change in the vocal production system during human evolution was the descent of the larynx from its normal mammalian position high in the throat to a lower position in the neck (Negus. C. Despite these caveats. 106. most mammals appear to lower the larynx during vocalization (Fitch. Biological Journal of the Linnean Society.58 Part I: Voice Figure 1. Vocal tract length and formant frequency dispersion correlate with body size in rhesus macaques. In the 1960s. The existence of nonhuman mammals with a descended larynx raises the possibility that this trait initially arose to exaggerate size in early hominids and was later coopted for use in speech (Fitch and Reby. and Ditelberg. (2002). (1993). See also vocalization. This change may be associated with an increase in breathing control necessary for singing and speech in our own species.. neural mechanisms of. T. 205–218.. Lung ventilation in salamanders and the evolution of vertebrate air-breathing mechanisms. J. J. 57. has a huge larynx (gray) enlarged to fill the thoracic cavity. Examples of unusual vocal adaptations among vertebrates (not to scale). E. speech scientists realized that this ‘‘descended larynx’’ allows humans to produce a wider variety of formant patterns than would be possible with a high larynx (Lieberman. Male red deer Cervus elaphus have a permanently descended larynx. (1999). (2000b). T. E. u/ seem to be impossible to attain unless the tongue body is bent and able to move freely within the oropharyngeal cavity. resulting in an elongated ‘‘two-tube’’ vocal tract (shown in gray).

and palilalic iterations (Brown. 1988. A comparative approach to the ¨ nonhuman primate vocal tract: Implications for sound production. The evolution of human speech: The role of enhanced breathing control. 407– 418. 1861 ¨ (Pteropodidae. Electrical stimulation of the ACG in monkeys elicits vocalization and autonomic responses (Jurgens. 1988). 1215–1226. The biology and evolution of language. R. Cambridge. Although there are little supporting empirical data. which lies on the mesial surface of the frontal cortex just above and anterior to the genu of the corpus callosum. (1994). I.. King. M. Damage to the ACG in humans results in akinetic mutism that is accompanied by open eyes. 91. (2001). Negus. and Kelemen. and the supplementary motor area (SMA) (Muller-Preuss. 105–192). a patient’s ability to communicate gradually returns. 1185–1187. New York: Academic Press.. the vocalizations lack prosodic features and are characterized as expressionless (Jurgens and von Cramon. These observations ¨ support the view that the ACG controls motivation for primitive forms of behavior. (1989). Principles of voice production. However. H. The vocal organ of the howling monkey (Alouatta palliata). MA: Belknap Press/Harvard University Press. Patterns of sounds. G. Newman (Eds. Larson. (1992). Newman. the superior temporal gyrus. How cats purr. or repetitive utterances. then with vocalization. Kelemen. McLelland (Eds. W. In E. and Sade. Paleobiology. 109. Journal of the Acoustical Society of America. The limbic system...-J. S. (1973). B. A.. 1988). S. and nonreactance to painful stimuli (Jurgens and von ¨ Cramon. D. P. hesitation. D. Weishampel.. (1969). Vocal tract limitations on the vowel repertoires of rhesus monkey and other nonhuman primates. Electrical stimulation of the ACG in humans may also result in oral movements or postural distortions representative of an ‘‘archaic’’ level of behavior (Brown. Laryngocoele. Neural Mechanisms of mammalian vocal production. 7.). (1991). 63. 268. Formant frequency discrimination by Japanese macaques (Macaca fuscata). Journal of Zoology (London). and Maran. A.. American Zoologist. first as a whisper. 123–140. poor initiation of speech. the posterior cingulate gyrus. New York: Plenum Press. Suthers. Mammalia). 67–78. B. Monkeys become mute ¨ when the ACG is lesioned. I. Frazer Sissom. 3499–3510. D.. Current topics in primate vocal communication (pp. Science. and Wilson. Schneider. T. E.. J. R. (1949). Electrical stimulation of the SMA elicits ¨ vocalization. Zimmerman and J. In A. Sound production in the Salientia: Mechanism and evolution of the emitter. G. (1984). Moody. American Zoologist. Prosen. 1980). a group of neural structures controlling motivation and emotion. The Comparative anatomy and physiology of the larynx. New York: Hafner. patients often go through a period in which the production of . P. H. 1988). G. (1975). 1179–1194. W. The descended larynx is not uniquely human. D.. Lieberman. lack of limb movement. Lieberman. Physiologic and acoustic di¤erences between male and female voices. Zeitschrift fur ¨ wissenschaftliche Zoologie. and single neurons in the ACG become active with vocalization or in response to vocalizations from conspecifics (Sutton. During recovery. Neural Mechanisms of The capacity for speech and language separates humans from other animals and is the cornerstone of our intellectual and creative abilities. C. NJ: Prentice Hall.. G. Biological Sciences. Megachiroptera. MA: Harvard University Press. R. (1981).).. C. R. and Reby. 89. and Fattu. A. Journal of Laryngology and Otology. A. 1994). K. Muller-Preuss. Englewood Cli¤s. The ACG has reciprocal connections with several cortical and subcortical sites. Mechanisms of sound production in echolocating bats. H. Kuhn. Schon Ybarra. E. W.Vocalization. D. 1982). 175. 164. (1989). M. 1–53. and Hewitt. (1960). Damage to the SMA may result in mutism. Stell. (1973). (1999). D. F. A. 1974. King and J. American Journal of Physical Anthropology. Journal of Morphology. G. distortions. D. 13. H. 341–363. and during recovery. many human emotional vocalizations probably involve the limbic system. and Stebbins. 185–198). By studying these mechanisms in animals that represent stages of phylogenetic development. 223.). P. Ventilation. (1985). UK: Cambridge University Press. and Lindeman.. Fitch. Functional vertebrate morphology (pp. Liem. S. C. J. 13. Titze. These symptoms reflect a lack of drive to initiate vocalization and many other behaviors (Brown. Der Larynx des mannlichen Hypsignathus monstrosus Allen. In M. 1982). is considered part of the limbic system (Fig. West and Larson. Titze. Journal of the Acoustical Society of America. Proceedings of the Royal Society. we can gain insight into the neural control of human speech that is necessary for understanding many disorders of human communication. Form and function in birds (pp. 915–924. and ¨ Jurgens. lack of apparent a¤ect. Rice. A. D. ¨ 1995). and Peters. 107. also controls most mammalian vocalizations. Vocalization is an integral part of speech and is widespread in mammalian aural communication systems. Sommers. Acoustic analysis of potential vocalization in lambeosaurine dinosaurs (Reptilia: Ornithischia). 1699–1707. (1984). Cambridge. 252–261. a fixed gaze. V. (1995). 59 Vocalization. I.. This capacity evolved from rudimentary forms of communication in the ancestors of humans. 1). Klatt. This discussion considers the limbic system and those neural mechanisms thought to be necessary for normal speech and language to occur. (1967). Gans. 85. 185–209). Hildebrand (Ed. Functional anatomy of the syrinx. The anterior cingulate gyrus (ACG). M. M. including prelinguistic vocalization. including a premotor area homologous with Broca’s area. Maddieson. Animal Behaviour. speech arrests. Cambridge. MacLarnon. 1669–1675.

facial. vocalization is less frequently a¤ected than speech articulation or language (Du¤y. The perisylvian cortex is reciprocally connected to the ACG. propositional speech remains severely impaired but nonpropositional speech (e.60 Part I: Voice Figure 1. Electrical and chemical stimulation of the PAG in many animal species elicits species-specific vocalizations (Jurgens.. Additional evidence linking the insula to vocalization comes from recent studies of apraxia in humans (Dronkers. respiratory.. 2000). aphonia may arise from widespread damage. Starkstein. 1958). ¨ 1994). singing. The perisylvian cortex also includes the right superior temporal gyrus and Heschl’s gyrus. or psychogenic etiology (Sapir and Aronson. Mutism seems to occur more frequently when the opercular region of the pre. ¨ 1982.. A variety of techniques have shown that ¨ PAG neurons. Kirzinger. insula) are im- portant for vocalization. which projects to midbrain mechanisms involved in vocalization. 1988. and recovery following therapy may suggest a di¤use. 1988). an area important for speech and ¨ language. Damage to Broca’s area may cause total or partial mutism. Berthier. and perhaps control of the voice by self-monitoring auditory feedback (Perry et al. 1994). as both are remembered and require proper sequencing..and postcentral gyri is damaged bilaterally or when the damage extends deep into the cortex. along with expressive aphasia or apraxia (Du¤y.. 1999). and Leiguarda. a¤ecting the insula and possibly the basal ganglia (Jurgens. it is necessary to know whether mutism results from psychogenic or physiological mechanisms. activate or suppress coordinated groups of oral. ¨ 1994). 1999. Newman. utilizing excitatory amino acid transmitters (glutamate). 1997). Studies of other motor systems in primates suggest that the SMA is involved in selection and initiation of a remembered motor act or the correct sequencing of motor acts (Picard and Strick. The lateral and mesial surface of the human brain. counting) remains relatively una¤ected (Brown. Jurgens. In some cases. The specific pattern of activation or suppression is determined by descending inputs from the ACG and limbic system. perception of one’s own voice. and von Cramon. motivational. Output from the SMA to other vocalization motor areas is a subsequent stage in the execution of vocalization. The other widely studied limbic system structure known for its role in vocalization. 1994). Further research is necessary to determine whether the opercular cortex alone or deeper structures (e. is the midbrain periaqueductal gray (PAG) (Jurgens. The perisylvian cortex also projects directly to the medulla. 1995). where motor neurons controlling laryngeal muscles are located (Kuypers. Du¤y.g. 1996).g. and laryngeal muscles for species-specific vocalization (Larson. 1991. ¨ and Jurgens. 1995). The ACG is also connected with the perisylvian cortex of the left hemisphere (Muller-Preuss. Belin et al. The perisylvian cortex may control vocalization by one or more pathways to the medulla. 1987). 1980). along with sensory feedback from the . Speech and vocalization fall into these categories. and the e¤ect is usually temporary. 1995). In specific cases. which are preferentially active for perception of complex tones. Lesions of the ¨ PAG in humans and animals lead to mutism (Jurgens. However. These neuroanatomical projections are supported by observations of a short time delay (13 ms) between stimulation of the cortex and excitation of laryngeal muscles (Ludlow and Lou. 1996) and findings of increased blood flow in the insula during singing (Perry et al.

A. one that is primitive and found in most animals. Holstege. 1979). Zhang. 2000). U. M. 1993. Behavioural Brain Research. Journal of Comparative Neurology. P. by way of the NRA (Holstege. 159–161. 1992). 77–86. Zatorre. and Davis. and lesions of the NA abolish vocalizations elicited by PAG stimulation (Jurgens and Pratt. Finally. Sensory feedback for the reflexive control of laryngeal muscles flows through the superior and recurrent laryngeal nerves to the nucleus of the solitary tract and spinal nucleus of the trigeminal nerve (Tan and Lim. 309–312. and stimulation of the NRA elicits vocalization (Zhang. Motor neurons in the NA control laryngeal muscles during vocalization. Motor speech disorders. Corticobulbar connexions to the pons and lower brain-stem in man. and von Cramon. 409. 1999). In J. Voice-selective areas in human auditory cortex. 2000). R. H. (1994). 1997. (1999).. R. (1995). (1993). Larson. 81. R. Brown.. (1989). Jurgens. An anatomical study on the final common pathway for vocalization in the cat. See also vocal production system: evolution. NRA. P. Lesions of the NRA eliminate vocalizations evoked by PAG stimulation (Shiba et al. it is unknown whether this pathway is involved in normal. J. C. (1982). A new brain region for coordinating speech articulation. and respiration (Yajima and Larson. Structures outside the dashed box may be found only in humans and perhaps anthropoid apes.. Y. swallowing. The ¨ e¤ects of deep-reaching lesions in the cortical face area on phonation: A combined case report and experimental monkey study. and lesions alter the acoustical structure of vocalizations (Luthe. and one that is found only in humans and perhaps anthropoid apes (Fig. F. Davis. (2000). The NRA in turn projects to the nucleus ambiguus (NA) and spinal cord motor neurons of the respiratory muscles. Structures inside the dashed box are involved in vocalization in other mammals as well as in humans. G. 15. S. Nature. The pathway found in all mammals extends from the ACG through the limbic system and midbrain PAG to medullary and spinal motor neurons. 1958). aided by sensory feedback. 2). St. P.. Nature. found primarily in humans.. The resultant vocalizations convey the a¤ective state of the organism. Pulmonary and upper airway a¤erent influences on the motor pattern of vocalization evoked by excitation of the midbrain periaqueductal gray of the cat. Brain Research. 1997). and Jurgens. and seems to control most emotional vocalizations. Damirjian. —Charles R. the NRA lies functionally between the PAG and motor neurons of laryngeal and respiratory muscles controlling vocalization and may play a role in coordinating these neuronal groups (Shiba et al. Dronkers. Journal of Comparative Neurology. U. Du¤y. J. R. U. and Pike. Neurons of the PAG project to several sites in the pons and medulla. periaqueductal gray. Cortex. Figure 2.. The role of the periaqueductal grey in vocal ¨ behaviour. Hausler. Laryngeal a¤erent stimulation enhances fos immunoreactivity in the periaqueductal gray in the cat. Although this system probably is responsible for emotional vocalizations in humans.. Jurgens.. Details of how these two parallel pathways are integrated are unknown. (1958). and Bandler.. Kirzinger. and Ludlow. NA. H. and von Cramon. P. RF. 284. 552. Bandler. Jurgens. D. and Pratt. 107–117. On the relation of PAG neurons to laryngeal and respiratory muscles during vocalization in the monkey. 364–388. (1991). Louis: Mosby. G.). 61–80. Brain Research. Cingulate gyrus and supplementary motor correlates of vocalization in man.. 411–423. nucleus retroambiguus. Brain. (1982). 18. Brain and Language. reticular formation. J. Zhang. 1995). Block diagram and arrows indicating known connec- tions between principal structures involved in vocalization.. Ahad. 367–378. 384. the NA contains laryngeal motor neurons and is crucial to vocalization. Belin. laryngeal and respiratory systems (Davis. Voluntary vocal control. 125–140. J. U. The tendency for vocalization and human speech to be strongly a¤ected by emotions may suggest that all vocalizations rely at least in part on the ACG-PAG pathway. and Bandler. vocalization is controlled by two pathways. may be exerted through a direct pathway from the motor cortex to the medulla. nucleus ambiguous. (1988). Thus.. Tanaka. (1979). . where neurons modulate their activity with temporal and acoustical variations in monkey calls. 1993).Vocalization. These data suggest ¨ that the parvocellular reticular formation is important for the regulation of vocal quality and pitch. 1989). Brain Research. The physiological control of mammalian vocalization (pp.. New York: Plenum Press. D. 403. Role of the periaqueductal ¨ grey in vocal expression of emotion. 227–243). 62. nonemotive speech and language. 167. or directly from the cerebral cortex (Kuypers. P. Ladaille. B. In summary. Luthe. D. Larson References Ambalavanar. 607. The NA receives ¨ projections either indirectly from the PAG. Jurgens. 234–248. PAG. 242–252.. On the role of the ¨ anterior cingulate cortex in phonation: A case report. Hausler. L. N. C. Newman (Ed. (1996). 1989). Kuypers. one of which is the nucleus retroambiguus (NRA) (Holstege. ¨ The PAG also projects to the parvocellular reticular formation. Neural Mechanisms of 61 auditory. M. R. Ambalavanar et al.. and Jurgens. R..

(1995). K. and Strick. Aronson... cardiac. (1982).. A. (1999). U. Gandour. Ludlow. E. Brain Research. 213–217. 104. A. M. Ortega. Seattle.. L. C. Acta Anatomica. and Jurgens. New York: Academic Press. C.. Journal of the Acoustical Society of America. On the location and size of laryngeal motoneurons in the cat and rabbit. 513–519. Experimental Brain Research. C. Journal of Comparative Neurology.). 9. Sapir.. 70. Abnormalities in long latency responses to superior laryngeal nerve stimulation in adductor spasmodic dysphonia. C.62 Part I: Voice Brown. Bilateral opercular syndrome and crossed aphemia due to a right insular lesion: A clinicopathological study. Marshall. (1985). 467–508. and Mesulam. 3453–3458. Lamandella. N. 13–32. B. 306–308. Gemba. Whitaker and H. (1987). Role of the human anterior cingulate cortex in the control of oculomotor.. Umezaki. Bandler. pp. 8. Brain Research. (1971). Journal of Neurophysiology. C. New York: Grune and Stratton. 230. 189–196. 245–262). 109.. C. Ludlow. (2000). Perry. Evans. 2197–2201. R. and Deleyiannis. Petrides. Neuronal ¨ activity in the medulla oblongata during vocalization: A single-unit recording study in the squirrel monkey. Fujimura (Ed. and Luschei. Localization of a pontine vocalization¨ controlling area. E. S. Journal of Comparative Neurology. 74. U. P. L. 233. A. and Aronson. Davis and N. Kirzinger. H. J. 636–642. 34. (1995).. K. Muller-Preuss. pulmonary.. 1393–1396. 307–315. K. Unpublished doctoral dissertation. H.). D. and Larson.. In J. S. L. Localization of cerebral activity during simple singing. Davis. E¤ects of cerebellar lesions on conditioned monkey phonation. Y. Experimental mutism resulting from periaqueductal lesions in cats. In E.. (1988). The supplementary motor region and speech. G. and Jurgens. (1974). Brain Research. Muller-Preuss. . R. Jurgens... 2. manual and speech responses: A positron emission tomography study. and Jurgens. C. Starkstein. (1988). (1984). Clinical voice disorders. (1980). 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(1983). and Jurgens.. C. E. 202. Kirzinger. M. and Davis. L.. (1985).. H. Newman. A. 115. and Lim. S. and Laryngology.. C. The physiological control of mammalian vocalization (pp. 73–80. 71. Preliminary observations on cortical and brainstem mechanisms of laryngeal control. R. (1987). Cortical lesion e¤ects ¨ and vocalization in the squirrel monkey. In J.. Zatorre. and Evans. Alivisatos.. 22. (1991). Barris. Y. 69.). Yajima. U. Vocal fold physiology: Contemporary research and clinical issues. R. Berthier. Neural correlates of audio-vocal be¨ havior: Properties of anterior limbic cortex and related areas.. 157–222). E. P. D. Neurology. Park. J. Journal of Neurophysiology. W. 928–935. 108. C. Bilateral anterior cingulate gyrus lesions. 545–560. NeuroReport. 103. (1976). L. Muller-Preuss.. D. Studies in neurolinguistics (vol. 61–75. ¨ ¨ Anatomical and physiological evidence for a relationship between the ‘‘cingular’’ vocalization area and the auditory cortex in the squirrel monkey. M. J. K. and Sasaki.. International Journal of Neurology. R. 143–151. 45–81). R. Selective impairment of phonation: A case study. Projections from the ¨ ¨ ‘‘cingular’’ vocalization area in the squirrel monkey. N. W. B. G. Laryngeal. U. and Schuman. 453–469. 197–210. San Diego: Singular Publishing Group. (2000). Brain Research. C. In O. M. 19–28). J. Wilson. 44–52. Brain stem integration of vocalization: Role of the nucleus retroambigualis. Brainstem projections of sensory and motor components of the vagus complex in the cat: II. New York: Raven Press. Cortical field potentials preceding vocalization and influences of cerebellar hemispherectomy upon them in monkeys. A. J. (1997). Larson. Larson.. E. H. M. (1997).. (1993). C. S. 84. and Windsor. and Larson. R. Picard. U.. R. U. Zhang. New York: Thieme-Stratton.. CA: College-Hill Press. in the mechanisms of speech and language.. K. Zheng. E. Neurons of the anterior mesial cortex related to faciovocal behavior in the awake monkey.-B. San Diego. R. Observations on human laryngeal muscle control. J. and Miller. Paus. F. Vocal physiology: Voice production.. Darby (Ed. and Zwirner.. 1156–1169. M. (1980). Botez. Brain and Language. (1992). (1959). Bless and J. A. A. D. D. Jonas. The frontal lobes revisited. Rhinology. The nucleus retroambigualis controls laryngeal muscle activity during vocalization in the cat. and gastrointestinal branches. (2000). Jurgens. Luthe. Kalia. Neurological basis of language processing. J. (1953).. (1988). Schulz. mechanisms and functions (vol. 241. Role of subcortical structures. 143.. R. University of Washington. Vocal fold physiology: Controlling complexity and chaos (pp. and Perecman. and O’Leary. 3. Neurology. J. S. E. and particularly of the thalamus. (1988). Abbs (Eds. 529–540. A. C. 313–339. DeRosier. P.. 74. Yamashita. and Lou. Journal of Neurophysiology. 3.). 2500–2512. Experimental Brain Research. Fletcher (Eds.. and Leiguarda. J.. Miki. In J. 29–43. 70... M. (1977). Petrides. A. Journal of Neurophysiology. Hausler. and Jurgens. P.). A. 193. Jurgens. Central projection of the sensory fibres of the recurrent laryngeal nerve of the cat. (1995). Speech and language evaluation in neurology: Adult disorders (pp.. British Journal of Disorders of Communication. R. H. Multifunctional properties of ambiguous neurons identified electrophysiologically during vocalization in the awake monkey. J.). Perecman (Ed. and Larson. Journal of Neurophysiology. Whitaker (Eds. Brain Research. M. Vocalization-correlated ¨ single-unit activity in the brain stem of the squirrel monkey.

289–317. Role of the right temporal neocortex in retention of pitch in auditory short-term memory. B. 13–23. Liljencrants.. The anterior cingu¨ late cortex and the phonatory control in monkey and man. 1A).. and then reaches a maximum negative value. the impedance of the glottal opening is usually large compared with the impedance looking into the vocal tract from the glottis. as depicted in Figure 2. Thus. (1948). When a nonnasal vowel is produced. Ward. During the open phase of the cycle. 114. K. The volume velocity at the lips is Um (t). The sound pressure pr is related to Um by a radiation characteristic R( f ). 7.e. 423–425. U. 1). 1985). Thus the output sound pressure can be considered to be the result of filtering Us0 (t) by the vocal tract transfer function T( f ). Each pulse has a sequence of two components: (1) an initial smooth portion where the waveform is first positive. and Lin. The frequency of this source waveform varies from one individual to another and within an utterance. D. The amplitudes of the harmonics at high frequencies decrease as 1= f 2 . For the ideal or modal volume-velocity waveform (Fig. The supplementary motor area of the cerebral cortex. a positive pressure below the glottis will cause the vocal folds to vibrate. 1A). The periodic nature of this waveform is reflected in the harmonic structure of the spectrum (Fig. J. and there is a relatively abrupt discontinuity in slope at the time the volume velocity decreases to zero. a change in frequency is represented in the number of pulses per second. the frequency is represented by the spacing between the harmonics. When the position and tension of the vocal folds are properly adjusted. von Cramon. where f ¼ frequency.Voice Acoustics Penfield. at about À12 dB per octave. Thus we have pr ( f ) ¼ Us ( f ) Á T( f ) Á R( f ): The magnitude of pr ( f ) can be written as r : (3) 4pr The expression jUs ( f ) Á 2pf j is the magnitude of the Fourier transform of the derivative Us0 (t). in the frequency domain (Fig. this derivative has the form shown in Figure 3A (Fant.. and during an utterance the shape can be modified depending on the position within the utterance and the prominence of the syllable. Archives of Neurology and Psychiatry. Journal of Neurophysiology. (1951). the volume velocity is zero in the time interval between the pulses. S. The shape of the individual pulses can also vary with the speaker.. Idealized waveform of glottal volume velocity Us (t) for modal vocal fold vibration for an adult male speaker. 1B). and (2) a second portion where the waveform returns abruptly to zero. (1983). multiplied by a constant. 1B). Brain. R. i. . the airflow is modulated. 1). and Samson. For modal vocal fold vibration. in most cases it is reasonable to represent the glottal source as a volumevelocity source that produces similar glottal pulses for di¤erent vocal tract configurations. This source Us (t) is filtered by the vocal tract. The cingular gyrus: Area 24. In the time domain (Fig. defined as the ratio Um ( f )=Us ( f ). Zatorre. 2403–2417. The magnitude of this radiation characteristic is approximately r Á 2pf . is an all-pole transfer function. That is. and Welch. 66. and the output sound pressure at a distance r from the lips is pr (t). Neurosciences and Biobehavior Review. 63 Voice Acoustics The basic acoustic source during normal phonation is a waveform consisting of a quasi-periodic sequence of pulses of volume velocity Us (t) that pass between the vibrating vocal folds (Fig. A. Spectrum of waveform in A. A. A. corresponding to the discontinuity in jpr ( f )j ¼ jUs ( f ) Á 2pf j jT( f )j Á (2) Figure 1. (1) jR( f )j ¼ 4pr where r ¼ density of air. 11. the vocal tract transfer function T( f ). (1991). and Jurgens. As the crosssectional area of the glottis changes during a cycle of vibration. the derivative Us0 (t) can be viewed as the e¤ective excitation of the vocal tract. then passes through zero (corresponding to the peak of the pulse in Fig. The magnitudes of the spectral components of Us ( f ) and pr ( f ) are shown below the corresponding waveforms in Figure 2. W.

The principal acoustic excitation of the vocal tract occurs at the time of this discontinuity. 1989). the excitation of the vocal tract and the overall amplitude of the output are decreased.64 Part I: Voice Figure 2. At the right is the waveform pr (t) and spectrum pr ( f ) of the sound pressure. 3B) at high frequencies decreases as 1= f . reflecting the discontinuity at closure. Derivative Us0 (t) of the modal volume-velocity waveform in Figure 1. 1964. The inertia of the air in the glottis and supraglottal airways prevents the occurrence of the Figure 3.e. although the subglottal pressure also influences the frequency. First. Spectrum of waveform in A. (Adapted with permission from Stevens. Tanaka and Gould. For normal speech production. i. Second. more specifically. Changes in the configuration of the membranous and cartilaginous portions of the vocal folds relative to the modal configuration can lead to changes in the waveform and spectrum of the glottal source. 1994. At the left of the figure both the source waveform Us (t) and its spectrum Us ( f ) are shown. which is radiated to obtain the sound pressure pr (t) at some distance from the lips. at À6 dB/octave. For some speakers and for some styles of speaking. introducing several acoustic consequences. there are several ways in which the glottal waveform can di¤er from the modal waveform (or its derivative). One obvious attribute is the frequency f 0 of the glottal pulses. . the e¤ect on the derivative waveform Us0 (t) is that the maximum negative value is reduced (that is.) slope of the original waveform Us (t) at the time the vocal folds come together. the speed with which the vocal folds approach the midline is reduced. The magnitude of the glottal excitation 3/2 increases roughly as Ps (Ladefoged and McKinney.. the spectrum (Fig. the vocal folds and arytenoid cartilages are configured such that the glottis is never completely closed during a cycle of vibration. Thus. it is less negative). or. which is controlled primarily by changing the tension of the vocal folds. Isshiki. there is continuing airflow throughout the cycle. For this ideal or modal derivative waveform. Increasing or decreasing the subglottal pressure Ps causes increases or decreases in the amplitude of the glottal pulses. B. 1983). A. 1963. Schema showing how the acoustic source at the glottis is filtered by the vocal tract to yield a volume velocity Um (t) at the lips. particularly when the folds are relatively slack (Titze. in the magnitude of the discontinuity in slope at the time of glottal closure.

It is most apparent in the first formant range and results in an increased bandwidth of F1. 1981). The derivative waveform Us0 (t) then has a shape that is schematized in Figure 4. causing a reduction in A1. since the noise component is weak in this frequency region. Liljencrants. there is an aspiration noise source with a continuous spectrum (Klatt and Klatt. Figure 6 shows spectra of a vowel produced by a speaker with modal glottal vibration (A) and the same vowel produced by a speaker with a somewhat abducted Figure 5. The corresponding waveform Us (t) is shown below the waveform Us0 (t). the harmonics are well defined. In contrast to the periodic source. the noise source has a spectrum that tilts upward with increasing frequency. 1985). 1998). The spectrum of the periodic component is represented by the amplitudes of the harmonics.Voice Acoustics 65 Figure 4. The three consequences just described lead to a vowel for which the spectrum amplitude A1 in the F1 range is reduced and the amplitudes of the spectral prominences due to higher formants are reduced relative to A1. 1990). Figure 5A shows estimated spectra of the periodic and noise components that would occur during modal phonation. Rather. . the noise source is also modulated. This increased flow causes an increased amplitude of noise generated by turbulence in the vicinity of the glottis. A third consequence of a somewhat abducted glottal configuration is an increased loss of acoustic energy from the vocal tract through the partially open glottis and into the subglottal airways. This energy loss a¤ects the vocal tract filter rather than the source waveform. Schematized representation of volume velocity waveform Us (t) and its derivative Us0 (t) when the glottis is never completely closed within a cycle of vibration. Since the flow is modulated by the periodic fluctuation in glottal area. 5B). and is generated only during the open phase of glottal vibration. however. abrupt discontinuity in Us0 (t) that occurs at the time of vocal fold closure in modal phonation (Rothenberg.’’ The aspiration noise source can be represented as an equivalent acoustic volume-velocity source that is added to the periodic source. This type of phonation has been called ‘‘breathy-voiced. Phonation with a more abducted glottis of the type represented in Figure 4 leads to greater noise energy and reduced high-frequency amplitude of the periodic component. there is a non-zero return phase following the maximum negative peak. The spectrum of the noise is calculated with a bandwidth of about 300 Hz. around 2–4 kHz (Stevens. the amplitude of the first-formant prominence in the spectrum (Hanson. The noise component is relatively weak. during which Us0 (t) gradually returns to zero (Fant. The spectral consequence of this non-zero return phase is a reduction in the high-frequency spectrum amplitude of Us0 (t) relative to the low-frequency spectrum amplitude. in addition to the quasi-periodic source. Schematized representation of spectra of the e¤ective periodic and noise components of the glottal source for modal vibration (A) and breathy voicing (B). 1997). With breathyvoiced phonation. Still another consequence of glottal vibration with a partially open glottis is that there is increased average airflow through the glottis. At low frequencies. as shown in the Us (t) waveform in Figure 4. and the noise component may dominate the periodic component at high frequencies (Fig. the individual harmonics corresponding to the periodic component may be obscured by the noise component at high frequencies. and Lin. Thus. It appears to have a broad peak at high frequencies.

In addition. 1990). As the vocal folds are adducted. Below the spectrum are waveforms of this vowel before and after being filtered with a bandpass filter centered on F3. and may occur aperiodically (glottalization). Spectrum of the vowel /e/ produced by a male speaker with approximately modal phonation. The noise in the waveform in the F3 region (and above) obscures the individual glottal pulses. Filtered waveforms of this type have been used to highlight the presence of noise at high frequencies during phonation by a speaker with a breathy voice (Klatt and Klatt. The spectra are from Hanson and Chuang (1999). Therefore. Adduction of the vocal folds relative to their modal configuration can also lead to changes in the source waveform. The individual glottal pulses as filtered by F3 of the vowel are evident. 2002). glottis (B). These di¤erences lead to significant . the transglottal pressure required to maintain vibration (phonation threshold pressure) increases. Comparison of the two spectra in Figure 6 also shows the greater spectrum tilt and the reduced prominence of the first formant peak associated with an abducted glottis. The above description of the glottal vibration pattern for various degrees of glottal abduction and adduction suggests that there is an optimum glottal width that gives rise to a maximum in sound energy (Hanson and Stevens. As the average glottal area increases. B. in which the glottal pulses are narrower and of lower amplitude than in modal phonation. phonation-threshold pressure increases. for a given subglottal pressure an increase in the glottal area can lead to cessation of vocalfold vibration. eventually reaching a point where the folds no longer vibrate. See text. as already noted. The waveforms below are as described in A. There are substantial individual and sex di¤erences in the degree to which the folds are abducted or adducted during phonation.66 Part I: Voice Figure 6. with a bandwidth of 600 Hz. Below the spectra are waveforms of the vowel before and after being filtered by a broad bandpass filter (bandwidth of 600 Hz) centered on the third-formant frequency F3. A. pressed voicing occurs. The noise is also evident in the spectrum at high frequencies for the speaker of Figure 6B. Spectrum of the vowel /e/ produced by a male speaker who apparently phonated with a glottal chink. This optimum configuration has been examined experimentally by Verdolini et al. (1998).

W. Q. Journal of Speech and Hearing Research. —Kenneth N. Journal of Voice. (Adapted with permission from Hanson and Chuang. A fourparameter model of glottal flow. S. Hillman. (1983). Rothenberg. and Gould. Note the substantial ranges of 20 dB or more within each sex. there is airflow through the glottis. a measure that reflects the reduction of the high-frequency spectrum relative to the lowfrequency spectrum. (1988). Liljencrants. I.. P. for male (black bars) and female (gray bars) speakers. In K. Introduction to communication sciences and disorders (pp. B. E. but careful control of stimuli and a good knowledge of laryngeal physiology make airflow and air pressure measurements invaluable tools. synthesis. Journal of the Acoustical Society of America. Journal of the Acoustical Society of America. The asterisks indicate that corrections have been applied to H1 and A3. Hillman. R. Stevens. and Samawi. 305–323). . For example. Glottal airflow and transglottal air pressure measurements for male and female speakers in soft. (1997). Ladefoged. Regulatory mechanism of voice intensity variation.. 1999. and Klatt.. 511– 529. as described in the text. 87. (1998). Scientific substrates of speech production. 1316–1321. the amount of References Fant. 466–481. Tokyo: University of Tokyo Press. Speech Transmission Laboratory Quarterly Progress and Status Report. (1998). (1964).) Distributions of values of H1*-A3* are given in Figure 7 for a population of 22 female and 21 male speakers. and McKinney. K. Relationships between vocal intensity and noninvasively obtained aerodynamic parameters in normal subjects. (1989). S. Journal of the Acoustical Society of America. (1981). S. A quasiarticulatory approach to controlling acoustic source parameters in a Klatt-type formant synthesizer using HLsyn.. N. MA: MIT Press. 12. Isshiki. and in A3 due to the influence of the frequencies of the first and second formants. San Diego. 399–437). H. Glottal characteristics of female speakers: Acoustic correlates.Voice Disorders in Children 67 Figure 7. R. Vocal fold physiology (pp. and consequently in the spectral characteristics of vowels generated by these sources (Hanson. 820–857. normal. H. Titze. Drucker. N. Klatt. 35. Journal of the Acoustical Society of America. Minifie (Ed. H1 is the amplitude of the first harmonic and A3 is the amplitude of the strongest harmonic in the F3 peak. suggesting a somewhat less abrupt glottal closure during a cycle and a greater tendency for lack of complete closure throughout the cycle. 1094–1077. 1999). and Lin..) di¤erences in the waveform and spectrum of the glottal source.. and Stevens. Glottal characteristics of male speakers: Acoustic correlates and comparison with female data. 4. 112.. (1999).. 17– 29. Journal of the Acoustical Society of America. (The asterisks indicate that corrections are made in H1 due to the possible influence of the first formant. N. and Chuang. C. J. 1–13. K. When the vocal folds are open. With other physiological events held constant. G. Voice Disorders in Children Investigations of voice using aerodynamic techniques have been reported for more than 30 years.). H.. Investigators realized early on that voice production is an aeromechanical event and that vocal tract aerodynamics reflect the interactions between laryngeal anatomy and complex physiological events. G. Journal of the Acoustical Society of America. On the relation between subglottal pressure and fundamental frequency in phonation. and perception of voice quality variations among female and male talkers. M. Journal of the Acoustical Society of America. Stevens and Helen M. 84. J. 85. airflow through the glottis (Vg) is an excellent indicator of whether the vocal folds are open or closed. at a simple level. Stevens. 1158–1182.. Cambridge. Hanson Hanson. (1985). and loud voice. N. E. there is zero airflow. Hanson. E. The female speakers appear to have a greater spectrum tilt on average.). (1994). N. Hanson and Chuang. H. 454–460. Distributions of H1*-A3*. In F. 315–327. M. CA: Singular Publishing Group. Aerodynamic events do not always have a one-to-one correspondence with vocal tract physiology in a dynamic biological system. D. Tanaka. 73. (1963).. 901–912. Acoustic phonetics. Palmer. Hanson. J. 1997. M. D. 7. P. N. and subglottal pressure in speech. and when the vocal folds are completely closed. Hirano (Eds. G. P. (2002). Journal of the Acoustical Society of America. Stockholm: Royal Institute of Technology. D. Stevens and M. and Perkell (1988) using di¤erent measurement techniques. M. One acoustic measure that reflects the reduction of the high-frequency spectrum amplitude relative to the lowfrequency spectrum amplitude is the di¤erence H1*-A3* (in dB) between the amplitude of the first harmonic and the amplitude of the third-formant spectrum prominence.. Acoustic interaction between the glottal source and the vocal tract. Airflow (rate of air movement or velocity) and air pressure (force per unit area of air molecules) in the vocal tract are good reflectors of vocal physiology. 101. Verdolini. Analysis. H. 106. M. Holmberg. sound pressure. Laryngeal adduction in resonant voice. Similar observations have also been made by Holmberg. K. L. Loudness. K. (1990). and Perkell.

1966. Stathopoulos and Weismer. Opening . Assuming that pressure is the same across all speakers. it would appear that the greater peak intraoral air pressure in children should lead to a greater magnitude of oral airflow. During voice production. Subglottal air pressure will increase when the size of the lungs is decreased. von Leden. Other intraoral air pressure distinctions in children are similar to the overall trends described for adult pressures. and Moore (1958). Worth. and I ¼ laryngeal airflow (V). Hillman. 1971. Measures of flow and pressure were used to reflect laryngeal and respiratory function. the closed time of the vocal folds. permitting detailed. children produce lower average airflow than adults. 2. and I ¼ current. 1986). Intraoral air pressure: Measured peak pressure during the voiceless [p] to obtain an estimate of subglottal pressure. a smaller supraglottal or glottal opening yields a higher resistance at the constriction and therefore a restricted or lower flow of air. 1977). where R ¼ resistance. the overall shape of the vibratory waveform. The findings related to intraoral air pressure have indicated that children produce higher intraoral air pressures than adults. 1972. Van Hattum and Worth. Measures made using the Smitheran and Hixon (1981) technique include the following: 1. 1986). 1988): 1. Bernthal and Beukelman. because it is responsible for generating the pressure di¤erential causing vocal fold vibration (the pressure that drives the vocal folds). The open time of the vocal folds (defined as the interval of time between the instant of opening and the instant of closing of the vocal cords) is divided by the period of the glottal cycle. Thus. R ¼ V=I. Theolke and Cowan. and Kitzing. (2) prevocalic compared to postvocalic consonants. Subglottal pressure is also important for controlling sound pressure level and for contributing to changes in fundamental frequency— all factors essential for normal voice production. Measures made using the derived glottal airflow waveform important to vocal fold physiology include the following (Holmberg. two important aerodynamic techniques relative to voice production were developed that stimulated new ways of analyzing children’s aero- dynamic vocal function. especially because they tend to speak at higher sound pressure levels (SPLs). Opening and closing instants on the airflow waveform are taken at a point equal to 20% of alternating airflow (OQ-20%). and laryngeal and articulatory configuration. Supraglottal and glottal airway opening most likely account for the di¤erent average airflow values as a function of age and sex. The derived volume velocity waveform provides airflow values. Arkebauer. children tend to speak at a higher SPL than adults. (3) stressed compared to unstressed syllables. Beckett. subglottal pressure will decrease when the size of the lungs is made larger. Like adults. Speed quotient: The speed quotient is determined as the time it takes for the vocal folds to open divided by the time it takes for the vocal folds to close. In the 1970s and 1980s. A small number of classic studies used average airflow and intraoral air pressure to investigate voice production in children (Subtelny. It is likely that children’s smaller glottal and supraglottal areas substantially counteract the potentially large flows resulting from their high intraoral air pressures. The second aerodynamic technique developed was for the estimation of subglottal pressure and laryngeal airway resistance (Rlaw) through noninvasive procedures (Lofqvist. V ¼ subglottal pressure (P). Carlborg. The first technique was inverse filtering of the easily accessible oral airflow signal (Rothenberg. Changes in subglottal air pressure are mainly regulated through muscular forces controlling the size of the rib cage. Children were found to be capable of maintaining the same linguistic contrasts as adults through manipulation of physiological events such as lung cavity size and driving pressure. Hixon. V ¼ voltage. and Hardy. and boys tend to produce higher average airflow than girls of the same age. The measures made from the derived volume velocity waveform can be related to the speed of opening and closing of the vocal folds. Subglottal air pressure is of primary importance. Subglottal air pressure directly reflects changes in the size of the subglottal air cavity. R ¼ laryngeal airway resistance. the amplitude of vibration. Diggs. 3. The higher pressures produced by children versus adults reflect two physiological events. In the speech system. conversely. A simplified version of Boyle’s law predicts the relationship in that a particular pressure (P) in a closed volume (V) of air must equal a constant (K). Smitheran and Hixon. and second.68 Part I: Voice airflow can be an excellent indicator of the degree of opening between the vocal folds. Estimated laryngeal airway resistance: Calculated by dividing the estimated subglottal pressure by estimated laryngeal airflow. 1982. R ¼ P=V. K ¼ PV. and Perkell. Intuitively. First. 1967. 1981). quantifiable analysis of vocal fold physiology. and Sakuda. Airflow open quotient: This measure is comparable to the original open quotient defined by Timcke. 1967. that is. The estimation of Rlaw o¤ers a more general interpretation of laryngeal dynamics and can be used as a screening measure to quantify values outside normal ranges of vocal function. and the degree of glottal opening during the closed part of the cycle. This calculation is based on analogy with Olm’s law. 1978. children’s airways are smaller and less compliant than adults’ (Stathopoulos and Weismer. 2. and (4) stops compared to fricatives. children produce higher pressures during (1) voiceless compared to voiced consonants. with glottal resistance or glottal flow used to help increase or decrease the pressures (the glottis can be viewed as a valve that helps regulate pulmonary flows and pressures). Average oral air flow: Measured during the open vowel /A/ at midpoint to obtain an estimate of laryngeal airflow. Rothenberg’s procedure allowed derivation of the glottal airflow waveform.

Their MFDRs range from about 250 cc/s/s for comfortable levels of SPL to about 1200 cc/s/s for quite high SPLs. Anatomical di¤erences in the upper and lower airway will a¤ect the aerodynamic output of the vocal tract. It is indicative of airflow leak due to glottal opening during the closed part of the cycle. As seen in Figures 2A and 2B. In adults. 1988). hence the higher alternating glottal airflows for adults. 1980). 7. Estimated subglottal pressure: Children produce higher subglottal pressures than adults. men and boys increase their amplitude of vibration during the high SPLs more than women and children do. Fundamental frequency: This measure is obtained from the inverse-filtered waveform by means of a peak-picking program. Because the anatomical structure in children is constantly growing and changing. The data are discussed in relation to their physiological implications. It is the lowest vibrating frequency of the vocal folds and corresponds perceptually to pitch. SPLs (Fig. Many of the measures listed above have been used to derive vocal physiology. 2000). and all speakers produce higher pressures when they produce higher Figure 1. Alternating glottal airflow: Fourteen-year-old boys and men produce higher alternating glottal airflows than younger children and women during vowel production for the high SPLs (Fig. That is. which show data from a wide age span and both sexes. boys and men functionally group together. MFDR increases as SPL increases (Fig. Additionally. 3. From these cross-sectional data as a function of children’s ages. In children and adults. After that age. a clearer picture of child vocal physiology has emerged. Estimated subglottal pressure as a function of age and sound pressure level. 3).Voice Disorders in Children 69 and closing instants on the waveform are taken at a point equal to 20% of alternating air flow. 4). Younger children also increase their . Stathopoulos and Sapienza (1997) empirically explored applying objective voice measures to children’s productions and discussed the data relative to developmental anatomical data (Stathopoulos. Additional measures important to vocal fold physiology include the following: 6. Greater SPLs result in greater lateral excursion of the vibrating vocal folds. Alternating glottal airflow: This measure is calculated by taking the glottal airflow maximum minus minimum. Minimum flow: This measure is calculated by subtracting minimum flow from zero. Airflow open quotient (OQ-20%): Open quotient has traditionally been very closely correlated with SPL. physiological. 4. The increased airway resistance in children could substantially increase tracheal pressures (Muller and Brown. Increasing MFDR as SPL increases a¤ects the acoustic waveform by emphasizing the highfrequency components of the acoustic source spectra (Titze. We can interpret the flow data to indicate that older boys and men produce higher alternating glottal airflows because of their larger laryngeal structures and greater glottal areas. The flow measure corresponds to how fast the vocal folds are closing. and neurological components and from the complex coordination of these biological systems. 1). Maximum flow declination rate: The measure is obtained during the closing portion of the vocal fold cycle and reflects the fastest rate of airflow shut-o¤.’’ Figures 1 through 7 show cross-sectional vocal aerodynamic data obtained in children ages 4–14 years. 5. it is widely believed that as SPL increases. only adults and older teenagers produce lower open quotients for higher SPLs. Sound pressure level: This measure is obtained at the midpoint of the vowel from a microphone signal and corresponds physically to vocal intensity and perceptually to loudness. children continually alter their movements to make their voices sound ‘‘normal. The measure reflects how fast the vocal folds are opening and closing and the asymmetry of the opening and closing phases. the vocal folds remain closed for a longer proportion of the vibratory cycle as vocal intensity increases. regardless of vocal intensity. Maximum flow declination rate (MFDR): Children and adults regulate their airflow shut-o¤ through a combination of laryngeal and respiratory strategies. Di¤erentiating the airflow waveform and then identifying the greatest negative peak on di¤erentiated waveform locates the fastest declination. indicating that the vocal folds are open for a longer proportion of the cycle than in men and older boys. One of the striking features that emerge from the aerodynamic data is the change in function at 14 years of age for boys. Voice production arises from a multidimensional system of anatomical. while women and children seem to have more in common aerodynamically and physiologically. the open quotient decreases. This measure reflects the amplitude of vibration and can reflect the glottal area during vibratory cycle. It is notable that the younger children and women produce higher OQ-20%.

B. and sound pressure level. Fundamental frequency: As expected. A. Figure 3.and 6-year-olds produce unusually high f0 values when they increase their SPL to high levels (Fig. Laryngeal airway resistance: Children produce voice with higher Rlaw than 14-year-olds and adults. amplitude of vibration when they increase their SPL. B. and all speakers increase their Rlaw when increasing their SPL (Fig. Since Rlaw is calculated by dividing subglottal . An interesting result predicted by Titze’s (1988) modeling data is that the 4. 5). Changes in fundamental frequency are more easily e¤ected by increasing tracheal pressure when the vocal fold is characterized by a smaller e¤ective vibrating mass.70 Part I: Voice Figure 2. The interpretation is somewhat complicated by the fact that younger children and women have a shorter vocal fold length and smaller area (Flanagan. Figure 4. Airflow open quotient as a function of age and sex. and we would assume an increase in the alternating flow values. 1958). older boys and men produce lower fundamental frequencies than women and younger children. Maximum flow declination rate (MFDR) as a func- tion of age. 6). thereby limiting airflow through the glottis. Alternating glottal airflow as a function of age and sound pressure level. Alternating glottal airflow as a function of age and sex. as in young children ages 4–6 years. Airflow open quotient as a function of age and sound pressure level. sex. A.

and Cowan. The fact that subglottal pressure increases for high SPLs but flow does not increase clearly indicates that Rlaw must be increasing. R. (1982). References Arkebauer. Intraoral air pressure during the production of /p/ and /b/ by children. Journal of Speech and Hearing Disorders. male larynges continue to increase in size to approximate the size of adult male larynges. 13–17. whereas larynges in teenage girls plateau and approximate the size of adult female larynges (Fig. British Journal of Disorders in Communication. W. Bernthal. 21. In sum.. Stathopoulos sound pressure level. 361–371. 6. M. and physiological models of normal voice need to be referred to for the diagnosis and remediation of voice disorders. B. H. since the average glottal airflow is the same across age groups.. Figure 6.. J.. C. Physiologically. Intraoral air pressure for selected English consonants: A normative study of children. the shape and configuration of the laryngeal airway must be decreasing in size to maintain the constant airflow in the setting of increasing subglottal pressures.. Initial validation of an indirect measure of subglottal pressure pressure by laryngeal airflow. Figure 7. and Perkell. Carlborg. A. and Kitzing. 84. Purdue University.. T. L. that glottal airflow will increase when subglottal air pressure increases if laryngeal configuration/resistance is held constant. B. Diggs. R. Laryngeal airway resistance as a function of age and —Elaine T. It is not merely coincidental that at 14 years. Beckett. A general scan of the cross-sectional data discussed here shows a change in . Hillman. C. (1978). Journal of Speech and Hearing Research. P.. Journal of Speech and Hearing Research. children and adults alike continually modify their glottal airway to control the important variables of subglottal pressure and SPL. The cross-sectional aerodynamic data. 7). (1988). Hixon. Length of vocal fold as a function of age and sex. See also instrumental assessment of children’s voice. (1958). Normative study of airflow in children. Indiana. (1967). A. and Beukelman. it is clear that use of an adult male model for depicting normal vocal function is inappropriate for children. J.and sex-appropriate aerodynamic. B. E. vocal function at age 14 in boys. sex. C. J. E. L. Flanagan. 99– 116. 10. normal. 1. L. and in particular the flow data. Regardless of whether it is size or other anatomical factors a¤ecting vocal function. and sound pressure level. Fundamental frequency as a function of age. youths. A basic assumption needs to be discussed here. Glottal airflow and transglottal air pressure measurements for male and female speakers in soft. (1971). acoustic. and that is. Lofqvist. Unpublished master’s thesis. (1972). Holmberg. and Hardy. D. Lafayette. Age. Theolke. J. and loud voice. Some properties of the glottal sound source. J. 511– 529. make a compelling argument that the primary factor a¤ecting children’s vocal physiology is the size of their laryngeal structure. Journal of the Acoustical Society of America. R.. the high Rlaw for high SPL is largely due to higher values of subglottal pressure..Voice Disorders in Children 71 Figure 5. J. 196–208. Peak intraoral air pressure during speech. and adults.

since prescription and nonprescription drugs are used disproportionately by the elderly (Linville. 9. 137–147. particularly in later stages of old age. Titze. The reason why women are at greater risk than men for developing pathological epi- . mechanisms. 633–635. velopharyngeal closure. 1986. focal dystonia. Language. 1986. Voice Disorders of Aging Voice disorders a¿ict up to 12% of the elderly population (Shindo and Hanson. (1977). However. White (Ed. Journal of Speech and Hearing Research. Woo et al. A number of pathological conditions that a¤ect voice are prevalent in the elderly population simply because of advanced age. Oral airflow and air pressure during speech production: A comparative study of children. A clinical method for estimating laryngeal airway resistance during vowel production. C. Estimates of the incidence of peripheral laryngeal nerve damage in elderly dysphonic patients range from 7% to 21%. Timcke. Variations in the supraglottal air pressure waveform and their articulatory interpretation.. (1997).. and diplophonia. a thorough medical examination and history are required to rule out pathological processes a¤ecting voice in elderly patients (Hagen. E. In P. coordination of respiratory and phonatory systems. postural changes. 68.. 1992). 595–614. 318–389. T. and Brown.. reflux. Colton. 1997). T. von Leden. central neurological disorders such as stroke. 152–159. instability of vibration. P. Lyons. (1981). Stathopoulos. In addition. S.. I.. 37. M. Although the etiology of Reineke’s edema and polypoid degeneration is uncertain. R. H. Zeitels et al. augmentative communication strategies might be used. (1988). J. In some cases. (2000). inflammatory processes. After age 60. and Brewer. J. Journal of Acoustical Society of America. The specific site of the edema is the superficial layer of the lamina propria... Journal of Speech. Measurement of airflow in speech. 40. Some degree of edema and epithelial thickening is a normal accompaniment of aging in some individuals. distinguishing between pathology and normal age-related changes can be di‰cult. and Hearing Research. A review of the development of the child voice: An anatomical and functional perspective. speech prosody. and rib cage may also be compromised and may require treatment. unilateral sessile polyp. 1986. Such conditions include neurological disorders.. Subtelny. R.. Stathopoulos. E. and Worth.. Treatment may focus on vocal fold movement patterns. Reineke’s edema and polypoid degeneration occur more commonly in women and are characterized by chronic. and Hearing Research. 155–176. Woo et al. Interestingly. (1986). R. which occurs infrequently (Morrison and Gore-Hickman. Symptoms of peripheral paralysis include glottic insu‰ciency. Laryngeal vibrations: Measurements of the glottic wave. 46. including Reineke’s edema. or medical treatment may be combined with speech or voice therapy to improve outcomes (Ramig and Scherer.). and Nuss. Sweden: KTH Voice Research Centre. Therefore. (1966). Airflow rates in normal speakers. D. Functioning of the velopharynx.72 Part I: Voice during vowels. New York: Raven Press. 1–19. Language.. Treatment for central disorders involves attention to specific deficits in vocal fold function such as positioning deficits. 2001). 1992). and Weismer. (1980). multiple etiologic factors related to a voice disorder are more common in elderly patients than in younger adults. 227–238). Van Hattum. reduced loudness. respiratory support. as opposed to idiopathic peripheral paralysis. T. Developmental changes in laryngeal and respiratory function with variations in sound pressure level. R. 138–146. although more commonly it is diagnosed between the ages of 50 and 70 (Leon et al. A variety of benign vocal lesions are particularly prevalent in the elderly. 72.). E. Woo et al. youths. and benign epithelial lesions with variable dysplastic changes (Morrison and Gore-Hickman. and Hixon. Child voice. M. Elderly patients often exhibit neurological voice disorders. and endocrine disorders (Morrison and Gore-Hickman. G. benign lesions. Regulation of vocal power and e‰ciency by subglottal pressure and glottal width. Intraoral air pressure and rate of flow during speech. 1995. Woo. E. Indeed. International Symposium. peripheral paralysis in the elderly tends to be associated with disease processes associated with aging (such as lung neoplasm). W. abdomen. and incoordination of movements. 1990). diaphragm. and Sakuda. and vocal abuse/misuse have been mentioned as possible causal factors (Koufman. 4.. Smitheran. Journal of Speech and Hearing Research. and functions (pp. and essential tremor also occur frequently. 1996). Folia Phoniatrica. trauma. (1967). lips. J. Speech and Language Advance in Basic Research and Practice. 1992). Casper. stroboscopic examination of the vocal folds is recommended to detect abnormalities of mucosal wave and amplitude of vocal fold vibration that a¤ect voice production (Woo et al. H. tongue. and adults. and Moore. polypoid degeneration. M. breathiness. Vocal fold physiology: Voice production. H. 498–515. 2001). Fujimura (Ed. AMA Archives of Otolaryngology. cigarette smoking. Alzheimer’s disease. Journal of Speech. elderly persons are at increased risk for laryngeal side e¤ects from pharmacological agents. In addition. Generally. M. 4. and Sapienza. 1992). Voice therapy for peripheral paralysis frequently involves increasing vocal fold adductory force to facilitate closure of the glottis and improving breath support to minimize fatigue and improve speech phrasing. Stathopoulos. 1992). J. di¤use edema extending along the entire length of the vocal fold. Cleft Palate Journal. 1992). or speech intelligibility. T. Voice disorders in elderly persons can result from normal age-related changes in the voice production mechanism or from pathological conditions separate from normal aging (Linville. 20. (1958). Parkinson’s disease. Muller. J. Carcinoma of the head and neck occasionally occurs late in life.. Stockholm. 1986. Rothenberg. Worth. 1998). jaw. a number of investigators have concluded that the vast majority of elderly patients with voice disorders su¤er from a disease process associated with aging rather than from a disorder involving physiological aging alone (Morrison and Gore-Hickman. J.. In O.

such as visible tension in the cervical muscles. These factors result in considerable variation in phonatory characteristics. Francis and Wartofsky. 1992). Age-related laryngeal changes such as mucous gland degeneration might be a factor in development of laryngitis sicca (Morrison and GoreHickman. 2001). even if the procedure is uncomplicated (e. Physical conditioning is also important in nonsingers to prevent dysphonia in later life (Satalo¤. 2000). Inflammatory conditions such as pachydermia. Richter. Smoking also has a definite e¤ect on the larynx and alters laryngeal function. The incidence of functional hypertensive dysphonia among elderly speakers is disputed. enhanced nerve conduction velocity. Kahane and Beckford. it is a more complicated disease in this group. and agility. Gastroesophageal reflux disease (GERD) is another inflammatory condition that is reported to occur with greater frequency in the elderly (Richter. 1987). They also di¤er in lifestyle.. Lifestyle factors can either postpone or exacerbate the e¤ects of aging on the voice. 1983). high laryngeal position. De Vito et al. and increased blood flow (Spirduso. or from neuropathic disturbances resulting from diabetes (Maceri. voice changes are possible with thyroidectomy. burns. 2001). Smoking amplifies the impact of normal age-related changes in both the pulmonary and laryngeal systems. Satalo¤. The rate and extent of decline in motor and sensory performance with aging varies both within and across elderly individuals (Finch and Schneider. In addition. Age-related changes in the endocrine system also affect the voice. there is evidence that variability on measures of phonatory function in elderly speakers is reduced by controlling for a speaker’s physiological condition (Ramig and Ringel.. however.. Some investigators report significant evidence of phonatory behaviors consistent with hypertension.. 2000). Physical conditioning programs that include aerobic exercise often are recommended for aging professional singers to improve respiratory and abdominal conditioning and to avoid tremolo. Since GERD has been present for a longer time in the elderly in comparison with younger adults. 1991). Debruyne et al. 1992). Trauma might manifest as granuloma or scar tissue from previous surgical procedures requiring general anesthesia. The e¤ects of smoking coexist with changes related to normal aging in elderly smokers. elderly patients may be at increased risk for traumatic injury to the vocal folds. inflammatory processes. 1996. such as hyperactivity of the ventricular vocal folds in the elderly population (Hagen. and nonspecific laryngitis also are diagnosed with some regularity in the elderly (see infectious diseases and inflammatory conditions of the larynx). a report of increased phonatory e¤ort. 1998. Morrison and Gore-Hickman. 1986). Emerich. 1999). That is. reflux. Lyons. Clinicians also must be mindful of the overall health status of older patients presenting with voice disorders. Vocal fold scarring may be present as a consequence of previous vocal fold surgery. intubation. as well as relatively few cases of functional dysphonia without tissue changes (Woo et al. medications. The benefits of daily exercise include facilitated muscle contraction. 1986). A healthy lifestyle that includes regular exercise may also positively influence laryngeal performance. even if no pulmonary disease is detected (Hill and Fisher. that elderly patients need to be evaluated for evidence of hypertensive phonation and provided with therapy to promote more relaxed phonatory adjustments when evidence of hypertension is found. Woo et al. and neurological changes. Lifestyle factors and variability among elderly speakers often blur the distinction between normal and disordered voice. 2001). perhaps the most controllable and potentially significant lifestyle factors are physical fitness and cigarette smoking. 1993. and respiratory function capabilities among elderly speakers (Linville. Secretion disorders of the thyroid (both hyperthyroidism and hypothyroidism) occur commonly in the elderly and often produce voice symptoms. Spiegel. laryngitis sicca. Often elderly patients report less severe heartburn but have more severe erosive damage to the esophagus (Katz.. a pattern of glottal attack. although di¤erences in vocal use patterns could be a factor. physiological. 1986. Others report a low incidence of vocal fold lesions commonly associated with hyperfunction (vocal nodules. either as a consequence of altered hormone levels or as a result of increased pressure on the recurrent laryngeal nerve. 1997). 2001). 1997).Voice Disorders of Aging 73 thelial changes as they age is unknown. Although a potentially limitless combination of environmental factors combine to a¤ect aging. Elderly dysphonic patients often are in poor general health and have a high incidence of systemic illness. accuracy. or radiation therapy for glottic carcinoma (Morrison and Gore-Hickman. and Hoover. 1986. and Nuss. 1997. These conditions might arise as a consequence of smoking. 1985. Because of advanced age. 1992. Finch and Schneider. Declines in motor performance are directly related to muscle use and can be minimized by a lifestyle that includes exercise. Elderly smokers demonstrate accelerated declines in pulmonary function. as well as to improve endurance. pedunculated polyps). or poor hydration and often coexist with vocal fold lesions that may be either benign or malignant. Lee et al. 1997. Elderly persons di¤er in the rate and extent to which they exhibit normal age-related anatomical. articulatory precision habits. although a direct link has yet to be established (Ringel and Chodzko-Zajko. 1985). Clinicians are in agreement. and Rosen. Clinicians must consider smoking history in assessing an elderly speaker’s voice (Linville. Elderly persons also may experience vocal symptoms as a consequence of hypoparathyroidism or hyperparathyroidism. However. Pulmonary disease and hypertensive cardiac disease have been cited as particularly prevalent in elderly voice . 1982. Linville. elderly women may be more likely to develop hypertensive phonatory patterns in an e¤ort to compensate for the age-related pitch lowering that accompanies vocal fold thickening and edema (Linville. or from other traumatic vocal fold injuries. and/or anteroposterior laryngeal compression..g. The elderly population is extremely variable in fitness levels.

and Abitbol. Spirduso. Speech breathing in women. 35. T. Lyons. J. et al. Fahn. C.). 15. P. New York: Igaku-Shoin. (1997). and Laryngology. R. CA: Singular Publishing Group.. 368–373. Seminars in Speech and Language. 19)... D. (1993).. and Chodzko-Zajko. and Sidransky. Emerich. 120–151).. W.. 102. Ringel. F.. Koufman. Fahn.. The aging motor system (pp. and K. H..). (1998). J. T.).. Mahler (Ed. Acta Oto-Rhino-Laryngologica (Belgium). S. Boyle. (1992). and Hoover. Laryngoscope. Endocrine dysfunction. C.. X. and Sakaguchi. Physical fitness in relation to motor aging.). (1996). Ball (Eds.. Archives of Biochemistry and Biophysics... In Proceedings of the Research Symposium on Communicative Sciences and Disorders and Aging (ASHA Reports No. (1997). elderly dysphonic patients may be less compliant in following therapeutic regimens. D.. A. 309–316. R.. Hillman. Mortimer. P. the diagnosis and treatment of voice disorders are more complicated if multiple medical conditions are present (Linville. 2001). Hill. N. Kent and M. S. In R. Brennan. V. Ageing of the vibratory tissue of human vocal folds. D. Journal of Otolaryngology. P. The e¤ects of age on the voice. (1983). 1558–1565. Gould (Eds. Benjamin.. Korovin and W. Gastroesophageal disease in the older patient: Presentation. J. W. F. Kahane. K. Journal of Speech and Hearing Research. 1209–1215. Annals of Otology. Professional voice: The science and art of clinical care (pp. Finucane.. Glottal gap configurations in two age groups of women. 72–77. New York: Thieme Medical Publishers. R. 32. De Vito. 30. 268–277.. 63. J. or treatment for voice problems may need to be postponed.. Hirano.. 51. P. Gastroesophageal reflux and voice disorders. S. 107. CA: Singular Publishing Group. (1987). Gonzalez. Sasaki. Dysphonia in the elderly: Diagnosis and management of age-related voice changes. (1992). P. C. 106. R. (1992). W. (1997). Austin. Journal of Speech and Hearing Research.. Professional voice: The science and art of clinical care (pp. Ramig. E. J. R. Vocal indices of biological age.). San Diego. Handbook of geriatric communication disorders. Felici. Journal of the American Geriatrics Society. J.). Geriatric voice and laryngeal dysfunction. Katz.. (1997). 37. Journal of Speech and Hearing Research. Koch. Bastian. P. . 135– 141.. Postgraduate Medicine. D. 351–366. 424–446. Smoking cessation in the older chronic smoker: A review.. 533–543. Journal of Speech and Hearing Research. (1995). Drugs and Aging. W. In C. Lung biology in health and disease (vol. Further Readings Abitbol. Vocal aging. and Morgan. Rockville. (1996). (1999). Journal of Voice. E¤ects of physiological aging on selected acoustic characteristics of voice. The aging larynx and voice. If multiple health problems are present. F. Delaere. Agudelo.. (1989). Otolaryngology–Head and Neck Surgery. J. New York: Van Nostrand Reinhold. Satalo¤. M. C. 353–365. 291–297). T. Finch. Casper. and Ringel. 22–30. F. 362. Influence of age on laryngeal carcinoma. and Beckford.. 259–267). T. M.. Kahane.). Satalo¤ (Ed. Speech therapy for neurologic disorders of the larynx. (1987). Lu. Koufman.. S. Neurologic disorders of the larynx (pp. 19. 31–37. —Sue Ellen Linville References Debruyne. S. 161–175). Acta Otolaryngologica. Journal of Voice. and Anderson. treatment. Wellens. 89. 23... Shindo. In D. M. Lopez-Pousa. M.. 6. V. Woo. F. H. (1999). Bunting. Ramig.. 115. D. (1986). Altman. Zhang.. 18. CA: Singular Publishing Group. M. and Scherer. New York: Praeger. Journal of Sports Medicine and Physical Fitness. 75–87. (2001). (1990). and Gore-Hickman. Quer.. S.. In A. S. Ostyn. Brin. C. MD: American Speech-Language-Hearing Association. J. Patel. D. 95. S.. Hoit. R. Voice disorders in the elderly. Satalo¤. (1991). 231–234. (1982). R.. and Vaughn. TX: Pro-Ed. M. Pirozzolo.. In J. 163–181). In R. Ripich (Ed. J. 164–169. San Diego. 121. Reineke’s edema: Phonatory mechanisms and management strategies. Dysphonia in the aging: Physiology versus disease. Lee. H.. J. M. (1992). In R. Ford. Hixon. Maceri. 26. and Laryngology. Rhinology. (1997). (1998). E. Archives of Otolaryngology–Head and Neck Surgery. Low intensity physical training in older subjects.. and Schneider. Francis... Kurita. Benninger.. and Fisher. Liu. Linville. Vocal fold scarring: Current concepts and management. and Decoster. L. and Rosen. (1997). pp. 474–482. Hoit. and Figura. (1986). and Hixon... J. Morrison. Zeitels. R. L.. and Wartofsky... P. 225.. M. Harris (Eds. 13. New York: Marcel Dekker. (1989). R. Otolaryngologic Clinics of North America. Sex hormones and the female voice. and G. M. 262–265. G. J. 107. E. patients (Woo et al. Annals of Otology..74 Part I: Voice Richter. 46. 204–207. (1995).. D. CA: Singular Publishing Group.. (1995). Maletta (Eds. Speech production of normally aging adults. Satalo¤ (Ed.. 137–140. American Journal of Gastroenterology. Southern Medical Journal. Age and speech breathing. Voice quality measurement (pp.. Squamous cell carcinoma of the head and neck in the elderly. and Brewer. Head and neck manifestations of endocrine disease. Leon. Age-related changes in the peripheral speech mechanism: Structural and physiological changes. (1990). (2000). Colton. E. S. Linville. Archer. W. San Diego.. C. Common thyroid disorders in the elderly. The aging voice. et al. Diagnosis and treatment of voice disorders (pp. 92. and complications. 139–144. 189–218).. Otolaryngologic Clinics of North America. 359–376). R. E. J. B.. Lim.. C. 1992). Temporary voice changes after uncomplicated thyroidectomy. 1. Alessi.. Blitzer. Hagen. Concurrent increase of oxidative DNA damage and lipid peroxidation together with mitochondrial DNA mutation in human lung tissues during aging: Smoking enhances oxidative stress on the aged tissues. Gastroesophageal reflux disease. G. Hernandez. (1985). Abitbol. W. (2000). and Hanson. In D. 1035–1044. F. J. In general. Spiegel. and Nuss. 428–433. Diez. B. Linville. and Burgues. Handbook of the biology of aging. 171–180. De Juan. pp. D.). Rhinology.. San Diego. L. Thyroid disease in older patients: Diagnosis and treatment. S.

(1998). a su‰cient transglottal pressure will set them into oscillation. Kashima.. M. Gerontology: An interdisciplinary perspective (pp. this equation is used for each mass proposed. J.. Glottal configuration associated with fundamental frequency and vocal register. In multimass models of phonation (e. F. S. Kacker. 514–518. G. and optimizing pharmacotherapy. 12. Willey.).. x 0 is the velocity of the tissue. 544–551. 1992) for the prevailing conditions of the vocal fold tissues and adduction. R. Austin.. viscosity. Journal of Voice. S. 106. Casiano.. and Throat Journal. (2) where L is the vibrating length of the vocal folds. In D. Each term on the right-hand side characterizes forces in the tissue. Criner. This article discusses some of the mechanistic aspects of phonation. Kacker.. Koopermann (Eds. G. Whitbourne (Eds. D. 547–553. Fretwell. Hirano... and C. 1994) and da .. In J. H. 53. Ramig. L. k is a spring constant coe‰cient. Comparison of diaphragm strength between healthy adult elderly and young men. and they are balanced by the external air pressure forces acting on the vocal folds. velocity. N. and McMullen. Lundy. D. Tanaka. Decker. TX: Pro-Ed. and yet not too overly compressed.. Luschei. When the vocal folds are lengthened by rotation of the thyroid and cricoid cartilages through the contraction of the cricothyroid (CT) muscles. Phonosurgery in the elderly: A review. and Blaugrund. K.. Muza. and sti¤ness each play a role in the motion (normal or abnormal) of the vocal folds. and Blaugrund. J. M.. and Woodson. (1999). L. K. Tolep. (1990). and Rosenbek. S. 53. Scherer.. voice. Otolaryngology–Head and Neck Surgery. (2) The space created by the intercartilaginous glottis determines the ‘‘constant’’ opening there through which some or all of the dc (baseline) air will flow. Murry. and Xue. 45. P35–P45. The aging voice: A review. 78. (1991). K. Nose. Glottal adduction has three parts.. 103. the vocal folds must be within the phonatory adductory range (not too far apart. Slavit. Handbook of geriatric communication disorders. Evaluation and management of voice disorders in the elderly. (1) How close the vocal processes are to each other determines the posterior prephonatory closeness of the membranous vocal folds. D. sp is the passive tension of the tissue in motion. 76–79. 118. x is the position of the tissue from rest. Vocal evaluation of thyroplasty type I in the treatment of nonparalytic glottic incompetence. T. American Journal of Respiratory and Critical Care Medicine. D.. C. Folia Phoniatrica et Logopedica.. Morrison.C. 44–49. Buder. A. (1999).. Drugs and Aging. or density increases. Ishizaka and Flanagan.. Slavit. R. Owens. (1994). 1972). that these are associated with the acceleration. and r is the density of the tissue in motion. (3) The closeness of the membranous vocal folds partly determines whether vocal fold oscillation can take place. Weismer.. and will tend to fall if the length.. and Liss. Titze. da =d is the ratio of the depth of the thyroarytenoid (TA) muscle in vibration to the total depth in vibration (the other tissue in motion is the more medial mucosal tissue). K. G. M.. 4. and Laryngology. (1998). D. (1998). Speech motor control and aging. Increasing subglottal pressure increases the lateral amplitude of motion of the vocal folds. S. and the transglottal pressure must be at or greater than the phonatory threshold pressure (Titze. Sinard.. E.. (1998). Xu..). A. 103. Geriatric otorhinolaryngology. Distinguishing between the fit and frail elderly. and Laryngology. related to the pitch of the voice. (1998).. The aging voice: How to di¤erentiate disease from normal changes.g. and Hall. This oscillation produces cycles of airflow that create the acoustic signal known as phonation. 65–90). Goldstein. and x 00 is the acceleration of the tissue. 357–362.. S. The most general expression to date for pitch control has been o¤ered by Titze (1994). L. thus increasing sp (via greater passive stretch. 108. (1994). the voice signal. Lu. Higgins. Rhinology... K. S. Some aspects of vocal fold bowing. Annals of Otology. 47– 55. 481–485. b is a viscous coe‰cient. and Chijiwa. (1995). J.. mass. Rammage.. R. Ear. C. Omori. . thereby increasing Voice Production: Physics and Physiology When the vocal folds are near each other. and Kelsen. Omori. M. aTA is the activity level of the TA muscle. 152. the passive stretching of the vocal folds increases their passive tension. (1) where F (x) is the air pressure forces on the vocal fold tissues. J. Lundy. (2001). the voicing sound source. Silva. 252–265. sam is the maximum active stress that the TA muscle can produce. H. K. New York: Oxford University Press. Lu.. Luborsky. or more generally. and the left-hand side represents the external forces.. Philadelphia: B. The fundamental frequency F0. and Xue. Cavanaugh and S. This equation emphasizes the understanding that mass. Selected acoustic characteristics of speech production in very old males. Matos. Geriatrics.. D. D. J. et al. To permit oscillation. and Laryngology. Weismer. Rhinology. Laryngoscope. H.. Rhinology. Corbin-Lewis. and displacement of the tissue. Ripich (Ed. S. and Murphy. 75 The most general expression of forces in the larynx dealing with motion of the vocal folds during phonation is F (x) ¼ mx 00 þ bx 0 þ kx. 1995). G. Influence of size and etiology of glottal gap in glottic incompetence dysphonia. (1989). 505–512.. will tend to rise if the tension of the tissue in motion increases. Kojima.. Annals of Otology. Casiano.. 677–682. Vocal fold atrophy: Quantitative glottic measurement and vocal function. Culture and aging.. D. F. (1997). Cause of hoarseness in elderly patients. N. Annals of Otology. Journal of Gerontology Psychological Sciences..). In J.Voice Production: Physics and Physiology Liss. m is the mass of the tissue in motion. treatment data and familial and genetic perspectives. C.. J. respectively. Gray. viz.. S. Baker. Slavit. pffiffiffiffiffiffiffiffiffiffiffiffi F0 ¼ (0:5=L) (sp =r) Ã (1 þ (da =d ) Ã (sam =sp ) Ã aTA ) 0:5 . and thus L and sp tend to counter each other. with sp being more dominant (F0 generally rises with vocal fold elongation). E. and Nichol.

MFDR is the maximum flow declination rate (derivative of the flow). need to be established in the human larynx for the wide range of possible phonatory and vocal tract acoustic conditions. including the di¤erentiated contraction of the complex TA muscle. Leanderson. along with the alternation of the internal forces of the vocal folds. the intensity of the first formant region (at least). The flow peak. 1969. An increase in the subglottal pressure during phonation can a¤ect the cyclic glottal flow waveform (Fig. Intensity increases with an increase in subglottal pressure. The vocal tract filter function will augment the spectral intensity values of the glottal flow source in the region of the formants (resonances). and Vennard. and the pressures on the walls of the lower glottis are negative because of this shape (Fig. The transglottal pressure was 10 cm H2 O in this illustration. 1983). and vocal tract aspects. Glottal entrance is at the minimum diameter position for the divergent glottis. One cycle of glottal airflow. F0. 1994). 2). and von Euler. Glottal adduction level greatly a¤ects the source spectrum or quality of the voice. The length of the glottal duct was 0. F0 control. 2000). This positive pressure separates the folds during glottal opening. which itself depends on both lung volume reduction (an increase in air pressure in the lungs) and adduction of the vocal folds (which o¤ers resistance to the flow of air from the lungs). Liljencrants. 1989). Uac is the varying portion of the waveform. both having a minimal glottal diameter of 0.76 Part I: Voice Figure 1. and corner sharpness respectively increase the intensity of F0. Ohala. and the sharpness of the baseline corner when the flow is near zero (or near its minimum value in the cycle). is a combination and coordination of respiratory. During glottal closing. . Supraglottal pressure was taken to be atmospheric (zero). Thus. 2001). and Kucinschi. 1995). The intensity of voiced sounds.04 cm (using a Plexiglas model of the larynx. wider in the upper glottis). 1985. and corner sharpness are all important for the spectral aspects of the flow pulse (see text). This alternation in glottal shape and intraglottal pressures. the maximum rate that the flow shuts o¤ as the glottis is closing). 2).3 cm. laryngeal. both of which would raise F0 but at the same time decrease the passive tension (sp ) and the depth of vibration (da ). cricoid tilt via tracheal pull (Sundberg. and Udc is the o¤set or bias flow. The flow peak is the maximum flow in the cycle. MFDR. and subglottal pressure. The convergent glottis shows positive pressures and the divergent glottis shows negative pressures throughout most of the glottis. and Lin. Titze. Figure 2. as well as the changing shape of the glottis and the changing intraglottal air pressures during each cycle. increasing the maximum flow declination rate (MFDR. MFDR. Scherer and Shinwari. During glottal opening. typically located on the right-hand side of the flow pulse. and the associations with adduction and vocal quality all need much study. 1) by increasing its flow peak. which would decrease F0. The radiation away from the lips will increase the spectrum slope (by about 6 dB per octave). Greater peak flow. Pressure profiles within the glottis. Maintenance of vocal fold oscillation during phonation depends on the tissue characteristics mentioned above. 1989). the shape of the glottis is divergent (narrower in the lower glottis. maintains the oscillation of the vocal folds. the shape of the glottis corresponding to the vibrating vocal folds is convergent (wider in the lower glottis. Increasing the contraction of the TA muscle (aTA ) would tend to sti¤en the muscle and shorten the vocal fold length (L). DeWitt. the primary control for F0 is through the coordinative contraction of the TA and CT muscles. The curvature at the glottal exit of the convergent glottis prevents the pressures from being positive throughout (Scherer. narrower in the upper glottis). anterior pull by the hyoid bone (Honda. and the intensity of the higher partials (Fant. related to the loudness of the voice. and negative throughout the glottis when there also is rarefaction (negative pressure) of the supraglottal region. and the corner curvature at the end of the flow pulse describes how sharp the corner ‘‘shut-o¤ ’’ is. and will decrease their inten- sity values in the valleys of the resonant structure (Titze. Gau‰n and Sundberg. The upper trace corresponds to the data for a glottis with a 10 convergence and the lower trace to data for a glottis with a 10 divergence. and the pressures on the walls of the glottis are positive due to this shape and to the (always) positive subglottal pressure (for normal egressive phonation) (Fig. large changes in F0 are associated with increased contraction of both the CT and TA muscles (Hirano. 1994). increasing the negative slope of the spectrum as one changes voice production from highly compressed voice (a relatively flat spectrum) to normal adduction to highly breathy voice (a relatively steep spectrum) (Scherer. The exact glottal shape and intraglottal pressure changes. however. Typically.

and approaches for phonosurgery. S. (1996). Alipour. and Scherer. from more resistance (decreasing the flow if the false folds are quite close) to less resistance (increasing the glottal flow when the false folds are in an intermediate position) (Agarwal and Scherer. Berry. G.. and Berke. quality. and Titze. 1976. Vocal fold physiology: Controlling complexity and chaos (pp. W.... R. J. Abbs (Eds. The most complete approach so far is to combine finite element modeling of the tissue with computational fluid dynamics of the flow (to solve the Navier-Stokes equations. and glottal shape (via vocal fold length. . creating roughness. In D. one vocal fold may not vibrate like the other one.Voice Production: Physics and Physiology 77 Figure 3. Rothenberg. 1983). J. but also closer to physiological reality. G. CA: Singular Publishing Group. Combined simulation of airflow and vocal fold vibrations. Computer modeling needs to be practical.. I. 556–565. glottal flow resistance (transglottal pressure divided by the airflow). Scherer. When the two medial vocal fold surfaces are not mirror images of each other across the midline.. When lung volume reduction is then employed. and radiation from the lips. F.). Journal of Voice. (1983). —Ron Scherer References Agarwal. Ishizaka. Baken. 1972). if there is tissue asymmetry. 108. 2001). TA. in press). 2002) and therefore di¤erent driving forces on the two sides. subharmonics. Spectral correlates of glottal voice source waveform characteristics. A four-parameter model of glottal flow. 3003–3012. and the output spectra (quality) and intensity (loudness) result from the combination of the glottal flow. 14. and modeling remain unclear for both normal and abnormal phonation. (1969).. S66. Scherer et al. San Diego. Also. 1993.. 1233–1268. Alipour. (in press).. 2001. 4. the glottal flow is a¤ected by the resonances of the vocal tract (pressures acting at the glottis level) and the inertance of the air of the vocal tract (to skew the glottal flow waveform to the right.. Journal of Speech and Hearing Research. and Lin. 1991. A finiteelement model of vocal-fold vibration. B. Bell System Technology Journal. and Hollien. 616–628. 1995). The glottal flow (the volume velocity flow) is considered a primary sound source. and cyclic groupings (Isshiki and Ishizaka. 1–13. Journal of the Acoustical Society of America. The function of the laryngeal muscles in regulating fundamental frequency and intensity of phonation. aeroacoustics. the geometric asymmetry creates di¤erent pressures on the two sides (i. Hirano. Stockholm: Royal Institute of Technology. (1989). The false vocal folds: Shape and size in coronal view during phonation. R. F. Alipour and Scherer.e. and adduction). 1996). Vocal fold bulging: E¤ects on phonation using a biophysical computer model.. posterior cricoarytenoid.. See also voice acoustics. 17–29). R. M.. Ohala. that is. J. Fletcher (Eds. 32. J. 2000). phonation styles and types. San Diego. Many basic issues of glottal aerodynamics. adduction (via TA. K. Bless and J. Factors leading to pitch. Steinecke and Herzel. as in finite element modeling (Alipour. Source characteristics of diplophonia... Figure 3 summarizes some basic aspects of phonation. and the fundamental frequency (and pitch) of the voice. R.. K. Synthesis of voiced sounds from a two-mass model of the vocal cords. as well as for providing rehabilitation and training feedback for clients. However. M. Honda. Journal of the Acoustical Society of America... we still need models of phonation that are helpful in describing and predicting subtle aspects of laryngeal function necessary for di¤erentiating vocal pathologies. and Vennard. and TA rounding e¤ect). (1985). 83. Berry. Gerratt et al. and Titze. and Flanagan. Liljencrants. With the vocal tract included. H. Precoda. C. resonance.. 12. H. Journal of Voice. See text. Fant. and interarytenoid muscle contraction). J.). tension (via CT. (2000). The false vocal folds themselves may contribute significant control of the flow resistance through the larynx. and Titze. 51. R. Journal of Speech and Hearing Research. K. and the presence of the false vocal folds may interfere with the glottal jet and create a secondary sound source (Zhang et al. as in twomass modeling (Ishizaka and Flanagan. pressure asymmetries. and loudness pro- duction.. (1988). The upper left suggests muscle contraction e¤ects of vocal fold length (via CT and TA action). 2001). lateral cricoarytenoid. A. F. Relationship between pitch control and vowel articulation. Speech Transmission Laboratory Quarterly Progress and Status Report. The turbulence and vorticities of the glottal flow may also contribute sound sources (Zhang et al. I. and Sundberg. Gerratt. Vocal fold physiology: Contemporary research and clinical issues. (1972). (2000). L. adduction. D. 1988. C. M. and Herzel.. Q. In P. glottal airflow and subglottal pressure are created. D. Hanson. if the two vocal folds themselves do not have equal values of tension (sti¤ness) and mass. CA: College-Hill Press. Wong et al. Alipour and Titze. Gau‰n. 2000. Titze. Davis and N. resulting in motion of the vocal folds (if the adduction and pressure are su‰cient). 470–483. Alipour.

3. and Titze. listeners evaluate voices on the scales Grade (or extent of pathology). R. Steinecke. In D. Activity relationship between diaphragm and cricothyroid muscles. Computational aeroacoustics of phonation: E¤ect of subglottal pressure. Bless and J. Most techniques for assessing voice quality fall into one of two general categories: perceptual assessment protocols. B.. DeWitt. Perceptual Evaluation of Voice quality is the auditory perception of acoustic elements of phonation that characterize an individual speaker. In perceptual assessments. Frankel. (1992). R. vocal abuse. 1874–1884. L. Zhao. Vocal fold physiology: Contemporary research and clinical issues (pp. S. T. For example. Zhang... (2001). both clinically and experimentally. 383– 394.. Wong. brassiness. Kucinschi. 89. R. CA: Singular Publishing Group. Titze. K.. Diagnosis and treatment of voice disorders (pp. Researchers from other disciplines are also interested in measuring vocal quality. and sweetness. For example.. 1981). pitch. Scherer. Evaluation of vocal quality is an important part of the diagnosis and treatment of voice disorders. R. Shinwari. Many other similar protocols have been proposed.). M. Observation of perturbations in a lumped-element model of the vocal folds with application to some pathological cases. and loudness. 17 parameters) and Laver (approximately . pitch.. Shinwari. Abbs (Eds. K. and Afjeh. Intraglottal pressure profiles for a symmetric and oblique glottis with a uniform duct. R. Sundberg. for example. R. Laryngeal function during phonation. Zhang. 112(4). In the GRBAS protocol (Hirano. 110. (1995). Journal of the Acoustical Society of America. M. 97. Fairbanks (1960) recommended that voices be assessed on 5-point scales for the qualities harshness... R.). R.. brilliance. San Diego. H. Ito. Ancient writers on oratory emphasized voice quality as an essential component of polished speech and described methods for conveying a range of emotions appropriately. Rothenberg. (2002). (1989). for review). and breathiness. C. Phonation threshold pressure: A missing link in glottal aerodynamics. 107. a nasal voice indicated a spiteful and immoral character. creakiness. CA: College-Hill Press. pitch breaks.. and W. (2001). (1991). I.. (1983). and Herzel. 60. D. I. and Mongeau. 143–188). but in general. 1253–1256. M. laxness. H. The e¤ect of exit radii on intraglottal pressure distributions in the convergent glottis. and law enforcement o‰cials need to assess the accuracy of speaker identifications. Kucinschi. Thus. A. (1976). and most often they judge the success of treatment for the voice problem by improvement in their voice quality. pitch instability. and ventricular folds. R. A 13-scale protocol proposed by Hammarberg and Gau‰n (1995) includes scales for assessing aphonia (lack of voice). Journal of the Acoustical Society of America. C. (2001). 1998) has expanded it to GIRBAS by adding a scale for Instability.). In J. Zhang. Baken. 109.78 Part I: Voice Isshiki. Asthenicity (weakness or lack of power in the voice). 2267–2269. or protocols employing an acoustic or physiologic measurement as an index of quality. (1994). For example. (1993). N.. glottal oscillation frequency. rate. Journal of the Acoustical Society of America. I. N. and Shinwari. a listener (or listeners) rates a voice on a numerical scale or a set of scales representing the extent to which the voice is characterized by critical aspects of voice quality. D.. Even more elaborate protocols have been proposed by Gelfer (1988. voice breaks. or shrillness (see Laver. A.. Journal of the Acoustical Society. In I. Roughness. Voice Quality.. Scherer. C. with each scale ranging from 0 (normal) to 4 (severely disordered). K. R. Titze.. Journal of the Acoustical Society of America. D. and von Euler. tension. Journal of the Acoustical Society of America. nasal emission. 1616–1630. psychologists are concerned with the perception of emotion and other personal information encoded in voice. R. and Kucinschi.. A.. Patients usually seek clinical care because of their own perception of a voice quality deviation.. Breathiness. The ancient Greeks asso- ciated certain kinds of voices with specific character traits. Titze (Ed. J. laryngeal tension. C. and overall vocal e‰ciency. 155–165). Scherer. linguists are interested in how changes in voice quality can signal changes in meaning. Journal of Voice. Journal of the Acoustical Society of America. I. Journal of the Acoustical Society of America. diplophonia (perception of two pitches in the voice). H. falsetto. Scherer. H. C. K. Computer simulation of pathological vocal cord vibration. C. J. Satalo¤. and Ishizaka. 2412 (A). A clinician may also judge success by documenting changes in laryngeal anatomy or physiology. (1995). A recent revision to this protocol (Dejonckere et al. and for avoiding undesirable characteristics like roughness. Leanderson.04 cm. breathiness. Bifurcations in an asymmetric vocal-fold model. Voice quality has been of interest to scholars for as long as people have studied speech. and Afjeh. B. roughness. New York: Igaku-Shoin. Principles of voice production. R.. Despite this long intellectual history and the substantial cross-disciplinary importance of voice quality. 109. R. Korovin. vocal inflections. Titze. J. Glottal pressure profiles for a diameter of 0. 2905 (A). Gould (Eds. R. 2926–2935. De Witt. 225–232. hoarseness. 86– 104). (2000). engineers seek to develop algorithms for signal compression and transmission that preserve voice quality. it is an interaction between the acoustic speech signal and a listener’s perception of that signal. S.. Intraglottal pressure profiles for a symmetric and oblique glottis with a divergence angle of 10 degrees. the Wilson Voice Profile System (Wilson. R. W. S. Scherer. resonance. 1977) includes 7-point scales for laryngeal tone. An interactive model for the voice source. C. Vocal fold physiology: Frontiers in basic science (pp. measurement of voice quality is problematic. San Diego. 91. loudness.. Journal of the Acoustical Society of America. G. D. C. C. Cox. patients are more concerned with how their voices sound after treatment. B. for cultivating power. B. R. 1193–1198. and Strain. Evidence of chaos in vocal fold vibration. NJ: Prentice Hall. gratings. Englewood Cli¤s.. DeWitt. diplophonia. J. 1981... and Herzel. Rubin. I.

The usefulness of such protocols for perceptual assessment is limited by di‰culties in establishing the correct and adequate set of scales needed to document the sound of a voice. correlation does not imply causality: simply knowing the relationship of an acoustic variable to a perceptual one does not necessarily illuminate its contribution to perceived quality. and contribute to listener disagreement (see Gerratt and Kreiman. Thus. or the acoustic signal for these flawed perceptual measures. This approach reflects the prevailing view that listeners are inherently unable to agree in their perception of such complex auditory stimuli. we cannot know the perceptual importance of particular aspects of the acoustic signal without valid measures of that perceptual response. Further. listeners can manipulate acoustic parameters and hear the result of their manipulations immediately. and may vary substantially across listeners as well as within a given listener. more than 60% of the variance in ratings of voice quality is due to factors other than di¤erences between voices in the quality being rated. fails to provide useful insight into the perceptual process. and validly specify the voice quality of interest. severity of vocal deviation. Such a set could obviate the need for voice quality labels. di‰culty isolating individual dimensions in complex perceptual contexts. This process helps listeners focus attention on individual acoustic dimensions. In addition. acoustic measures that purport to quantify vocal quality can only derive their validity as measures of voice quality from their causal association with auditory perception. internal standards appear to vary with listeners’ previous experience with voices (Verdonck de Leeuw. Perceptual Evaluation of 79 50 parameters. suggesting that such instrumental measures are not stable indices of perceived quality. These factors (and possibly others) presumably all add uncontrolled variability to scalar ratings of vocal quality. They measured vocal quality by asking listeners to copy natural voice samples with a speech synthesizer. 1998) and with the context in which a judgment is made. airflow. parsimonious set of acoustic parameters that successfully characterizes all possible normal and pathological voice qualities. for review). consistent correlations have never been found between perceptual and instrumental measures of voice. e. given the great variability in perceptual strategies and habits that individual listeners demonstrate in their use of traditional rating scales.Voice Quality. In response to these substantial di‰culties. scale ratings may vary depending on variable listener attention. listeners vary speech synthesis parameters to create an acceptable auditory match to a natural voice stimulus.g. Methods like visual-analog scaling (making a mark on an undi¤erentiated line to indicate the amount of a quality present) or direct magnitude estimation (assigning any number—as opposed to one of a finite number of scale values—to indicate the amount of a quality present) have also been applied in e¤orts to quantify voice quality. However. the synthesis settings parametrically represent the listener’s perception of voice quality. 1996). Further. allowing researchers and clinicians to replace quality labels with acoustic parameters that are causally linked to auditory perception. 1998). the nature of that contribution would not be revealed by a correlation coe‰cient. the overall correlation between acoustic and perceptual variables. Much more research is certainly needed to determine a meaningful.. they need not refer to internal standards for particular voice qualities. In addition. and di¤erences in listeners’ previous experience with a class of voices (Kreiman and Gerratt. because voice quality is by definition the perceptual response to a par- ticular acoustic stimulus. and that tools can be devised to measure perception reliably. Even if an acoustic variable were important to a listener’s judgment of vocal quality. presumably because this analysis-synthesis method controls the major sources of variance in quality judgments while avoiding the use of dubiously valid scales for quality. averaged across samples of listeners and voices. using a measure of acoustic frequency perturbation as a de facto measure of perceived roughness (see acoustic assessment of voice). completely. for example.) Gerratt and Kreiman (2001) proposed an alternative solution to this dilemma. Practically. These idiosyncratic. —Bruce Gerratt and Jody Kreiman . 2000. In this method. Greene and Mathieson. Evidence suggests that on average. reducing the perceptual complexity of the assessment task and the associated response variability. Ratings may be made with reference to ‘‘anchor’’ stimuli that exemplify the di¤erent scale values. and some evidence suggests that di¤erences between listeners in perceptual strategies are so large that standardization e¤orts are doomed to failure (Kreiman and Gerratt. where external stimuli (the voices) are compared to stored mental representations that serve as internal standards for the various rating scales. Researchers have never agreed on a standardized set of scales for assessing voice quality. di‰culty isolating single perceptual dimensions within a complex acoustic stimulus. (See Kreiman and Gerratt. some researchers suggest substituting objective measures of physiologic function. or with reference to a listener’s own internal standards for the di¤erent levels of a quality. For example. Theoretically. 2001. When a listener chooses the best match to a test stimulus. Preliminary evaluation of this method demonstrated near-perfect agreement among listeners in their assessments of voice quality. and factors like lapses in attention can also influence perceptual measures of voice (de Krom. Finally. how such protocols will function in clinical (rather than research) applications remains to be demonstrated. listeners are apparently unable to agree in their ratings of voices. 1989). for an extended review of these issues. Theoretical and practical di‰culties also beset this approach. and whose levels objectively. Because listeners directly compare each synthetic token they create with the target natural voice. 1994). Evidence suggests that traditional perceptual scaling methods are e¤ectively matching tasks. These results indicate that listeners do in fact agree in their perceptual assessments of pathological voice quality.

Vocal characteristics following conservation laryngectomy are a consequence of anatomical influences and the resultant physiological function of the postsurgical laryngeal sphincter. San Diego.. Leeper. (1996).. (2001). Consistency and reliability of voice quality ratings for di¤erent types of speech fragments. G. Utrecht.). 73–102). (1998). M. B. B. Hammarberg... 985–1000. J. Sources of listener disagreement in voice quality assessment. and Reynolds. D. L. 119. (2000). J.). Perceptual analysis of voice quality: Trained and naive raters. This may then call attention to the voice. Greene. Measuring vocal quality with speech synthesis. and Kreiman. 1984. I. and Gerratt. Voice quality measurement. 1997). Measuring vocal quality. Kempster. B.). Revue de Laryngologie Otologie Rhinologie. However.. In G. Journal of Speech and Hearing Research.. and Gau‰n. Fairbanks. In O.. Laver. H. and Coleman. (1994). B. tutorial. 1990. J. with varied degrees of social pen- Further Readings Gerratt. and Mathieson. Fujimura and M. Retention of adequate valvular function allows conservation of some degree of vocal function and safe swallowing. 104. the degree of air leakage through the reconstructed laryngeal sphincter. Doyle. 1867–1879.. J. Verdonck de Leeuw. 1992. Hirano. San Diego. Journal of the Acoustical Society of America. R. G. and a framework for future research. M. New York: Springer-Verlag. Leeper. appear to play a significant role in compensatory behaviors influencing auditory-perceptual assessments of voice quality (Doyle. Dejonckere. 1995.. C. 1981). R. (1998). (2000). S. Kreiman. (2001).. and Kreiman. and Millet. Similarly.). Fresnel-Elbaz. Voice Rehabilitation After Conservation Laryngectomy Partial or conservation laryngectomy procedures are performed not only to surgically remove a malignant lesion from the larynx. Doyle et al. Voice and articulation drillbook. Clinical examination of voice. 1994). The voice and its disorders. 110. J. G. The perceptual structure of pathologic voice quality. E. Kreiman. Heeneman.. F. Ball (Eds. compensatory adjustments in respiratory volume in an e¤ort to drive a noncompliant voicing source characterized by postsurgical increases in its resistance to airflow may negatively influence auditory-perceptual judgments of the voice by listeners. Heeneman. with disruption of the vibratory integrity of at least one vocal fold (Bailey. B. the primary goal of conservation laryngectomy procedures is cancer control and oncologic safety. 21–40. 1990. San Diego. Gerratt. and Doyle. P. Kent. (1998). Hoasjoe et al. Wilson.. (2000). 1984. 79–99). Leeper. B. CA: Singular Publishing Group. (1989). and Doyle. London: Whurr. Woisard. 1787–1795. Kreiman. but data clearly indicate perceived changes in voice quality. vibratory.. R. Keith. M. Hirano (Eds. 1983. In R. 320– 326. B. Changes in laryngeal structure result in aerodynamic. A. and Reynolds. as well as secondary physiological compensation. (1981). 108. this level of compensation may facilitate the communicative process. 2560–2566. (1993). 1997). with a secondary goal of maintaining upper airway sphincteric function and phonatory capacity postsurgery. M. L. . From the standpoint of voice production. B. Journal of Voice. Schecter. (1995). 110. Toward a history of phonetics (pp. New York: Harper. J. volitional. Austin. 2. Rizer. Proceedings of Voicedata98 Symposium on Databases in Voice Quality Research and Education (pp..80 Part I: Voice References de Krom. any degree of laryngeal tissue ablation has direct and potentially highly negative implications for the functional capacity of the postoperative larynx.. Gerratt. J. R. 2560–2566. but in other instances such compensations may be detrimental to the speaker’s communicative e¤ectiveness (Doyle.. R. conservation laryngectomy will always necessitate tissue ablation. TX: Learning Concepts. Journal of Speech and Hearing Research. the appearance of compensatory hypervalving. V. 100.. but also to preserve some functional valving capacity of the laryngeal mechanism. Edinburgh: Edinburgh University Press. 37. R. Vocal fold physiology: Voice quality control (pp.. Excessive closure of the laryngeal mechanism at either glottic or supraglottic (or both) levels might decrease air escape. Kreiman. (1960). Remacle. 36. the Netherlands: Utrecht Institute of Linguistics. Perceptual attributes of voice: Development and use of rating scales. G. In some instances. Doyle et al. 1995. J. 247–248. Perceptual observations following a variety of conservation laryngectomy procedures have been diverse. 283–303).. Journal of the Acoustical Society of America. M. Kent and M. Gerratt. and Berke. As such. (1988). de Krom (Ed. Journal of the Acoustical Society of America. CA: Singular Publishing Group. and Gerratt.. B. and ultimately acoustic changes in the voice signal (Berke. Crevier. Two factors in particular. Henderson (Eds. Validity of rating scale measures of voice quality. Reliability and clinical relevance of perceptual evaluation of pathological voices. Gelfer. (1981). (1977). and Gerratt.. Journal of the Acoustical Society of America. and Hanson. and other features (Blaugrund et al. Erman. 1996. and self-ratings. R. The analysis of vocal quality: From the classical period to the 20th century. D. Voice quality measurement (pp. but may also create abnormalities in voice quality due to active (volitional) hyperclosure (Leeper. 1996). R. Journal of the Acoustical Society of America. Asher and E. 1997). Kreiman. Perceptual evaluation of voice quality: Review. Voice disorders. 12–15). L. Keith. and Ball. M. J. J.. Measuring vocal quality with speech synthesis. Doyle. and Gerratt. 1598–1608. B. In R. CA: Singular Publishing Group. glottic insu‰ciency and the relative degree of compliance and resistance to airflow o¤ered by the reconstructed valve. Perceptual and acoustic characteristics of quality di¤erences in pathological voices as related to physiological aspects. J. P.

Voice analysis of the partially ablated larynx: A preliminary report. In such cases of hypofunctional behavior. and whether changes in voice quality may be the result of multiple factors. the clinician should be able to discern functional (physiological) changes to the sphincter that may have a direct influence on voice quality. Common facilitation methods may involve the use of visual or auditory feedback. Further treatment goals should focus on (1) enhancing residual vocal functions and capacities. 1997). T. The clinical evaluation of individuals who have undergone conservation laryngectomy initially focuses on identifying behaviors that hold the greatest potential to negatively alter voice quality. However. J. The physical and psychological demands placed on the patient during initial attempts at voicing might increase levels of tension that ultimately may reduce the individual’s phonatory capability. 502–508. (2) a slow. J. clinical tasks that focus on reducing overcompensation (i. 1742–1771. and Hanson. Partial laryngectomy and laryngoplasty. For example. ear training. (1977). Although the rationale for such ‘‘abnormal’’ behavior is easily understood. 1990). A comprehensive framework for the evaluation and treatment of voice alterations in those who have undergone conservation laryngectomy is available (Doyle. it may be preferable for some speakers when compared to a breathy voice quality. Boone. G. (3) increasing the length of utterance in conjunction with consistently easy phonation. Doyle References Bailey. Colton and Casper.’’ The intent is to improve vocal e‰ciency and generate the best voice quality without excessive physical e¤ort. and Laryngology. (1981). Because active glottic hypofunction is infrequently noted in those who have undergone conservative laryngectomy. S.. This is of particular importance when evaluating goals and potential voice outcomes relative to the speaker’s sex. Annals of Otology. Gould. Laryngoscope. 1997).g. Such compensations may remain when the discomfort has resolved. Many individuals who have undergone conservative laryngectomy may demonstrate considerable e¤ort during attempts at postsurgical voice production. primary treatment targets will frequently address changes in voice quality and/or vocal e¤ort. Otolaryngology–Head and Neck Surgery. Maladaptive compensations following conservation laryngectomy often tend to be hyperfunctional behaviors. and may result in perceptible limitations in verbal communication. J. or intermittent voice stoppages may be experiencing problems that result from postoperative physiological overcompensation because they are struggling to produce voice. Boone and McFarland. 91. W. Metzler. the ultimate postsurgical e¤ects of conservation laryngectomy on voice quality may result in unique limitations for men and women.. hyperfunctional closure) are more commonly used.. 1977. the speaker’s attempt to increase vocal loudness may create a level of hyperclosure that is detrimental to judgments of voice quality. 1995). NJ: Prentice Hall. Until recently. Rhinology. Colton and Casper. Englewood Cli¤s. or simply to initiate the generation of voice. Doyle. only limited comprehensive data on vocal characteristics of those undergoing conservation laryngectomy have been available. Those auditoryperceptual features that most negatively a¤ect overall voice quality should form the initial targets for therapeutic intervention. Careful. . An acoustic analysis of the e¤ects of surgical therapy on voice quality. and as such require clinical consideration. Blaugrund. 1994). Clinical assessment should determine whether voice change is due to under. Clinical goals that focus on ‘‘easy’’ voice production without excessive speech rate are appropriate targets. B. and auditoryperceptual assessment. 81. strained voice quality are commonly observed (Doyle et al. (1983). and (4) control of speech rate via phrasing. B. Depending on the auditory-perceptual character of the voice.).e. Increased e¤ort may be compensatory in an attempt to alter pitch or loudness. Excessive vocal e¤ort and a harsh. 93. the contributions of volitional compensation.. 1977. productive transition to voice generation at the initiation of voice and speech production. The voice and voice therapy (2nd ed. Doyle (1997) has suggested that therapy following conservation laryngectomy should focus on ‘‘(1) smooth and easy phonation. R.Voice Rehabilitation After Conservation Laryngectomy 81 alty.. Voice therapy strategics for those who have undergone conservation laryngectomy have evolved from strategics used in traditional voice therapy (e. M.. Although a ‘‘rough’’ or ‘‘e¤ortful’’ voice may be judged as abnormal. A weak voice requires the clinician to orient therapy tasks toward systematically increasing glottal resistance. T. excessively aperiodic voices. Gerratt. particularly early during treatment..or overcompensation for the disrupted sphincter. 311–317. In this regard.. 1990. strategies for voice therapy must address changes in anatomical and physiological function. Berke. Bloch. Thus. Haji. Those individuals who exhibit increased fundamental frequency.. 1994. D. voice therapy is usually directed toward facilitating increased approximation of the laryngeal valve by means of traditional voice therapy methods (Boone. D. and Baer. systematic perceptual assessment has direct clinical implications in that information from such an assessment will lead to the definition of treatment goals and methods of monitoring potential progress. R. (1984). and respiration training (Boone. the speaker must understand the relative levels of penalty it creates in a communicative context. and (2) e¤orts to reduce or eliminate compensatory behaviors that negatively alter the voice signal (Doyle. Boone and McFarland. —Philip C. G. a subgroup of individuals may present with weak and inaudible voices because of pain or discomfort in the early postsurgical period. See also laryngectomy. Therefore. C. S. aerodynamic. 1977). Standard evaluation may include videoendoscopy (via both rigid and flexible endoscopy) and acoustic..

. 92. J.. more lung volume per phrase. Normal Breathing When assessing and planning therapy for disorders of the voice... Hawkins. pharyngeal. F. 1984. Microacoustical measures of voice following near-total laryngectomy. For example. DeSanto. 111. the breathing behavior observed in the women with nodules was most likely in response to ine‰cient valving at the larynx and did not cause the nodules. (1996). B. A. and McFarlane. F. R.. Some clinical inferences from the study of serial laryngeal sections. M. Voice Therapy: Breathing Exercises Breathing—the mechanical process of moving air in and out of the lungs—plays an important role in both speech and voice production. and Martin.. H. base-of-tongue.. J.. However. then. Leeper. 109. Minni. A. K. R. J. O. 6. R. J. and Rabanal. L. (1998). 1995). Vocal function after vertical partial laryngectomy with glottic reconstruction by false vocal fold flap: Durational and frequency measures. Crevier-Buchman. (1999).. (1990). and Olsen. C. They found that the women used more air per syllable. 21. Gallo. L. Doyle. Hoasjoe. A.). Journal of Otolaryngology. A histological demonstration of the development of laryngeal connective tissue compartments. 113. 2–7. Tucker. Stemple.. H. 62–67. San Diego. Yoo. H. C. Otolaryngology–Head and Neck Surgery. (1994). Although breathing exercises are advocated by some. F. 635–638. The data that do exist generally describe the breathing patterns that accompany voice disorders. Doyle. H. and Wong. Understanding voice problems: A physiological perspective for diagnosis and treatment... Supracricoid partial laryngectomies: Oncologic and functional results. 504–509.. Journal of Medical Speech-Language Pathology. the emphasis placed on breathing exercises relative to voice disorders in the published literature is mixed. Speech results and complications of near-total laryngectomy. 356–360. 1980. K. Otolaryngology–Head and Neck Surgery. Otolaryngology–Head and Neck Surgery. 93. Prim. 39–43. A. J. C. 118. Growth and spread of laryngeal cancer as related to partial laryngectomy... Kataoka. there is a paucity of data on the relationship of breathing to voice disorders. (2001).. M. (1984). A.. Submucosal compartmentalization of the larynx.. and Doyle. Vocal function following vertical hemilaryngectomy: A preliminary investigation. Wuyts. F. J. 98. P. Hans. 729–733.. 1516–1521. Houghton-Jones... 73. Foundations of voice and speech rehabilitation following laryngeal cancer. O. C. Laryngoscope. P. A comparative acoustic analysis of voice production by near-total laryngectomy and normal laryngeal speakers. Englewood Cli¤s. Rhinology. K. S. Baltimore: Williams and Wilkins. Further Readings Biacabe. 85. Rizer. Boone and McFarlane. Sapienza.. F. Heeneman. Perceptual characteristics of hemilaryngectomized and near-total laryngectomized male speakers. H. A. Heeneman. A. E. Takeuchi. others do (e. and Brasnu. and Laryngology. D.. Fung.. H. Leeper. K. and Brasnu. and Kitajima. H. 105. 1920–1924. W. Colton. I. 98.. 594–599. Pressman. Gavilan. P. (1998). Leeper. A. The voice and voice therapy (5th ed. 301–305. Archives of Otolaryngology. Cooper. either directly or indirectly. Feasibility of subtotal laryngectomy based on whole-organ examination.. Herranz. Vocal function following radiation for non-laryngeal versus laryngeal tumors of the head and neck. (1989). Martin. 19. F.. 66. C. Laryngoscope. Doyle. R.82 Part I: Voice Kirchner.. CA: Singular Publishing Group. 1996). P. Glaze. A. (1975). Heeneman. Acta Otolaryngologica. (1998). Annals of Otology. D. Laccourreye. C. Hanamitsu. (1995). 661–667. 118. Doyle. K. J. (1984). 3.. it is important to know what normal function . and Laryngology. American Journal of SpeechLanguage Pathology. (1989).. and Brown (1997) studied breathing kinematics during reading in ten women with vocal fold nodules. (1956). Larynx preservation: The discussion is not closed. H. G. Rhinology. 131–143. Pearson. 20. (1999).. Annals of Otology. 65. Reed (1980) noted the lack of empirical evidence that breathing exercises were useful in ameliorating voice disorders. A. (1964). De Vincentiis. (1985).. P. as the authors point out. Comparative study of vocal function after near-total laryngectomy. in disorders of the voice. C. Kirchner. and Gerdeman. 109. Annals of Otology. J. 308–318. T. W. H.. Colton and Casper. C. and Michaels. C. R. D. S. (1990). What have whole organ sections contributed to the treatment of laryngeal cancer? Annals of Otology. Utility of near-total laryngectomy for supraglottic. Head and Neck. and Coleman. G. 728–748. 766–773. (1997). 111. Rhinology. (1996). M. G. Schecter.. 1973.. Rhinology. 2000. L. Laryngoscope.. C. L. Lefebvre. L. and other cancers. F. D. Laryngoscope. P. Monfrais-Pfauwadel.. A review of voice therapy techniques by Casper and Murray (2000) did not suggest any breathing exercises for voice disorders. 389–393. Crevier-Buchman. L.. G. R.. G. and Laryngology. Transactions of the American Academy of Ophthalmology and Otolaryngology. B. M. Doyle. Voice quality and intelligibility characteristics of the reconstructed larynx and pseudolarynx. Kirchner. 698–704. Leeper. Annals of Otology. Laryngoscope. (1994). Some books on voice and voice disorders have no discussion of changing breathing behavior relative to voice disorders (Case. D. S. P. 698–694. Rhinology. J. (1982). et al. Boone. Stathopoulos. Robbins. NJ: Prentice Hall. H. At present. J. and DiNardo. Keith. (1992)..g.. and Casper. and initiated breath groups at higher lung volumes than women without vocal nodules. Laccourreye. Journal of Otolaryngology. and Reynolds. Pathways and pitfalls in partial laryngectomy. Voice refinement following conservation surgery for cancer of the larynx: A conceptual model for therapeutic intervention. Aronson... and Smith. Pillot. L. Tucker. and Laryngology. little is known about the role played by breathing. and Laryngology. Comparison and evolution of perceptual and acoustic characteristics of voice after supracricoid partial laryngectomy with cricohyoidoepiglottopexy. however. S.. 27–35. 1320–1323. but there are no data on what kind of breathing behavior might contribute to voice disorders.

in the supine position there is little or no muscular activity of the abdomen during speaking. Pressure is generated by both muscular and inherent recoil forces. the following apply. Han. 1976). 1964. and the interworking of these forces depends on the level of lung volume (Hixon. only one breathing technique to improve voice production is usually described: The client is placed supine and increased outward movement of the abdomen is observed as the client breathes at rest. and Goldman. Saltzman.. In the upright body position. Stegen. 1973). or wasted motion. it consists of muscle fiber types that are able to generate fast and accurate pressure changes. supine position would generalize to an upright body position. 2001.4–0. beginning at 60% VC and ending at around 40% VC (Hixon. this inward abdominal position as it is maintained provides a platform against which the diaphragm and rib cage can push in order to produce the necessary pressures and flows for speech. Hixon and Putnam . it seems unwarranted to position an individual supine to teach ‘‘natural’’ breathing for speech and voice. for a comprehensive tutorial). it would be forced outward and would move in a paradoxical manner during expiration. the abdomen is smaller and the rib cage is larger relative to relaxation (Hixon. Kelso.Voice Therapy: Breathing Exercises 83 is. Stathopoulos and Sapienza. Hoit et al. Clement. As a result. 1995. and Mead. and Mead. Second. In light of the mechanical and neural control issues discussed earlier. and breathing exercises are known to be beneficial in reducing heart rate and blood pressure (Grossman et al. The changes that occur in speech breathing with a switch from the upright position are numerous and reflect the di¤erent e¤ects of gravity (see Hoit. This allows quicker and more forceful contractions for both inspiration and expiration while using less neural energy. body configuration refers to the size of the abdomen relative to the size of rib cage. The volumes used for speech are usually within the midvolume range of vital capacity (VC). when this patient laughed. For example. Thus. This di¤erence in timing reflects the speaker’s desire to maintain the flow of speech in his or her favor. and Goldman. or 0. his abdominal wall was displaced inward and displayed a great amount of movement. it seems unlikely that techniques for changing breathing behavior learned in a resting.. audible inspiratory turbulence was evident during her broadcasts. For conversational speech in the upright body position. what else might be done with the breathing apparatus to ameliorate voice disorders? Perhaps modifying lung volume would be useful. Hixon.. It may be that this technique does not change breathing behavior but is e¤ective in relaxing individuals with voice disorders. Pressure (translaryngeal pressure) is related to the intensity of the voice (Bouhuys. The abdomen not only produces lung volume change in the expiratory direction. The change of body configuration from the upright position to the supine position means that rib cage volume decreases and abdominal volume increases. Mead. Goldman. The rib cage is e‰cient in displacing lung volume because it covers a greater surface area of the lungs. First. This action positions the expiratory muscle fibers of the rib cage and muscle fibers of the diaphragm on a more favorable portion of their length-tension curve. Mead. 1976). 1988). Although she had a normal voice and no positive laryngeal signs. Mead. and Woestijne. the pressure generated by the rib cage would alter the shape of the breathing apparatus and would not assist in developing as rapid and as large an alveolar pressure change (Hixon and Weismer. 1993). Hixon and Putnam (1983) described breathing behavior in a 30-year-old woman (a local television broadcaster) with a functional voice problem. 1974). Pressure for conversational speech is typically around 4–7 cm H2 O. Valck. This volume range is e‰cient and economical. Reference to flow is in the macro sense and denotes shorter inspiratory durations relative to longer expiratory durations.7 kPa (Isshiki. 1973. Lung volume is the amount of air available for speaking or vocalizing. in that extra e¤ort is not required to overcome recoil forces (Hixon. Hixon (1982) showed kinematic data from a patient with Friedreich’s ataxia whose abdominal wall was assumed to be paralyzed because it showed no inward displacement and no movement during speech. and it is well endowed with spindle organs for purposes of sensory feedback. whereas in the upright body position the abdominal muscles are quite active (Hixon. little of this information has found its way into the clinical literature and been applied to voice therapy. In supine speech breathing involves approximately 20% less of VC. 1996). It seems curious why this technique is advocated. 2000. Greene and Mathieson. Using breathing kinematic measurement techniques. If the abdomen did not o¤er resistance to the rib cage during the expiratory phase of speech breathing. Hoit et al. Proctor. However. and Tuller (1986) hypothesize that the control of speech is task-specific. 1995). The upright body configuration provides an economical and e‰cient mechanical advantage to the breathing apparatus. 1976. pressure. and Goldman. 1976. 1989). Paradoxical motion results in reduced economy of movement. flow. 1973). 1966). Other Approaches If learning breathing techniques in the supine position is not useful. Mead. With regard to breathing at rest. 1989). Hixon (1975) provides a useful parameterization of breathing for speech that includes volume. E¤ects of Posture Although much is known about speech breathing. inward abdominal placement lifts the diaphragm and the rib cage (Goldman. As Hoit (1995) points out. and body configuration or shape. it also optimizes the function of the diaphragm and rib cage. It does so in two ways. For speech production in the upright body position. it should be noted that this task is not specific to speech. This modification changes the mechanics of the breathing muscles and requires a di¤erent motor control strategy for speech production. Relaxation techniques have been advocated to reduce systemic muscular tension in individuals with voice disorders (Boone and McFarlane. and Goldman. Most lung volume exchange for speech is brought about by rib cage displacement and not by displacement of the abdomen (Hixon.

hearing. F.. The dynamic perspective on speech production: Data and theory. T.. W. Hoit. Plassman and Lansing (1990) showed that with training. Minifie. it is possible the telecaster’s noisy inspirations could have been eliminated or reduced if she were to produce speech at higher (more normal) lung volumes. J.. Hoit. and abdomen. S. D. Breathing-control lowers blood pressure. Abdominal muscle activity during speech production. 78–115. (1999). The voice and its disorders (5th ed.. between 45% and 10%. 353–365. 341–347. Garlitz. Bouhuys. Paper presented at the Veterans Administration Workshop on Motor Speech Disorders. Otolaryngologic Clinics of North America. Baltimore: Williams and Wilkins. Journal of Applied Physiology. (1980). (1975). 983–1002. A. J. They believed the noisy inspirations were due to the turbulence created by increased resistance in the lower airways that occurs at low lung volume. (2000). E‰cacy research is of great importance because of the reluctance of third-party insurers to cover voice disorders. Mechanical coupling of the diaphragm and rib cage. Voice therapy methods in dysphonia. Solomon.. E.. 45. A. 16. UK: Pergamon Press. and McFarlane. Mead. Pengally. 1960). and that her voice seemed to be much lighter when she spoke at higher lung volumes. 263–269. R. J. Casper. Laryngeal function associated with changes in lung volume during voice and speech production in normal speaking women. (1964). D. T. (1989). (1983). J. Journal of Applied Physiology. Stathopoulos. and W. J. Sapienza.. and Casper. In L. 297–356. B. 29–59. 14. Modern techniques of vocal rehabilitation.). 69. Voice abnormalities in relation to respiratory kinematics. Unpublished dissertation. and Tuller. T. and Milbrath. Speech motor control (pp. J. NJ: Prentice-Hall. J. A. Speech breathing in women. University of Arizona. individuals can produce consistently higher lung volumes during inspiration. Reed (Eds. Boston: Allyn and Bacon. (1976). 50–63).. and A. the woman said that when she spoke at lower lung volumes. D. S. London: Churchill Livingstone. abdomen. E. 7.. (1974).84 Part I: Voice Greene. and Putnam. there was a tendency for laryngeal airway resistance to be reduced during syllable production at high lung volumes compared with low lung volumes. Hixon. 41.. Garlitz. 14. (2000). 483–496. 157–169. More research in this area is decisively needed. J. Valck. T..C. and Gavish. MD: Aspen. 32. When a person inspires to higher lung volumes. New York: B. C. Cooper. Perceptual cues used to reproduce an inspired lung volume. T. 217–231. Williams (Eds. Journal of Human Hypertension. Lindblom. Journal of Voice. Hixon. In F. In S. J.). Thomas. J. (2000). R. 17–29. T. Tucson. B.... Journal of Voice. D. (1997). W. B. Hixon. 2656– 2664. Dynamics of the chest wall during speech production: Function of the thorax. Grillner. Rebuk.). However. 42–60. 33.. The voice and voice therapy (6th ed. G. Even after the call by Reed (1980) more than 20 years ago for more empirical data on breathing exercises to treat voice disorders. (1966). Clement. Clinical voice disorders: An interdisciplinary approach. Influence of body position on breathing and its implications for the evaluation and treatment of voice disorders. the authors did not report any attempts to modify lung volume. R. and C. Regulatory mechanisms of voice intensity variation.. Decker. L. 5. 19. Hixon. Oxford. (2001).. M. T. Plassman. 11. the laryngeal area appeared more dilated and the larynx was in a lower vertical position in the neck than during phonation at lower lung volumes.. 9. Persson (Eds. Kinematics of the chest wall during speech production: Volume displacements of the rib cage. Goldman.. E. Grossman.. Zimlichman. Schein. Speech breathing kinematics and mechanism inferences therefrom. Altman. Perspectives on the Edinburgh study of speech breathing. J. (1973). J. M. Understanding voice problems (2nd ed. and this pulling is believed to generate passive adductory forces on the vocal folds (Zenker and Zenker. Reed. her voice sounded more authoritative. Journal of Psychosomatic Research.. Of note. J.. Seminars in Speech and Language. Kinetic aspects of singing. J.. Hixon. Brown. D. R. 481–493.. D. M. (1986). Boone. M. little has been done. and Lansing. Proctor. L. the downward movement of the diaphragm pulls on the trachea.). C.). Then researchers should examine what techniques are viable for changing this abnormal breathing behavior—if it exists. rib cage. Journal of Speech and Hearing Research. Hixon. using video-endoscopic and breathing kinematic analysis. T. . and lung. A. 21. (1996). and Mathieson. London: Whurr.. (1996). Respiratory-laryngeal evaluation. and Mead. and Hixon. Springfield: Charles C. and language.. B. N. and van de Woestijne. (1995). A. Journal of Voice. and Goldman. (1982). and Morgan. Therefore. Respiratory and laryngeal contributions to maximum phonation duration. Speech breathing during reading in women with vocal nodules. Research e¤orts should focus first on how and whether abnormal breathing behavior contributes to voice disorders. Stegen.. T.. Lansing. —Peter Watson References Aronson.. Saltzman. Rockville. (1995). and Mead. Milstein. J. J. 331–340. Journal of Speech and Hearing Research. (1973).. D. M. and Milbrath (2000) found that in men. Clinical management of voice disorders. C. Respiratory function in speech. E. Grossman. Loaded breathing (pp. 65. Journal of Phonetics. (1988). M. found that at high lung volumes. Journal of Speech and Hearing Disorders. Hixon. B. Han. R. and Weismer.. N. Hoit. Isshiki. Colton. T. and Murray. T. L. M. (1980). J. J. (1984). Journal of Speech and Hearing Research. diaphragm. C. anxiety and breathing pattern in patients with hyperventilation syndrome and anxiety disorders. Plassman. 75–93). 1123–1130. T. K.. Normal aspects of speech. 195–201. A.. S. Madison. Case. J. and F. Englewood Cli¤s. Solomon. Hixon. WI. K. Journal of Speech and Hearing Research. J. (1989). J. 38. M. (1990). Voice therapy: A need for research. Journal of Applied Physiology. Goldman. S. J. Milstein (1999). Lubker. Hixon. Kelso. Influence of breathing therapy on complaints. (1973). 14. found that this person spoke in the lower range of her VC. D. Journal of Speech and Hearing Research.).

. pp.).. Respiratory sensation. and linguistic factors. A. and Loring. Watson. K. J. Studies in speech production: A Festschrift for Katherine Sa¤ord Harris (pp.. (1996).. 49–56. (1986). Respiratory kinematics in female classical singers.. P. E. and coordination among these and the supraglottic resonators (pharynx. H. Williams. Watson. DC: American Institute of Physics. Macklem and J. Hixon. T. 1–25).. Bethesda. Journal of Speech and Hearing Research. W. Folia Phoniatricia. Nonetheless. Respiratory and laryngeal function of women and men during vocal intensity variation. Journal of Applied Physiolgy. Journal of Speech and Hearing Research. T. Hixon. Loring. J. D. Macklem and J. and may manifest in vocal fold tone. P. 120–128... 535–556. 85 Further Readings Agostoni. The following discussion considers the use of Vocal Function Exercises to strengthen and balance the vocal mechanism. E. speech intensity. A. Dynamics of breathing. or psychological. Glaze. A... (1989).. D. MD: American Physiological Society. Handbook of physiology (vol. J... and Gerdeman. Journal of Speech and Hearing Research. E. (1996). R. Measurement of the separate volume changes of rib cage and abdomen during breathing. and Klaben. N. 93–104. and approximation. and Hixon. and Davis. In a double-blind.. Finally. Cognitivelinguistic demands and speech breathing. B. 2000). 2000). D. These physiological events are measurable and may be modified by voice therapy. J.. T.). J.. S. this is considered holistic voice therapy. J. Voice Therapy: Holistic Techniques Whenever a voice disorder is present. 159–169.). 36. McFarland. Ellis. and Smith. (1967). Roy et al. Konno. Activity of respiratory muscles in upright and recumbent humans. R. and Hixon. Porter. Hogue. and Adams.. 1–36. (1968). In P. T. 28. Uber die Regelung der Stimmlippenspannung durch von aussen eingreifende Mechansimen.Voice Therapy: Holistic Techniques Stathopoulos.. and Bruce. The significance of breathing in speech. 4. Macklem and J. 657–667. a change in the normal functioning of the physiology responsible for voice production may be assumed. 411–427). In P. Stathopoulos. and Sullivan. C. vol. Normal voice production depends on a relative balance among airflow. 40. Loring.. Journal of Speech and Hearing Research. S. and Maher. P. (1986). J. balance. Mitchell. 2000). F. 10. Hoit. vol. (1995). A. neurological. Winkworth. J. Journal of Voice. (1993). Dynamic analysis of speech and non-speech respiration. Journal of Speech. 1994. J. J. and flow. R. In L. one management approach is direct modification of the inappropriate physiological activity through direct exercise and manipulation. 51. the Accent Method of voice therapy (Kotby. 1995. ¨ Zenker. 1961–1970. laryngeal muscle strength. Davis. coordination. 2000). C. T. J. In F. 387–409). In Psycholinguistics: Experiments in spontaneous speech (pp. J. Glaze. New York: Academic Press. . J. Language.). oral cavity. W. Harris. Clinical voice pathology: Theory and management (2nd ed. Stemple. 1. (1967). (1987).. MD: American Physiological Society. When all three subsystems of voice are addressed in one exercise. T. power. The respiratory system (3rd ed. Smith... 22. (1960). and Mead. Mead (Eds. pp. M. Watson. 2001). J. Lansing. Guz (Eds. The respiratory system (3rd ed. J. P. and Banzett... 1552–1561. A. 64–75.. Journal of Voice. (1994). (1985).. 3. and Zenker. R. Handbook of physiology (vol. Hoit. 429–442). Examples of holistic voice therapy include Vocal Function Exercises (Stemple. Journal of Voice. (1986). Journal of Applied Physiology. E. and Environment. 3. T. W. W. 32. Variability and consistency in speech breathing during reading: Lung volumes. Passive mechanical properties of the chest wall. nasal cavity). as well as several e‰cacy studies (Stemple. pp. T. Disturbances may occur in respiratory volume. 59. Lee. and Watson. pressure.. Dependence of diaphragmatic length on lung volume and thoracoabdominal configuration. and the Lee Silverman Voice Treatment (Ramig. New York: Marcel Dekker. J. 104–122. H. In P. E. MD: American Physiological Society. Goldman-Eisler. B. L. Lansing. Respiration. (1985). Mead. 3. Raphael (Eds. supplied by the respiratory system. Psychophysical methods in the study of respiratory sensation. Watson... E¤ects of verbal decision behavior upon respiration during speech production. Adams and A. Resonant Voice Therapy (Verdolini.. The Vocal Function Exercise program is based on an assumption that has not been proved empirically. and Sharp. Sabol. and Hearing Research. (1989).. and Agostoni.). 1994). mass. L. R. (1990). 12.. T. Surface recordings of respiratory muscle activity during speech: Some preliminary findings. J. Betheseda. CA: Singular Publishing Group. Mead (Eds. pp. N. Journal of Speech and Hearing Research.). Macklem and J. Mead (Eds. and Tobey. P. MD: American Physiological Society.. 3. 24–31. Webb.). and Sapienza. E. P. H. 39. and Stemple. P. 269–272. and Griscom. Washington. T. L. J. Bethesda. Abdominal muscle activity during classical singing. Statics of the respiratory system. 37. Any disturbance in the relative physiological balance of these vocal subsystems may lead to or be perceived as a voice disorder. flexibility. Winkworth. sti¤ness. Journal of Applied Physiology. (1986). The overall causes of vocal disturbances may be mechanical. R. D. Whatever the cause. 100–106).. T. (1997). J. F. Methods for study of the chest wall. and stamina. Respiratory kinematics in classical (opera) singers. 3. (1981). this assumption and the clinical logic that follows have been supported through many years of clinical experience and observation. Journal of Speech and Hearing Research. and Mead. the coupling of the supraglottic resonators and the placement of the laryngeal tone may cause or be implicated in a voice disorder (Titze. M. T. Druz. (1994). S. 415–428). H. E. 407–422. D. Mead (Eds. 1995.. San Diego. Betheseda.. and Minifie. Bell-Berti and L. Speech breathing and the lombard e¤ect. To breathe or not to breathe—that is the question: An investigation of speech breathing kinematics in world-class Shakespearean actors. Mead. S. In P. R.

Sabol. Seldom are they modified by more than two scale steps in either direction. and a sympathetic vibration should be felt on the lips. (2001) studied the e‰cacy of Vocal Function Exercises in a population with voice pathology. and connective tissue. Lee. the goal is based on reaching 80–100 mL/s of airflow. the patient is encouraged to continue the glide without hesitation. The immobilization is followed by assisted ambulation. experimenting with the value of Vocal Function Exercises in the practice regimen of singers. It stretches the vocal folds and encourages a systematic.. When the knee is injured. The primary physiological e¤ects were reflected in increased phonation volumes at all pitch levels. twice a day. laryngeal muscle activity. and increased maximum phonation time. in the form of systematic exercise. Frequency ranges were extended significantly in the downward direction. (A lip trill. A series of laryngeal muscle exercises was first described by Bertram Briess (1957. almost but not quite nasal. decreased airflow rates. The word knoll encourages a forward placement of the tone as well as an expanded open pharynx. When the voice breaks at the top of the current range and the patient typically has more range. similar in concept to physical therapy. 1995). Indeed. When airflow measurements are not available. This is considered a warm-up exercise. using illustrations as needed or the patient’s own stroboscopic evaluation video. preferably morning and evening. The voice must be engaged. and the therapy program often is successful in returning the patient to normal voice production. Briess’s exercises concentrated on restoring the balance in the laryngeal musculature and decreasing tension of the hyperfunctioning muscles. many assumptions Briess made regarding laryngeal muscle function were incorrect. For 6 weeks the experimental groups followed their respective therapy programs and were monitored by speechlanguage pathologists trained by the experimenters in the two approaches. The concept of direct exercise to strengthen voice production persisted. cartilage. The patient is then taught a series of four exercises to be practiced at home. rehabilitation includes a short period of immobilization to reduce the e¤ects of the acute injury. Jacobson et al. slow engagement of the cricothyroid muscles. Rehabilitation of the voice may also involve a short period of voice rest after acute injury or surgery to permit healing of the mucosa to occur. if the flow volume is 4000 mL. decreased airflow rates. patients are not fully rehabilitated because an important step was neglected—the systematic exercise program to regain the balance among airflow. Subjects in the control group rated themselves worse. the goal is 40–45 s. even in this group of superior voice users. when presented appropriately. All exercises are produced as softly as possible. Indeed. These exercises were modified and expanded by Stemple (1984) into Vocal Function Exercises. the glide may be continued without voice as the . whether the disorder is one of vocal hyperfunction or hypofunction. and supraglottic placement of the tone. the goal is equal to the longest /s/ that the patient is able to sustain. many patients are enthusiastic to have a concrete program. Placement of the tone should be in an extreme forward focus. and Stemple (1995). Both the knee and the larynx consist of muscle. So.86 Part I: Voice placebo-controlled study. These exercises include the following: 1. F below middle C for males. including increased airflow volume. The patient’s lips are to be rounded. the analogy that we often draw with patients is a comparison of knee rehabilitation with rehabilitation of the voice. Teachers who reported experiencing voice disorders were randomly assigned to three groups: Vocal Function Exercises. (Pitches may be modified up or down to fit the needs of the patient. 2. Barnes (1977) described a modification of Briess’s work that she termed Briess Exercises. 1997) revealed significant improvement in the Vocal Function Exercise group. and then the primary rehabilitation begins. This exercise is designed to strengthen and balance all of the supportive knee muscles for the purpose of returning the knee as close to its normal functioning as possible. or the word whoop may also be used. The exercises are simple to teach and. The patient may then begin conservative voice use and follow through with all of the management approaches that seem necessary. two times each. When breaks occur. (1994) demonstrated that Vocal Function Exercises were e¤ective in enhancing voice production in young women without vocal pathology.) The goal of the exercise is based on airflow volume. and his therapy methods were not widely followed. and control groups. The exercise program strives to balance and strengthen the subsystems of voice production. during which they may plot the progress of their return to vocal e‰ciency. Full voice use is then resumed quickly. Roy et al. Pre. In our clinic. The program begins by describing the problem to the patient. 1959). Significant improvements in the physiologic measurements of voice production were achieved. Glide from your lowest note to your highest note on the word knoll. Sustain the /i/ vowel for as long as possible on a musical note: F above middle C for females and boys. however. and no improvement in the vocal hygiene group.) Voice breaks will typically occur in the transitions between low and high registers. Briess suggested that for the voice to be most e¤ective. and a subsequent increase in maximum phonation times. tongue trill. The glide requires the use of all laryngeal muscles. vocal hygiene. Often. The laryngeal mechanism is similar to other muscle systems and may become strained and imbalanced for a variety of reasons (Saxon and Schneider. Unfortunately. seem reasonable to patients. Stemple et al. but not breathy. the intrinsic muscles of the larynx must be in equilibrium.and post-testing of all three groups using the Voice Handicap Index (VHI. used graduate students of opera as subjects. The goal is to achieve no voice breaks.

The patient is asked to breathe in deeply. (1957). Briess. no growl is permitted. an octave below middle C for men. The range should be around middle C for females and boys. Seldom. 2 times each. and so on. Assessment of laryngeal function. Instrumentation in voice assessment and treatment: What’s the use? American Journal of Speech-Language Pathology. because of normal daily variability. and Orliko¤. or a tape recording of live voice doing the exercises may be given to the patient for home use. The quality of the tone is also monitored for voice breaks. attention is paid to the glottal onset of the tone. the vocal subsystems will receive a better workout than if louder tones are produced. October). tongue trill. This is considered a stretching exercise. wavering. 1 time each. (A lip trill. Many patients find the tape-recorded voice easier to match than the pitch pipe. Extreme care is taken to teach the production of a forward tone that lacks tension. therefore. 1 time per day (morning) Full program. It is similar to other recognizable exercise programs: the concept of physical therapy for the vocal folds is understandable. Some patients experience minor laryngeal aching for the first day or two of the program. 66. Cincinnati. —Joseph Stemple References Barnes. The following systematic taper is recommended:        Full program. 9–16. which is a means of plotting progress. B. The patient is instructed to feel a half-yawn in the throat throughout this exercise. When the patient has reached the predetermined therapy goal. 2 times per day Full program. 6(4). The shape of the pharynx in respect to the lips is like an inverted megaphone. and then initiating the exercise gesture without a forceful glottal attack or an aspirated breathy attack. . In fact. OH. Tone quality improves as times increase and pathologic conditions begin to resolve. systematic engagement of the thyroarytenoid muscles without the presence of a backfocused growl. sympathetically vibrating lips. Voice therapy: Part 1. Archives of Otolaryngology. 2 times each. 1 time per day (morning) Exercise 4. Briess exercises. they are encouraged to continue the program through the discomfort should it occur. All exercises are done as softly as possible. This exercise may be tailored to the patient’s present vocal ability. Finally. Identification of specific laryngeal muscle dysfunction by voice testing. Although some professional voice users choose to remain in peak vocal condition. D. laryngeal muscle activity.. then a tapering maintenance program is recommended. The goal is the same as for exercise 1. Sustain the musical notes C-D-E-F-G for as long as possible on the word knoll minus the kn. 3 times per week (morning) Exercise 4. patients are encouraged not to compare today with tomorrow. As this discomfort will soon subside. (Even aerobic exercise does not improve lung capacity. 61–69. 1 time per week (morning) Each taper should last 1 week. Times do not increase with improved lung capacity. It is explained to the patient that maximum phonation times increase as the e‰ciency of the vocal fold vibration improves. Ford and D. Bless (Eds. The goal is to achieve no voice breaks. R. J. 3. The estimated time of completion for the program is 6–8 weeks. otherwise they should move up one step in the taper until the 85% criterion is met. (1997). The program appears to benefit patients with a wide range of voice disorders because it is reasonable in regard to time and e¤ort. 91–122). It is much more di‰cult to produce soft tones. The -oll is produced with an open pharynx and constricted. Vocal Function Exercises provide a holistic voice treatment program that attends to the three major subsystems of voice production. the downward glide encourages a slow. Glide from your highest note to your lowest note on the word knoll.) The musical notes are matched to the notes produced by an inexpensive pitch pipe that the patient purchases for use at home. and the voice quality and other vocal symptoms have improved. posturing the vowel momentarily.Voice Therapy: Holistic Techniques 87 folds will continue to stretch. By keeping the pharynx open and focusing the sympathetic vibration at the lips. Workshop presented at the Southwestern Ohio Speech and Hearing Association. Glides improve muscular control and flexibility. is the exercise shifted more than two scale steps in either direction. Rather. 1 time each. Behrman. many of our patients desire to taper the exercise program. Bless. Progress is monitored over time and. 1 time each. with attention paid to training abdominal breathing. however. which is inherently motivating. 4. patients are given a chart on which to mark their sustained times. In addition. (1991).). Phonosurgery (pp. and supraglottic placement. and it appears to balance and strengthen the relationships among airflow. Although the basic range of middle C (an octave lower for men) is appropriate for most voices. We have found that patients who think they are ‘‘tone deaf’’ can often be taught to approximate the correct notes well with practice and guidance from the voice pathologist. and breathiness. 1 time per day (morning) Exercise 4. This is considered a low-impact adductory power exercise. progress may be easily plotted. or the word boom may also be used. 2 times each. thus giving the sense of more air. 1 time each. 1 time per day (morning) Exercise 4. New York: Raven Press. Patients should maintain 85% of their peak time. similar to the muscle aching that might occur with any new muscular exercise. the exercises may be customized up or down to fit the current vocal condition or a particular voice type. In C. (1977.) This is considered a contracting exercise. weekly comparisons are encouraged. but rather the e‰ciency of oxygen exchange with the circulatory system. A.

286–296. 1989. Stemple. A classic situation is the need to distinguish between functional and neurogenic conditions. or phonotrauma. hydration. Harris. breathy voice’’ (Casper et al. San Diego. Principles of voice production. and Schneider. Silbergleit. 271–278. B. I. Vocal Biomechanics. CA: Singular Publishing Group. Another large group of diagnostic conditions involves hypoadduction of the vocal folds. (1959). examples are use of a ‘‘quiet. K.88 Part I: Voice Briess. Voice therapy can be characterized with reference to several di¤erent classification schemes. 9. (1994). CA: Singular Publishing Group. However. Stemple (Ed. or diagnostic considerations. N. should be reduced by it. S. Lee. Functional issues are the usual indication. Journal of Voice. San Diego. However. C. Englewood Cli¤s.. The value of vocal function exercises in the practice regimen of singers. Vocal exercise physiology. B. Dove.). NJ: Prentice-Hall. The Voice Handicap Index (VHI): Development and validation. Glaze. San Diego. Titze. B. health-related. Ramig. 1993). (2000). 69. and by the same token.. and Pickup.. (1995). Phonotraumatic lesions such as nodules. polyps. Stemple (Ed. 61–69.. or emotional domains. C.). physical disease such as cancerous. Lack of voice restoration suggests the need for further clinical studies to rule out neurological causes. Here we review voice therapy in relation to (1) vocal biomechanics and (2) a specific therapy approach—roughly the ‘‘what’’ and ‘‘how’’ of voice therapy. The traditional approach to hyperadduction and its sequelae has targeted the use of widely separated vocal folds and smallamplitude oscillations during voice production. J. 1993) or quiet ‘‘yawn-sigh’’ phonation (Boone and McFarlane.. 1994). Corbin-Lewis. individuals may also restrict their use of a quiet. impact stress appears to be a primary cause of phonotrauma (Titze. pp. 1995). H. Functional voice assessment: What to measure and why. pp. Adduction causes monotonic increases in impact stress (Jiang and Titze. Casper. 1995). (1991). CA: Singular Publishing Group. Johnson. CA: Singular Publishing Group. Stemple (Ed. Many of the conditions listed in the various classifications map to several di¤erent voice therapy options. Voice therapy: Clinical studies (2nd ed.. see Hillman et al. Essential treatment phases of laryngeal muscle dysfunction. B.).. (1995). Hicks. 6(3). San Diego.. 76–81). Bethesda. 27–36. MD: National Institute of Deafness and Other Communicative Disorders. Journal of Speech and Hearing Research. physical. inflammatory. and Stemple. S. communicative. and nonadducted hyperfunction (muscle tension dysphonia. precancerous. paresis. Archives of Otolaryngology. bowing. B. in that vocal fold impact stress.).. The accent method of voice therapy. MD: National Institute of Deafness and Other Communicative Disorders. and nonspecific inflammation consequent on voice use are traceable to hyperadduction resulting from vocal fold impact stress. and Klaben. E‰cacy of vocal function exercises as a method of improving voice production. Jacobson. The preponderance of voice problems that are amenable to voice therapy involve some form of abnormality in vocal fold adduction. Resonant voice therapy. Voice therapy: Part II. The restoration of a normal or near-normal voice with therapy may suggest a functional origin of the problem. Adults with voice problems often experience significant functional disruptions in occupational. G.. breathy voice extraclinically because it is functionally limiting (Verdolini-Marston et al. J. In Assessment of speech and voice production: Research and clinical applications (pp. In J.. Health-related concerns are less common precipitants of voice therapy in adults. An evaluation of the e¤ects of two treatment approaches for teachers with voice disorders: A prospective randomized clinical trial. (2001). Stemple (Ed. breathy voice approach is e¤ective in reducing signs and symptoms of phonotraumatic lesions for individuals who use it outside the clinic (Verdolini-Marston et al. and phonotrauma. In Assessment of speech and voice production: Research and clinical applications (pp. D.). Voice therapy: Clinical studies (2nd ed. Clinical voice pathology: Theory and management (3rd ed.). In J. I. Voice therapy: Clinical studies (2nd ed. Gray. voice therapy may be indicated in cases of diagnostic uncertainty. San Diego. Stemple. In turn. M. M. (2000). 1994). voice therapy is e¤ective in reducing such disruptions. Thus. 46–62).... There is evidence that the quiet. J. Columbus. Voice Therapy for Adults Voice therapy for adults may be motivated by functional. (2000). Sabol.. Verdolini. Benninger. (1984). and Newman. social. which results in a certain amount of nosological confusion. The accent method of voice therapy. Lee Silverman voice treatment for individuals with neurological disorders: Parkinson disease. L. Treatment that increases vocal fold closure is indicated in such cases. J.. Clinical voice pathology: Theory and management (1st ed. In J.. (2000). Examples include vocal fold paralysis. J. D’Amico. Measurements for assessment of voice disorders.. pp... 204–209). each therapy option maps to multiple classifications.. Lee. K. K. Grywalski.. American Journal of Speech-Language Pathology. Voice therapy may be a useful adjunct to medical or surgical treatment in these cases. 8. 44. Roy. atrophy. 66–70. (1994). L. tions. Stemple. N. Vocal function exercises. (1991). diet. Titze. L. Journal of Voice. (2000). Simon. for a discussion. San Diego. J. 1989). or neurogenic disease may exist and may be exacerbated by behavioral factors such as smoking. 62–75). (1995). In J.. J. CA: Singular Publishing Group. Voice therapy addresses adductory deviations using a variety of biomechanical solutions. CA: Singular Publishing Group. and Stemple. Saxon. Bethesda.. (1997). Finally.. Kotby.. CA: Singular Publishing Group. A. Jacobson. This general approach is sensible for the reduction of hyperadduction and thus phonotraumatic changes. Stemple. C. and in selected popula- . Voice therapy: Clinical studies (2nd ed.. San Diego. L. 42–49). pp. therapy targeting a reduction in adduction is indicated in cases of hyperadduction. 34–46). OH: Merrill. A.

Titze. and laryngeal appearance (VerdoliniMarston et al.. 1998). the medical condition involves cricothyroid paresis. in addition to addressing laryngeal kinematics. Critical aspects of LSVT that may contribute to its success include a large number of repetitions of the target ‘‘loud voice’’ in a variety of physical contexts.. 2000).. Moreover. However. and Fennell. 1995). LSVT utilizes a predetermined hierarchy of speech tasks in 16 therapy sessions delivered over 4 weeks. vocal hygiene programs alone in voice therapy apparently produce little benefit if they are not coupled with voice production work. 1994).. 1993). The configuration involves barely separated vocal folds. Countryman et al. interest has emerged in cognitive mechanisms involved in skill acquisition and factors a¤ecting patient compliance as related to voice training and therapy models. 1997). Hamdan et al. 2001). such as altering the tongue position. hydration regimens are appropriate for individuals with voice problems and dehydration (Verdolini-Marston.’’ perceptually corresponding to anterior oral vibratory sensations during ‘‘easy’’ voicing (Verdolini et al. Several programmatic approaches to voice therapy have been developed. which is ‘‘ideal’’ because it optimizes the trade-o¤ between voice output strength (relatively strong) and vocal fold impact stress. including inflammatory and even neurogenic and malignant disease. The traditional approach is eclectic and entails implementing a series of facilitating techniques such as the ‘‘yawn-sigh’’ and ‘‘push-pull’’ techniques. An example is the Lee Silverman Voice Treatment (LSVT). some of which have been submitted to formal clinical studies. There is increasing support for the view that laryngopharyngeal reflux plays a role in a wide range of laryngeal diseases. but also prosodic and articulatory deficiencies in individuals with Parkinson’s disease.g. Voice therapy can play a supportive role to the medical or surgical treatment of laryngopharyngeal reflux by educating patients regarding behavioral issues such as diet and sleeping position. Verdolini. However. The clinical consensus is that voice therapy generally is useful in treating mutational falsetto. 1994. changing the loudness of the voice. A more recent approach to treating adductory abnormalities has focused on the use of a single ‘‘ideal’’ vocal fold configuration as the target for both hyperadduction and hypoadduction. and others. Sapir. such as falsetto and breathy voicing. 1988. A relatively small number of clinical cases involve vocal fold elongation abnormalities as the salient feature of the vocal condition. Another programmatic approach to voice therapy. LSVT has increased vocal loudness and voice inflection for as long as 2 years following therapy termination (Ramig. Brief courses of aggressive laryngeal massage by skilled practitioners have dramatically improved voice in individuals with this condition (Roy et al.g. and Titze.. Sandage. voice therapy usually also addresses nonphonatory aspects of biomechanics that influence the vocal fold mucosa. Fox et al. presumably hyperfunctional dysphonia. Thus. Other elongation abnormalities are functional. 1995). the Lessac-Madsen Resonant Voice Therapy (LMRVT). Boone and McFarlane. Some data are consistent with the view that control of laryngopharyngeal reflux can improve both laryngeal appearance and voice symptoms in individuals with a diagnosis of laryngopharyngeal reflux (Shaw et al. . 2001). using chant talk. 1994). An exception is digital manipulation. Such issues are addressed in voice hygiene programs (see voice hygiene).. Mucosal performance and mucosal vulnerability to trauma are the key concerns. breathy voice’’ because it is functionally tractable (Verdolini-Marston et al. as well as other maneuvers.. Voice produced with this intermediate laryngeal configuration has been called ‘‘resonant voice. used for idiopathic. Specific Therapy Approach.. 1995). although thyroarytenoid paresis may also be implicated. This treatment uses ‘‘loud’’ voice to treat not only hypoadduction and hypophonia. as in mutational falsetto. there is evidence that individuals use this type of voicing outside the clinic more than the traditional ‘‘quiet. such as nodules. 2001. 2002).. may temporarily improve symptoms of adductory spasmodic dysphonia and increase the duration of the e¤ectiveness of botulinum toxin injections (Murry and Woodson.. Finally. Facilitating techniques are used by many clinicians and are generally considered e¤ective. specifically manual circumlaryngeal therapy (laryngeal massage). The primary issues targeted are hydration and behavioral control of laryngopharyngeal reflux. Voice therapy has been less successful in treating such conditions. and thus reduces the potential for phonotraumatic injury (Berry et al. 1996.. Sapir. Ramig. Speechlanguage pathologists may train individuals to acquire the basic biomechanical changes described in preceding paragraphs. and using digital manipulation. voice quality. Solomon and DiMattia. which should reduce the glottal gap (e. formal e‰cacy data are lacking for most of the techniques. was developed for individuals with either hyper. variants of ‘‘yawn-sigh’’ phonation. Indeed. Titze. Also. Often.or hypoadducted voice problems associated with nodules. Recent theoretical modeling has indicated that nonlinear source (vocal fold)– filter (vocal tract) interactions are critical in maximizing voice output germane to resonant voice and other voice types (Titze. Programmatic approaches to resonant voice training have shown reductions in phonatory effort.. Dehydration increases the pulmonary e¤ort required for phonation. 2001). whereas hydration decreases it and also decreases laryngeal phonotrauma (e. Recently. In comparison with control and alternative treatment groups. as well as reductions in functional disruptions due to voice problems in individuals with conditions known or presumed to be related to hyperadduction.Voice Therapy for Adults 89 The traditional approach to hypoadduction has involved ‘‘pushing’’ and ‘‘pulling’’ exercises. some data corroborate clinicians’ impressions that this approach can increase voice intensity in individuals with glottal incompetence (Yamaguchi et al. Resonant voice training may also be useful in improving vocal and functional status in individuals with hypoadducted dysphonia.

P. Measurement of vocal fold intraglottal stress and impact stress. Journal of Neurology. R. R. Combined-modality treatment of adductor spasmodic dysphonia with botulinum toxin and voice therapy.. Changes in vocal loudness following intensive voice treatment (LSVT) in individuals with Parkinson’s disease: A comparison with untreated patients and normal agematched controls. 271–276.. A. 44. paralysis. and functional status (Verdolini-Marston et al. Objective assessment of vocal hyperfunction: An experimental framework and initial results.. Accent Therapy.. NJ: Prentice Hall.. laryngeal appearance. Sharara. An evaluation of the e¤ects of two treatment approaches for teachers with voice disorders: A prospective randomized clinical trial. 6.. Countryman. vocal folds that are barely touching or barely separated. Ramig. A. D. Hillman. N. I.). 1976). and McFarlane. and better voice clarity than that achieved with vocal hygiene treatment alone (Roy et al. Stemple (Ed. S. LMRVT targets the use of barely touching or barely separated vocal folds for phonation. Gray. that is. Colton. Subjective. E¤ect of aggressive therapy on laryngeal symptoms and voice characteristics in patients with gastroesophageal reflux. A critical view of the yawn-sigh as a voice therapy technique. 1995). J. R. K. 10. S. Learning-induced dedi¤erentiation of the representation of the hand in the primary somatosensory cortex in adult monkeys. 28.. 79–83. J. and Titze. J. nonspecific phonotraumatic changes. (2001).. and Jenkins. Dove. Amin.. 16. 29–37. Care of the Professional Voice. 2001). (1993). G.. C. Laryngeal image biofeedback for voice disorder patients.. and Woodson.. —Katherine Verdolini References Bastian.g. D. Journal of Voice. L. 47.. 508–520. Hess. and Vaughan. New York. P. Merzenich. W. N. 44. G. Journal of Voice. (1996)... and Titze. A primate genesis model of focal dystonia and repetitive strain injury: I. S. and Woo. Intensive voice treatment (LSVT) for patients with Parkinson’s disease: A 2 year follow up. greater phonatory ease. Pawlas. Carryover exercises to conversational speech may also be used. Training emphasizes sensory processing and the extension of ‘‘resonant voice’’ to a variety of communicative and emotional environments. I. 2001). Koufman. The voice and voice therapy (5th ed. M. M. beginning with sustained consonants and progressing to phrases and extended speech. Investigation of selected voice therapy techniques.. A. D. Voice therapy: Clinical methods (pp. Another programmatic approach to voice therapy for both hyper. M. W. Jiang. S. Roy.. R. (2001). addresses the ideal laryngeal configuration—barely touching or barely separated vocal folds—in individuals with hyper. Younes. 132–144. Sapir.. E. Byl. paresis. Simon. J.. Boone. Byl. 410–418. Training consists of repeating maximally sustained vowels and pitch glides twice daily over a period of 4–6 weeks. and acoustic measurements of laryngeal reflux before and after treatment with omeprazole. Brewer. and McFarlane. M. 71.90 Part I: Voice polyps. Merzenich. 123. (2001).. specific clinical observations have been reported relative to ventricular phonation (Bastian.. 39–45). J. 121. Louis: Mosby–Year Book. S. N. Englewood Cli¤s. W. voice quality. A. C. . Smith. 493–498. I. and Miner. S. (1995). and Psychiatry. a configuration considered to be ideal because it maximizes the ratio of voice output intensity to vocal fold impact intensity (Berry et al. Berry. (2001). E. Stemple et al. Hoehn. St.. L... 1996). and Stemple. J... Training entails the use of specified rhythmic. Shaw.. B. R. Journal of Voice. C. Hamdan. 868–872. 385–388. Journal of SpeechLanguage-Hearing Research. Chan. Walsh.. and Jenkins. Casper. and Thyme. (1994). Electromyographic biofeedback has been reported to be e¤ective in reducing laryngeal hyperfunction and laryngeal appearance in individuals with voice problems linked to hyperadduction (nodules).). D. D. C. A quantitative outputcost ratio in voice production. Journal of Voice. Verdolini. 8.. 1994). Journal of Speech and Hearing Research.. Also. H. W. K. M. S. A 6week program of VFE in teachers with voice problems resulted in greater self-perceived voice improvement. L. and Countryman. 75–80. Young... H. 1987). Ramig.. N. (1996). 98–103. R. L. Acta Otolaryngologica. O. A. Paper presented at the 18th Symposium of the Voice Foundation. atrophy. K. Casper. Data on preliminary versions of LMRVT indicate that it is as useful as quiet. B. C. breathy voice training for sorority women with phonotrauma or the use of amplification for teachers with voice problems in reducing various combinations of phonatory e¤ort. Perkell. O.and hypoadducted conditions (Smith and Thyme. (1987). and Panetti. Searl. K.. Sapir. Murry. (2001). Corbin-Lewis. R. Relevance of reflux in 113 consecutive patients with laryngeal and voice disorders... Y. P. M. 32. R. M. S. Neurology.. J. Finally. for phonation. Journal of Voice. 373– 392. Repetitive strain injury involves decreased use of manual digits or voice and pain subsequent to overuse. Another program. J. Attention to sensory di¤erentiation in the treatment of repetitive strain injury is motivated by reports of fused representation for groups of movements in sensory cortex following extensive digit use (e. In J. and sulcus vocalis.and hypoadducted conditions is called Vocal Function Exercises (VFE. R.. A. This approach targets similar vocal fold biomechanics as LMRVT. Folia Phoniatrica. Movement Disorders. D. 7.. (1994). eight structured therapy sessions typically are delivered over 8 weeks. The Accent Method is more widely used in Europe and Asia than in the United States. Holmberg. In LMRVT. and Fuleihan. W. S.. 279–282. Neurosurgery. Fox. M. Journal of Speech-LanguageHearing Research. (1989).. visual feedback using videoendoscopy may be useful in treating numerous voice conditions. M. et al.. M. T. (1976). O’Brien. 1. Objective methods for the evaluation of vocal function. K.. (1989).. Otolaryngology–Head and Neck Surgery.. some clinicians have found that sensory di¤erentiation exercises may help in the treatment of repetitive strain injury—one of the fastest growing occupational injuries. (2000). (1993). Boone. A.. Statistic research on changes in speech due to pedagogic treatment (the accent method). prosodically stressed vocal repetitions. Montequin. J. 286–296. C. bowing. laryngoscopic.

Titze. CA: Singular Publishing Group. Verdolini-Marston. 1989.. (2000). Anatomical (Hirano. 1983). Understand voice problems: A physiological perspective for diagnosis and treatment (2nd ed. and McCoy. Voice therapy: Clinical studies (2nd ed. (1994). (1996). M. circulatory function. Dependence of phonatory e¤ort on hydration level. Englewood Cli¤s. K. Baltimore: Williams and Wilkins. L. Central nervous system changes include nerve cell losses in the cortex of the frontal. San Diego. Kobayashi. and Pickup. and Krebs. Ostrem. Verdolini. speed. B.. J. A. (2001). and Ramig. R. (2000). Regulating glottal airflow in phonation: Application of the maximum power transfer theorem to a low dimensional phonation model. a Further Readings Boone. K. M. K. (1999). 99–105. Stemple. (1998). Kahane. Voice therapy: Clinical studies (2nd ed. Titze. (2000).. Nair.. H. D’Amico. Mechanical stress in phonation. 341–362. 271–278.. The upper respiratory system.. Iowa City. Titze. Stemple. In J. (1994).).. and Yukizane. 8. Colton. I. Englewood Cli¤s. Watanabe. In G. 1997). E. San Diego. Glaze. R.. D. Nervous system changes are also associated with tremor. M. 8. C. S.. leading to increased sti¤ness. 46–62). 1975). Review: Occupational risks for voice problems. parietal. Hirose. L. I. P. N. is associated with decreased strength. (2002). R. (1994). (1994). This results in the slowing of motor movements (Scheibel and Scheibel. N. and Di Mattia. 37–46. 30–47. (1995). The vocal folds lose collaginous fibers.. Laryngeal adduction in resonant voice. E¤ects of a vocally fatiguing task and systemic hydration on phonation threshold pressure. Verdolini.. The e¤ects of normal aging are somewhat similar across organ systems. Y. Verdolini-Marston.Voice Therapy for Neurological Aging-Related Voice Disorders Solomon.. and Bless. (1993). K. CA: Singular Publishing Group. endurance. M. L. R. A thorough laryngological examination coupled with a complete voice assessment will likely reveal obvious voice disorders associated with aging. Journal of Voice. Lee. K. S. (1994).. N.. and Vocology. E‰cacy of vocal function exercises as a method of improving voice production. Sandage. Journal of Voice. J. Journal of Voice. and speed of articulation (Leonard et al. (1995). I. The vocal fold epithelium. It still remains for the clinicians along with the help of the patient to identify and distinguish normal age-related voice changes from voice disorders. CA: Singular Publishing Group.. Nerve conduction velocity also contributes to speed of voluntary movements such as pitch changes. NJ: Prentice Hall. E¤ect of hydration treatments on laryngeal nodules and polyps and related voice measures. Glaze. Voice production in the elderly is associated with other bodily changes that occur with advancing age (Chodzko-Zajko and Ringel. R. . Palmer. This article focuses on neurologically based voice disorders associated with general aging. Druker. larynx and respiratory systems).). like other organ systems. Stemple (Ed. (1995). Yotsukura.). Voice tradition and technology: A state-of-the-art studio (pp. Preliminary study of two methods of treatment for laryngeal nodules. 37. M. the larynx. Clinical voice pathology: Theory and management (2nd ed. (1998). K. as is Parkinson’s disease. 14. Verdolini.. Pushing exercise program to correct glottal incompetence. E. 12. organ system interaction (i. 74–85. 1965) clearly demonstrate that di¤erences in structure and function do exist as a result of aging. K.. C. pp.. J. 1987). Journal of Voice... The Accent Method of voice therapy. Hirosaku. although changes in specific organs may derive from various causes and mechanisms. Kotby. S. 315–327. IA: National Center for Voice and Speech. D. (1994). however.. Principles of voice production.. nerve conduction velocity. and Fennell. coordination. Verdolini. 1001–1007. vocal tract.. J.e. K. and Titze. In 1983. R. K. 227–239). Journal of the Acoustical Society of America.. and Gerdeman. and Samawi. Journal of Voice. Y. 8. Titze. The voice and voice therapy (5th ed. 26. R. Neurological. D. accuracy. Verdolini. increased loudness. Stemple. National Center for Voice and Speech’s guide to vocology.). Some considerations on the science of special challenges in voice training. K. Journal of Logopedics.. San Diego. Traumatic or idiopathic vocal fold paralysis is described in another entry. I. J. The neurological impact to the aging larynx includes central and peripheral motor nervous system changes. R. 250–256. H... H.). and Casper. 91 Voice Therapy for Neurological AgingRelated Voice Disorders Introduction The neurobiological changes that a person undergoes with advancing age produce structural and functional changes in all of the organs and organ systems in the body. 9.. CA: Singular Publishing Group. Kurita. L. musculoskeletal. I. do not necessarily result in abnormal voice quality. This entry describes neurological aging-related voice disorders and their treatment options. Journal of Voice. 1987) and histological studies (Luchsinger and Arnold. NJ: Prentice Hall. and circulatory remodeling account for changes in laryngeal function and vocal output in older adults. Case study: Resonant voice therapy. San Diego. 111. D. Journal of Speech and Hearing Research.. Yamaguchi. and Caldwell.. S.. K. and oral cavity all reflect both normal and abnormal changes that result from aging. C. and the muscles of the larynx change with aging. C. DeVore. K. Burke. CA: Singular/Thompson Learning. Journal of Voice. P. Verdolini. 7. McFarlane. Ramig and Ringel suggested that age-related changes of the voice must be viewed as part of the normal process of physiological aging of the entire body (Ramig and Ringel. Phoniatrics. and temporal lobes of the brain. Lessac. the layers of the lamina propria. These changes. San Diego.. G. Aging of the vocal organs. A. and chemical degradation at synaptic junctions. 367–376.

vocal fatigue. Excluding vocal fold paralysis. and to maintain a broad pitch range for singing. 1997) and decrease in distal and motor neurons. Acoustic. The most common symptoms reported by this group of patients are shown in Table 2. perceptual. diagnosis. and Chijina. resulting in decreased contractile strength and an increase in muscle fatigue (Doherty and Brown. These needs are met with vocal education including awareness of vocal hygiene. increased breathy quality during extended conversations. 1994).. and vocal use requirements. Finally. Treatments for Neurological Aging-Related Voice Disorders Treatments for elderly patients with mobile vocal folds presenting with dysphonia include behavioral. condition seen more in the elderly than in young individuals. 1987). The most common needs of patients with neurological age-related voice disorders are to increase loudness and endurance. pharmacological. The Most Common Voice Symptoms Reported by Patients 65 Years of Age and Older Symptom Loss of volume Raspy or hoarse voice Vocal fatigue Di‰culty breathing during speech Talking in noisy environments Loss of clarity Tremor Intermittent voice loss Articulation-related problems % of Patients 28 24 22 18 15 16 7 6 5 Total exceeds 100% as some individuals reported more than one complaint. or decreased hearing acuity resulting in excessive vocal force (Chodzko-Zajko and Ringel. Koufman (2000). presence of tremor. The total number of diagnoses is larger since some patients had more than one diagnosis. A review of surgical treatments can be found in Ford (1986). 1993). and pitch breaks (especially breaks into falsetto and hoarse voice quality). vocal volume deficiencies. Conversely. asymmetrical vibration. and physiological assessment of vocal function may reveal evidence of tremor. direct vocal exercises. dopaminergic changes which decline with aging may also a¤ect the speed of motor processing (Morgan and Finch. and surgical approaches. Voice Changes Related to Neurological Aging The central and peripheral degeneration and concomitant regenerative neural changes that occur with neurological aging may result in a number of voice disorders. the voice may be perceived as ‘‘old’’ not solely due to neurological changes in the larynx and upper airway. atrophy. if the neuromotor systems are intact and the elderly patient is healthy. scarring. certain aspects of voice production that are characteristically associated with agerelated neuropathy. previous surgeries. In the absence of suspected malignancies or frank aspiration due to lack of glottic closure. The use of medications and their relationship to vocal production and vocal aging can be found in the work of Satalo¤ and colleagues (1997) and Vogel (1995). Prior to voice therapy. 1963). Diagnoses of Subjects Age 65 and Older Seen at the University of Pittsburgh Voice Center Diagnosis Vocal fold atrophy Vocal fold paralysis Laryngopharyngeal reflux Parkinson’s disease Essential tremor Other neurological disorders Muscular tension dysphonia—primary Muscular tension dysphonia—secondary Edema Spasmodic dysphonia N 46 39 32 26 8 16 15 38 14 7 % 23 19 16 13 4 8 7 19 6 3 N ¼ 205. A careful examination of the elderly patient with a complaint about his or her voice consists of an extensive history including medications. the speaking and singing voice is not likely to be perceived as ‘‘old’’ nor function as ‘‘old’’ (McGlone and Hollien. There are. and changes in vibrato (Tanaka. . Postma (1998). Murry and Rosen reported on 205 patients 65 years of age and older. selective denervation of type II fast twitch muscle fibers (Lexell. voice therapy is the treatment of choice for most elderly patients with neurological aging-related dysphonias. Neurological changes to the voice accompanying aging are related to decreased neurological structure and function which result in patient perceived and listener perceived vocal dysfunction. cardiovascular changes (Orliko¤. but due to muscular weakness of the upper body (Ramig and Ringel. 1990). The peripheral changes that occur in the elderly are thought to be broadly related to environmental e¤ects of trauma (Woo et al. however. 1999). 1988). 1983). The clinical examination of elderly individuals who complain of voice disorders should specifically address and test for loss of vocal range and volume.92 Part I: Voice Table 1. increased breathiness. and as Table 2. these neurological changes account for disorders of voice quality and overall vocal output. Elderly singers should be evaluated for pitch inaccuracies. 1992). and current and previously diagnosed diseases. Examination of the larynx and vocal folds via flexible endoscopy as well as strobovideolaryngoscopy is essential to reveal vocal use patterns. tremor (of the larynx or other structures). Table 1 shows the diagnosis of this group (Murry and Rosen. Voice therapy for neurological aging-related voice disorders varies. or lesions. and Durson (1996). Indeed. to reduce hoarseness or breathy voice qualities. depending on the patient’s complaints. and management of the vocal environment. and/or vocal fatigue. Hirano.

and building muscle power. senior citizen residences. and Poburka. This treatment method of voice therapy may be the most promising of all for neurological aging-related voice disorders. odynophonia. hyperfunctional dysphonia. Roy and colleagues reported on their use of the massage technique in controlled studies (Roy. and Gerdeman. General body massage in which muscles are kneaded and manipulated is known to reduce muscle tensions. pitch range. One focus of the circumlaryngeal massage is to relieve the contraction of those muscles and allow the larynx to lower. 1994).. Bless. The technique was first proposed by Aronson (1990) and later elaborated by Morrison and Rammage (1993). Resonant voice. muscle wasting. or loudness that was present in earlier years. 1995). Leddy. Specific techniques for the aging voice have evolved from our understanding of the aging neuromuscular process. Vocal Education Vocal education coupled with vocal hygiene provides the patient with an understanding of the aging process as it relates to voice use. Burke. Confidential voice is the voice that one might typically use to describe or discuss confidential matters. 1995). and Lemke. Manual circumlaryngeal massage (manual laryngeal musculoskeletal tension reduction) is a direct. stretching and contracting of muscles. Nursing homes. (2) allow lesions such as vocal nodules to heal in the absence of continued pounding. it is necessary to push the entire . and Lessass. Recently. Theoretically. The softness of the productions is said to increase muscular and respiratory e¤ort and control. and paralysis. rigidity. of four sessions per week for 4 weeks specifically for patients with idiopathic Parkinson’s disease (Ramig. and system endurance may not restore the voice to its youthful characteristics. its disorders. Increased use of laryngeal imaging and knowledge of laryngeal physiology have provided a base for behavioral therapy that is increasingly focused on the specific nature of the observed pathophysiology. or a scarred vocal fold. Exercises to place the vocal mechanism in a specific manner coupled with humming help the patient identify to optimum pitch/placement for maximum voice quality. and vocal fatigue in the early postoperative period. Resonant voice therapy is described as being useful in the treatment of vocal fold lesions. Therapy focuses on the production of this voice primarily through feeling and hearing. and geriatric specialists should consider o¤ering this outline as the first step in patient education when patients complain of voice disorders. Glaze. Burke. Vocal function exercises are designed to pinpoint and exercise specific laryngeal muscles. This technique is most often used with patients who report neck or upper body tension or sti¤ness. The confidential voice technique is appropriately used to treat benign lesions. the Lee Silverman voice treatment program. Rather. usually refers to an easy voice associated with vibratory sensations in facial bones (Verdolini-Marston. The goal is to create healthier vocal folds and a neutral state from which healthy voice use can be taught and developed through a variety of other techniques (Verdolini-Marston. 1997). muscle tension dysphonia. Murry and Rosen published a vocal education and hygiene program for patients (Murry and Rosen. bradykinesia.Voice Therapy for Neurological Aging-Related Voice Disorders 93 part of the diagnostic process. If the patient wears a hearing aid or aids. and their treatment. or voice with forward focus. 2000). tenderness in the neck muscles. The exercises are hypothesized to restrengthen and balance laryngeal musculature. all of the systems that contribute to the aging of these organs are responsible for the final vocal output. (4) reset the internal volume meter. Since the voice is the product of respiratory and vocal tract functions. This program is an excellent guide for all aging patients with neurological voice disorders. Since then. and reduction in respiratory e¤ort. the e‰cacy of the treatment for this population has been extended to include aging patients and patients with other forms of progressive neurological disease. it is produced with minimal vocal fold contact. The recent explosion of knowledge about the larynx is matched by an equal growth of interest in its physiology. Samlan. Direct Voice Therapy Voice therapy is one treatment modality for almost all types of neurological aging-related voice disorders. 1997). he or she should wear them for the therapy sessions. hands-on approach in which the clinician massages and manipulates the laryngeal area in a particular manner while observing changes in voice quality as the patient phonates. the desired goals should be e¤ective vocal communication and forestalling continued vocal deterioration (Satalo¤ et al. and (5) force a heightened awareness of voice use and the vocal environment. conditions with incomplete glottal closure. (3) eliminate excessive muscular tension and vocal fatigue. and to rebalance airflow (Stemple. They reported almost normal voice following a single session in 93% of 17 subjects with hyperfunctional dysphonia. a thorough audiological assessment of the patient should be done. or those who demonstrate rigid postures. While treatment is designed to restore maximum vocal function. the aging process of weakness. The Lee Silverman voice treatment program is based on the principle that. Ramig and colleagues developed a structured intensive therapy program. 1995. endurance. to improve vocal fold flexibility and movement. An understanding of how all body organ systems are a¤ected by normal aging helps to explain why the voice may not have the same quality. mild vocal atrophy. and Lessass. functional voice problems. It is not appropriate for treatment of vocal fold paralysis. 1997). The confidential voice technique is used to (1) eliminate hyperfunctional and traumatic behaviors. This concept is adapted to massage the muscles in the laryngeal area. to counteract the physical e¤ects of reduced amplitude of motor acts including voice and speech production. The four steps address warmup of the muscles. Bonitati. and Heisey.

Journal of Voice. fatigue. The accent method. H. Tremor often accompanies many voice disorders having a neurological component. and in some cases with laryngeal framework surgery. 122. General physical conditioning. (1987). 14. 155–159. Laryngoscope. Superior laryngeal nerve paresis and paralysis. Advances for Speech-Language Pathologists and Audiologists. Asymmetry of the laryngeal framework: A morphologic study of cadaver larynges. endurance problems.. the laryngeal. (1993). (1997). and the ability to monitor voice change help to . See also voice disorders of aging. Journal of Gerontology.. Matsumoto. The estimated numbers and relative sizes of the nar motor units as selected by multiple point stimulation in young and older adults. It di¤ers from the work of voice and acting coaches. increased respiratory function exercises. Rhinology. T. originally developed by Smith. (1996). S. has been used to treat all types of dysphonias (Smith and Thyme. T. maintain voice or retard vocal weakness. Kurita. J. and McMillan. P.. which is available in published form. Acta Neurologica Scandanavica (Supplement). the respiratory system must provide more driving power. and loss of clear voice quality. T.. —Thomas Murry References Aronson. Connective tissue changes in the larynx and their e¤ects on voice. and Ringel. which requires only that a pill be taken or an injection received.. J. R. L. 206–211. 1997).. Vocal fold paresis. T. This method is useful for treating those individuals with vocal fatigue. Chodzko-Zajko.. (1987).. The specific therapeutic techniques presented in this article may also be helpful in reducing the perception of tremor especially those that focus on increasing vocal fold closure (i. N.. J. (1990). M. J. Otolaryngology–Head and Neck Surgery. G. (3) treatment is intensive. Clinical voice disorders. Ford. A. 1248–1257. and (5) productions and outcomes are quantified. Journal of Nutrition. They are primarily interested in rapid restoration of normal voice. (1972). it seems that the respiratory. (2) a high degree of e¤ort is required. To increase loudness. (1997). 1. The aging brain. Summary Progressive neurological aging-related disorders o¤er a challenge to the speech-language pathologist. and attention is paid primarily to an abdominal/diaphragmatic breathing pattern. sound absorption materials such as rugs and cushions are used in large meeting rooms. and Laryngology. Voice therapy di¤ers from the medical approach. C. Diedrich. R. 96. warmup. All voice therapy is a directed way of changing a particular behavior or set of behaviors.. Journal of Voice. Brody. Leddy. Kahane. It has been adopted more widely abroad than in the United States and focuses on breathing as the underlying control mechanism of vocal output and uses accentuated and rhythmic movements of the body and then of voicing. (1997). 1011S– 1013S. Finally. wherein the surgeon does the work. M. Vocal tremor has been treated in the past with medications. and Speigel. Vocal Tremor One neurological aging-related disorder that often resists change is vocal tremor. Postma.. 15. Journal of Voice. Changes in neural modulation and motor control during voluntary movements of older individuals. Lexell. The scope of this article does not permit inclusion of the extensive literature available on this method or an extensive description of the therapy protocol. M.. Doherty. 16. (1986).. (1989). 135–140. 40–44. Diagnosis. The program is highly structured and involves five essential concepts: (1) voice is the focus. It di¤ers from the surgical approach. 98. Hollien. 355–366. which identifies the vocal use habits of the patient is critical to identify strategies and the specific exercises needed to maintain and/or improve voice production.. Cummins. Durson. Voice use is maximized in environments where background noise is minimal. 127. 18. when vocal fold atrophy is also diagnosed. voice therapy demands the cooperation of the patient in ways that may be novel and unusual. or overall volume weakness. 1976). the patient with mobile vocal folds and a neurological disorder may benefit from specific exercises to maintain vocal communication. M320–M325. (2000). Speaking fundamental frequency and chronological age in males. 27–30. W.e. New York: Thieme-Stratton. Evidence for nervous system degeneration with advancing age.. N.. (1992). the treatment of aging-related dysphonias should include techniques used in training singers and actors (Satalo¤ et al. R. Histologic studies on the fate of soluble collagen injected into canine vocal folds. Satalo¤. J.94 Part I: Voice phonatory mechanism to exert greater e¤ort by focusing on loudness. Muscle and Nerve. C. a task that cannot always be accomplished. The vocal environment should not be ignored as a factor in communication for patients with neurological aging-related voice disorders. E. and Brown. M. Koufman. and the articulatory mechanisms all benefit from the e¤ort to increase loudness. and the vocal folds must adduct more completely. K. A. Lee Silverman voice treatment and the Accent Method). who work to enhance and strengthen a normal voice. 137. 52A. and proper lighting is available to help with visual components of communication. and Poburka.. and Shipp. Indeed. Voice clinicians work with individuals who never thought about the voice until they acquired a voice disorder. (4) the patient’s self-perception must be calibrated. Medical Sciences. R. W. J. Annals of Otology. Journal of Speech and Hearing Research. Leonard. 18–26. Samlan. In the absence of surgery for vocal fold paralysis. P. G. D. Regardless of the methods used. and Blalock. Easy voice production with an openthroat feeling is stressed. 10. and Yukizane. Physiological aspects of aging. C. H. E¤ective treatments for hyperfunctional voice disorders. Hirano. 537–541. B.

Rosen and T. T. clergy.Voice Therapy for Professional Voice Users Luchsinger. H. M. Orliko¤. G. Scheibel. The relationship of age and cardiovascular health to certain acoustic characteristics of male voices. and Lemke. Morgan. Morrison. M.. R. 164–170. (1995). 22–30. 428–434. C. speech. and Lessas. Bonitati. Symptoms of repetitive strain injury typically begin in the fingers after keyboard use. K. Manual circularyngeal therapy for functional dysphonia: An evaluation of short. one of the fastest growing occupational injuries in the United States in general.. J. Part III. E. K. At any given time. Laryngoscope. Professional voice (pp. and Scheibel. R. A new occupational hazard for voice problems has recently surfaced in the form of repetitive strain injury. Postma. L. M. (1990). 11.). T. F. 108. D. Hawkshaw. and Ramage. K.. and Koufman. (2000). D. Smith. O. (1994)... Emerich. air tra‰c controllers. (1994). 321–331.). Voice treatment for patients with Parkinson’s disease: Development of an approach and preliminary e‰cacy data. D. 74–85. and auctioneers are among those who use their voices significantly in their line of work. J. P. M. (1988). However. C. A. 191–209. 450–457. Journal of Voice. 2. teachers made up between 5% and 6% of the employed population in the United States. L. Agerelated change in the internal branch of the rat superior laryngeal nerve. firefighters...). Increasingly. New York: Raven Press. police. (1963). 115. J. (1999). Malmgren. (1976). L. The consequences of voice problems for professionals are not trivial and may include temporary or permanent loss of work. J. Brody (Ed. San Diego. Satalo¤ (Ed. Vocal aging: Treatment options (abstr. M. Blalock. J. phonotrauma is considered an occupational hazard in these populations (Villkman. 78–86. Statistic research on changes in speech due to pedagogic treatment (the accent method). Oates. ˜ Murry. language: Clinical communicology—Its physiology and pathology. 357–362. G. A. San Diego. A. Central Neuronal Alterations Related to Motor Behavior Control in Normal Aging: Basil Ganglia. Other occupations at risk for voice problems are lawyers. Typically. A. E. Dsyphonia in the aging: Physiology versus disease. Annuals of the New York Academy of Sciences. R. P. 156–160.). The goal of treatment for professional voice users is to restore the best possible voice use—and. C.. Otolaryngologic Clinics of North America. Conservative estimates of costs associated with voice problems in teachers alone are on the order of $2 billion annually in the United States (Verdolini and Ramig. lawyers. However. K. Bless. The e¤ects of drugs on communication disorders. 11. Glaze. Endocrine dysfunction... Ramig. C.. 102. J. Folia Phoniatrica. Journal of Voice. M. Journal of Voice. Rhinology. C. involves weakness and pain from somatic overuse. (1997). Bilateral medialization laryngoplasty. B. and Arnold. (1975). A. (1998). Vocal education for the professional voice user and singer.. 967–982. (1997).. 145–159. and Finch. CA: Singular Publishing Group. special considerations may be required in therapy for professional voice users because of their job demands. 98–103. C. In Proceedings of 2nd World Voice Congress. 139–144. (1995). Stemple. Thus. and possibly even counselors and social workers. and Laryngology. C. Journal of Medical Speech-Language Pathology. M. (1995). Vocal pitch characteristics of aged women. D. 33. Voice Therapy for Professional Voice Users A professional voice user is a person whose job function critically depends on use of the voice. (1992). Satalo¤. (1983). Rosen. Hirano.. D. N.. E¤ects of physiological aging on selected acoustic characteristics of voice. E. and Spiegel. Annals of Otology. Voice. Casper. Muscle misuse voice disorders: Description and classification. and Hollien.. (1997). Laryngoscope. Sao Paulo. (1989). Rosen. T... A preliminary study on two methods of treatment for laryngeal nodules. D. where relevant.. This condition. 103. Journal of Speech and Hearing Research. 1993. N. A.. A. R. at about the same rate as in the population at large. Woo. San Diego. L.. Dopaminergic changes in the basal ganglia: A generalized phenomenon of aging in mammals. and Ringel. 1429–1434. T. Acta Otolaryngologica. (1993). R. A. Clinical morphological and neuromechanical aspects of the aging nervous system.. telemarketers. In H. Journal of Speech and Hearing Research.and long-term treatment outcomes. Murry (Eds. 1998. between one-fifth and one-half of teachers in the United States and elsewhere are experiencing a voice problem (Sapir et al. T. voice problems can be devastating both occupationally and personally to many professional voice users. Smith et al. L. In 1999. Rosenburg.. Colton. 6.. Russell. laryngeal symptoms may develop if the individual replaces the keyboard with voice recognition software. Not only singers and actors but teachers. CA: Wadsworth. P. counselors. R.. 33. and Gerdeman. Satalo¤.. S. 1998). D. Ramig. Clinical voice pathology (2nd ed. Brazil. and Heisey. In C. The teaching profession is at highest risk for voice problems.. Belmont. and Rosen. D. and Greenwood. L. 9. Archives of Otolaryngology–Head and Neck Surgery. Structural changes in the aging brain. The aging adult voice. clergy. Tanaka.).. 28. In R. Probably the preponderance of professional voice users who seek treatment for voice problems have voiceinduced conditions. 95 Vogel. and Woo. S. R. The full range of non-use-related vocal pathologies may occur in professional voice users as well. and Thyme. R.. K. Journal of Speech and Hearing Research. 2001). Voice problems appear to occur at about the same rates among singers. Some aspects of vocal fold bowing. 2000). and Brewer. 113. and Chijina. K.. anatomy and physical function—relative to the job . Burke.. T. Murry. Roy. Verdolini-Marston. (1965). such conditions involve either phonotrauma or functional problems.. H. and Hoover. A. 291–299). S.. 26.. CA: Singular Publishing Group. McGlone. CA: Singular Publishing Group. and Carter. telemarketers.

including hydration and reflux control.96 Part I: Voice in question. 316–317). systematic fading of biofeedback support appears critical for transfer. and flow mode therapy (see.. The voice therapist may need to address special challenges in the physical and political environments of performers. which occurs during ongoing performance (Armstrong. In respect to training modalities. individuals are limited at least as much by the treatment as by the disease. However. and lifestyle issues. Another political issue has to do with directors’ drive toward meeting commercial goals. measurable goals.. and alveolar-size quartz sand (Richter et al..g. over an extended period of time or at sustained loudness. Biofeedback may be a useful adjunct to voice therapy and training. theatre and increasingly singing training and voice therapy incorporate general body work (alignment. Voice therapy for performers often replicates voice pedagogy methods. An intermediate vocal fold configuration. Specific noxious substances that have been measured on stages include aromatic diisocyanates. Open-air performing environments can present particular vocal challenges to performers. Performers are threatened with loss of income. career. 1997. pp. Hoß. performers may find themselves contractually linked to heavy performance schedules without the possibility of rest if they are ill or vocally indisposed. and Prinz. 1999.g. movement) as a central part of training. loss of health care benefits. The most comprehensive technical framework for professional voice training in general has been proposed by Estill (2000). provided after the completion of performance. and more emotionally variable. Directors and producers may sometimes show little concern for performers’ vocal health. 1970. Politically. and performers are subject to a suite of special personality. mental attitude toward performance plays a central role in the performing domain. Gau‰n and Sundberg. plays a role in most treatment programs for professional voice users (see vocal hygiene). The ¨ motor learning literature also clearly indicates the need for special attention to transfer in training. Vocal Function Exercises (Stemple et al. that is. Training in this general laryngeal configuration appears to be more e¤ective than vocal hygiene intervention alone and more e¤ective than intensive respiratory training in reducing self-reported functional problems due to voice in at least one class of professional voice users. the mainstay of intervention for voice problems is behavioral work on voice production. than many individuals in the population at large.g.. including Lessac-Madsen resonant voice therapy (Verdolini. see also Wulf. Smith and Thyme. appears relevant to this goal (Berry et al. and to prevent new ones. 2001). Also. 2002). Linklater. The literature describes a critical dependence of motor learning on sensory processing and deemphasizes mechanical instruction (Verdolini.g. which may be complicated by pathology. involving slight separation of the vocal processes during phonation. Such goals may dictate vocal practices that are at odds with performers’ best interest. contributes to greater learning than on-line feedback. Surgical management may be appropriate in selected cases. 2001). Traditional therapy for phonotrauma in professional groups that use the voice quantitatively (e. false vocal fold position. The motor learning literature indicates that the performers may be right. for most professional voice users. teachers. and aryepiglottic space. especially if these are unmiked. Titze. 2000). 1976).. Voice training for acting tends to be less technically oriented and more ‘‘meaning driven’’ than singing training (e. Skills acquired in a clinic or studio may transfer poorly to untrained stimuli in untrained environments if less specific transfer exercises are used. the voice training of singers and actors is not standardized. 1989). on average. The primary di¤erences are an emphasis on injury reduction and a shorter-term intervention. Stage environments can be frankly toxic. or voice therapy. Heavy costumes weighing 80–90 lb or more and unusual. palatal position. Vocal performers have exacting voice needs. clergy. 2002). few scientific studies on training e‰cacy exist. Moreover. 1997). attorneys). e. 1998). that are independently varied to create ‘‘recipes’’ for a variety of sung and spoken voice qualities. for many reasons. cobalt and aluminum (pigment components). A variety of training methods are available for this approach to vocalization.. All of these factors make many speech-language practitioners feel that a specialty focus on vocology is important in working with performing artists. Terminal biofeedback. teachers (Roy et al. however. The system identifies 11 or 12 physical ‘‘degrees of freedom. cautions exist. has emphasized voice conservation. and loss of professional reputation if they refuse to perform when they should not. Vocal hygiene.’’ such as voice onset type. contorted postures required during vocal performance may add further challenges and may even contribute to injury. however. Also. However. It is probably safe to say that individuals who are drawn to vocal performance are more extroverted. In this approach. laryngeal height. The principles of sports psychology fully apply to . with specific. Therapy for individuals with qualitative both qualitative voice needs recognizes that a special sound of the voice is required occupationally. 1994). in voice therapy. exceptions exist. and compromising to vocal and overall physical health. Research conducted thus far has corroborated some aspects of the approach (e. Therapy for performers—singers and actors—with voice problems is conceptually challenging.. The vocal practitioner should be comfortable dealing with performers’ individual personal styles. because numerous vocalists are available to replace injured ones who are unwilling or unable to perform. cited in Schmidt and Lee. the Accent Method (S. The system recently has gained currency in voice therapy as well as vocal pedagogy. Penicillium frequentans and formaldehyde in cork granulate. The current emphasis is on training individuals to meet their voice needs while they recover from existing problems. traditional speechlanguage pathology models tend to be more analytical and less experiential than typical performing arts models of training.

Champaign. and Lee. References Berry.. speech-language pathologist. Journal of Speech-LanguageHearing Research. CA: Singular Publishing Group. The vocal vision (pp. 271–278. Regulating glottal airflow in phonation: Application of the maximum power transfer theorem to a low dimensional phonation model. S. Folia Phoniatrica. and Pickup. K. and Stemple. New York: Applause. (2001). Sapir. (1976). 44. 26. 111(1 Pt 1). K. First prize: Putting under stress. 480–499. convergent e¤orts are required across specialities. and Prinz. J. tend to maximize physical performance. A.. Lessac. D. IL: Human Kinetics. Smith. Rather. 129–135.). J.. Lessac. Knapp. A.. Mountain View. Exercise and fresh air may be restricted.. N. In M. Verdolini. C.. 145–150. J. The speech-language pathologist and voice teacher generally work together on technical issues. K. 32. Wulf. including right-hemisphere activity consistent with imagery and target awareness (Crews. depending on the issues at hand. 27. B.. A robust finding is that intermediate anxiety levels. M. Acker (Eds. implying verbal analytic thinking and evaluative self-awareness. Keidar. B. Hampton and B. M. W. voice teacher or coach. Frequency of voice problems among teachers and other occupations. (1998). D’Amico. According to some reports. Corbin-Lewis. Estill. New York: Applause. New York: Theatre Arts Books. The use and training of the human voice: A practical approach to speech and voice dynamics (3rd ed. (1997). and Ho¤man.. Russell. Voice problems at work: A challenge for occupational safety and health arrangement. 94–96. 169–179. Richter. I. Villkman.). . San Diego. E. patient.. K. High-level performers tend to show more distributed brain activation. W. Mountain View. K. Di¤erent individuals take the lead.. Review: Occupational risks for voice problems. The importance of communication across individuals within the team cannot be overemphasized. (1996). Verdolini. Also. A. the direction of attention appears key for distinguishing ‘‘chokers’’ (people who tend to perform poorly under pressure) from persons who perform well under high stress... Instructions for ¨ motor learning: Di¤erential e¤ects of internal versus external focus of attention.. 12. Journal of Voice. Professional speaking voice training and applications to speech-language pathology. (1997). Lee. Journal of Motor Behavior. Vocal attrition in teachers: Survey findings.). Vocal performers with voice problems often cannot pay for treatment because their voice problems lead to lack of employment and thus lack of income and benefits. Weikert. Hess. Spectral correlates of glottal voice source waveform characteristics. A quantitative outputcost ratio in voice production. Journal of Voice. B. R. Kirchner. 6. I. Hoß. R. Logopedics. E. and Greenwood. 16. The voice teacher is the most appropriate person to address career issues with the performer. Principles of skill acquisition: Implications for voice training.. (1998). 43. (1998). Gau‰n. 46–62). O.. (2001). M. In M. Touring groups literally may live on buses. CA: Estill Voice Training Systems. Vocology. The use and training of the human voice: Bio-dynamic approach to vocal life. Pay may be poor and sporadic. 28. 367–376. In J. T. Case study: Resonant voice therapy. Simon. Dove. Level one primer of basic figures. 3–12). (2000). and Sundberg. J. D. (2002). E. Gray. Benefits often are not provided unless the performers belong to a union. Lemke.. M. 120–125. 29–37. Santa Rosa. 98–103..). particularly issues that bear on a potential mismatch between the individual’s aspirations and capabilities. 467–479. J. (1997). K. Journal of the Acoustical Society of America.. K. Freeing the natural voice.). M. as opposed to low or high anxiety. 65–80). (2000). M. C. D. K. 37–46. B. K. —Katherine Verdolini Linklater. A. (1999). Taylor. 30. Hampton.. (1976). H.. An evaluation of the e¤ects of two treatment approaches for teachers with voice disorders: A prospective randomized clinical trial. Phoniatrics... Statistic research on changes in speech due to pedagogic treatment (the accent method). CA: Mayfield. Many other findings from the sports psychology literature are applicable to attitude issues in vocal performance. R.). The vocal vision: Views on voice (pp.. D. (1989).Voice Therapy for Professional Voice Users 97 the performing arts. Journal of Speech and Hearing Research. Daily routines may be nonexistent. and Titze. M. Journal of Voice. 44. therapy and the art of voice. Current Opinion in Otolaryngology–Head and Neck Surgery.. Voice therapy: Clinical studies (2nd ed. Schmidt. Vocal performers may have erratic lifestyles that are linked to their jobs. W. Hampton and B. 52. pp. (2000). J. S. J. G. B. (1993). The physician is responsible for medical issues. New York: Applause. A. Folia Phoniatrica et Logopaedica. Stemple. Machlin. Motor control and learning: A behavioral emphasis (3rd ed.). Chan. The vocal vision: Views on voice. Golf. 12. K. Verdolini. Journal of SpeechLanguage-Hearing Research. E‰cacy of vocal function exercises as a method of improving voice production. Journal of Voice. Stemple (Ed. Linklater. 2001). (Eds. Crews. Clinics wishing to work with professional voice users should be equipped to provide some form of fiscal support for treatment. and Acker. 556–565. Further Readings DeVore. 83. K. D. Verdolini. chokers tend to show a predominance of left hemisphere activation when under the gun. Roy. Titze. 72–80. Practitioners working with vocal performers agree that no single individual can fully assist a vocalist with voice problems. and Verdolini. (1992). 286–296.. (1998). Thoughts on theatre. S. J. Prevalence of voice problems in teachers. K. Harmful substances on the opera stage: Possible negative e¤ects on singers’ respiratory tract. Montequin... Verdolini. Schlomicher¨ ¨ Their. E. Speech for the stage (rev. European Journal of Disorders of Communication.. (1994).. R... B. and Thyme. L. Smith.. A. Lohle. and Marthers-Schmidt. and... (2001). M. Performers need to find ways to establish intermediate arousal states and stay there even in high-stress situations. ed. CA: Mayfield. New York: Drama Book Specialists. L. H. (2002). to minimally include an otolaryngologist. Oates. and Ramig. L. Acker (Eds. H. (2001)..

Speak with distinction (rev. (1977). London: Thames and Hudson. IA: National Center for Voice and Speech. San Diego. The actor speaks. (1987). (1977. Thurman. Ostrem. IL: Human Kinetics.. 203–205). A. E. Body mind and voice: Foundations of voice education. G. In pursuit of excellence. National Center for Voice and Speech’s guide to vocology. Sundberg. 37–46. New York: Applause. San Diego. (1999). The Alexander technique: The essential writings of F.. J.. Nair. DeKalb. (1990). Satalo¤ (Ed. R.. and Lee. The science of the singing voice. CA: Singular Publishing Group. San Diego. pp. Voice tradition and technology: A state-of-theart studio. Champaign. T.. ed. Metuchen. . Verdolini. T. Scientific American. German and Italian techniques of singing: A study in national tonal preferences and how they relate to functional e‰ciency. Verdolini. and Mansell. S. Professional voice: The science and art of clinical care (2nd ed. (1974). D. MN: VoiceCare Network.. and Ramig. Logopedics. Vocology. and Welch. P. CA: Singular Publishing Group. Schmidt. Phoniatrics. Skinner. E. 26. French. Monich. (1998). Review: Occupational risks for voice problems. N.). L. Sundberg. J. and McCoy.).). T. Matthias Alexander. English. L. In R. Champaign. Collegeville. IL: Northern Illinois University Press.98 Part I: Voice Satalo¤.). K. T.. Iowa City. Professional voice: The science and art of clinical care (2nd ed. R. The acoustics of the singing voice. IL: Human Kinetics. March). (1997). DeVore. 82–91. Rodenburg. CA: Singular Publishing Group. T. 236. Miller. (2001). K. Orlick. (1997). B. G. J. NJ: Scarecrow Press. Maisel. (2000). Raphael. (1997). Special considerations relating to members of the acting profession. Motor control and learning: A behavioral emphasis (3rd ed. (1997). L. R. London: Methuen Drama.. K. (1999).. O.

Part II: Speech .


Although this motor speech disorder has a languorous and tortuous theoretical and clinical history and is frequently confused with other motor speech disorders and with phonemic paraphasia. Because Darley defined AOS as a disorder of motor programming. 1984) do not show a single site or common cluster of lesion sites responsible for the disorder. Marquardt and Sussman’s (1984) prospective study of 12 subjects with AOS also failed to reveal a consistent relationship among lesion location (cortical . He found that 50% of his AOS subjects (N ¼ 18) had a lesion in the frontal lobe and 50% had posterior lesions. they are not localizable to one part of the motor control architecture and.. AOS-producing lesions subtending Broca’s area (Mohr et al. with a tendency to make errors on more stressed than unstressed syllables. an AOS/limb apraxia comorbidity of 67%. (3) relatively consistent trial-to-trial location of errors and relatively nonvariable error types. Without doubt. and may not be representative of other patient care sites. anticipatory. Luria (1966) proposed that the frontal lobe mechanisms for storing and accessing motor plans or programs for limb gestures or for speech segments were represented in Broca’s area. Deutsch (1984) was perhaps the first to conduct a prospective search.6% prevalence of AOS. language. a first-pass estimate of some of its epidemiological characteristics has been presented by McNeil. 1997.or programming-generated mechanisms and are attributable to the phonological encoding mechanism. Aronson.g. 9% were unspecified. and Sommers. especially in Broca’s area. Darley. Sound distortions serve as evidence of a motor-level mechanism or influence in the absence of an anatomical explanation. Retrospective studies of admittedly poorly defined and poorly described persons purported to have AOS (e. and exchange) errors that cross word boundaries are not compatible with motor planning. Doyle. Errors are relatively consistent in location within the utterance and invariable in type. Acoustically well-produced (nondistorted) sound-level serial order (e. an AOS/limb apraxia and oral-nonspeech apraxia comorbidity of 83%. and (4) impaired measures of coarticulation. aphasia. intersegment transitionalization resulting in extended durations of consonants. Marquardt and Sussman. do not di¤erentiate AOS from the dysarthrias. AOS may be the most infrequent. limb apraxia. an AOS/ aphasia comorbidity of 81%. AOS. In 15% of cases the AOS was traumatically induced (12% neurosurgically and 3% concomitant with closed head injury). or oral-nonspeech apraxia is extremely rare. kinesthetic. and Wambaugh (2000) indicated an AOS/oralnonspeech apraxia comorbidity of 68%. 1990) have received support. and Wambaugh (2000). Comorbidity estimates averaged across studies and summarized by McNeil. tactile. aphasia. 1978) as well as those in the postcentral gyrus (Square. resulting in (2) abnormal prosody across multisyllable words and phrases. Du¤y reported that 58% had a vascular etiology and 6% presented with a neoplasm. resulting in intra. Although apraxic speakers may produce a preponderance of sound substitutions. perseverative.. and in the remaining cases the cause was undetermined or was of mixed etiology. and Brown (1975) proposed it as a neurogenic speech pathology that is theoretically and clinically di¤erent from aphasia and the dysarthrias. the responsible lesion has been sought in the motor circuitry. The lesion responsible for AOS has been studied since Darley (1968) and Darley. 4% were associated with dementia. with a result that set the stage for most of the rest of the results to follow. He also proposed the facial region of the postcentral gyrus in the parietal lobe as a critical area governing coordinated movement between gestures (speech or nonspeech). McNeil et al. and other neurogenic speech. and an AOS/dysarthria comorbidity of 31%.. Its occurrence unaccompanied by dysarthria.. and cognitive disorders. One per- cent presented with a seizure disorder and 16% had a diagnosis of degenerative disease. taken alone. Prospective studies of the AOS-producing lesion have been undertaken by a number of investigators.g. however. 1982. syllables and words. 1984. vowels and time between sounds. proprioceptive. and Schmidt. It is characterized by distortions of segments. p. including dysarthria. including CreutzfeldtJakob disease and leukoencephalopathy (of the remaining. These distortions are often perceived as sound substitutions and the misassignment of stress and other phrasal and sentence-level prosodic abnormalities. Based on retrospective analysis of the records of 3417 individuals evaluated at the Mayo Clinic for acquired neurogenic communication disorders. Du¤y (1995) reported a 4. Based on this same retrospective analysis of 107 patient records indicating a diagnosis of AOS. Kertesz. or language information. Among all of the acquired speech and language pathologies of neurological origin. 329) The kernel perceptual behaviors that di¤erentiate apraxia of speech (AOS) from other motor speech disorders and from phonological paraphasia are (1) lengthened segment (slow movements) and intersegment (segment segregation) durations (overall slowed speech). and 3% were associated with primary progressive aphasia). nor to deficits in the processing of auditory. these proportions are influenced by the type of patients typically seen at the Mayo Clinic.and inter-articulator temporal and spatial segmental and prosodic distortions. (McNeil.Apraxia of Speech: Nature and Phenomenology Apraxia of speech is a phonetic-motoric disorder of speech production caused by ine‰ciencies in the translation of a well-formed and filled phonologic frame to previously learned kinematic parameters assembled for carrying out the intended movement. Robin. Doyle. these substitutions do not serve as evidence of either AOS or phonemic paraphasia. It is not attributable to deficits of muscle tone or reflexes. Its frequent co-occurrence with other disorders and its frequent diagnostic confusion with those disorders that share surface features with it suggest that the occurrence of AOS in isolation (pure AOS) is extremely rare.

McNeil. McNeil. however. using the indirect route. and (4) reduced coarticulation. and physiological features. LaPointe. It is clear. In this theory. Motor programs.. normal speech production involves the retrieval from storage of verbal motor patterns for frequently used syllables (the direct route). Whiteside and Varley (1998) proposed a deficit of the direct phonetic encoding route to account for AOS. the apraxic speaker with a reduced bu¤er capacity is required to reload or reprogram the appropriate (unspecified) bu¤er in a feature-by-feature. there are competing theories. and Rosenbek.. Van der Merwe (1997) proposed a model of sensorimotor speech disorders in which AOS is defined as a disorder of motor planning. motor plans carry information (e. When it occurs. The diagnosis can be confidently applied when assurance can be obtained that the person has the cognitive or linguistic knowledge underlying the intended movement and the fundamental structural and sensorimotor abilities to carry out the movement. Doyle. Although AOS is predominantly viewed as a disorder of motor programming (Wertz. while two of three subjects with phonemic paraphasia (diagnosed with conduction aphasia) had a lesion in the insula. the majority of practitioners view AOS as a disorder of previously learned movements that is di¤erent from other speech movement disorders (i.102 Part II: Speech versus subcortical. In this model. It is classified as a motor speech disorder in the scientific literature. with a reliance on the indirect encoding route. or motor-control-variable-by-motor-control-variable fashion. raising or lowering of the tongue tip. Mayer. (2) syllable segregation. Based on experimental evidence that the phonological similarity e¤ect should not be present in persons with AOS. Rogers and Storkel (1998. In this account. lip rounding. writing (agraphic). and rate of movement) of specific muscles or muscle groups. That is. McNeil et al. interarticulator phasing/coarticulation) that is articulator-specific. AOS is therefore proposed to be a deficit of the direct encoding route. Dronkers (1997) reported that 100% of 25 individuals with AOS had a discrete left hemispheric cortical lesion in the precentral gyrus of the insula. These criteria are generally consistent with those used for the identification of other apraxias. syllable-by-syllable. are said to share many of the core features of apraxic speakers.. One hundred percent of a control group of 19 individuals with left hemispheric lesions in the same arterial distribution as the AOS subjects but without the presence of AOS were reported to have had a complete sparing of this specific region of the insula. Other theoretical accounts of AOS include the overspecification of phonological representations theory of Dogil. 1999) hypothesized a reduced bu¤er capacity as the mechanism responsible for AOS. range. Though their view is expanded from the traditional view of AOS as simply a disorder of motor programming. The diagnosis requires that patients display the ability to process the language underlying the movement. and limb apraxia. acoustic. Motor plans are derived from specific speech sounds and specify the spatial and temporal goals of the planned unit. 2000). that the major anterior/posterior divisions common to aphasiology and traditional neurology as sites responsible for nonfluent/ fluent (respectively) disorders of speech production are challenged by the AOS/lesion data that are available to date. disorders of motor programs result in the dysarthrias and cannot account for the di¤erent set of physiological and behavioral signs of AOS. on the other hand. muscle tone. Two of the four AOS subjects had involvement of the insula. Additionally. For Van der Merwe. and the presence or absence of AOS. and Wambaugh (2000) argue that a combined motor planning and motor programming impairment as specified by Van der Merwe (1997) is required to account for the array of well-established perceptual. and Vollmer (1994) and the coalitional/ dynamical systems breakdown theory of Kelso and Tuller (1981). such as (1) articulatory prolongation. the dysarthrias).e. including oral nonspeech (buccofacial).g. This requirement would give rise to essentially the same observable features of AOS as those commonly used to define the entity and consistent with the observable features discussed earlier. specify the movement parameters (e. not muscle-specific. sound-by-sound.g. The attributes ascribed to motor plans in this model are consistent with the array of cardinal behavioral features of AOS. force. Doyle. glottal closure. and Wambaugh. (3) inability to increase the speech rate and maintain articulatory integrity. The only common lesion site for these ‘‘pure’’ apraxic speakers was in the facial region of the left postcentral gyrus. Speech produced by normal speakers for infrequently occurring syllables. it is frequently accompanied . The unambiguous results of the Dronkers study notwithstanding. AOS is an infrequently occurring pathology that is clinically recognized by most professionals dedicated to the management of speech production disorders. the lesions responsible for AOS remain open to study. anterior versus posterior). 1984). derived from its historical roots based in other apraxias (particularly limb-kinetic apraxia. direction. Two of the four subjects with AOS and one of the three subjects with conduction aphasia evinced involvement of Broca’s area. Critical to this view is the separation of motor plans from motor programs. lesion volume. jaw depression. These accounts have received considerably less examination in the literature and will not be described here. or the patterns are calculated anew (presumably from smaller verbal motor patterns) by an indirect route. Theoretical Accounts The study of and clinical approach to AOS operate under a scientific paradigm generally consistent with the mechanisms ascribed to apraxia. most definitions of apraxia suggest an impairment of movements carried out volitionally but executed successfully when performed automatically. (1990) reported computed tomographic lesion data from four individuals with AOS unaccompanied by other neurogenic speech or language pathologies.

New York: Thieme. J. An analysis of the productive errors made by pure apractic speakers with di¤ering loci of lesions. P. kinematic. Darley. (1966). Boston: College-Hill Press. and B. D. A. A representational account for apraxia of speech. R. S.. 231–249. Broca aphasia: Pathological and clinical. S. Neurology. H. S. J. Code. A. Mlcoch. J. 255–268. Keele. aphasic and articulatory disorders in speech production: A move towards sound theory. Speech production models as related to the concept of apraxia of speech.. F. B. D. Conduction aphasia (pp. and McNeil. Motor representation and control (pp.. A. D. H. W. Motor speech disorders. Journal of Speech and Hearing Research. 224–245. 221–231. In J. E. In S. Selective phonological impairment: A case of apraxia of speech.. and electromyographic studies. McNeil. and Kent. and Schmidt. Aphasia and language: Theory to practice (pp. 181–220). Whiteside. and Vollmer.. R. The lesions responsible for acquired AOS remain a matter for future study. L.. Phonology. Robin. A.). Aphasiology.). 77–110). P. (1990).. Kent. Apraxia of speech: Physiology. management (pp. (1990). L. Clinical Linguistics and Phonetics. F. P. (2001). In J. Reprogramming phonologically similar utterances: The role of phonetic features in pre-motor encoding. 33. R. (1984). Apraxia of speech in adults: The disorder and its management. and apraxic disorders. T. 15. 311–324. Journal of Speech and Hearing Research. 73–90). J. McNeil. C. McNeil. (1994). H. and A. Cohen.. L. Dronkers.). In M. Attention and performance: XIII. I. Rosenbek. (1984). Wertz. acoustics. 15. K. and Storkel. F. S. D. and A. E. Van der Merwe. R. Jeannerod (Ed. 14. Pessin.. linguistics. A. and Sommers. J.... di¤erential diagnosis and management. Aphasiology. acoustics. R.. R. linguistics. Hammond (Ed. (1975). 793–805.. C. Deutsch. CA: College-Hill Press. D. L. (1982). NJ: Erlbaum. (1984). C. aerodynamic. Cortex. R. 39. Clinical management of sensorimotor speech disorders (pp. Mayer.). 221–266). P. Luria. 384. Ryalls (Ed. 201–238). J. Adams. and A. American Scientist. 41. CA: College-Hill Press. Darley. R. Models. Hillsdale. Subcortical lesions and verbal apraxia. New York: Harper. W. Geshwind. E. Journal of Speech and Hearing Research. 13. LaPointe. J. Hillsdale.. Croot. J. and Mulligan. R. 12. A. N.). Phonetic approaches to speech production in aphasia and related disorders (pp. management (pp. Marquardt. R. Oral structure nonspeech motor control in normal dysarthric aphasic and apraxic speakers: Isometric force and static position control. 47–65. (1990). The elusive lesionapraxia of speech link in Broca’s aphasia. M. 91–112). S.. Apraxia of speech: 107 years of terminological confusion. and Brown. 113–134). Amsterdam: North-Holland. M. (1998). In J. 1–25). The apraxias: Neural mechanisms of disorders of learned movement. (1998). In S.). acoustics. San Diego. Goodglass. M. linguistics. Granier. See also apraxia of speech: treatment.. E. (1995). LA. FL: Grune and Stratton. 4.. M. 143–188. J. Rogers. G. R. 63. S. Motor speech disorders: Substrates. —Malcolm R. (1987). M. (1998). (1990). T. In N. G. 245–250. St. R.. Integrating the investigation of apraxic. Crosson (Eds. 258–274. Paper presented at the American Speech and Hearing Association Convention. 188–195. D. Understanding the nature of apraxia of speech: Theory. 311–344). Aronson (Eds. 159–161. R. acoustic. H. C. 28. Kelso. Clinical Aphasiology. and Davis. C. McNeil (Ed. pp. Kohn (Ed.. McNeil and Patrick J. Du¤y. J.. management (pp. Relative timing of sentence repetition in apraxia of speech and conduction aphasia. A. Dogil. Brain and Language.). Weismer. A. R. R. Doyle References Darley. In M. Diagnosis of conduction aphasia.. analysis and treatment. Lebrun.. (1997). and Varley. Its defining features are not widely agreed upon. Cerebral control of speech and limb movements (pp. and Mayer. 12. and Noll. Aronson (Eds. McNeil. M. J.. A theoretical framework for the characterization of pathological speech sensorimotor control. (1978). informed by recent models of speech motor control and phonological encoding. J. Y. Human brain and psychological processes. McNeil. Speech and language: Advances in basic research and practice (vol. 58–62. Motor programs: Concepts and issues.. Kertesz. M. R. Apraxia of speech: A treatable disorder of motor planning and programming. A. D. Motoric characteristics of adult aphasic and apraxic speakers. have led to clearer criteria for subject/patient selection and a resurgence of interest in its proposed mechanisms. H. Apraxia of speech: Physiology. Clinical management of sensorimotor speech disorders (pp. Louis: Mosby. 26. Journal of Speech and Hearing Disorders. In G. K. K. A new brain region for coordinating speech coordination. NJ: Erlbaum. 969–995. . S. (1980). and Ivry. Nature. and Storkel. Rosenbek. Apraxia of speech: Physiology. New Orleans. R. language. R. C. M. M. H. 3–50). (1984). (1968). and Sussman. 34. 349–386). (1983). Toward a theory of apractic syndromes. and Robin. Prediction of site of lesion from speech apraxic error patterns. Rosenbek. L. A. In M. (1997). K. Martin.). Aronson. Rogers.). and Rosenbek. G. F. R. New York: Guilford Press. N. theories and heuristics in apraxia of speech. however. Apraxia of speech: A critical review. Philadelphia: Saunders. L. and Rosenbek. (1997). L. Apraxia of speech: Definition. R. Lass (Ed. (2000). Further Readings Ballard. New York: Thieme. and treatment. and Wambaugh.. Paper presented at the Fourth Symposium of the International Clinical Phonetics and Linguistics Association.. San Diego. (1998). CA: College-Hill Press. Denver. G. In J. 5. M. Square.. A. 53– 64.. Acoustic patterns of apraxia of speech. 10.). (1975). A. J.). (1974). San Diego. R. (2000). M.. Orlando. McNeil (Ed. G. developmental apraxia of speech. (1981). J. McNeil. Planning speech one syllable at a time: The reduced bu¤er capacity hypothesis in apraxia of speech. A.. Aphasiology. M. A. and Tuller. di¤erentiation. Doyle. evidence from perceptual. McNeil. Mohr. A reconceptualisation of apraxia of speech: A synthesis of evidence. Neurolinguistics. New York: Academic Press. A. (1992). Funkenstein. P. Some objections to the term apraxia of speech.. (1999). Duncan. J. Dogil.. E.Apraxia of Speech: Nature and Phenomenology 103 by other speech.. Finkelstein. 379–406. E. Nadeau. E. Aronson (Eds. Gonzalez Rothi. Kent.

and (4) minimal pairs contrasts.. Disturbed coarticulation in apraxia of speech: Acoustic evidence. (1985). 1988) for the purposes of specifying the structure of AOS treatment sessions have been proposed. most of these studies su¤ered from methodological limitations. linguistics. and (2) segmental sequencing of longer speech units (Square-Storer and Hayden. McNeil. In addition. L. J. and positive maintenance e¤ects of targeted sounds at 6 weeks posttreatment. Ziegler. and minimal pair contrasts in 11 well-described subjects with AOS (Wambaugh et al. Specifically. Explanatory models consistent with these observations have been proposed (Van der Merwe. Rogers. and Doyle. Dyspraxia and its management. C.). 1998. 15. Overwhelmingly. The empirical support for each approach to treatment is reviewed here. (Ed. Holtzapple and Marshall. W. and Whiteside. 39–84. McNeil. or voicing features from the other member of the pair. N. L. P. the e¤ects of these facilitative techniques on speech production. 15. syllable and word durations. (2) progressive approximation. and pre-experimental research designs. and electromyographic features that characterize AOS (cf. D. N. A. D. Rockville. Wambaugh. What is the underlying impairment in acquired apraxia of speech? Aphasiology. 1997. Rosenbek. UK: Psychology Press. two subjects showed positive Apraxia of Speech: Treatment In the years since Darley (1968) first described apraxia of speech (AOS) as an articulatory programming disorder that could not be accounted for by disrupted linguistic or fundamental motor processes. and word levels.. 29.104 Part II: Speech Miller. based on evidence that such principles facilitate learning and retention of motor routines involved in skilled limb movements (Schmidt. Square-Storer. and Wambaugh. W. R. R. East Sussex. (1989). 15. L. Apraxia of speech is not a lexical disorder. (2001). K. In J. and LaPointe. (1986). and A. Aphasiology. 1984. (Ed. the misassignment of stress. A. 1997). S. and Schmidt. 117–130. Darley and apraxia of speech in adults. which involves the gradual shaping of targeted speech segments from other speech segments. arguments supporting the application of motor learning principles (Schmidt. 15. Enhancing Articulatory Kinematics at the Segmental Level. Apraxia: The neuropsychology of action. and movement. K. 1983. kinematic. 1991). Apraxia of speech: An overview and some perspectives. 1984). Ziegler. Such movement distortions are realized as extended segmental. and Spencer. which employ visual models. A. (McNeil.. Amsterdam: North-Holland. J. Wambaugh and Cort. 1989). 1996. Several early studies examined. Miller.. acoustic. phonetic placement. Robin... 1999. C. (1986). (2001). nonreplicable treatment protocols. J. M. the evidence supports a conceptualization of AOS as a neurogenic speech disorder caused by ine‰ciencies in the specification of intended articulatory movement parameters or motor programs which result in intra.). E. Neuropsychological studies of apraxia and related disorders. and von Cramon. Spoken word production without assembly: Is it possible? Aphasiology. 15. and von Cramon. 261–273. However. C. A. in a series of investigations using singlesubject experimental designs Wambaugh and colleagues examined the e¤ects of a procedurally explicit treatment protocol employing the facilitative techniques of integral stimulation. and reported positive treatment responses (Rosenbek et al. 68–74. 1977. 1973. LaPointe. Wambaugh. P. 1–72). and are frequently perceived as sound substitutions. MD: Aspen. (1997). and Heilman. 329) Traditional and contemporary conceptualizations of the disorder have resulted in specific assumptions regarding appropriate tactics and targets of intervention. 1998. including inadequate subject selection criteria. Brain and Language. Brain and Language. 1978. and other phrasal and sentence-level prosodic abnormalities. Kent. These studies revealed positive treatment e¤ects on targeted phonemes in trained and untrained words for all subjects across all studies. 2000). LaPointe. Aphasiology. (Eds. which precluded firm conclusions regarding the validity and generalizability of the reported treatment e¤ects. Robin. West. acoustics. Doyle. (1984).. R. Varley. phasing of the articulators at the segmental and syllable levels.). CA: College-Hill Press. syllable. (1985). 1998. 62–68. and a number of treatment approaches have been proposed that seek to enhance (1) postural shaping and . Thompson and Young. 74–77. These techniques include (1) phonetic derivation. W. (2001).. Anticipatory coarticulation in a patient with apraxia of speech. management (pp. (2001).and interarticulator temporal and spatial segmental and prosodic distortions. Wertz. in isolation or in various combinations. E. Aronson (Eds. Contemporary investigations have addressed these methodological shortcomings and support earlier findings regarding the positive e¤ects of treatment techniques aimed at enhancing articulatory kinematic aspects of speech at the sound. D. and Schmidt. aerodynamic. Apraxia of speech: Physiology. San Diego. verbal descriptions and physical manipulations to achieve the desired articulatory posture.). Rosenbek. 1997. 3–47. London: Taylor and Francis.. 2000). which refers to the shaping of speech sounds based on corresponding nonspeech postures. Roy. considerable work has been done to elucidate the perceptual. McNeil. (3) integral stimulation and phonetic placement. Rosenbek. Several facilitative techniques have been recommended to enhance postural shaping and phasing of the articulators at the segmental and syllable levels and have been described in detail by Wertz. Dual or duel route? Aphasiology. 26. G. p. Deal and Florance. Ziegler. place. Acquired apraxia of speech in aphasic adults. M. M. which requires patients to produce syllable or word pairs in which one member of the pair di¤ers minimally with respect to manner. More recently. and Rosenbek (1984). intersegmental transitionalization. (2001). Rothi.

research on motor learning in limb systems has shown that practicing several di¤erent skilled actions in random order within training sessions facilitates greater retention and transfer of targeted actions than does blocked practice of skilled movements (Schmidt. and stress manipulations on the production of longer speech units in adults with AOS is limited. 1985). Dworkin et al. clinical management of AOS has long espoused intensive drill of targeted speech behaviors (Rosenbek. KP provides information regarding aspects of the movement that deviate from the intended action and how the intended action is to be performed. and retention of skilled movements (i. 1975). In addition. in the frequency. in the behaviors targeted for intervention. among the reports cited. untrained phrases). 1987). Three such principles are particularly relevant to the treatment of AOS: (1) the need for intensive and repeated practice of the targeted skilled movements. generalized e¤ects) were evaluated. 1997. and little attention has been paid to the structure of drills used in treatment. These results provide initial experimental evidence that treatment strategies designed to enhance postural shaping and phasing of the articulators are e‰cacious in improving sound production of treated and untreated words. transfer. As with studies examining the e¤ects of techniques designed to enhance articulatory kinematic aspects of speech at the segmental level. and context in which the various facilitative techniques were applied. General Principles of Motor Learning. KR provides information only with respect to whether the intended movement was performed accurately or not.e. Whereas each of these studies reported positive results. these facilitative techniques are most frequently used as antecedent conditions to enhance target performance. have also been reported. The habituation. the e¤ects of similarly motivated treatment programs. However. 1978). That is.. Chumpelik. vibrotactile stimulation (Rubow et al. only five subjects were studied under conditions that permit valid conclusions to be drawn regarding the relationship between application of the facilitative technique and the dependent measures reported (Southwood.Apraxia of Speech: Treatment 105 generalization of trained sounds to novel stimulus contexts (i.e. there is limited evidence that for some patients and some sounds. 1982). the limited available evidence suggests that techniques that reduce the rate of articulatory movements and highlight rhythmic and prosodic aspects of speech production may be e‰cacious in improving segmental coordination in longer speech units. knowledge of results (KR) and knowledge of performance (KP). prolonged speech (Southwood. and intersystemic facilitation (i. generalization to untrained contexts may be expected. and one subject showed positive generalization to untrained sounds within the same sound class (voiced stops).. Enhancing Segmental Sequencing of Longer Speech Units.e. and greater transfer of treatment e¤ects to novel movements (Schmidt. Ballard. retention. 1988. it is di‰cult to compare them because of di¤erences in the severity of the disorder. 1984).e. The contemporary explication of AOS as a disorder of motor planning and programming has given rise to a call for the application of motor learning principles in the treatment of AOS (McNeil et al. As such. The final principle to be discussed concerns the nature and schedule of feedback employed in the training of skilled movements.. and transfer of speech movements. 2001). This research has led to the specification of several principles regarding the structure of practice and feedback that were found to enhance retention of skilled limb movements posttreatment. and Adams. and response-contingent feedback frequently takes the form of KR. With respect to the first of these principles. 2000. their generalizability remains unknown.. melodic intonation therapy (Sparks. Dworkin and Abkarian. 1999). and in the extent to which important aspects of treatment e¤ectiveness (i. 2001) and surface prompts (Square. Treatment programs and tactics grounded in this framework employ techniques designed to reduce or control speech rate while enhancing the natural rhythm and stress contours of the targeted speech unit. 1996.. and (3) the nature and schedule of feedback. However. Schmidt and Lee (1999) argue that KP is most beneficial during the early stages of training but that KR administered at low response frequencies promotes greater retention of skilled movements. Abkarian. Both types of feedback are frequently employed in the treatment of AOS.. (2000) in two adult subjects with AOS in the only study to date to experimentally manipulate random versus blocked practice to examine acquisition. 1991). 1999). This finding has been replicated by Knock et al.. Dworkin and Abkarian. 1990) and temporal constraints (Kent and Adams. . and Johns. 1978. These include metronomic pacing (Shane and Darley. The e¤ects of several such specific facilitative techniques have been studied. Wambaugh and Martinez.. 1991). 1988. based on the premise that the sequencing and coordination of movement parameters required for the production of longer speech units (and other complex motor behaviors) are governed by internal oscillatory mechanisms (Gracco. Further. The e¤ects of the nature. the facilitative techniques of integral stimulation and phonetic placement provide the type of information that is consistent with the concept of KP. Wambaugh et al. Indeed. However. 1996. Wertz et al. Dworkin. duration. 1987. motor learning) and their controlling variables have been studied extensively in limb systems from the perspective of schema theory (Schmidt. finger counting) (Simmons. (2) the order in which targeted movements are practiced. the empirical evidence supporting the facilitative e¤ects of rhythmic pacing. Two types of feedback have been studied. 1989). Several facilitative techniques have been recommended to improve speech production in persons with AOS. 1978. until these findings can be systematically replicated. no studies have examined the e¤ects of manipulating the number of treatment trials on the acquisition and retention of speech targets in AOS. That is. rate control..

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. L. M. L. 725–743. (1980). R. and West.. L.. D. P.. R. Clinical Aphasiology Conference proceedings (pp. European Journal of Disorders of Communication. 294–301). An environmental manipulation approach to treating apraxia of speech. Lee.. L. Shea. New conceptualizations of practice: Common principles in three paradigms suggest new concepts for training. K. and Bjork. H. Square-Storer. (1994). 285–293). P. M. J. In P. McNeil. Brookshire (Ed. When forgetting benefits motor retention. and Rogers. (1977). 348–361. Wertz. M. Raymer. Aprosodia Prosody consists of alterations in pitch. Square.). Clinical Aphasiology Conference proceedings (pp. C. (1994). R. Prescott (Ed. Square-Storer (Ed. Minneapolis: BRK. A. E. Rabidoux. J. Wulf. The locus of contextual interference in motor-skill acquisition. Wertz. 1987). Journal of Motor Behavior. C. R. L. L. In R. In R. 11.. Facilitating communication skills in adult apraxics: Application of blisssymbols in a group setting. N.. W. R. Sound production treatment for apraxia of speech: Overgeneralization and maintenance e¤ects. and Wright. (1991). Kalinyak-Flizar. Prosody is thus crucial to conveying and understanding communicative intent.). 24. J. M. acoustics. and transfer of a motor skill. 157–167. R. but also invests spoken language with linguistic and emotional meaning. and Rosenbek. 20. and Bollier. Singing as therapy for apraxia of speech and aphasia: Report of a case. The nature and treatment of neuromotor speech disorders in aphasia. J. and Morgan. The use of a Handi Voice in the treatment of a severely apractic nonverbal patient. R. intensity. CA: College-Hill Press. E¤ects of treatment for sound errors in apraxia of speech and aphasia. London: Taylor and Francis. (1983). Brookshire (Ed. 41. management (pp.).. Aphasiology. Florance. Rabidoux. and Aronson. Aphasiology. (1992). and timing.. Lane... Wambaugh. Rosenbek. 730–746. Clinical Aphasiology Conference proceedings (pp. 9. (1996). and Thompson. TX: Pro-Ed. Orlando. S. (1980).. T. and Doyle. D.. M. Feedback-induced variability and the learning of generalized motor programs. H. 483–488.. and duration across words.). 30.. Doyle. and McCauslin. Journal of Experimental Psychology: Human Learning and Memory. L. Clinical Aphasiology. LaPointe.. C. Minneapolis: BRK.. Robin. 365–372. Journal of Communication Disorders. and Magill. E.. E. 1981. 467–499). M. phrases. B. K. Freed. 731–743. R. A. and Varley. Brain and Language. San Diego. 821–837. R. M. C. Shea. P.). H. 12. Therapeutic approaches to apraxia. R. 26. T. 1. E¤ects of verbal plus gestural treatment in a patient with aphasia and severe apraxia of speech.. Clinical Aphasiology Conference proceedings (pp. S. P. It resurfaced in the 1980s in the work of Ross and his colleagues to refer to the attenuated use of and decreased sensitivity to prosodic cues by right hemisphere damaged patients (Ross and Mesulam. Ross. Chumpelik. 14. Prescott. Simmons. Prosodic deficits in expression or comprehension can accompany a variety of cognitive. J. Choice of stimulus modes in treating apraxia of speech: A case study.. Psychological Science. L. 151–171). and McCauslin. linguistics. J. L. 41.. Austin... J. Martinez. McNeil. 302–307). R..... (1975). and psychiatric conditions. 107 Further Readings Dabul. H. Marshall.. Research Quarterly for Exercise and Sport. (1989). V.. and Frazier. and Martin. and Martinez.. Wambaugh.. A. D. H. D. Schmidt. 2.). Apraxia of speech in adults: The disorder and its management. In R.. (1979). P. EPG in therapy: Using electropalatography to treat severe acquired apraxia of speech. (1976). Aphasiology. Clinical Aphasiology Conference proceedings (pp. C. D. (1999). 14. In R. In R. J. L. E. (1986). Clinical Aphasiology. 603–617.. E. Minneapolis: BRK. J. A. and sentences. J. E. A. West. and Schmidt. C. Chapey (Ed. L. 19–22. Howard. Clinical Aphasiology. E‰cacy of the PROMPT system of therapy for the treatment of acquired apraxia of speech: A follow-up investigation. and Doyle. Response to treatment in patients with apraxia of speech. Journal of Speech and Hearing Disorders. J. and A. (1998). L. stress. L. and Samples. Wambaugh. 3. The long-term e¤ectiveness of PROMPT treatment in a severely apractic-aphasic speaker. Florance. An application of electro-myographic biofeedback to aphasia/ apraxia treatment. West. E.). 293–301. L. 62. and Lemme. In T. S. D. It is the variation in these parameters that not only provides the melodic contour of speech. 5. T. C. Brookshire (Ed. Acquired apraxia of speech in aphasic adults. Wambaugh. Journal of Speech Language and Hearing Research. (1976). M. (1981). P. 207–217. Language intervention strategies in adult aphasia (pp. 268–276. Treatment for acquired apraxia of speech: A review of e‰cacy reports. (1994). E. P. T. A. and Doyle. 285–298. Memory. 221–226). J. The term ‘‘aprosodia’’ was first used by MonradKrohn (1947) to describe loss of the prosodic features of speech. FL: Grune and Stratton. Morningstar. Contextual interference e¤ects on the acquisition retention. A.Aprosodia Wambaugh. M. A. R. 1979. Developmental apraxia of speech: Just another motor problem. In J. Aphasiology. P. (1984). L. (1999).. 13. A minimal contrast treatment for apraxia of speech.). 231–243. Brookshire (Ed. Gorelick and Ross. Traditional therapies for AOS: Reviewed and rationalized. Kalinyak. R. (1984). Apraxia of speech: Physiology. A. American Journal of SpeechLanguage Pathology: A Journal of Clinical Practice. Aronson (Eds. These same parameters are defined acoustically as fundamental frequency.). linguistic. Brookshire (Ed. L. Treatment for apraxia of speech: E¤ects of targeting sound groups. Minneapolis: BRK. Journal of Experimental Psychology: Learning. H. Keith. (1992). E¤ects of rate and rhythm control on sound production in apraxia of speech. L. R. 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Ko¤. With the exception of site of lesion. which adds a subjective component. or some combination of conditions. Holtas et al. Federo¤. body language. 1990. monotonic. chronic alcoholism. Linguistic tasks include discriminating between nouns and noun phrases based on contrastive stress patterns (e. and attenuated animation in facial expression subsequent to RHD. these variables have rarely been taken into account in research design. 1995. and identifying sentence types based on prosodic contour (e. for example. Patients may be taught to attend more carefully to other forms of emotional expression (e. however. in imitation. as well as right hemisphere damage (RHD) (Du¤y. depression. Fichtner et al. the presence or absence of neglect and dysarthria. and methods of data analysis. and sentence level. using stress patterns to identify sentence meaning (Joe gave Ella flowers versus Joe gave Ella flowers).g. Borod. typically refers to the prosodic impairments that can accompany RHD from stroke.g. facial expression). It is not clear the extent to which expressive aprosodia is a motor problem. It is important to note that receptive and expressive prosodic processing can be di¤erentially a¤ected in aprosodia. The condition often. Subjects with unilateral left or right brain damage have been asked to produce linguistic and emotional prosody in spontaneous speech. a more general form of reduced environmental responsivity. 1998). 1994). Even the disturbed prosody of other illnesses. Bradvik. or to some as yet unspecified mechanism. In some studies it has been based on perceptual judgments by one or more listeners. Thus. and Ross.. data are . areas considered important to prosodic impairment subsequent to RHD (Sweet. but also because of their limbic and frontal connections which may influence the expression of emotion in motor action. facial expression) and to signal mood by explicitly stating their mood to the listener. Blonder. such as schizophrenia. patients may have problems both encoding and decoding the tone of spoken messages and the intention behind the message as conveyed through both linguistic and emotional prosody. The extensive literature supporting a particular role for the right hemisphere in processing content generated the central hypotheses guiding prosodic laterality research. aprosodia may last for months and even years when other signs of RHD have abated. 1975. Monnot. Severity of neglect. greenhouse versus green house). independent of their function (emotional or linguistic) (Van Lancker and Sidtis. Much of the research in prosodic processing has been conducted to answer questions about the laterality of brain function. Subjects across and within studies may vary in terms of time post-onset. subject selection criteria. Ross et al. or progressive neurologic disease with a right hemisphere focus. play a role in prosodic processing (Cancelliere and Kertesz. Price et al. and in the absence of motor programming deficits typically associated with apraxia of speech. been at least one report of successful symptomatic treatment using pitch biofeedback and modeling (Stringer... Research findings have varied as a function of task type. in the absence of depression or other psychiatric disturbances.g. Aprosodia can occur in the absence of dysarthria and other motor speech disorders. Dravins. 2001). gesture. however. In rare cases. Treatment has been somewhat limited by uncertainty about the underlying mechanisms of aprosodia. a pragmatic problem. 1996).. Lovallo. intrahemispheric site of lesion. Data analysis has varied across studies. Even then. aphasia. 1985. the rising intonation pattern for interrogatives versus the flatter pattern for declaratives). The clinical presentation of expressive aprosodia is a flattened. patients with aprosodia are usually unaware of the problem until it is pointed out to them. In others. reduced sensitivity to the paralinguistic features of communication (gesture. Patients with persistent aprosodia may be aware of the problem but feel incapable of correcting it. but not always. Bowers. First observed in the emotional domain. 1998. and Heilman. 2001). Another hypothesis holds that prosodic cues themselves are lateralized. accompanies flat a¤ect. aprosodia has also been found to occur in the linguistic domain. Nixon. Myers. may be the result of alterations in right frontal and extrapyramidal areas. Finally. Cancelliere and Kertesz (1990) speculated that the basal ganglia may be important not only because of their role in motor control.. Similarly. and in reading tasks at the single word. Expressive aprosodia is easily recognized in patients with flat a¤ect. particularly if they su¤er from other forms of denial of deficit. Deficits in prosodic perception and comprehension are less apparent in clinical presentation. it is not clear whether receptive aprosodia is due to perceptual interference in decoding prosodic features. In receptive tasks they have been asked to determine the emotional valence of expressive speech and to discriminate between various linguistic forms and emotional content in normal and in filtered-speech paradigms. There has. Treatment of aprosodia is often limited to training patients to adopt compensatory techniques. Myers.. a resource allocation problem. The first hypothesis suggests that a¤ective or emotional prosody is in the domain of the right hemisphere (Heilman. phrase. 1991). Primeau. Because it is associated with damage to the right side of the brain. 1995. In the acute stage. The emphasis on laterality of function has helped to establish that both hemispheres as well as some subcortical structures contribute to normal prosodic processing.. stilted prosodic production characterized by reduced variation in prosodic features and somewhat uniform intersyllable pause time. somewhat robotic. has been found to correlate with prosodic deficits (Starkstein. and mania. schizophrenia. head injury. 1998. Scholes.108 Part II: Speech speech disorders. 1991). 1992). lesion localization studies have found that certain subcortical structures. and Watson. Lorch et al. and severity of attentional and other cognitive deficits.. it usually occurs in the absence of linguistic impairments (Du¤y. the basal ganglia in particular. they may deny it. The term aprosodia. to restricted attention (which may reduce sensitivity to prosodic cues).

Behrens. X. 1986. Dravins. Ko¤. K. S. Robin et al. Borod. Motor speech disorders.. However. The role of the right hemisphere in the production of linguistic stress. C. Sidtis and Volpe. 290–396. impairment. In particular. 1987). A. (1987). S. H. E.. (1992). Ponglorpisit. and Heilman. 33. 1992). I. the data pool on which we rely for conclusions about the nature of RHD prosodic deficits consists largely of subjects with and subjects without prosodic impairment. Khunadorn. which may explain why impaired production of emotional prosody appears particularly prominent in aprosodia. Robin et al. S. A. 379–383. 1988. These issues will remain unclear until a working definition of aprosodia is established and descriptive studies using that definition as a means of screening patients are undertaken. B. 1992). L. 32. For example. R... Colsher. Brain and Language. 1987. Prosodic perception or comprehension deficits associated with aprosodia tend to follow the pattern found in production. 37. J. and Gra¤-Radford. Thus. Lexical . Myers References Baum. 1989. Intonation variability in the speech of right-hemisphere damaged patients. A. S. W.g. 1997. Van Lancker and Sidtis. Chinese. (1995). the data are supported by data from dichotic listening and other studies that have investigated temporal versus time-independent cues such as pitch information (Chobor and Brown. the focus on laterality has had some drawbacks for understanding aprosodia per se. 345–348. Brain. Boongird. See also prosodic deficits. L. (1990). 114. Lorch. Behrens. which a¤ords increased objective control but in some cases may not match listener perception of severity of impairment (Ryalls. W. Brain and Language. its mechanisms. Pell. RHD patients are minimally if at all impaired in the production of emphatic stress. Chobor. E. 1989. Although a study by Pell and Baum (1997) failed to replicate these results. 1987. they are not screened for prosodic impairment... Boonklam. 1987. Brain and Language. 37. 177–198.. Emmory. 1990. K. Tranel. Dechongkit. M. 114–126. Duration and timing cues are considered to be in the domain of the left hemisphere (Robin.. S. The role of the right hemisphere in emotional communication. 104–127. N. Gandour. S. M. P. Thai. Blonder. Characterizing sentence intonation in a right hemisphere-damaged population.. 30. and Brown. Gandour et al. 11.. Disturbances of speech prosody following right hemisphere infarcts. Archives of Neurology.. 1997). and Potisuk.. Interestingly. Phoneme and timbre monitoring in left and right cerebrovascular accident patients. R. R. and Gra¤-Radford. Brain and Language. 1989. J. St.and left-hemisphere-damaged patients used di¤erent cues to identify emotional stimuli. M. Pell. and Feldman. Divenyi and Robinson. J. Ryding. Du¤y.. and Norwegian) in which pitch patterns in individual words serve a semantic role. 84. acoustic analyses of prosodic productions by RHD patients supports the theory that prosody is lateralized according to individual prosodic cues rather than according to the function prosody serves (emotional versus linguistic). D. The body of laterality research has established that pro- sodic deficits can occur in both left as well as right hemisphere damage.... Bowers. and Damasio. 30. J. P. Ryalls and Reinvang. (1987). Patients with RHD tended to base their decisions on durational cues rather than on fundamental frequency variability while left-hemisphere-damaged patients did the opposite. in the case of tonal languages (e. rather than a functional (linguistic versus emotional). The characteristics of aprosodia. Van Lancker and Sidtis. Aphasiology. they may have an abnormally flat pitch pattern in declarative sentences. L. Non-temporal properties such as pitch appear to be more problematic than time-dependent properties such as duration and timing (Divenyi and Robinson. D. In general. 1990). J. 78–284. K. Baum and Pell. Rosen. and Nicholas. Lesion localization in acquired deficits of emotional expression and comprehension. Emmory. Cooper. less than normal variation in pitch for interrogative sentences. 305– 320. 1990. 1999a). Brain and Cognition. and Ingvar.. Brain and Language. and Kertesz. M. Divenyi.. frequency of occurrence in the general RHD population. Production of a¤ective and linguistic prosody by brain-damaged patients. (1989). Cooper. (1987).. and may produce emotionally toned sentences with less than normal acoustic variation (Behrens. S.... Acta Neurologica Scandinavica. Pitch variation is crucial to signaling emotions. Baum and Pell. 1986. C. and Robinson. and the presence/absence of other RHD deficits that may accompany it have yet to be clearly delineated. Research suggests that reduced pitch variation and a somewhat restricted pitch range appear to be significant factors in the impaired prosodic production of RHD subjects (Colsher. However. (1988).. Louis: Mosby. D. Bradvik. 42. P. pitch has been found to be a left hemisphere function (Packard. and Pell. The main problem is that while subjects in laterality studies are selected for unilateral brain damage. 1988. 133–147. rather than describing the characteristics of prosodic problems in patients known to have prosodic deficits. E. (1985). pitch cues are considered to be in the domain of the right hemisphere. (1989). These data suggest a perceptual. (1991). Cancelliere. Van Lancker and Sidtis (1992) found that right. duration. J. D. L. (1991). 1992. Holtas. Channels of emotional expression in patients with unilateral brain damage. 1999). 181–200. The neurological substrates for prosodic aspects of speech. 13. —Penelope S. J. Joanette. Almost all studies of prosodic deficits have focused on whether unilateral brain damage produces prosodic deficits. P. and has furthered our understanding of the mechanisms and di¤erences in prosodic processing across the hemispheres. Brain and Language...Aprosodia 109 submitted to acoustic analysis. right hemisphere language disorder. F. 1115–1127. B.. E. Behrens. right hemisphere language and communication functions in adults. (1997). Nonlinguistic auditory compatabilities in aphasia.

g.. and Reinvang. Alcoholism: Clinical and Experimental Research. Stringer. Tranel. and Feldman. low. H. 29... T. J. 389–398. (1975). and Ross. Auditory perception of temporal and spectral events in patients with focal left and right cerebral lesions.. Altered emotional perception in alcoholics: Deficits in affective prosody comprehension.. Burgard. T. Price. 1988). G. R. S. Y. Journal of Neurology. AAC systems are typically described as hightechnology. M. Journal of Speech and Hearing Research. Dissociation of a¤ect recognition and mood state from blunting in patients with schizophrenia. Brain and Language. Brain and Language. Lutz. 39. Brain and Language. (1990). and sign language. 144–148. An acoustic comparison of normal and right-hemisphere-damage speech prosody. D. S. Ross. Low. 81. M. (1987).. and Buck. P. A.. C. 235–245.. 561–569. such as body movements. AAC is considered multimodal. M. but also the establishment. E.. 1998. Pell. 35. without the use of specific aids or devices.. 405–415. 73– 90). Journal of Neurology. Individuals at any point across the life span and in any stage of communication ability may use AAC (see the companion entry.. Ross. and (4) social etiquette (Light. 50. E. M. and/or written communication is temporarily or permanently . I. D. 13. T. 38.. (1981). The identification of a¤ective-prosodic stimuli by left. Lovallo. Brain and Language. D.-M. Brain and Language. amyotrophic lateral sclerosis) (American Speech-Language-Hearing Association [ASHA]. D. (1999b). (2001). traumatic head injury. 581–608. 685–694. Neurosurgery. Adults with severe communication disorders benefit from AAC. and Watson. gestures. and Damasio. Neuropsychological and neuroradiologic correlates of emotional prosody comprehension. M. 212–223. D. maintenance. speech.. 23. H. and aided communication. D.. and as such it incorporates the full communication abilities of the adult.. S. S. J... H. and social etiquette. mental retardation). R. and development of interpersonal relationships using information transfer. 70. 25. Y. Sidtis. Myers. 29. Leiguarda. (2001). and no-technology in respect to the aids used in implementation. and Ross. D. (1994).. J.. These four functions broadly encompass all communicative interactions. 44. E. L. Cortex. Fundamental frequency encoding of linguistic and emotional prosody by right hemisphere damaged speakers.. J. Sweet. (1998). M. Hightechnology AAC systems use electronic devices to support digitized or synthesized communication strategies. Primeau. (1986). 161–192. (1947). Packard. (1988). R. R. E. Tone production deficits in nonfluent aphasic Chinese speech. 963–970. Dysprosody or altered ‘‘melody of language.. Aphasiology. acquired disabilities (e. 43... G. G. M. (1996)..’’ Brain.. and Psychiatry. Pell.. A no-technology system involves the use of strategies and techniques. (1998). Functional lateralization of linguistic tones: Acoustic evidence from Norwegian. Psychiatry Research. The aprosodias: Further functional-anatomical evidence for the organization of a¤ective language in the right hemisphere. gestures. (1999).. Hansel. W. Augmentative and Alternative Communication Approaches in Adults An augmentative and alternative communication (AAC) system is an integrated group of components used by individuals with severe communication disorders to enhance their competent communication.g. E. of which we can isolate four: (1) communication of wants and needs. 362–369. (3) social closeness. stroke). Orbelo. Federo¤. B. (1992). including congenital disabilities (e. Neurosurgery. Monnot. D. and the acoustic cues to prosody. multiple sclerosis. Joanette. (1986). Journal of Neurology. Mohrad-Krohn. Auditory a¤ective agnosia: Disturbed comprehension of affective speech. p. L. 62. Competent communication serves a variety of functions. The aprosodias: Functional-anatomic organization of the a¤ective components of language in the right hemisphere. R.and right-hemispheredamaged subjects: All errors are not created equal. M. and Mesulam. Further Reading Baum. P. Language and Speech. Scholes. Heilman. Gorelick. Cortex. Treatment of motor aprosodia with pitch biofeedback and expression modelling. 539–555. (1979). (1987). The neural bases of prosody: Insights from lesion studies and neuroimaging. Unilateral brain damage. and Pell. It includes any existing natural speech or vocalizations. AAC is used to assist adults with a wide range of disabilities. J. augmentative and alternative communication approaches in children). D. R.g. and light pointing devices. and Psychiatry. Starkstein. A. 583–590. Robin. S.. 1). and Baum. 34. and Robinsn.. 195–214. p. Brain and Language. 10) describes these people as ‘‘those for whom natural gestural. Brain Injury. Neurosurgery. S.. Archives of Neurology. 10. 1989). Ryalls. (1999a). Nixon. San Diego. Fichtner. K. (1997).. R. 553–560.or light-technology systems include items such as communication boards (symbols). Neurology. Selective loss of complex pitch or speech discrimination after unilateral lesion. and degenerative conditions (e. 69–72. J. D. M. Cartwright. D. 57. An appropriate AAC system addresses not only basic communication of wants and needs. E. The temporal organization of a¤ective and non-a¤ective speech in patients with right-hemisphere infarcts. In Right hemisphere damage: Disorders of communication and cognition (pp. C. ASHA (1991. 301–308. cerebral palsy.or light-technology. communication books. tones in Thai after unilateral brain damage. G. Testa.110 Part II: Speech Van Lancker. (2) information transfer. Dominant language functions of the right hemisphere? Prosody and emotional gesturing. Prosodic deficits. J.. 163–182. Ryalls. J. B. ‘‘AAC allows individuals to use every mode possible to communicate’’ (Light and Binger. A. R. formal sign language. 275–307. 35. social closeness. 38. Pell. CA: Singular. 70. Archives of Neurology. 597–604. 516–522. M. Ross. J. and Volpe. 36. D. prosodic comprehension deficits. and Sidtis. P. A¤ectiveprosodic deficits in schizophrenia: Profiles of patients with brain damage and comparison with relation schizophrenic symptoms. and Psychiatry. J.

speech symptoms typically occur early in the disease progression. 103). Many adults with severe communication disorders demonstrate some ability to communicate using natural speech. In the early phase. speech intelligibility in this (bulbar) group declines precipitously approximately 10 months after diagnosis. speech-supplementation. recovery of cognitive functioning is categorized into phases (Blackstone. it is likely a result of chronic motor control and language impairments. If they do not become speakers by the end of this phase. and Gutmann.. it is likely the result of specific motor or language impairment. vocational. The cause is unknown. optimizing any available contextual information through AAC techniques will increase the comprehensibility of the message. Generally.’’ An important consideration is that ‘‘although some individuals may be able to produce a limited amount of speech. AAC intervention is typically described in five stages (Beukelman and Mirenda. and reduced ability to control the muscles of the face. 2000). For those whose impairment begins in the lower spine. while others may be unable to speak. a drop in speaking rate predicts the onset of the abrupt drop in speech intelligibility (Ball. Traumatic brain injury (TBI) refers to injuries to the brain that involve rapid acceleration and deceleration. Beukelman. it is important that individuals who use natural speech. 10). low-technology. intelligibility is not a good measure to use in determining the timing of an AAC evaluation. people. the person is minimally responsive to external stimuli. On average. Amyotrophic lateral sclerosis (ALS) is a disease of rapid degeneration involving the motor neurons of the brain and spinal cord that leaves cognitive abilities generally intact. which results in compromised neurological function (Levin. Some individuals are dysarthric but able to communicate partial or complete messages. AAC goals during this phase address providing a way to indicate basic needs and giving a response modality that increases participation in the evaluation and treatment process. p. AAC intervention makes use of both low. and Tice. it is inadequate to meet their varied communication needs’’ (ASHA. As the quality of the acoustic signal and the quality of environmental information improve. 2001). or notechnology interventions to express needs. The goal of AAC in TBI is to provide a series of communication systems and strategies so that individuals can communicate at the level at which they are currently functioning (Doyle et al. and larynx voluntarily or reflexively. Beukelman. 2000). Frequent objective measurement of speaking rate is important to provide timely AAC intervention. mouth. Because the drop in intelligibility is so sudden. ACC approaches for a few adult severe communication disorders are described here. poorquality acoustic signals and poor environmental information result in a deterioration in message comprehensibility. AAC intervention strategies usually involve nonelectronic. Intervention goals address provision of functional ways to interact with listeners in a variety of settings and to assist the individual to participate in social. In the middle phase. Communication symptoms vary considerably with the extent of damage. Persons with aphasia. AAC goals include providing support to respond to one-step motor commands and discriminate one of an array of choices (objects. the person exhibits improved consistency of responses to external stimuli. In the late phase. AAC applications during this phase include low-technology pictures and communication boards and choices of real objects to support communication. locations). or CVA) disrupts the circulation serving the lower brainstem. an AAC evalua- tion should be completed when an individual reaches 50% of his or her habitual speaking rate (approximately 100 words per minute) on a standard intelligibility assessment (such as the Sentence Intelligibility Test. Yorkston. It is in this phase that persons who are unable to speak because of severe cognitive confusion become able to speak. 2000. Clinically. 1989). ‘‘Given that communication e¤ectiveness varies across social situations and listeners. Similarly. AAC may also be used to support comprehension and cognitive abilities by capitalizing on residual skills and thus facilitating communication.Augmentative and Alternative Communication Approaches in Adults 111 inadequate to meet all of their communication needs. because the speaking rate declines more gradually. and Pattee. p.and high-technology strategies in this phase of recovery. Natural speech is more time-e‰cient and linguistically flexible than other modes (involving AAC). Benton. Some individuals maintain functional speech much longer. The result is often severe dysarthria or anarthria. Parkinson’s disease. Brainstem stroke (cerebrovascular accident. As a group. 1998). and there is no known cure. 1990). if the person continues to be nonspeaking. In stage 1. Guillain´ Barre syndrome. whereby the brain is whipped back and forth in a quick motion. 1982). When a speaker experiences reduced acoustic speech quality. Rather. and recreational settings. comprehensibility—intelligibility in context—of messages is enhanced (Lindblom. 1996). and Grossman. Access to a communication system is increasingly important as ALS advances (Mathy. 80% of individuals with ALS eventually require use of AAC. Speech supplementation AAC techniques (alphabet and topic supplementation) used in conjunction with natural speech can provide extensive contextual knowledge to increase the listener’s ability to understand a message. traumatic brain injury. The patterns of communication disorders in adults vary from condition to condition. and numerous motor speech impairments benefit from using AAC (Beukelman and Mirenda. 1991. the person exhibits no functional speech. 1998). speech intelligibility declines precipitously approximately 25 months after diagnosis. The goal of intervention is to provide early communication so that . AAC intervention may be complicated by coexisting cognitive deficits. For those whose initial impairments are in the brainstem. educational. and AAC strategies learn to switch communication modes depending on the situation and the listener’’ (Hustad and Beukelman. Yorkston. multiple sclerosis.

Children who are unable to meet their daily needs using their own speech require alternative systems to support their communication interaction e¤orts (Reichle... TX: Pro-Ed. and Yorkston. 5). F. 31. References American Speech-Language-Hearing Association. K. Levin. S.).).. Beukelman. 2(3). In K. (2000). Reichle (Eds..). (1992). AAC for individuals with amyotrophic lateral sclerosis.. Journal of Neurological Sciences. B. D. D.). Augmentative communication following traumatic brain injury. velopharyngeal. Yorkston. 66–82. and Reichle. P. Brookes. and Beukelman. K. Beukelman. D. DeRuyter. 317–365).. or stable. Blackstone. Baltimore: Paul H. Collier. G.. Mathy. (1992). (2001). In stages 4 and 5.. Augmentative communication in the medical setting. (1998). AAC for Huntington disease and Parkinson’s disease: Planning for change. M. Klasner. NE: Tice Technologies. G. P. The AAC intervention focuses on intelligibility.. In D. and Culp. AZ: Communication Skill Builders. D. Hustad. (1998). 2001). and Mirenda. In summary. and J. Brookes. Augmentative Communication News. Brookes. Brookes. (1988). D.. Garrett. Brookes. In stage 3. Reichle (Eds. and motor impairments (pp... —Laura J. Baltimore: Paul H.. (1995). E.. Building communicative competence with individuals who use augmentative and alternative communication.. Baltimore: Paul H. with alphabet supplementation used early. 139–243). 220–230. and Kimelman. Yorkston. New York: Oxford University Press. Communication disorders following traumatic brain injury: Management of cognitive. and Kennedy.. and J. Sentence Intelligibility Test. adults with severe communication disorders are able to take advantage of increased communication through the use of AAC. and Tice. Augmentative and alternative communication for adults with acquired neurologic disorders (pp. In K. M. Benton. D. 191. ASHA. Baltimore: Paul H. and Grossman. Yorkston. D. Yorkston. Baltimore: Paul H. Yorkston. Canada: William Bobek Productions. Baltimore: Paul H. (1991). and Light. Brookes. D. Beukelman and K. Beukelman. 183–229). the person can respond to yes/no questions. Kennedy. American Speech-Language-Hearing Association. 83–106). AZ: Communication Skill Builders. and J. C. R. remitting. (2000).). 9–12. initial choice making. Miller. AAC and aphasia: Cognitive-linguistic considerations. Integrating AAC strategies with natural speech in adults. Jausalaitis. Early in this stage. and Pattee. late in this stage persons are able to convey an increasing percentage of messages with natural speech. Tucson. 5(3). 1–3. 107–110. In stage 2. M. For consumer: Societal rehabilitation. Augmentative and alternative communication for adults with acquired neurologic disorders (pp.). The staging of AAC interventions is influenced by the individual’s communication abilities and the natural course of the disorder. R. In K. language. Austin. In K. 233–270). (1989).). (2000). J. Augmentative and alternative communication: Management of severe communication disorders in children and adults. and Phillips. Yorkston (Eds. and Bersani. whether advancing. ASHA. (2000). Fried-Oken. Reichle (Eds.. A. San Antonio. Lincoln.. 33(Suppl. Brookes. K. K. See what we say: Vocabulary and tips for adults who use augmentative and alternative communication. B.. M. J. Yorkston (Ed. Augmentative communication in the medical setting (pp. and Binger. Management of speech and swallowing in degenerative diseases. 339–374). Augmentative communication with the traumatically brain injured population. Yorkston. phonatory. Augmentative and Alternative Communication. Yorkston. Light. (1996).112 Part II: Speech Lindblom. pointing. (1991). the AAC system will support the majority of interactions. Speaking up and spelling it out: Personal essays on augmentative and alternative communication. K. Brookes. (2000). and J. Ball Further Readings Beukelman. and Strand. K. Ontario. (2000). R. L. 6. however. and Gutmann. Augmentative and alternative communication for adults with acquired neurologic disorders (pp. Baltimore: Paul H. the goal is to reestablish speech by working directly to develop control over the respiratory. J. Augmentative and Alternative Communication. Baltimore: Paul H. E. (2000). B. Interaction involving individuals using augmentative and alternative communication systems: State of the art and future directions. 271–304). North York. Ladtkow. (1989). D. Tucson. Neurobehavioral consequences of closed head injury. and articulatory subsystems. M. Yorkston. Beukelman. Beukelman. On the communication process: Speakerlistener interaction and the development of speech. and J. D. the person no longer needs to use an AAC system.. TX: Psychological Corporation. An augmentative and alternative communication (AAC) system is an . M. bidirectional process of interactions between speaker and listener. Beukelman. Reichle (Eds. Doyle. Yorkston. AAC and traumatic brain injury: Influence of cognition on system design and use. Competencies for speech-language pathologists providing services in augmentative communication. M. In K. In D. Augmentative and alternative communication for adults with acquired neurologic disorders (pp. but later only to resolve communication breakdowns. Reichle (Eds. In this stage. A protocol for identification of early bulbar signs in ALS. the use of AAC may become necessary only to support writing.. Brookes. K. Yorkston.. (1997).. (1990). H. Beukelman. (1982). K. Beukelman. H. the person exhibits independent use of natural speech. Light. Baltimore: Paul H. 43–53. and introduction of a multipurpose AAC device. Augmentative and alternative communication for adults with acquired neurologic disorders. K. Ball. Report: Augmentative and alternative communication. Augmentative and Alternative Communication Approaches in Children The acquisition of communication skills is a dynamic. Augmentative and alternative communication for adults with acquired neurologic disorders (pp. Beukelman.

Calculator and Bedrosian noted that ‘‘communication is neither any more nor less than . The resulting motor speech disorder (dysarthria) may be so severe that AAC technology is required to support communication. Children with severe cerebral palsy primarily experience motor control problems that impair their control of their speech mechanisms. and work) that appear before the age of 18 (Luckasson et al. A secondary support team might include orthotists. academic participation. leisure. Home talk is used with familiar persons to meet needs and develop social closeness. 1985. p. teachers. For children with communication impairments. An AAC system must be designed to support literacy and other academic skill development as well as peer interactions. who are preliterate. as well as to assist parents in understanding their child. in which they speak with relatively unfamiliar adults in order to acquire knowledge. health and safety. and community activities (Beukelman and Mirenda. Large numbers of persons with cerebral palsy successfully use AAC technology (Beukelman. community use. and pediatric ophthalmologists. or school to post-school (vocational) will attain optimal participation when consideration is made for integration. Early interventions allow children to develop the linguistic. messages within their AAC systems must be represented by one or more symbols or codes. 391). It includes any existing natural speech or vocalizations. and Smith. have not yet developed reading and writing skills. Generic small talk refers to messages that can be used without change in interaction with a variety of di¤erent listeners. which includes four variables that can be manipulated to achieve appropriate participation for any child. AAC systems are used by children with a variety of severe communication disorders. home living. p. self-care. In addition. social participation. and ‘‘Leave me alone!’’ Extensive instructional resources are available to school-age children. ‘‘AAC allows individuals to use every mode possible to communicate’’ (Light and Drager. 2001). or mental retardation. Intellectual disability. and aided communication. e¤ective AAC systems that are age appropriate and context appropriate serve as critical tools for academic success (Sturm. from preschool through high school. It must be appealing to children so that they find the system attractive and will continue using it (Light and Drager. when in preschool and at home (Ball et al. Typically. 2001). in the form of the Individuals with Disabilities Education Act. and independence. The earlier that graphic and gestural mode supports can be put into place. academics. In addition to the communication/AAC specialist. rehabilitation engineers. ‘‘What’s that?’’. AAC interventionists facilitate transitions from the preschool setting to the school setting by ensuring comprehensive communication through systematic planning and establishing a foundation for communication. and physical growth throughout their formative years. Yorkston. ‘‘What are you doing?’’. Cerebral palsy is a developmental neuromuscular disorder resulting from a nonprogressive abnormality of the brain. gestures. it provides a foundation for language development and facilitates literacy development (Light and Drager. A framework for integrating children into general education programs may be implemented by following the participation model (Beukelman and Mirenda. Public policy changes have been adopted in numerous other countries to address resources available to children with disabilities. AAC support is provided to these children by a team of interventionists. Examples include ‘‘Hello’’. selfcontained to departmentalized programs. Very young children. 1998. educational. so that they will be prepared to communicate e¤ectively as they mature.. Because participation in the general classroom requires many kinds of extensive communication. ‘‘I like that!’’. Children experience significant cognitive. In the United States. Careful analysis of environmental and communication needs is used to develop vocabulary for the child’s AAC system. social skills. self-direction. 1992). The goal of AAC support is to provide children with access to the power of communication. exchange information. Children transitioning from preschool to elementary school. This vocabulary selection assessment includes examination of the ongoing process of vocabulary and message maintenance. Timeliness in implementing an AAC system is paramount (Reichle. Many young children and those with severe multiple disabilities cannot use traditional spelling and reading skills to access their AAC systems. including school talk. while older children with severe cognitive impairments may remain nonliterate. and provides a legal basis for AAC interventions. 1989). For individuals who are not literate. With children. is characterized by significantly subaverage intellectual functioning coexisting with limitations in adaptive skills (communication.Augmentative and Alternative Communication Approaches in Children 113 integrated group of components used by a child to enhance or develop competent communication. and participate in social. The vocabulary needs of children comprise contextual variations. 1). AAC support for children must address both their current communication needs as well as predict future communication needs and abilities. linguistic. formal sign language. language. who have been found to use generic small talk for nearly half of their utterances. the greater will be the child’s ability to advance in communication development. 2001). Mirenda and Mathy-Laikko. 1999).. 1998). and Light. technologists. it is important to engage in AAC instruction and interactions in natural rather than segregated environments. and parents. This power allows them to express their needs and wants. and literacy. 1998). and social competencies necessary to support their participation in academic settings. the federal government has mandated publicly funded education for children with disabilities. develop social closeness. Beukelman. 1998. operational. early communication development focuses on vocabulary that is needed to communicate essential messages and to develop language skills. An example of vocabulary needs is exhibited by preschool children. the primary team often includes occupational and physical therapists.

1997). Unpublished doctoral dissertation. J. San Diego.. with and without accompanying physical impairments. P. AAC interventionists may need to work with professionals whose views di¤er from their own.114 Part II: Speech a tool that facilitates individuals’ abilities to function in the various activities of daily living’’ (1988. interests. children with severe communication disorders benefit from using AAC systems. (1994). Generic small talk use by preschool children. Brookes. Calculator. and communication is extremely important (Dawson and Osterling. and Parnes. Their phonological systems are impaired because of their di‰culties in managing the intense motor demands of connected speech (Strand and McCauley. Diagnostic and statistical manual for mental disorders (4th ed. Caruso. Augmentative and alternative communication: Management of severe communication disorders in children and adults (2nd ed. and significant speech production disorder. 110–125. . 2000). and Mirenda. repetitive. Lincoln. Camarata. Children who are unable to speak because of cognitive limitations. University of Nebraska. L. 1996).unl. from a variety of perspectives.. Cumley.. Collier. Brookes. Ball. Articulation and phonological disorders (3rd ed. Camarata. (1988). E. 15. N. 1985a.). (1997). Lasker.). A web site (http://aac. New York: Thieme. DC: Author. Bernthal. (1996).. 1993. Olley. 1. G. These disorders occur as a spectrum of impairments of di¤erent causes (Wing. Koegel and R. Englewood Cli¤s. Augmentative and Alternative Communication. (1998). K. Developmental apraxia of speech and augmentative communication: A case example. (1993). have demonstrated considerable success using AAC strategies involving high-technology (electronic devices) and low-technology (communication boards and books) options (Light. 1997.. Augmentative and Alternative Communication. CA: College-Hill Press. Positive behavioral support: Including people with di‰cult behavior in the community (pp. language. A range of intervention approaches has been suggested. Children with a pervasive developmental disorder may have cognitive. Autism and pervasive developmental disorders are described with three main diagnostic features: (1) impaired social interaction. Ball References American Psychiatric Association. (1999). In L. D. Introduction of augmentative and alternative modality: E¤ects on the quality and quantity of communication interactions of children with severe phonological disorders. Early intervention with an emphasis on speech. background. Augmentative and Alternative Communication. and Swanson. Children with DAS have a guarded prognosis for the acquisition of intelligible speech (Bernthal and Bankson. Thirdparty payer response to requests for purchase of communication augmentation systems: A study of Washington state. D. particularly during the early elementary grades. and Rupp. they did not reduce their speech efforts.. language. social intervention.. 333–351).. (1989). Cumley (1997) studied children with DAS who were provided with AAC technology. Children with an assortment of clinical disorders are able to take advantage of increased communication through the use of AAC. J. 1–28). Baltimore: Paul H. These arguments have changed little in the last 20 years. and speechintelligibility training. 1987. communication problems that limit e¤ective social interaction. Culp. Marvin. and as a result. and processing impairments. and Smith. 1999). 1994). and (3) restricted. but rather used the technology to resolve communication provides current information about AAC resources for children and adults. D. and Strand. 104). (1985). J. Beukelman. DASrelated speech disorders may result in prolonged periods of unintelligibility. 145–155. Some children with DAS have been treated with phonologically based interventions and others with motor learning tasks. Children with suspected DAS have di‰culty performing purposeful voluntary movements for speech (Caruso and Strand. Developmental apraxia of speech (DAS) results in language delays. social participation. NJ: Prentice Hall. Beukelman. Washington.). the need to provide these children with some means to communicate so that they can successfully participate socially and in educational activities is becoming increasingly accepted. S. communication problems that influence academic performance. and a theoretical framework. and ultimately independence. C. Cumley and Swanson.. 1996). The provision of AAC intervention is influenced by the child’s communication abilities and access to memberships. Strand (Eds. Dawson and Osterling. When children with DAS with low intelligibility scores used AAC technology.). The use of AAC strategies to support the communicative interactions of children with such severe DAS that their speech is unintelligible is receiving increased attention (Culp. 15. (2) impaired communication. On the importance of integrating naturalistic language. Cumley. 5– 9. and stereotypical patterns of behaviors.. p. S. Caruso and E. K. In A. and Bedrosian. and Bankson. 1993). (1999). Membership involves integration. 1989. 1985c). D. 5. 27–34. academic participation. G. Freeman. 1999). The negative e¤ect of reduced speech intelligibility on social and educational participa- tion has been documented extensively (Kent. Yorkston.). He reported that the group of children with lower speech intelligibility scores used their AAC technology more frequently than children with higher intelligibility. Augmentative and alternative communication options for children with developmental apraxia of speech: Three case studies. social/communicative. Baltimore: Paul H. Beukelman. Some interventionists support very intense schedules of interventions. A. thus necessitating considerable collaboration (Simeonsson. Clinical management of motor speech disorders in children (pp. and Rosenthal. Communication assessment and intervention for adults with mental retardation. In summary. There is ongoing debate over the best way to manage suspected DAS. (2000). and activities (American Psychiatric Association. Motor speech disorders in children: Definitions.. S. Koegel (Eds. 1997). Augmentative and Alternative Communication. —Laura J. D. However. 1985b.

D. 391–424).. Birmingham. G. In M. J. individually administered IQ testing is administered. symbolic communication. Elder. Baltimore: Paul H. Baltimore: Paul H. Sturm. . (1988). The autistic spectrum: A guide for parents and professionals. (1996). Park City. E..).. S. E. Light. 15(2). 125–133. (1989). and Light. 110–125. Luckasson. 115 Bristow. 13. (1985a). New York: Academic Press. AL: Southeast Augmentative Communication Conference Publications.. Brookes. Beukelman.). and Williams. R. P. J. Early intervention in autism. Augmentative and Alternative Communication. Polloway. Modes of communication. E. Communicative function. and Parnes. J. Dowden. E¤ects of test adaptations on test performance. Educational inclusion of AAC users. 2). 1(3).. (1992). Collier. Paper presented at a meeting of the United States Society of Augmentative and Alternative Communication. and Drager. D. In A. Journal of Applied Behavioral Analysis.. Baltimore: Paul H. P. et al. (1997).. Mirenda. J. (1996). and Osterling. Culp. (1999). S. individuals with autism do show unusual scatter in their abilities. (1997). 73–108). Simeonsson. Light. Olley. When developmentally appropriate. Light. (1993). classification. K. New York: Thieme. Discourse patterns. (1996). M. J. Coulter.. Engineering training environments for interactive augmentative communication: Strategies for adolescents and adults who are moderately/severely developmentally delayed. In D. 179–185. Paul. CA: Mayer-Johnson. D. Augmentative and alternative communication decision making for children with severely unintelligible speech. R. 24. Augmentative and Alternative Communication.. P.). Early intervention for children with autism.. R. R. T. Kaiser and D. Collier.. Mirenda (Eds.). but who were missing the social motivation toward communication and interaction that is typically present even in children with severe intellectual deficits. 15. (1998). 171. 1(4). Goossens. Crain. Strand. Brookes. unlike the performance seen in children with other kinds of retardation. Despite their obvious impairments in social communication. Augmentative and alternative communication options for children with developmental apraxia of speech: Three Case Studies. J. P. 3). (2001).. Baltimore: Paul H. Building communicative competence with individuals who use augmentative and alternative communication. Engineering the preschool environment for interactive. Journal of the Association for Persons with Severe Handicaps. J. (1997). Brookes. Augmentative and Alternative Communication. (2002). Augmentative and Alternative Communication. 4. P. D. J. L. S. P..Autism Dawson. 2). Brookes. Kent. 3–14. Enhancing children’s communication: Research foundations for intervention. and systems of support (9th ed. and Swanson. Augmentative and Alternative Communication. Exemplary practices for beginning communicators: Implications for AAC (vol. Reiss. P.. (1992). R. 1(2). visually based performance often significantly exceeding verbal skills. (1987).. Bennett (Eds. UT: Creative Communicating. Baltimore: Paul H.. P. J. symbols. and Drager. Brookes. and Parnes. Autism The term autism was first used in 1943 by Leo Kanner to describe a syndrome of ‘‘disturbances in a¤ective contact. 48–58. the children Kanner observed did surprisingly well on some parts of IQ tests. Augmentative and Alternative Communication. (1998). P. Baltimore: Paul H. Augmentative and Alternative Communication. Snell. Light.. Exemplary practices for beginning communicators: Implications for AAC (vol. 27(6).. Kanner’s observation about intelligence has been modified by subsequent research.. B. B. approximately 80% of people with autism score in the mentally retarded range. Solana Beach.. 3–21. Washington. S. Reichle.’’ which he observed in 11 boys who lacked the dysmorphology often seen in mental retardation. Augmentative and alternative communication: Management of severe communication disorders in children and adults (2nd ed. K. B.. However.. (1998). Communication interaction between young nonspeaking physically disabled children and their primary caregivers: Part II. and Parnes. M. Speech intelligibility and communicative competence in children. leading Kanner to believe they did not have mental retardation. 13.. (1997). P. Collier. Guralnick and F.. Aug. Reichle. Communication alternatives to challenging behavior: Integrating functional assessment and intervention strategies (vol. Strand (Eds. Baltimore: Paul H. Assessment procedures for treatment planning in children with phonologic and motor speech disorders. B. and Light. St. 641–651. pp. J. and Mathy-Laikko. Mirenda. Communication options for persons with severe and profound disabilities: State of the art and future directions. (1993). Beukelman and P. Freeman. Schalock. Light. The e¤ectiveness of early intervention for at-risk and handicapped children (pp. Reichle. (1985b). Iacono. Augmentative and Alternative Communication. Augmentative and alternative communication applications for persons with severe congenital communication disorders: An introduction.. D. (1993). Caruso and E. In A. 98–107.. (1999). London: Constable. Further Readings Bedrosian. and Rosenthal. G. (2001. Communication interaction between young nonspeaking physically disabled children and their primary caregivers: Part I... G. J... MN. Wing. King-Debaun. Light. Mental retardation: Definition. (1990). 5(1). ChalkTalk: Augmentative communication in the classroom. special needs children. 1994). Brookes. Clinical management of motor speech disorders in children (pp. 275–293).. with nonverbal. 74–83. 369–378. Storytime just for fun: Stories. Language acquisition in young AAC system users: Issues and directions for future research. and Fristoe. 2). J. Cumley. and scores remain stable over time (Rutter et al. J. (1985c). J. Journal of Autism and Developmental Disorders. J. Improving the design of AAC technologies for young children. Anchorage: Assistive Technology Library of Alaska. DC: American Association on Mental Retardation. and emergent literacy activities for young.). C. Guidelines for evaluating intervention programs for children with autism. Communication interaction between young nonspeaking physically disabled children and their primary caregivers: Part III. Building communicative competence with individuals who use augmentative and alternative communication. B. Gray (Eds. R. Brookes. and McCauley. whose scores are comparable across all kinds of tasks. and Elder. Beukelman.

and cognitive di‰culties expressed in varying degrees in parents. and the use of maladaptive and self-injurious behaviors to express desires (Donnellan et al. Although genetic factors appear to contribute to some degree to the appearance of autism. This is the hallmark of the autistic syndrome. but forms for expression are aberrant. Few references are made to mental states. Hobson. as in normal development. showing. Some examples are pulling a person toward a desired object without making eye contact. radio. such as responding to questions they do not understand (Prizant and Duchan. and they rarely attempt to direct others’ attention to objects or events they want to point out. Impairment in communication. Impairment in social interaction. 1995). seen in normal preverbal children. Pragmatic. and other relatives of individuals with autism. according to the Diagnostic and Statistical Manual of the American Psychiatric Association (4th ed. (1994).. and . The range of communicative intentions expressed is limited to requesting and protesting. or delayed echolalia. here/there). 1981). Words are assigned to the same categories that others use (Minshew and Goldsein. Forty percent of people with autism exhibit echolalia. and so on. 1997). More recent research suggests that the flexibility required to shift referents and di‰culty assessing others’ state of knowledge are more likely to account for this observation (Lee. The primary diagnostic criteria for autism include the following: Early onset. and establishing joint attention. Formal aspects of language production are on par with developmental level. and waving. The rate of initiation of communication is low (Stone and Caro-Martinez. Similar research on diagnostic criteria for other pervasive developmental disorders is not yet available. Nonverbal communication. you/I. but language development lags behind nonverbal mental age (Lord and Paul. Wants and needs are expressed preverbally. and Howlin. or gestures to engage in social interaction as other children do. 1984). Communicative di¤erences in autism include the following: Mutism. Children with autism do not use facial expressions. is greatly restricted (Paul. and often appear content to be left on their own to pursue their solitary preferred activities. instead of pointing. showing. and di‰culty is seen with deictic terms (i.. However. 1994). The diagnostic criteria for autism are more explicitly stated in DSM-IV than the criteria for other pervasive developmental disorders. Many parents first become concerned at the end of the first year of life.e. depending on the point of view of the speaker). The field trial showed that the criteria specified in DSM-IV exhibit reliability and temporal stability. There may also be unusual preoccupations with objects (e. Tuberous sclerosis (a disease characterized by abnormal tissue growth) is associated with autism with higher than expected prevalence. high-functioning adults with autism show higher than expected rates of speech distortions (Shriberg et al. both verbal and nonverbal forms of communication are impaired. At this period of development. a direct parroting of speech directed to them. Showing o¤. Language and communicative di‰culties are also core symptoms in autism. They show only fleeting interest in peers. 1994). in which they repeat snatches of language they have heard earlier. an intense interest in vacuum cleaners) or actions (such as twanging rubber bands) that are not like the preoccupations of other children at this age. siblings. body posture. communicative. Articulation is on par with mental age in children with autism who speak.. This vulnerability may be expressed in a range of social.. 1997). an imitation of speech they have heard— either immediate echolalia. eye contact. as evidenced by di‰culty with saying I.g. For people with autism who do develop speech. 1997). whose meaning changes. and turntaking are significantly reduced. however. 1993). are absent in this population. and Chiat. interpersonal uses of language present the greatest challenges to speakers with autism. The co-occurrence of autism and fragile X syndrome (the most common heritable form of mental retardation) is also higher than would be expected by chance. 2001).  Autism is considered one of a class of disabilities referred to as pervasive developmental disorders. This was first thought to reflect a lack of self. perhaps including echoing that is far in advance of what can be produced in spontaneous or meaningful contexts.. Echolalia decreases. They are less interested in sharing attention to objects and to other people. labeling. with increases in language comprehension. and speech is often idiosyncratic and contextually inappropriate (Lord and Paul. too. The criteria for autism are the result of a large field study conducted by Volkmar et al. acknowledging. from other people or on TV. Maywood. when a child does not start talking. Dykens and Volkmar (1997) reported the following:    Approximately 25% of individuals with autism develop seizures. Word use is a major area of deficit in those who speak (Tager-Flusberg. A significant delay in comprehension is one of the strongest distinctions between people with autism and those with other developmental disabilities (Rutter. the condition can also be associated with other medical conditions. Children with autism are similar to mental age– matched children in the acquisition of rule-governed syntax. less use of communicative gestures such as pointing. and scores on vocabulary tests are often a strength. Pointing. words may be used with idiosyncratic meanings. 1990). children with autism also show reduced interest in other people. 1987).. Both kinds of echolalia are used to serve communicative functions.116 Part II: Speech  Recent research on the genetics of autism suggests that there are heritable factors that may convey susceptibility (Rutter et al. 1992). and noncommunicative sound making. Approximately half of people with autism never develop speech.

and some are e¤ective at treating certain symptoms (see McDougle. and Lockyer. In adolescence. In the vast majority of cases. 1998). prevalence estimates rose to 1 per 1000 (Bryson. they generally progress toward more. 1998) and on the use of environmental compensatory supports. intonation. and Le Conteur. primitive strategies such as imitation are used to continue conversations (Tager-Flusberg and Anderson. Very talkative people with autism are impaired in their ability to use language in functional. and of approaches that are some hybrid of the two (Prizant and Wetherby. Until recently. 1998). Children with autism are more impaired in symbolic play behaviors than in other aspects of cognition.g. 2000). current prevalence estimates range from 1 in 500 to as low as 1 in 300 (Fombonne. The most widely used for research purposes are the Autism Diagnostic Interview (Lord. Abnormal preoccupations with objects or parts of objects are characteristic of autism. that provide separate documentation of aberrant behaviors in each of the three areas that are known to be characteristic of the syndrome: social reciprocity. For individuals at the highest levels of functioning. Stereotyped motor behaviors. there is a great deal of debate about incidence and prevalence. Using this broad definition. 1973). repetitive behaviors. However. communication. Approximately 75% of adults with autism require high degrees of support in living. For higher functioning and older individuals with autism. Delays in imaginative play. either interview or observational. There is little awareness of listeners’ lack of interest in extended talk about these topics.Autism 117 people with autism have di‰culty inferring the mental states of others (Tager-Flusberg. autism was thought to be a rare disorder. nor is there one diagnostic test that definitely identifies this syndrome. 1987). whose language use improves with increased amount of speech. children with autism grow up to be adults with autism. 1995). Still. As children with autism grow older. with good outcomes almost always associated with IQs above 60 (Rutter. 1997).000 (Lotter. The use of pragmatic stress in spontaneous speech and speech fluency are also impaired (Shriberg et al. Recent innovations focus on the use of alternative communication systems (e.. and Wetherby. Although clinicians see more children today who receive a label of autism than they did 10 years ago. with stereotypic behaviors and a great need to preserve sameness—is most characteristic of the preschool period. unlike other kinds of children with language impairments. Current assessment methods make use primarily of multidimensional scales. for a review). 1967). Only 1%–2% of cases have a fully normal outcome (Paul. such as stacking and nesting (Schuler. It is a major contributor to listeners’ perception of oddness (Mesibov. these prevalence figures were based on identifying the disorder in children who. 1994) and the Autism Diagnostic Observation Scale (Lord et al. with only about 20% gainfully employed (Howlin and Goode. as is a need for routines and rituals always to be carried out in precisely the same way. 2001). There are proponents of operant applied behavior treatments (Lovaas. this is likely to be due to a broadening of the definition of the disorder to include children who show some subset of symptoms without the full-blown syndrome. growth in both language and cognitive skills can be seen (Howlin and Goode. 1996). Paralinguistic features such as voice quality. Outcome in adulthood is related to IQ. Prizant. particularly about whether incidence is rising significantly. As it became recognized that the social and communicative deficits characteristic of autism could be found in children along the full range of the IQ spec- trum. The development of functional speech by age 5 is also a strong predictor of good outcome (DeMyer et al. 1997). with prevalence estimates of 4–5 per 10. communicative ways (Lord and Paul. Early intervention. Although a variety of pharmacological agents have been tried. Major changes have taken place in the treatments used to address autistic behaviors. Although there is some debate about the precise ratio. There is ongoing debate about the best methods of treatment. Rutter. though still aberrant. 1991). most interventions are derived from more . when provided with a high degree of intensity (at least 20 hours per week). had IQs within normal range. to facilitate communication and learning (Quill. and restricted. 1966). 1999). Although all of these approaches have been shown to be associated with growth in young children with autism. 1997. 1981). The classic image of the autistic child—mute or echolalic. of naturalistic child-centered approaches (Greenspan and Wieder. although strengths are seen in constructive play. Deficits are seen in providing relevant responses or adding new information to established topics. and stress are frequently impaired in speakers with autism. with continued intervention. has proved particularly e¤ective (Rogers. such as hand flapping. 10%–35% of children with autism show some degree of regression (Gillberg and Schaumann.. such as visual calendars. Currently. 1997). the primary forms of treatment for autism are behavioral and educational. no definitive study has yet compared approaches or measured long-term change.. conversation is often restricted to obessive interests. 1998). 1998). like the classic patients described by Kanner. 1997). are also typical but are related to developmental level and are likely to emerge in the preschool period. Children with autism become exceedingly agitated over small changes in routine. particularly for lower functioning children. Bondi and Frost. Greenfield. There is no medical or biological profile that can be used to diagnose autism. 1992). 1997). social involvement. autism is more prevalent in males than in females (Bryson.. Monotonic intonation is one of the most frequently recognized aspects of speech in autism. 1987). Stereotypic patterns of behavior. Di‰culty is seen in adapting conversation to take into account all participants’ purposes.

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(1994). Hillsdale. To be able to make accurate diagnoses. C. T. G. MA: Harvard University Press. and Schopler. Solving behavior problems in autism. (2000). (1994). MA: Harvard University Press. In the former case. (1995).. (1995). Albany. Pacific Grove. Fragile success. Children with autism: A parents’ guide. and Anderson.. it is impossible to rule out interference. CA: Academic Press. (1989). K. Dawson. even if the child seems to be a dominant speaker of one of the languages. E. Bauman. The neurobiology of autism. Classic readings in autism. P. Baron-Cohen. and Volkmar. New York: Plenum Press. B. P. F. (1962). Bilingualism defies delimitation and is open to a variety of descriptions and interpretations. Rutter. For example. and the specific dialect features. 1123–1143. and Capps. Szatmari. (2000). Sperry. M. New York: AppletonCentury-Crofts. (1998). D. and each should be examined in detail. speechlanguage pathologists must use information from interference patterns. UK: Oxford University Press. Cohen. Happe. Siegel. U. Assessment tools that are designed for English. UK: Cambridge University Press. B. and the range of interference from the dominant language forms a continuum. (Eds. The development of contingent discourse ability in autistic children. Hogdon. CA: Brooks/Cole. The di¤erent patterns that a bilingual child reveals in speech may not necessarily be the result of interference. and the influence of one language on the other is more evident. Baltimore: Paul H. NJ: Erlbaum.. Schopler. Stone. Autism in children and adults. NY: Delmar. concluded that it is not possible to formulate a single neat definition. L. S. F. Cambridge.. and Bolton.. 175–194). 1361–1367. 44. Volkmar. will not be Further Readings Baron-Cohen. et al. and treatment. L. A. Donnellan. and Caro-Martinez. New York: Brunner/Mazel. MD: Woodbine House. Sigman. Frith... (1989). Journal of Autism and Developmental Disorders. when the child goes to school). Autism and pervasive developmental disorders. Glidden. Quill. 1097–1115.. F.. Troy. Autism: Nature. M. More children become bilingual successively. 32. Powers. Journal of Speech. may su¤er speech and/or language disorders. L. both languages should be the focus of attention. all phonemes of the languages should be assessed in different word positions. Yet even here there is no uniformity among speakers. H.). Journal of Child Psychology and Psychiatry. Handbook of autism and pervasive developmental disorders. Thus. Cambridge. Cambridge. UK: Cambridge University Press. no matter how perfect they are. Matson. (1998). Morgan. Autistic children. International review of research in mental retardation: Autism. New York: Wiley. W.Bilingualism. 20. Beatens-Beardsmore (1982). Tager-Flusberg (Ed. (1995).. normal and disordered phonological development in general as well as in the two languages. (1991). (1997). When autism strikes. and Kempter. L. Rimland. Brookes. M. like their monolingual counterparts. 119 Bilingualism. (1999). B. is acquired earlier. it is crucial to determine whether these nonconforming patterns are due to the influence of the child’s other language or are indications of a speech-language disorder. F. and the other language is acquired. the earlier acquired language may put its imprint on the one acquired later. Lord.. and Prizant. an anterior question that must be answered is who qualifies as bilingual. Naturalistic observations of spontaneous communication in autistic children. Constraints on language acquisition: Studies of atypical children (pp. Teaching children with autism. L. Wetherby. Autism. Oxford. (2000). J.. Current issues in autism (series). Autism: Explaining the enigma. (1997). Wing. (1978). Cambridge. San Diego. Baltimore: Paul H. In H. 437–453. observing a wide range of variations in di¤erent contexts. S. Field trial for autistic disorder in DSM-IV. G. American Journal of Psychiatry. when children who grow up with more than one language produce patterns that are erroneous with respect to the speech of monolingual speakers. Language. and phonotactic patterns should be evaluated. Oxford. (1993). Autistic spectrum disorders. for example. Bethesda. New York: Teachers’ College Press. in the latter. H. (1996). and stated that bilingualism as a concept has ‘‘open-ended semantics. Baltimore: Johns Hopkins University Press. M. Bilingual children. Klin. New York: Guilford Press. Scholars have struggled with this question for decades.’’ It has long been recognized that bilingual individuals form a heterogeneous population in that their abilities in their two languages are not uniform. Dissociations in form and function in the acquisition of language by autistic children. (1989). Autism: An introduction to psychological theory. the great majority are not balanced between the two languages. MI: QuirkRoberts Publishing. Bloomfield (1933) required native-like control of two languages. V. A. (1994). (1985–2000).. M. Autism: The facts. and Hearing Research. R. Children with autism. this may happen because of di¤erent degrees of exposure to the two languages. Tager-Flusberg. (1972). and Mesibov. Whether a child becomes bilingual simultaneously (two languages are acquired simultaneously) or successively (one language. (1990). Volkmar. UK: Blackwell. Mindblindness. Speech Issues in tioning adolescents and adults with autism and Asperger syndrome.. Adults with autism. To this end. Infantile autism. (1995). Tager-Flusberg. . (1985).). In assessing the phonological development of a bilingual child. while Weinreich (1968) and Mackey (1970) considered as bilingual an individual who alternately used two languages. The result is interference from the dominant language. H. Cambridge. New York: Plenum Press. Although some bilingual speakers may have attained a native-like production in each language. diagnosis. Catalano. 151. New York: Plenum Press. Speech Issues in In evaluating the properties of bilingual speech. Brookes. M. generally the home language. MA: MIT Press. A.

This occurs when one or more of the developmental processes are also the patterns followed by the first (dominant) language. made more errors overall. substitutions may reflect certain developmental simplification processes that are universally phonetically motivated and shared by many languages. these processes are among the commonly occurring developmental processes that occur in the speech of children in many languages. suppress such patterns over time more slowly. Thus. with confidence. Any assessment of the child’s speech must be made with respect to the norm of the particular variety she or he is learning. Turkish. fricative gliding. frication of stops. 1993). American. because these common simplification processes are usually suppressed in normally developing children by age 6. Certain cases lend themselves to obvious identification of interference. Polish. if a 6-year-old child bilingual in Spanish and English reveals processes such as final obstruent devoicing (e. and African American Vernacular in the United States). Accordingly. a bilingual child is assessed with two procedures. Because none of these varieties or dialects of a given language is or can be considered a disordered form of that language. Spanish. 1996) and bilingual children with a suspected speech disorder (Dodd. they will also need to consider not only the languages of the client. as in [v0n] for ban. as in [wIg] for fig. Compared with their monolingual peers. In such instances we must attribute these patterns to universally motivated developmental processes that have not been eliminated according to the expected timetable. because Spanish has no voiced obstruents in final position and no consonant clusters that do not follow sonority sequencing.g. Language skills in bilingual persons have almost always been appraised in reference to monolingual standards (Grosjean. and Wei. the result is a natural tendency that receives extra impetus from the rule of the primary system. as in [ren] for train (instead of the expected [ten]).or underdiagnosis. Studies that have examined the phonological patterns in normally developing bilingual children (Gildersleeve. distorted more sounds. Indian) and even within one country (New England variety. we can. it is also a feature of the languages listed. For example. [b0k] for ‘‘bag. For example. and are likely to have uncommon processes.’’ [pIt] for ‘‘spit’’). other languages also show dialectal variation. As speech-language pathologists become more adept at di¤erentiating common and uncommon phonological patterns and interference patterns in bilingual children. Last but definitely not least is the desperate need for information on phonological development in bilingual children and assessment procedures unique to these individuals. however. or Finnish. As for the di¤erence between normally developing bilingual children and bilingual children with phonological disorders. We may also encounter a third situation in which the seemingly clear distinction between interference and the developmental processes is blurred. Not accounting for dialect features may either result in the misdiagnosis of a phonological disorder or escalate the child’s severity rating. British. each phonological system of a bilin- . and the change of /t/ to [tS ] before /i/ is a rule of Portuguese phonology.’’ [bEt] for ‘‘bed’’) and/or deletion of clusters that do not follow sonority sequencing ([tap] for ‘‘stop. Besides the interference patterns and common developmental processes. Australian. these processes may not have surfaced until age 6 because none of these patterns are demanded by the structure of Spanish. This assumes that a bilingual individual is two monolingual individuals in one person. Russian. Italian. that are designed to evaluate monolingual speakers of these languages. we cannot claim that these changes are due to Spanish interference.’’ whereby target /t/ turns into [tS ]. In this case. it appears that children with phonological disorders manifest more common simplification patterns. may occur in children with phonological disorders. and if the first language of the child does not have the opportunities for such processes to surface. General American. and Stubbe. as in [p0k] for pat. Rather. However. or Portuguese. because of the constant interaction of the two languages. The decision is not always so straightforward. and backing. as such substitutions are not commonly observed in developmental phonologies. if we encounter in the English language productions of a Portuguese-English bilingual child forms like [tSiz] for ‘‘tease’’ and [tSIp] for ‘‘tip. 1997) indicate that children in both groups exhibit patterns di¤erent from matched. 1992).. However. Dodd. Other examples that could be included in the same category would be consonant cluster reduction in children whose primary language is Japanese. If a bilingual child’s speech reveals any such processes.g. speech-language pathologists must be watchful for some unusual (idiosyncratic) processes that are observed in children (Grunwell. Canadian. but also the specific dialects of those languages. then it would be very di‰cult to identify the dominant language as the culprit and label the situation as one of interference. Holm. For example. one for each language. the child’s dialectal information is essential. monolingual peers.120 Part II: Speech appropriate for the other language and may be the cause of over.. and single obstruent coda deletion in children whose primary language is Japanese. Davis. An example is final obstruent devoicing in the English language productions of a child with German. normally developing bilingual children and bilingual children with phonological disorders had a lower overall intelligibility rating. Southern variety. this particular situation suggests a delay or disorder. or Turkish as the first language. it is impossible to refer to the first language as the explanation. In other words. Just as there are several varieties of English spoken in di¤erent countries (e. and produced more uncommon error patterns. Processes such as unusual cluster reduction. 1987. South African. say that these renditions were due to Portuguese interference. Although final obstruent devoicing is a natural process that even occurs in the early speech of monolingual English-speaking children.

Bilingual speech-language pathology: An Hispanic focus. In F. (1976). UK: Tieto. See also bilingualism and language impairment. Deuchar.). Phonological patterns in Puerto Rican Spanish-speaking children with phonological disorders. (1991). Needham Heights. Grosjean. New York: Oxford University Press. H. Developmental studies of dysphonology in children.g. Phonological processing in two languages. (Ed. New York: Elsevier. Magnusson. Yavas.). 825–834). Mackey. perception and awareness. B. (1970). Phonological patterns in normally developing Spanish speaking 3. Linguistics: Disorders and pathologies (pp. Speech. A. Watson..Developmental Apraxia of Speech 121 gual child may. and Quay.). However. In G. CA: Singular Publishing Group. Holm. C. Washington. Kelly. Marshall. WA. W. B. Austin. Clinical Linguistics and Phonetics. Because bilingual speakers’ abilities in the two languages vary immensely from one individual to another. Department of Speech and Hearing Sciences. Lund. In E.. Stoel-Gammon. Davis. and in most cases will. New York: Wiley. San Ysidoro. (2000). VOT patterns in bilingual phonological development. and Wei. M. Dodd. and Iglesias. (1997). integration and the synchronic fallacy. Dittman. and Hodson. as information on phonological development in bilingual children is the real key to understanding bilingual phonology. Harris (Ed. 7. Seattle. CA: Singular Publishing Group. and Lamprecht. Bilingualism and language contact. detailed information on both languages being acquired by the children is indispensable. Phonological assessment of child speech. R.). E. M. 229–243.. not necessarily be acquired in a way identical to that of a monolingual child (Watson. Sweden: Gleerup. MD: Aspen. L. W. Phonological development: Models. B. (1996a). and Bankson. Lund. H. (1998). (1991). Wallesh (Eds. TX: National Education Laboratory Publishers. and Dodd.). L. and Paden. Weinreich. Language. CA: San Ysidoro School District. (1995). and C. (1987). Hodson. Hodson. (1983). implications. Cognitive processing in bilinguals (pp. Goldstein. Grimm. and Stubbe. Bloomfield. Bilingualism: Basic principles.. Languages in contact. R. (1977). I. data on the developmental patterns in two languages separately would not be adequate. San Diego. Jordon. MD: York Press. C.). Brazil: Artes Medicas. (1993). Clinical Linguistics and Phonetics. Berlin: De Gruyter. A. Another view of bilingualism. Sweden: Gleerup. M.. Investigations in clinical linguistics (pp. (1992). C. Porto Alegre. B. M. (1933).. Cantonese Segmental Phonology Test. NJ: Erlbaum. Spanish-speaking children’s phonologies: Assessment and remediation of disorders. Mahwah.. Mason.). J. The acquisition of phonology by Cantonese speaking children. In R. Avaliacao fonologica da Crianca (Phonological assessment tool for Brazilian Portuguese). U. Southwest Spanish Articulation Test. M. (1995). Clinical phonology (2nd ed. (1968).. (Eds. Alatis (Ed. 5. 27. Targeting intelligible speech (2nd ed. So. Cheng. Developmental Apraxia of Speech Developmental apraxia of speech (DAS) is a developmental speech disorder frequently defined as di‰culty in programming of sequential speech movements based on presumed underlying neurological di¤erences. B. (1994). and Dunn. Speech disorder in preschool children exposed to Cantonese and English. L. Theoretical constructs motivating understanding of DAS have been quite diverse. Speech sound di¤erences and disorders in first and second language acquisition: Theoretical issues and clinical applications. Interference. Language processing in bilingual children. Toronto.. J. (1987). UK: Cambridge University Press.). Motor-based or pre-motor planning speech output deficits (e. (1985). (1985). and Hearing Services in the Schools. The phonology of language disordered children: Production. Cambridge. Grunwell. Timonium. —Mehmet Yavas References Beatens-Beardsmore. J. E. London: Croom Helm.. (1996b). Gildersleeve. When monolingual rules don’t apply: Speech development in a bilingual environment. C. 1991).. (1991). Goldstein. MA: Allyn and Bacon. and Hinshaw. Yavas. (1998). Articulation and phonological disorders (4th ed. Hewlett (Eds. developing assessment tools for phonological development is a huge task. Bortolini. N. research. (1991). Bilingual acquisition. Assessment of phonological processes in Spanish. B. B. 15. Menn. and N. Keyser.. In J. Seminars in Speech and Language. Phonology: Development and disorders. 473–495.. 22. In order to characterize bilingual phonology accurately. A. B. D. A. L. American Journal of Speech and Language Pathology. Grunwell.. L. 1–12. Yavas. L. 82–90. Journal of Communication Disorders. L. Mann. P. W. Windsor. perhaps the biggest challenge for the field. P.. M. San Diego. and Leonard. Blanken. Rockville. Language. and Stoel-Gammon. L. and Iglesias. (Eds. Smith. A. C. and Goldstein. The Hague: Mouton. Dodd. E. 341–350). M. 51–62). Medida Espanola de Articulacion. 367– 387. CA: Los Amigos. Ferguson. M. J. H. Yavas. F.. Bialystok (Ed. Clevedon. E. TX: Pro-Ed.. Hernandorena. (1986). (1996).. (1998).. TX: Pro-Ed. (1983).and 4-year-olds of Puerto Rican descent.. Austin. (2002). 137–147. The speech of phonologically disordered children acquiring Italian.)..). C. Journal of Child Language. Nettelbladt. Further Readings Bernthal. W. London: Nfer-Nelson. Normal and disordered phonology in children. 11. Assessing Asian language performance: Guidelines for evaluating limited-English-proficient students. and . Austin. B.). Hall. Speech disordered children. U. U. So. DC: Georgetown University Press. Paper presented at the annual convention of the American Speech-Language-Hearing Association. 29. S. Hong Kong University. (1992). (1992). B. San Diego. (1982).

Little coherence and consensus is available in this literature at present..g. Sussman. In contrast to developmental disorder categories such as hearing impairment or cleft palate. Aram. In every instance. and developmental articulatory dyspraxia. Crary. 1992. while others explicitly exclude these deficits (e. Aram. from preschoolers (Bradford and Dodd. Cautious application of the diagnostic label should be the norm. 1984. 1993). and valid theory building to understand the underlying nature of the disorder. see Vihman. a review of the range of behavioral correlates presently in use is of crucial importance to careful definition and understanding of DAS. 1997). Reflecting these varied views of causality.. 1997). or empirical evidence precisely defining behavioral correlates. If no single defining characteristic or complex of characteristics emerges to define DAS. a disorder category based on acquired brain damage resulting in di‰culty in programming speech movements (Broca. In addition. despite nearly 40 years of research. 1992). Clinically. and Robin. Such practice continues to cloud the issue of precise definition of the presence and prevalence of the disorder in child clinical populations. Despite the lack of consensus on theoretical motivation.. the di¤erential diagnosis of DAS is complicated (Davis and Velleman. Morley. In the case of very young clients. The relationship of behavioral correlates to di¤erential diagnosis from ‘‘functional’’ speech disorder or delay is of primary importance to discriminating DAS as a subcategory of functional speech disorder. Guyette and Deidrich (1981) have suggested that DAS may not be a theoretically or clinically definable entity. specific issues with available research will be reviewed briefly. Despite the foregoing critique. 1999. and Davis. Jakielski..g. founded on a clear understanding of positive benefits to the client in discerning long-term prognosis.122 Part II: Speech Robin. appropriate decisions regarding clinical intervention. 1993). Evidence for a neurological etiology for DAS is based on behavioral correlates that are ascribed to a neurological basis. The characterization of DAS was originally derived from apraxia of speech in adults.g. Thoonen et al. predominant use of simple syllable shapes or variability in production patterns at the onset of meaningful speech. and Miller (1954) first applied the term dyspraxia to children based on a proposed similarity in behavioral correlates with adult apraxic symptoms. lack of a link of underlying cause or theoretical base with behavioral correlates results in an ‘‘etiological’’ disorder label with no clearly established basis. and Kwiatkowski. or deficits in neural tissue with organizational consequences (e. no currently available theoretical constructs specifically disprove other possible theories for the origins of DAS (see Davis.g. A consequence of this inconsistency is lack of consensus on severity level appropriate to the DAS label. thus achieving a circular argument structure for neural origins (Marquardt. Hall. LeNormand et al. 1992.. as current empirical evidence does not produce any behavioral symptom not overlapping with other categories of developmental speech disorder or delay. p. Use of DAS as an ‘‘umbrella term for children with persisting and serious speech di‰culties in the absence of obvious causation. Associated language and praxis behaviors are included as di¤erential diagnostic correlates in some studies (Crary and Towne. Aram. 1997).g. In addition. the large available literature on DAS suggests some consensus on behav- . Jordon. phonologically based deficits in representation (e. 1993). It should be emphasized that behavioral inclusion criteria are not consistently reported and di¤ering criteria are included across studies. 1984). It thus represents an incompletely understood disorder that poses important challenges both to practicing clinicians and to the establishment of a consistent research base for overall understanding. In other reports (e. Shriberg. Criteria for inclusion in studies then become recognized symptoms of involvement. the basis for assigning severity judgments is inconsistent across studies. others do not (Horowitz. Velleman and Strand. Severity is not reported consistently. 2000). 1996) to adults (Ferry. a variety of terms have been employed: developmental apraxia of speech. DAS can manifest as mild. Accordingly.g. and Kwiatkowski. 30) is to be avoided. When it is reported. A neurological etiology was implied by the analogy but has not been conclusively delineated. In some reports. moderate. the defining characteristic is severe and persistent disorder (e. 2000). 2000). Stackhouse. Dodd. 1995). there is some consensus among practicing clinicians as well as researchers (e. regardless of the precise nature of their unintelligibility’’ (Stackhouse. 1998). developmental verbal dyspraxia. 1997) that DAS exists.. 1984). 1861). and Hicks. etiology. 1975). the utility of the label is seriously questionable for either clinical or research purposes. di¤erential diagnostic correlates and range of severity levels characterizing DAS remain imprecisely defined. Shriberg.. In the latter conceptualization. accordingly.. Subject ages vary widely. be based on awareness of the current state of empirically established data regarding theories and behavioral correlates defining this disorder.. Hall. a continuum of severity is explored. Court.g.. and Kwiatkowski. or severe speech disorder. 1988) have been posited. 1997. Shriberg. Sussman.g. even with increasingly sophisticated instrumental techniques for understanding brainbehavior relations (see Bennett and Netsell. for a review of normal phonetic and phonological development). achieving a circularity that is not helpful for producing valid characterization of the disorder (Stackhouse. and Marquardt. Before the clinical symptoms presently employed to define DAS are outlined. An ethical di¤erential diagnosis for clinical intervention and research investigations should. Some listed characteristics may be normal aspects of earliest periods of speech and language development (e. 1992. DAS has most often been defined by exclusion from functional speech disorder or delay using a complex of behavioral symptoms (e. Some studies include control populations of functional speech disorders for di¤erential diagnosis (Stackhouse. observed behaviors need to be evaluated against developmental behaviors appropriate to the client’s chronological age.

and Speech Research. not all clients show ‘‘groping postures of the articulators’’).Developmental Apraxia of Speech 123 ioral correlates that should be evaluated in establishing a di¤erential diagnosis. 6. J. TX: Pro-Ed. Seminars in Speech and Language. Circularity in the way in which etiology and behavioral correlates have been described and studied does not lend to precision in understanding DAS. (1995). (1981).e. (1998).-T.. Velleman and Shriberg. Long-term persistence of clinical symptoms in spite of intensive therapy has also frequently been associated with DAS. M. Remarques sur le siege do la faculte du language articule.. L.. Journal of Medical Speech-Language Pathology. Hall. 27–37. T. complicating understanding of the nature of the disorder and comparison across studies. 77–101.. (2) predominant use of simple syllable shapes. (5) altered suprasegmental characteristics (including rate. (6) variability and lack of consistent patterning in speech output. Austin. Phonological and phonetic correlates have also been listed. Ferry.. M. Marquardt.e. M. R. TX: Pro-Ed. Neurological findings in developmental verbal apraxia. M. and characterization of behavioral or neural correlates. The asynergistic nature of developmental verbal dyspraxia. cerebral palsy). Di¤erential diagnosis and treatment of children with speech disorders. Crary. Vogel and M. —Barbara L. (1999). Exclusionary criteria frequently noted include (1) no peripheral organic disorder (e. co-occurrence may be optional for a di¤erential diagnosis. The range of expression of these characteristics. Developmental apraxia of speech: Advances in theory and practice. Vaivre-Douret. B.. and Netsell. in vision or hearing).. B. L. However. Hall. Some characteristics are in common with functional disorders and thus do not constitute a di¤erential diagnostic characteristic (i.. Procedures for classification of sub-groups of speech disorder.. and Velleman. 1999) according to the theoretical perspective of the researcher. and Stokes. cognition. Treating disorders of speech motor control. not all symptoms are consistently reported as being necessary to a diagnosis of DAS (e.. 25–45. See also motor speech involvement in children. K. (7) increased errors on longer sequences. T. Developmental apraxia of speech. In N. Infant Toddler Intervention. (2000). T. (2000). Dilapidated speech: Developmental verbal dyspraxia. A. London: Whurr. Murdoch. 432–455. B. and Robin. W. Developmental dysarthria. (3) frequent omission of errors. suives d’une observation d’aphemie (peste de ´ la parole).. and (5) normal receptive language. (2000). Speech and language advances in basic practice (No. Davis References Bennett.. M. C. (1975). H. M. LeNormand. Aqttard. (1984). how limited does the consonant or vowel repertoire have to be to express DAS?). Bradford. (1984). Murdoch et al. and nasality). B. J. Clinical Linguistics and Phonetics. Devlopmental apraxia of speech: Determiners of di¤erential diagnosis. and (9) lack of willingness or ability to imitate a model.. J.g. Do all speech-disordered children have motor deficits? Clinical Linguistics and Phonetics.. 463–467. (1995). Language.. Australian Journal of Human Communication Disorders. A. In addition. Guyette.). (1999). (1954). S. 10(3).). In D. W. Neuromotor development and language processing in developmental dyspraxia: A follow-up case study.. Developmental Medicine and Child Neurology. Jakielski. C. 11). British Medical Journal... D. 42. because these characteristics have not been consistently tracked across available studies. Jordan. loudness.. Dodd. M. 71–83.. 6(2). Possible roles of the insula in speech and language processing: Directions for research. A. (2) poor volitional oral nonverbal skills. H. A. Phonological/phonetic correlates reported include (1) limited consonant and vowel phonetic inventory. and Towne. these behaviors should not be considered definitive but suggestive of directions for future research as well as guidelines for the practicing clinician based on emerging research.e. D. and (5) reading and spelling delays. Lass (Ed. P. etiology. Austin. S. 255–272. DAS is a problematic diagnostic category for both research and clinical practice. 12. 12. A critical review of developmental apraxia of speech. (4) normal IQ. Journal of Hearing. (3) inconsistent diadokokinetic rates. L. Feature analysis of segmental errors in children with phonological disorders. 330–337. (8) groping postures. K. Descriptive terminology varies from phonetic (e.. and Dodd. Phonological characteristics of developmental verbal dyspraxia. Accordingly. A. L. 1995) to phonological (Forrest and Morrisette. and Hicks. (2) no sensory deficit (i.. In addition. M. Impaired tongue strength and endurance in . and Marquardt. D. Broca.g. M. (1861). and Davis. cleft palate).. (4) delay in syntactic development. S. 1.. R. Exclusionary criteria for a di¤erential diagnosis have been suggested in the areas of peripheral motor and sensory function. pitch. 1999. L. E. Co-occurring characteristics frequently cited include (1) delays in gross and fine motor skills. and Morrisette. and receptive language. 177–192. D.. (1996). and Deidrich. Research utilizing consistent subject selection criteria is needed to begin to link understanding of DAS to ethical clinical practices in assessment and intervention and to elucidate the underlying causes of this disorder. E. M. P. Seminars in Speech and Language. 22. Cannito (Eds. E. 10. The range of expression of symptoms is not established (i. H. Davis. 187–194.. Journal of Clinical and Experimental Neuropsychology. 6(2). Dodd (Ed. little consensus exists on definition. W.. L. behavioral correlates have been established across studies with highly varied subject pools and di¤ering exclusionary criteria.. In B. Although it has long been a focus of research and a subject of intense interest to clinicians. has not been specified quantitatively. S.. P. L. and Cohen. 408–417. Court. Morley. 11–18. dysarthria. Payan.g. London: Academic Press. Forrest. Sussman. B. P. (4) a high incidence of vowel errors. and Miller. Ozanne. 7. Crary. Di¤erential diagnosis of developmental apraxia of speech in infants and toddlers. Horowitz. 2nd serie. (1993).. K. M. B. Co-occurring characteristics of DAS in several related areas have also been mentioned frequently. Clearly. Bulletin de la Societe d’Anatomique. Davis. J.). what types and severity of suprasegmental errors are necessary or su‰cient for the diagnosis?). L.g. 17. (1984). although frequently cited. (3) no peripheral muscle weakness or dysfunction (e.

P. and Kwiatkowski. Limb and oral praxic abilities of children with verbal sequencing deficits. 254–274. (1997). Gabreels. and Hearing Research. (1997).. Ingham. B. (2000). Williams. J. J. 25–252. Schreuder. (1995). Further Readings Aram. (1988). European Journal of Disorders of Communication. Language. 301–313. A. Sussman. Crary.. Treatment approaches for developmental apraxia of speech. Barriers to literacy development: I. and Rosenthal. Motor speech disorders: Advances in assessment and treatment. and Buekelman. D... 13. S. UK: Blackwell. The perception of phoneme sequence: A comparison of dyspraxic and normal children. 8. P. (1988). (2000). Hayden. (1988). R. Descriptive and theoretical perspectives. (1993).. In H. Di¤erential diagnosis of motor speech dysfunction in children. 173–215. Clinics in Communication Disorders. A subtype marked by inappropriate stress. (1999). Thoonen. L. J. (1999). and Debertine. European Journal of Disorders of Communication. Pollock. Shriberg. D. Language. K. Acoustic correlates of perceived lexical stress errors in children with developmental apraxia of speech. Clinician agreement of behaviors that identify developmental articulatory dyspraxia. R. 95–101. E. Strand. 40. 19–34.. M. St. Clinics in Communication Disorders. (1997). L. Wit. L. internal linguistic changes that occur within a language. M. Phonological processes and brain mechanisms.. morphology. The e‰cacy of integral stimulation intervention with developmental apraxia of speech. (1992). R.. Validity of maximum performance tasks to diagnose motor speech disorders in children. Baltimore: Paul H. 5. Aram. Acoustic validation of vowel error patterns in developmental apraxia of speech. and Pollock. J. (1992).. D. J. R. and Kwiatkowski. Thoonen. Clinical Linguistics and Phonetics. K.. M. (1994). 295–300. K. J. 1–23. 16–26. T. 265–276. A review and critique.. 22. In J. Wit. Velleman.). (1999). and Hearing Research. Square. A. Croce. Yorkston. M. R. Journal of Speech. 8. G.. Developmental motor speech disorders. 207–224. R. Child phonology: Characteristics. (1994). Maasen. San Diego. K. European Journal of Disorders of Communication. D. E. B. M. D. 8. Metrical analysis of the speech of children with suspected developmental apraxia of speech. Walton. Journal of Speech.. K. C. 91–101. The degree of mutual intelligibility that a speaker’s language has with a des- . M. 4.. 51–64. S. A. as well as lexical or semantic changes. (1994). Journal of Medical Speech-Language Pathology. D. Journal of Medical Speech-Language Pathology. M. What is developmental dyspraxia? Brain and Cognition. dialects reflect structural changes in phonology. 30.. Roy. An analysis of the vowel misarticulations of five children with developmental apraxia of speech. Regional Dialects or language varieties are a result of systematic. Bankson (Eds. The integrated use of maximum performance tasks in di¤erential diagnostic evaluations among children with motor speech disorders. 37–60. E.. B. A. British Journal of Communication. in which linguistic changes occur mainly at the phonological level.. K. S. A. Speech. (1993). 4. Journal of Speech. and Hearing Services in the Schools. 4.. and intervention with special populations.. Two cases of developmental verbal dyspraxia. 9. New York: Thieme. T. The occurrence of developmental apraxia of speech in a mild articulation disorder: A case study. Gabreels. G. (1982). Velleman. Language. 23–33. J.. Skinder. 279–284. F. 2.. (1996). 23. Journal of Medical Speech-Language Pathology. and de Swart. H. Thoonen.. Cognitive Neuropsychology. 151–161.. Perceptual and acoustic analysis of lexical and sentential stress in children with developmental apraxia of speech. Skinder. and Snowling. 32. M. Cambridge. D. 273–299.. G. Maasen. J.. (1994). H. 30. Austin. Packman. Thoonen. Developmental verbal dyspraxia. D. 10. A.. Clinics in Communication Disorders. M. Maasen. Language... 313–337. assessment.. 37. and Hearing Research. 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Journal of Medical Speech-Language Pathology. developmental verbal dyspraxia: A physiological analysis. Language. 42. and Wertz. M. (1989). H. 1424–1440. Journal of Communication Disorders. B. R. Bernthal and N. 33. D. (2000). 29. R. S. Clinical Linguistics and Phonetics. R. and Snowling. Maasen. (1994). J.. Stackhouse. and syntax. Research on speech motor control and its disorders: A review and prospective.. Developmental verbal dyspraxia: I. Journal of Speech. (1981). Till.. Strand. 273–285. 8. Gabreels. Towards a standardized assessment procedure for DAS of speech. Child language disorders. K. P. K.. Clinical Linguistics and Phonetics. M. G. Rosenbek. Dialect. Yorkston. CA: Singular Publishing Group. 40.. Journal of Communication Disorders. Buekelman. Dewey. Developmental apraxia of speech: I. An acoustic analysis of phonemic integrity and contrastiveness in developmental apraxia of speech. E. E. (1993). Sussman.. B. Hodge.. and Shriberg. 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dialect geography. and vice versa. D. or linguistic geography. Regional 125 ignated standard linguistic system is often used to distinguish dialect from language. B is adjacent to A and C. When multiple isoglosses. may not be mutually intelligible. Regional dialects are associated with geographical location or where speakers live. Regional dialect formation may also result from the presence of natural boundaries such as mountains. speakers may have the same language. others may be more dramatic. Regional dialects constitute a unique cluster of language characteristics that are distributed across a specified geographical area. The bundle of isoglosses on a linguistic map would indicate that people on one side produced a number of lexical items and grammatical forms that were di¤erent from the speech of those who lived outside the boundary. the dialects of the two towns at the extremes. Among these factors are settlement and migration patterns. each spoken in di¤erent geographical regions. this is used to designate dialect boundaries. For example. Concurrent with these technological advances. speakers may produce di¤erent languages but have mutual intelligibility. Although the construct of mutual intelligibility is frequently employed to di¤erentiate dialect from language. the morphological a-prefix in utterances such as ‘‘He come a-running’’ or ‘‘She was a-tellin’ the story’’ appears to be a retention from older forms of English that were prevalent in the seventeenth century.Dialect. there was increased interest in urban dialects. may not be mutually intelligible. For instance. Therefore. On the other hand. After the 1950s. in traditional dialect studies. Strong statistical analysis (dialectometry) has evolved since the 1970s and allows the investigator to explore large data sets with large numbers of contrasts. thereby creating a continuum. and interview tech- niques were used as primary mechanisms of data collection. specific sounds. yet speakers of these languages can easily understand one another. Some speech shifts may be subtle. Exploration of regional dialectal systems is referred to as dialectology. In other words. Regional and social dialects may co-occur within language patterns of the same speaker. and E and are serially adjacent to one another. A dialect continuum or dialect continua may account for lack of mutual intelligibility in a large territory. such as Boston. such as B and D. and swamps. data were mainly collected in rural areas. Speakers from the eastern region of England settled in New England. B. A field worker would visit an area and talk to residents using predetermined elicitation techniques that would encourage the speaker to produce the distinctive items of interest. dialects spoken in cities were thought of as prestigious. it is not easy to discriminate dialect precisely from language. video recordings were made of speakers in designated regions. or a bundle of isoglosses. between B and C. These methods generated a number of linguistic atlases that contained linguistic maps displaying geographical distributions of language characteristics. or grammatical forms. social and regional dialects are not mutually exclusive. Speakers of ‘‘Bawlamerese’’ live in ‘‘Merlin’’ (Maryland). C. On one hand. It is also possible that some of the intermediate dialects. and between D and E. Mutual intelligibility means that speakers of one dialect can understand speakers of another dialect. Dialects exist in all languages and are often discussed in terms of social or regional varieties. between C and D. For many years. Using mutual intelligibility as a primary marker of distinction should be considered relative to the territories of interest. eventually. Detroit. the dialect was more distinctive. Although Cantonese and Mandarin speakers consider these dialects. . C is adjacent to B and D. questionnaires. rivers. Because it was extremely di‰cult to traverse the Appalachian mountain range. Norwegian. surround a specific region. or isoglosses. Theoretically. A dialect continuum refers to a distribution of sequentially arranged dialects that progressively change speech or linguistic forms across a broad geographical area. Assume widely dispersed territories are labeled towns A. For example. Technological developments also led to more quantitative studies. The selected features could include vocabulary. whose state capitol is ‘‘Napolis’’ (Annapolis). whereas it is not completely valid in many other countries. but the dialects may not be mutually intelligible. there are counterexamples. A and E. Swedish. such as Cantonese and Mandarin. There will be mutual intelligibility between dialects spoken in A and B. audio and. However. and investigators began to explore diversity of dialects within large cities. Several factors contribute to the formation of regional dialects. owing to the continuous speech and language shifts that have occurred across the region. Each contributed di¤erent variations to the region in which they settled. and Danish are thought of as di¤erent languages. the two lack mutual intelligibility since those who speak only Cantonese do not easily understand those who speak only Mandarin. The field worker would then manually note whether the individual’s speech contained the distinctive linguistic features of interest. with a greater amount of bundling. as can be observed in the unique dialect of people in Baltimore. Data were used to determine where a selected set of features was produced and where people stopped using this same set of features. Social dialects represent a speaker’s social stratification within a given society or cultural group. For instance. Lines. For example. the concept of mutual intelligibility appears valid. regional English varieties began to appear in the United States as speakers immigrated from di¤erent parts of Britain. Maryland. Chinese has a number of dialects. inhabitants of the mountains were isolated and retained older English forms that contributes some of the unique characteristics of Appalachian English. and so on. Commerce and culture also play important roles in influencing regional dialects. in the United States. and London. Recordings allow a greater depth of analysis because they can be repeatedly replayed. New York. were drawn on a map to indicate the existence of specific features. Surveys. Because di¤erent conditions influence dialects. and those from Ulster settled in western New England and in Appalachia.

language has evolved to discuss employment. progressive. Although incidence and prevalence are not precisely known. New York: Cambridge University Press. While most people working ‘‘down a point’’ live in ‘‘Dundock’’ (Dundalk). 673–705. but sometimes they are the only manifestation of neurological disease. but mainly used in central and western Pennsylvania. and refer to Bethlehem Steel as ‘‘Bethlum.’’ where the boss will ‘‘har and far’’ (hire and fire) people. traumatic. as well as performance on tasks such as vowel prolongation and alternating motion rates (AMRs. The most commonly used intelligibility measures are the Computerized Assessment of Intelligibility in Dysarthric Speakers (Yorkston.. Many will say they work ‘‘down a point’’ or ‘‘down a mill. (1994). Studies using them have often . Kent et al. Yorkston et al. (1998). some may live as far away as ‘‘Norf Abnew’’ (North Avenue). W. Dialectology. 1985). weakness. Chambers. whereas others are primarily research tools. Dysarthrias: Characteristics and Classification The dysarthrias are a group of neurological disorders that reflect disturbances in the strength. and inflammatory causes are also possible. D. timing. Principles of linguistic change. Their course can be transient. pathological oral reflexes) and information from instrumental measures (e. A wide variety of acoustic. and anatomical imaging methods are available for assessment. pitch. dysphagia. Some are easily used clinically. resonatory.. K. or articulatory speech movements.’’ Because the ‘‘Bethlum’’ mill. 1990). Language in society: An introduction to sociolinguistics. Linn. with increased prevalence as the disease progresses (Logemann et al. located in Fells Point. and Tice.. approximately one-third of people with traumatic brain injury may be dysarthric. S. repetition of ‘‘puh. Visual and physical examination of the speech mechanism at rest and during nonspeech responses (e. and duration of voice. Gubbay et al. and Levita. improving. 1.’’ and ‘‘kuh’’ as rapidly and steadily as possible). has been a primary employer of many individuals.. and Traynor. Beukelman. but irregular in ataxic dysarthria). They are often accompanied by nonspeech impairments (e. but other measures are available for clinical and research purposes (Enderby. (1998). sentence repetition. D. P. speed. 1986. Handbook of dialects and language variation. and reading. but vascular.g. 1996). 1984) and the Sentence Intelligibility Test (Yorkston..126 Part II: Speech located next to ‘‘Warshnin’’ (Washington. (1992).g. Two other types of geolinguistic variables are often associated with regional dialects. adventitious movements.. 1983.. steadiness.g. hemiplegia). dysarthria often is present in a number of frequently occurring neurological diseases. M.. for example. J. the expression ‘‘take ’er easy’’ is known throughout the United States. subacutely. ‘‘yens’’ (you plural) and ‘‘yens boomers’’ (a group of people). 1978. For example. The clinical diagnosis is based primarily on auditory perceptual judgments of speech during conversation. AMRs permit judgments about the rate and rhythm of repetitive movements and are quite useful in distinguishing among certain dysarthria types (e. Beukelman. They result from central or peripheral nervous system conditions that adversely a¤ect respiratory. tone. 1977. or insidiously at any time of life. They are associated with many neurological conditions. Romaine. unique to western Pennsylvania. One variable is a set of linguistic characteristics that are unique to a geographical area or that occur only in that area. observations of asymmetry. and degenerative diseases are their most common cause in most clinical settings. endoscopic. Internal factors. e‰cient and intelligible speech. or stationary. infectious. acoustic. 2000). ‘‘Habberdy Grace’’ (Harve de Grace). For instance. 1992). For example. exacerbating-remitting. New York: Academic Press. Cambridge. It occurs in 25% of patients with lacunar stroke (Arboix and Marti-Vilata. or even ‘‘Klumya’’ (Columbia). and it probably represents a significant proportion of all acquired neurological communication disorders.g. MA: Blackwell. fasciculations. New York: Oxford University Press. and Trudgill. Labov. toxic-metabolic. physiological. 1995). 68.. (2000). Dysarthria probably occurs in 50%–90% of people with Parkinson’s disease. phonatory. speakers say ‘‘youse’’ (you singular). K.’’ ‘‘tuh. Language. Endogenous or exogenous events as well as genetic influences can cause dysarthrias. neoplastic. 1989). The second variable is the frequency of occurrence of regional linguistic characteristics in a specific geographic area. and it can be among the most disabling symptoms of the disease in some cases (Dewey. Dysarthria severity can be indexed in several ways. but quantitative measures usually focus on intelligibility and speaking rate. videofluorographic) often provide confirmatory diagnostic evidence. Vowel prolongation permits judgments about respiratory support for speech as well as the quality. Vol.C. J. they are typically slow but regular in spastic dysarthria. 1999). Mlcoch. with nearly double that prevalence during the acute phase (Sarno. atrophy. Dialect acquisition. Their neurological bases can be present congenitally or they can emerge acutely. Buonaguro. or accuracy of movements necessary for prosodically normal. —Adele Proctor Further Readings Chambers. In a large tertiary care center. range. Dysarthria emerges very frequently during the course of amyotrophic lateral sclerosis (ALS) and may be among the presenting symptoms and signs in over 20% (Rose.). dysarthria was the primary communication disorder in 46% of individuals with any acquired neurological disease seen for speech-language pathology evaluation over a 4-year period (Du¤y.

reduced loudness. Methods that show promise or that already have refined what we understand about the anatomical and physiological underpinnings of the dysarthrias include acoustic. Ataxic dysarthria is associated with lesions of the cerebellum or cerebellar control circuits. Hypokinetic dysarthria is associated with basal ganglia control circuit pathology. with each type representing a perceptually distinguishable grouping of speech characteristics that presumably reflect underlying pathophysiology and locus of lesion. or prosody. but sometimes they are worse during speech or activated only during speech. Its distinguishing characteristics are attributed to spasticity. functional magnetic resonance imaging. Often referred to as the Mayo Clinic system. Its specific characteristics depend on which nerves are involved. electromyography. but discrepancies that have been found make it clear that correspondence between perceptual attributes and physiology cannot be assumed (Du¤y and Kent. Its distinguishing characteristics include reduced loudness. to relatively rapid and predictable or unpredictable (chorea. electroencephalography. the method identifies dysarthria types. inappropriate variations in pitch. 1997. and their presumed underlying localization and distinguishing neurophysiological deficit. stridor. Some diseases are associated only with a specific mix. 2001). Parkinson’s disease is the prototypic disorder associated with hypokinetic dysarthria. because the locus of lesions they cause is less predictable (e. Its characteristics often overlap with varying combinations of those associated with flaccid. They occur more frequently than any single dysarthria type in many clinical settings. site of lesion.g. and their e¤ects on speech can be highly variable. and Brown (1969a. diplophonia. Its distinguishing characteristics are attributed primarily to incoordination... myasthenia gravis is associated only with flaccid dysarthria). and magnetoencephalography (McNeil. its distinguishing characteristics are a product of involuntary movements that interfere with intended speech movements. loudness. The dysarthrias can be classified by time of onset. but other conditions can also cause it. their primary distinguishing perceptual attributes. and duration. and its features seem mostly related to rigidity and reduced range of motion. or ‘‘blurred’’ articulation and AMRs. palatopharyolaryngeal myoclonus). Spastic dysarthria is usually associated with bilateral lesions of upper motor neuron pathways that innervate relevant cranial and spinal nerves. velopharyngeal. tics). flaccid-spastic dysarthria is the only mix expected in ALS. slow rate. Flaccid dysarthria is due to weakness in muscles supplied by cranial or spinal nerves that innervate respiratory. facial. whereas bilateral lesions or multiple nerve involvement can have devastating e¤ects on speech. Other diseases. Mixed dysarthrias reflect combinations of two or more of the single dysarthria types. In general. and because their prevalence in frequently occurring neurological diseases is high and their functional e¤ects are significant. severity usually is rarely worse than mild to moderate. Hyperkinetic dysarthria is also associated with basal ganglia control circuit pathology. 1975). articulation. face.Dysarthrias: Characteristics and Classification 127 yielded results consistent with predictions about pathophysiology from auditory-perceptual classification. The directions of clinical and more basic . voice. or ataxic dysarthria (Du¤y and Folger. Hartman and Abbs. Its manifestations vary across several causal movement disorders. short phrases. so sometimes the presence of a mixed dysarthria can make a particular disease an unlikely cause or raise the possibility that more than a single disease is present. positron emission tomography. All components of speech production are usually a¤ected. Kent et al. and imprecise and sometimes rapid. dysarthrias draw considerable attention from clinicians and researchers. Trigeminal. or lingual movement. unilateral lesions and lesions of a single nerve produce relatively mild deficits. radiography. or hypoglossal nerve lesions are associated with imprecise articulation of phonemes that rely on jaw. action myoclonus. Unilateral upper motor neuron dysarthria has an anatomical rather than pathophysiological label because it has received little systematic study. and etiology. slow but regular speech AMRs. Vagus nerve lesions can lead to hypernasality or weak pressure consonant production when the pharyngeal branch is a¤ected or to breathiness.. magnetic resonance imaging. and aerodynamic methods. The following summarizes the major types. Unlike hypokinetic dysarthria. When spinal respiratory nerves are a¤ected. and sometimes excess and equal stress across syllables. to irregular but relatively sustained (dystonia). hoarseness. 1969b. for example. or short phrases when the laryngeal branches are involved. computed tomography.g. and restricted pitch and loudness variability. traumatic brain injury). monopitch and monoloudness. Distinguishing characteristics usually reflect regular or unpredictable variability in phrasing. accelerating. Dysfluency and palilalia also may be apparent. Because of their potential to inform our understanding of the neural control of speech. 1996. Aronson. and alterations in breath patterning for speech may be evident. but the most widely used classification system in use today is based on the auditory-perceptual method developed by Darley. spastic. 2001). which can range from relatively regular and slow (tremor. and they often include a strained-harsh voice quality. Characteristics often include irregular articulatory breakdowns. laryngeal. and they are perceived most readily in articulation and prosody. tomography. kinematic. They may a¤ect any one or all levels of speech production. irregular speech AMRs. These movements may be a nearly constant presence. multiple sclerosis. breathy-tight dysphonia. or articulatory structures. course. Because the damage is unilateral. The presence of mixed dysarthria is very uncommon or incompatible with some diseases (e. may be associated with virtually any mix. 1992). It most commonly results from stroke a¤ecting upper motor neuron pathways. single-photon emission tomography.

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Laryngeal dysfunction in neurological disease: Amyotrophic lateral sclerosis.. J. L. and Yorkston. Motor speech disorders: Substrates. F. Computerized Assessment of Intelligibility of Dysarthric Speech. G. 28. and Brown. St. P. and Du¤y. R. 295–300. Frenchay dysarthria assessment.. Ahlskog (Eds. L. M. J. D. Gentil. Adler and J. Dysarthria associated with focal unilateral upper motor neuron lesion.. (1992). critique. (2001). J.g. 6. A. (1975). (1995). and Workinger. Weismer. C. anatomical.. Logemann. J. New York: Thieme. F.. J. D. A. G. (2000). J.. 1275–1289. J. J. Aronson. R. Weismer. H. F. Hammen. Journal of Speech. Journal of Medical Speech-Language Pathology.. Journal of Communication Disorders. Characteristics of verbal impairment in closed head injured patients. H. A. C. (1969a). G.. Kahana. Austin. and Thomas. neurology) working in concert to integrate clinical.. J. K.... 77–84). Koller (Ed. Louis: Mosby. Kent. Darley. J. Yorkston. Archives of Physical Medicine and Rehabilitation. D. Brooks. 2.. M. Emerging and future concerns in motor speech disorders.. E. New York: Grune and Stratton. W. Kent. 83–90. H. A. In C. and Brown. Darley’s contributions to the understanding.. L. Differential diagnostic patterns of dysarthria. G. (1998). Weismer. 221–238.. J. F. Kent. 47–57. G. New York: Marcel Dekker. 1215–1228. Fischer. and Marti-Vilata. F. F. Language. (1998). J. and Hearing Research. Kent. Motor neuron disease.. R. Kent. and Weismer. progress. related dysfunctions. L. Hartman. R. and management. J. 47. Journal of Speech and Hearing Disorders. and acoustic and pathophysiological correlates. 275–289. (2001).. and directions for research. Acoustic studies of dysarthric speech: Methods. (2001).. Kent. neural structures and circuitry. R. J. G. A. di¤erential diagnosis. 482–499. Neuromotor speech disorders: Nature. J. (1996). M. Enderby. R. and management. Further Readings Bunton. 253–262.. 27. 232. Sarno. J. A. The dysarthrias: Speech-voice profiles. Diagnosis and treatment of parkinsonian dysarthria. (1999). Kent. speech science. and Cooper.. Du¤y. (1996). Toward phonetic intelligibility testing in dysarthria. E. Darley.. M. B. Rose. E.). See also dysarthrias: management.. P. F. Clusters of deviant dimensions in the dysarthrias. J. 165–211. 273–302. Dysarthria associated with unilateral central nervous system lesions: A retrospective study. D. Kent. 3. Yorkston. R. S. R.. Lacunar infarctions and dysarthria. D. Kent... and Hearing Research. 36–39.). 12. 4. (1985). and neuropathology. R. Du¤y. and Bell. J. L. Gubbay. speech-language pathology... Beukelman. F. Philadelphia: Saunders. Journal of Speech. The relationship between perception and acoustics for a high-low vowel contrast produced by speakers with dysarthria. V. Quantification of motor speech abilities in stroke: Time-energy analysis of syllable and word repetition. D. and Clift. M. Clinicoanatomic studies in dysarthria: Review. Journal of Speech and Hearing Research. Du¤y.. Journal of Medical Speech-Language Pathology. R. E. R. Beukelman. Yorkston. European Journal of Disorders of Communication. (1995). Sentence Intelligibility Test. M. Parkinson’s disease. Murdoch. R. K. 249–269. 400–405. Ataxic dysarthria. Weismer. Kent. Rosenbek. J. 127. K. (1999).. (1999). 32. Zilber. C.. R. (1977). D. A. .. (1997). more precisely establishing the relationships among perceptual dysarthria types. A. S..

the physiological processes involved. (1994). Intelligibility refers to the degree to which the listener is able to understand the acoustic signal (Kent et al. LaPointe. Behavioral intervention for respiratory support focuses on achieving and maintaining a consistent subglottal air pressure level. M. Yorkston. Dysarthria and apraxia of speech: Perspectives on management. 7(2) (entire issue). Till. Strand. and Beukelman. Yorkston. Murdoch. resonance. Speech motor stability in IPD: E¤ects of rate and loudness manipulations.. L. and Hearing Research. Ball and M.. E. and articulation... A... R. 44. (1994). Tongue strength and endurance in mild to moderate Parkinson’s disease. Smith. R. The relationship of selected perceptual measures of diadochokinesis in speech intelligibility in dysarthric speakers with amyotrophic lateral sclerosis. O. Rodnitzky. L. and the expected course. A.. and Kennedy. Sustained phonation tasks are also used. Finally. D. D. Tongue function in subjects with upper motor neuron type dysarthria following cerebrovascular accident. early treatment may focus on maintaining intelligibility. 177–190. For patients with degenerative diseases such as ALS. Journal of Medical Speech-Language Pathology. and Ramig. R. allowing the patient to continue to use speech for a much longer period of time before having to use augmentative and alternative communication. Decisions regarding whether to focus treatment on intelligibility or on comprehensibility depend largely on the severity of the dysarthria. Journal of Medical SpeechLanguage Pathology. C. individuals are encouraged to produce sentences with appropriate Dysarthrias: Management Dysarthria is a collective term for a group of neurological speech disorders caused by damage to mechanisms of motor control in the central or peripheral nervous system. and Beukelman. 1996). P. contextual information becomes more critical for maintaining comprehensibility. O. (Eds. depending on the particular neuromotor systems involved. D. E. Brookes. listeners take advantage of environmental cues such as facial expression. Lefkowitz. B. Baltimore: Paul H. Moore. B. 27–40. Y.. and clinical characterization. (1991). M. Samlan. L. Kleinow. Disorders of motor speech: Assessment. Journal of Medical Speech-Language Pathology. Perceptual and acoustic methods in the evaluation of dysarthric speech. 4. 2. Later in the disease progression. 1982) often involve having the speaker blow and maintain target levels of water pressure (i. N. 129 nicative intent using speech plus the environment. and Wilson. Correlation of clinical deficits with anatomical lesions: Post-traumatic speech disorders and MRI. and augmentative aids. Management focus also depends on whether the dysarthria is associated with a condition in which physiological recovery is likely to occur (e. maximizing listener support and environmental cues. (2000). and Beukelman... Ziegler. cerebrovascular accident) versus one in which the dysarthria is likely to get progressively worse (e. (1999). (1994). W. and Luschei. 5 cm H2 O) for 5 seconds. D. Thompson. using the acoustic signal plus all information available from the environment (Yorkston.e. S. R.g. amyotrophic lateral sclerosis [ALS])... 15–26. Management for mildly dysarthric individuals focuses on improving intelligibility and naturalness.. K. A. 1979. Parkinson’s disease: Longitudinal changes in acoustic parameters of phonation. C.). (1994). E. J. P.Dysarthrias: Management King.g. treatment. K. Solomon. P. L. Hixon.. 3.. J. management of very severe dysarthria often focuses on augmentative communication. 1989). Murdoch. Baltimore: Paul H. (Eds.. D.. Lemke. and so on.). (2001). Robin.g. D. the focus of treatment is less on the acoustic signal and more on communicative interaction. gestures. or on helping the speaker convey more commu- . M.. Journal of Medical Speech-Language Pathology. Phonatory and laryngeal dysfunction following upper motor neuron vascular lesions. G. J. Journal of Medical Speech-Language Pathology. D. American Journal of Speech-Language Pathology. Intelligibility Deficits in intelligibility vary according to the type of dysarthria as well as the relative contribution of the basic physiological mechanisms involved in speech: respiration. 1–14. L. Journal of Speech. R.. severity. Brookes. the topic. Thompson. palatal lift).). context.. and behavioral interventions are used to improve the function of those physiological systems.. and Weismer. In conversational interaction. As the acoustic speech signal becomes more degraded. the situation. (Eds.. L. Robin. and Horii. (1995). The dysarthrias vary in nature. Management of the dysarthrias is generally focused on improving the intelligibility and naturalness of speech. Advances in clinical phonetics (pp. surgical. prosthetic (e. 1999). Finally. D. 1041–1051. giving the speaker feedback on maintained loudness. 91–114). B. (1995). M.g. (1996)... (1994). and Netsell. (1996). Motor speech disorders: Advances in assessment and treatment. pharmacological). In M. Amsterdam: John Benjamins. and Stokes. A. R. These issues include the type of dysarthria (reflecting the underlying neuromuscular status). phonation. 2. Methods to improve respiratory support (Netsell and Daniel. and Hartmann. 3.). Ramig.. Individuals with moderate levels of severity benefit from both intelligibility and comprehensibility approaches. E. 29–42. R. Journal of Medical SpeechLanguage Pathology. 9–13. Comprehensibility refers to the dynamic process by which individuals convey communicative intent. LaPointe. E. 8(4) (entire issue). Journal of Medical Speech-Language Pathology.. H. Yorkston (1996) provides a comprehensive review of the treatment e‰cacy literature for the dysarthrias associated with a number of di¤erent neurological disorders.. a number of issues are considered when devising a management approach for a particular patient. Consequently. D. Yorkston. C. allowing adequate loudness and length of breath groups (Yorkston et al. L. K. Duckworth (Eds. and Stokes.. J. Language. E. J. Baltimore: Paul H. Brookes. Hawley. 2.. Lorell. Medical (e.

1991).. and by allowing listeners more time to process the degraded acoustic signal. This medical management usually results in improvement in their voice and vocal fatigue. 1996) has been shown to be e‰cacious for individuals with Parkinson’s disease and is a commonly used therapy technique to reduce the hypophonic aspects of their dysarthria. or the hypokinetic dysarthria that accompanies Parkinson’s disease). but it also requires that the patient maximize respiratory pressures. Occasionally speakers may release too much airflow during speech. exercises to increase the patient’s awareness of e‰cient glottal adduction. which is a rigid appliance that covers the hard palate and extends along the surface of the soft palate. 1975. Palatal lifts should be considered for patients who are consistently unable to achieve velopharyngeal closure and who have relatively isolated velopharyngeal impairment. 1983). given the expiratory lung volume level. and Ishikawa. by facilitating more appropriate breath group units. Kuehn and Wachtel (1994) suggest the use of continuous positive airway pressure in a resistance exercise program to strengthen the velopharyngeal muscles. 1998). Strength training is sometimes advocated. but researchers and clinicians disagree as to their e¤ectiveness. is frequently used to improve the vocal quality of individuals with spasmodic dysphonia and laryngeal dystonias. behavioral approaches involve focusing the speaker’s attention on increased e¤ort for bigger and stronger movements. or hyperphonia. Behavioral approaches to the treatment of resonance problems focus on increasing the strength and function of the soft palate. respiratory treatment is focused on helping the speaker consistently initiate phonation at appropriate inspiratory lung volume levels. Behavioral treatment for hypophonia focuses on increasing glottal closure. but only when the speaker is habitually generating less force than is necessary for speech and has the capacity to increase strength with e¤ort. Rate control is most e¤ective for individuals with hypokinetic or ataxic dysarthria. 1985). words and phrases (Robertson. 2000). E¤ort closure techniques such as pushing and grunting may maximize vocal fold adduction (Rosenbek and LaPoint. usually the seventh cranial nerve (Daniel and Guitar. However. in which the vocal folds exhibit too much closure (as in spastic dysarthria). When specific work on improving articulatory function is warranted. without extraneous supraglottic tension. focusing on maintaining adequate respiratory pressure. Medical management. For individuals who exhibit discoordination (e. taking the next breath at the appropriate phrase boundary. Treatment focused on improving articulation often uses the hierarchical practice of selected syllable. Teflon and autogenous fat are also used to increase the bulk of a paralyzed or atrophied fold (Heikki. velopharyngeal insu‰ciency. Strengthening is most appropriate for speakers with flaccid dysarthria. Laryngeal system impairment frequently results in either hypophonia. The use of minimal contrasts (tie/sigh) or intelligibility drills (having the speaker produce a carefully selected set of stimulus words) focus the speaker’s attention on making specific sound contrasts salient and clear. in which patients are taught to use the inspiratory muscles to counter the elastic recoil forces of the respiratory system. in which muscular activity causes increasing weakness. Techniques to facilitate head and neck relaxation as well as laryngeal relaxation. Botulinum toxin has been used to improve speech in speakers with orofacial and mandibular dystonias (Schulz and Ludlow. because articulatory imprecision may be due to reduced respiratory support. in which the vocal folds do not achieve adequate closure for phonation (as in flaccid dysarthria. Netsell (1995) has suggested the use of inspiratory checking. 2001). but it may be appropriate for individuals with other types of dysarthria as well. 1978). strategies to maximize e‰ciency of the respiratory system. often with arytenoid adduction (Isshiki. its e¤ects on articulation are less clear (Du¤y. Medications to decrease tremor or chorea sometimes help improve speech by reducing the extraneous movement. A common prosthetic approach is to use a palatal lift. such as botulinum toxin injection. The Lee Silverman Voice Therapy Program (Ramig et al. Rate control is frequently the focus of treatment for dysarthric individuals. ataxic dysarthria). The most common procedure for medialization is a type I thyroplasty. . Individuals with lower motor neuron deficits involving the laryngeal muscles may benefit from surgical intervention either to medialize the vocal fold or to augment the bulk of the fold. (1999) point out that this variable alone may result in the most dramatic changes in speech intelligibility for some individuals. raising it to the pharyngeal wall. In each case. Okamura.g. Rate reduction improves intelligibility by facilitating increased precision of movement through the full range. are helpful. Compensatory strategies such as using a di¤erent place of articulation or exaggerating selected articulatory movements may be used (DeFao and Schaefer. the clinician works to focus the speaker’s attention and e¤ort toward taking in more air and using more force with exhaled air. and the use of postural control may be helpful. 1995. it is contraindicated for patients with disorders such as myasthenia gravis. the treatment of articulation is not always focused on improving the place and manner of articulatory contacts. 1995).. Patients with myasthenia gravis are typically successfully treated with anticholinesterase drugs or with a thymectomy. Surgical and medical management may also improve articulation. Treatment of phonation due to laryngeal spasticity is di‰cult. Although pharmacological treatment is frequently used to decrease limb spasticity. or rate control. Nasseri and Maragos.130 Part II: Speech phrase lengths. Yorkston et al. Patients with phonatory deficits due to laryngeal dystonia pose similar problems. Neural anastomosis is sometimes used to improve function to a damaged nerve. and for patients with degenerative disorders such as ALS. and behavioral intervention typically is not successful for this group of patients. For mild weakness.

and management.). K. Journal of Speech and Hearing Disorders. while working to avoid any diminution in speech naturalness. Netsell. and Wachtel.). Treatment e‰cacy in dysarthria. Till. Strand References Beukelman. Combination thyroplasty and the ‘‘twisted larynx’’: Combined type IV and type I thyroplasty for superior laryngeal nerve weakness. The e‰cacy of oro-facial and articulation exercises in dysarthria following stroke. Brown. (1989). D. Yorkston. Aronson. (1997). using predictable wording. N. Till. C. Laryngoscope. New York: Thieme. (1998). O’Brien. Motor speech disorders: Advances in assessment and treatment (pp. American Journal of Speech-Language Pathology. Further Readings Adams.). L. S. Brookes. In J. M. Baltimore: Paul H. Johns (Ed. 54.. Yorkston. R. and D. 48. Thompson. articulatory. In D. TX: Pro-Ed. R. A. Beukelman (Eds. 5. Motor speech disorders: Advances in assessment and treatment. Journal of Speech and Hearing Research. Kent. and D. Baltimore: Paul H. S. Clinical management of motor speech disorders. —Edythe A. prosthetic. EMG feedback and recovery of facial and speech gestures following neural anastomosis. Dysarthria and apraxia of speech: Perspectives in management (pp. and Tice. B.. (1990). Ramig. (2001). Yorkston. K. Such strategies include being sure to have the listener’s attention. and treatment. In W. 14. 47. Acta Oto-Laryngologica. 1496–1504. the dysarthric individual is often able to continue to use speech as a primary mode of communication.. 6–9. 43. Yorkston. and using alphabet board supplementation. The dysarthrias: Description.. Kent. Dysarthria in adults: Physiologic approach to rehabilitation. H.. and Tice. St. . S. and LaPoint. Hoehn. Netsell.. 36(Suppl.and long-term comparison of two techniques. providing (or asking for) the topic. increasing interword interval durations. (1975). K.. and Daniel. Schulz.. NE: Tice Technology Services. as the severity of dysarthria increases. Management strategies are designed to help the listener maximize the use of context to improve ability to understand even a very degraded acoustic signal. and Maragos. adding gestures if possible. 38. Language. Pacer/tally rate measurement software. Lincoln. Robertson.. (1983). and Hearing Research. and Horii. An around-thehouse device for the clinical determination of respiratory driving pressure: A note on making the simple even simpler. Berry (Ed. 465–473. Daniel. In delayed auditory feedback. R. Journal of Voice. Rosenbek. making eye contact. Neurology. Boston: Little. Journal of Speech. 413–415. 51–54. 108. A. 9–20.. Y. Accelerating speech in a case of hypokinetic dysarthria: Descriptions and treatment. A case study. Brookes. 227–242).. (1991). and Thompson. By working on communication interaction between speaker and listener. and Ishikawa. Archives of Physical Medicine and Rehabilitation.. E. G. C.).. K. Intensive speech treatment for patients with Parkinson’s disease: Short. Boston: Little. M. 1997). Motor speech disorders: Substrates. Toward phonetic intelligibility testing in dysarthria. S. 80. Yorkston. Comparison of two forms of intensive speech treatment for Parkinson disease. management focuses more on the communication interaction between the dysarthric speaker and his or her communicative partners. 482–499. DeFao. (1994). Clinical voice disorders. (1985).. Yorkston. or medical management. E. Instrumentation can also be helpful in rate control. (1996). 292–297. Bilateral facial paralysis in a preschool child: Oral-facial and articulatory characteristics. This technique typically slows the rate of speech and improves intelligibility. K. CPAP therapy for treating hypernasality following closed head injury. Yorkston. S. Weismer.. (1996). R. Baltimore: Paul H. In J. Brookes. reducing environmental noise. J. R. Heiki. Clinical management of neurogenic communication disorders (pp. and D.. 97–152). G. However. K. Journal of Speech and Hearing Disorders. T.Dysarthrias: Management 131 Behavioral approaches are geared toward slowing the rate by increasing consonant and vowel duration. Hawley. intelligibility is the primary focus of management. L. E. Hixon.. Brown. and Ludlow. Strand. R. signaling topic changes.. the speaker’s own voice is fed back to the speaker through earphones after an interval delay. R.. Countryman. J..). J. Comprehensibility When there is evidence that the individual is able to improve respiratory.). K. Autsin. E. Visual biofeedback is used to facilitate the speaker’s use of pause time and to slow the rate.. and Rosenbek. Beukelman (Eds. Isshiki.. and increasing pause time at phrasal boundaries. L. di¤erential diagnosis.. (1982). K.. 104–111.. (1999). K. Journal of Speech and Hearing Disorders. and Schaefer. D. (1995). M. Thyroplasty type I (lateral compression) for dysphonia due to vocal cord paralysis or atrophy. and Guitar. Neurophysiology and Neurogenic Speech Language Disorders. N.. Beukelman. 207–212). See also dysarthrias: characteristics and classification. Countryman. Yorkston. J. J. phonatory. 165–190). Nasseri. (1978). 502. Botulinum treatment for orolingual-mandibular dystonia: Speech e¤ects. B. using simple but complete grammatical constructs. 39. A. diagnosis. T. L. (1996). and Wilson. Kuehn. Computer screens can be used that cue the speaker to a target rate and mark the location of pauses (Beukelman. (2000). M. or resonating aspects of speech through behavioral. 60. 5. Du¤y. Louis: Mosby. Vocal fold augmentation by injection of autologous fascia. (1995). Beukelman (Eds. 55–66. D. and Bell. In C. (1979). C. Ramig. Also important is to adopt a consistent strategy for communication repair that is agreed upon by both speaker and listener.. Speech rehabilitation for individuals with unintelligible speech and dysarthria: The respiratory and velopharyngeal systems. S46– S57. Comprehensibility of dysarthric speech: Implications for assessment and treatment planning. Clinical dysarthria (pp. J. Moore. L. S.. 1232–1251. (1995). and Kennedy. International Journal of Language and Communication Disorders. Oscilloscopes can provide real-time feedback regarding rate over time. Strand. (1994). Okamura.

M. Boston: College-Hill Press. V. Recent advances in clinical dysarthria. the odds ratio of dying was 9. (1998)... and Beukelman. Austin. 48. The dysarthrias: Physiology. and management. Robin. M. Boston: College Hill Press. D.. (1996) studied the e¤ects of dysphagia on nutritional status in stroke patients who had similar nutritional status at the time of hospital admission. (1994). J. Dysphagia can result from unilateral or bilateral cortical insult. 2001). (Ed. D. D.. 550–561. (1986). Baltimore: Paul H. In M. D. et al. 26. Ramig. Dysphagia can result from anatomic variation or neuromuscular impairment anywhere from the lips to the stomach. Dworkin. 1992. acoustic perception.. San Diego. research as well as evaluation and treatment of dysphagia were directed primarily toward the esophageal stage. D. McNeil. M. Vogel. and Beukelman. and A. 39. VII. McHenry. (1989). Journal of Speech and Hearing Disorders.). Aronson. M. (1983). and Taylor.. Modification of breath patterning to increase naturalness of a mildly dysarthric speaker.2 times greater for patients who aspirated thickened viscosities than for those who did not aspirate or who aspirated only thin fluids.. and Brown. The role of phonation in speech intelligibility: A review and preliminary data from patients with Parkinson’s disease. Within the cortex. and Beukelman.. McNeil. Jankovic. 798–807. insula. Rubow. Vol. Yorkston. and Beukelman.. Dysphagia is associated with an increased risk of developing malnutrition and respiratory complications such as aspiration pneumonia. Management of speech and swallowing in degenerative neurologic disease. 246–269. Berry (Ed. D. Daniels and Foundas. and Beukelman. Motor speech disorders: A treatment guide. Daniels. 122–124. DAF speech modification in Parkinson’s disease: A report of two cases. One week after the stroke. (1990). Other portions of the cortical system have also been found to be active during swallowing (Hamdy et al.. Journal of Speech and Hearing Research. J. (1991). Rubow. D. the odds ratio that pneumonia would develop was 7. Adult Disorders. K.3% of patients who developed dysphagia while in the hospi- . and XII. Fahn (Ed. and Swift. Darley. Oral and Pharyngeal ‘‘Dysphagia’’ is an impaired ability to swallow.. J. and Traynor. Yorkston..6 times greater for stroke patients who were identified as aspirators than for stroke patients who did not aspirate.. acoustic perception. and Aronson.). (1985). CA: Singular Publishing Group. (1994). AZ: Communication Skill Builders. and Metter. Treating disorders speech motor control: For clinician.. A. Beukelman. Hanson. Rosenbek. Aronson (Eds. Neuropsychiatry. 7. Vogel and M. Darley.. J. St. M. J. (1975)... C.. and Dromey. J..). A. and Miller. and Brown. Cannito Dysphagia. Boston: College-Hill Press. (1995). (1997). 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65% of patients admitted with stroke and dysphagia were malnourished (Finestone et al. motor end-plate disease.6% of patients without dysphagia were malnourished. of those 24 patients. 1991). the extent of vallecular or pyriform sinus stasis. 2000).Dysphagia. Among young adults. The choice of method for a particular patient depends on the information that is sought. and larynx. medication e¤ects. (3) When 47 stroke patients with mixed sites of lesions were examined. (2) In a heterogeneous group of 1101 patients with dysphagia. and the presence of spillover or of delayed initiation of the pharyngeal stage of the swallow (Langmore. Aviv et al. The absence of any or all of these signs does not indicate that a patient has a safe swallow or that the patient is able to ingest an adequate number of calories by mouth to remain properly nourished. Therefore. cervical spine disease. can be saved when patients are properly evaluated. however. 11 (46%) were silent aspirators (Horner and Massey. systemic disease. the clinician will turn to one or more imaging modalities or other specific techniques. Videofluoroscopy is the most frequently used assessment technique because it provides the most complete body of information. Table 1 lists commonly observed clinical signs that are suggestive of dysphagia in the adult population. a diminished or absent gag has not been found to distinguish aspirators from nonaspirators (Horner and Massey. and impaired gastrointestinal function. Endoscopy permits the examiner to evaluate the status of vocal fold function. traumatic brain injury is a not uncommon cause of acquired dysphagia. radiation to the head and neck. with or without drooling Abnormal or absent laryngeal elevation during swallow attempts Choking or coughing during or after intake of food or liquid Wet-sounding cough Wet. Schatz. (4) In a study of 107 patients in a rehabilitation facility. whereas elderly individuals are more likely to acquire dysphagia as a result of illness. The already comprised patient can become increasingly comprised. young adults are also susceptible to the same causes of dysphagia as the elderly.. clinical evaluation identified only 18 (42%) of the aspirators (Splaingard et al. the view of velar function is superior to . the most frequent causes of dysphagia in adults include muscle disease. and the di‰culty of detecting it is suggested by the following: (1) Discriminant analysis of 11 clinical indicators resulted in identification of the presence of aspiration in only 66% of patients (Linden. particularly after eating or when lying down Heartburn or indigestion Unintended weight loss not related to disease 133 tal were malnourished. Furthermore.000–600. 1988). After stroke and neurological disease. The clinical examination provides important information that assists in the decision-making process. studies such as these support the argument that money. For most patients. gurgly voice quality Decreased oral sensation Weak sign of the cough Prolonged oral preparation with food Inability to clear the mouth of food after intake Absent gag reflex Food or liquid leaking from a tracheostomy site Fullness or tightness in the throat (globus sensation) Food or liquid leaking from the nose Regurgitation of food Sensation of food sticking in the throat or sternal region Xerostomia (dry mouth) Odynophagia (pain on swallowing) Repeated incidents of upper respiratory infections with or without a diagnosis of aspiration pneumonia Tightness or pain in the chest.000 persons per year experience dysphagia secondary to neurological disorders. Oral and Pharyngeal Table 1. 1995). Dysphagia can occur at any age across the life span. dementia. and the greatest percentage of these experience dysphagia secondary to stroke (Doggett et al. Clinical Signs Suggestive of Dysphagia in Adults Di‰culty triggering the swallow Di‰culty managing oral secretions. and Olsen. However. 276 (59%) of the 469 patients who aspirated were found to have silent aspiration (Smith et al. 1988). head and neck surgery. while only 13. Because of the additional expense encountered in caring for patients with respiratory or nutritional complications. which prolongs the hospital length of stay and increases medical costs. Kuhlemeier. this examination provides no information relative to the pharyngeal stage of the swallow and does not elicit adequate information to determine proper therapy. 43 (40%) were found to aspirate on videofluoroscopic examination. Certain clinical signs help to alert health care providers to the likely presence of dysphagia. Inadequate nutrition negatively a¤ects the ability of the immune system to fight disease and contributes to the development of respiratory and cardiac insu‰ciency. Evaluation and Treatment There are various methods for studying the swallow. In a study of the nutritional status of patients admitted to a rehabilitation service. and senescent changes in the sensorimotor system. this is the only instrumental procedure that will be performed. and Patterson. 1988). Interpretation of this examination is performed after observation of no less than two dozen events within the oral cavity. The incidence of silent aspiration is very high. the assessment begins with a clinical examination (Perlman et al. the formation of decubitus ulcers. 1993). patients who exhibit these signs and who have not been seen by a physician should be referred for medical examination. Additionally. Many of these signs can be indicative of a serious medical illness. traumatic brain injury. Therefore. 1988.. a significant number of patients who aspirate do so with no clinical indication. 24 (51%) of the patients were found to aspirate. When a patient is first seen. 1999). Although clinical indicators have been found to have a relationship to laryngeal penetration. For example. but it is not intended to identify the underlying variables that result in di‰culty with oral intake. Neurological disorders take a particular toll: it has been estimated that 300.... 2001). as well as life.. pharynx.

CA: Singular Publishing Group. The advantages to using ultrasound for assessing the oral stage of the swallow are the absence of exposure to ionizing radiation and the fact that the parent can hold an infant or small child and feed the child a familiar food while the examination is being performed. —Adrienne L. S. Horner. E.. G219–G225. M. S.. (1994). Miller. . B. or information on the larynx or pharynx during the moment of swallow is not observed with endoscopy. 7. Wilson. S... (1995).. Dysphagia. and Patterson. A. (1999). Diamond.. Lesion site in unilateral stroke patients with dysphagia. laryngeal. J. M.. Palmer. Dysphagia. Langmore. San Diego. Smith. Cerebral cortical representation of automatic and volitional swallowing in humans.. D. and pharyngeal muscles during swallowing. Ettema. P. because the tracheostomy tube prohibits good transducer placement.. K. D. TX: Pro-Ed. Hutchins.. (1988). Decisions regarding behavioral. and Pauloski. 86. Schatz. American Journal of Physiology. Halvorson. E. (1996). Videofluoroscopic evidence of aspiration predicts pneumonia and death but not dehydration following stroke. A. and VanDaele.. 1991). C.. Langmore. L. Perlman. and Brazer. Rademaker. Neurology. and Chaundhuri.. 216–219. G. Additionally. (1997). Fiberoptic endoscopic examination of swallowing safety: A new procedure. S. or surgical intervention are made once the evaluation has been completed. H. Thomson... Thompson... S. 1999). 6. (1998). and Sullivan. Gray.. Dysphagia. Splaingard. The probability of correctly predicting subglottic penetration from clinical observations. S. and Pelletier. Cortical activation during human volitional swallowing: An event-related fMRI study. (2000). Seminars in Speech and Language. L. This technique is presently being investigated to determine the physiological correlates of RDG output and to determine changes in the respiratory-swallowing pattern as a function of age and various medical diagnoses.). Evaluation and treatment of swallowing disorders (2nd ed. H. Cooper. S. H. Information relating to the oral stage of deglutition. S. M. Perlman. and Reding. Austin. Dysphagia. and Rothwell. (1997). J.). 2. 146–156.. (1988). A.. Aspiration after stroke: Lesion analysis by brain MRI. J.. and Olsen. Milianti. S. Journal of Stroke and Cerebrovascular Disease. 76. 9. Incidence and patient characteristics associated with silent aspiration in the acute care setting. 8... Finestone.. 277. D. Perlman et al. Respirodeglutometry (RDG) is a method for assessing the coordination of respiration and deglutition (Perlman. because needle electrodes can cause discomfort and the subject may alter the swallowing pattern. In the examination of swallowing. P. S. M. J.. 170–173. G. Dysphagia. Hamdy.. CA: Singular Publishing Group. R. B.. Perlman References Alberts. 85.. 12. 16.. E¤ect of malnutrition after acute stroke on clinical outcome. and Perlman. S. and Barkmeier. (1999). Dysphagia. A. The safety of flexible endoscopic evaluation of swallowing with sensory testing (FEESST): An analysis of 500 consecutive evaluations. J. et al. C. and Zenner. Daniels. E. Respiratory and acoustic signals associated with bolus passage through the pharynx. A. Iglesia. (1991). (1988). J. The information obtainable with ultrasound is restricted to the oral stage of deglutition. Management of adult neurogenic dysphagia. Prevention of pneumonia in elderly stroke patients by systematic diagnosis and treatment of dysphagia: An evidence-based comprehensive analysis of the literature. B. 15.. Foundas. In A. (1996).. (2001). E. Greene-Finestone.. V. and Raiv. A. the extent of elevation of the hyoid bone... 1663–1669. When a small child has a tracheotomy tube. 317–319. Colangelo. A. and Close. 69.. Comprehensive clinical examination of orophayngeal swallowing function: Veterans Administration procedure.. D. Sulton. W. it is advisable to use bipolar hooked wire electrodes. Henry. that obtained with videofluoroscopy. A. Electromyography in the functional and diagnostic testing of deglutition. J.... Daniels. et al. Aviv. H. Sonies. F. and Massey. 1028–1032. Schmidt. Soler. 938–950. Further Readings Huckabee. 1997. Malnutrition in stroke patients on the rehabilitation service and at follow-up: Prevalence and predictors.. 1–7. Gonzalez-Huix.134 Part II: Speech Davalos. R. J. K. Mikulis. Dysphagia. K. 89–94. Chapell. S. W. (1991). F. Perlman and K.. (1999).. R. J. Therapeutic intervention is determined as a function of the anatomical and physiological observations that were made during the evaluation process.. Goodyear. Doggett. Journal of Neurophysiology. J. B. Archives of Physical Medicine and Rehabilitation. Xue. 310–316. Spitzer. 279–295. Horner. Martin. 27. B. 38. Mitchell. 7–11.... M. Crawley. Muscle paralysis is best determined with intramuscular electromyography (Cooper and Perlman. R. it is often extremely di‰cult to obtain a good ultrasound image. Aspiration in rehabilitation patients: Videofluoroscopy vs bedside clinical assessment. Linden. Logemann.. Q. Marrugat. M. Ettema. 170–179. and Teasell. D. J. 30–34. T. Kuhlemeier.. J. The role of the insular cortex in dysphagia. (1993). Electromyographic activity from human submental.. A. G.. 39–44. and Barkmeier. N. S. J.. C. Ultrasound allows for observation of the motion of the tongue (Sonies. Dysphagia. the shadow reflected from the hyoid bone permits the examiner to observe and to measure the displacement of the hyoid. Archives of Physical Medicine and Rehabilitation. A. medical. Physiology and pathophysiology of the swallowing area of the human motor cortex. (1992).. L. Neural Plast. San Diego. L. Holas.. A. 14. L.. Logemann. (1999). 246–254. (2000).. New York: Springer-Verlag. M. and Foundas. Journal of Applied Physiology. R... Dysphagia. M.. Schulze-Delrieu (Eds.. Gati. L. (2001). 637–640.. 15. Ricart. Silent aspiration following stroke. 2000). 8.. D.. K. Lau.. Aziz.. Normal and abnormal swallowing: Imaging in diagnosis and therapy. R. Perlman. and Coates. Stroke. S. Kaplan. Deglutition and its disorders. P. (2001). W.. Specific treatments are beyond the scope of this discussion but can be found in textbooks listed in Further Readings. 12.. McCulloch. Tappe. Molins. Hamdy. Mills. A. L. 91–97.

When the inflammation results in the secretion of e¤usion... 1994. 122–133.g. OME accounts for little if any of the variance in developmental outcome measures (e.. studies have also di¤ered substantially in the measures used to document the outcome variable of speech development and in the extent to which e¤ect sizes for significant di¤erences on outcome measures are reported (cf. B. 15. Instrumental imaging technologies and procedures. the terms otitis media with e¤usion (OME) and middle ear e¤usion (MEE) are often used. 2000). A. 51. and small beneficial e¤ects (e... 1996b). 1997).. Middle ear e¤usion may be present during the period of acute inflammation (when it is known as acute otitis media). Casby. et al. C. J. Mayrand. Perlman. N. Roecker. 1996a) and evidence from several large studies supports this conclusion. For example.Early Recurrent Otitis Media and Speech Development Logemann. Studies also vary with respect to their ability to separate the contribution of OME to poor developmental outcome from the e¤ects of other variables with which OME is known to be associated.. (1997). J. J. Item reduction and preliminary scaling. Shriberg. and it may persist for some time after the acute inflammation has subsided (Bluestone and Klein. K.). McHorney. OME is significantly more prevalent in males than in females. H. (1999). San Diego. Coordination of respiration and swallowing: E¤ect of bolus volume in normal adults.. Statistical procedures are necessary to control for such confounding in order to distinguish the e¤ects of OME from those of other variables. et al. 263. A. P. such as sex and socioeconomic status. and Wood.. 2001). Rosenbek. (Eds. OME has been described as one of the most common infectious diseases of childhood (Bluestone and Klein. However. Paradise et al.. 1986). and Diamant. into the middle ear cavity. Aspiration: Cause and implications.. The gold standard for diagnosing OME is an examination of the tympanic membrane via pneumatic otoscopy. 135 Early Recurrent Otitis Media and Speech Development Otitis media can be defined as inflammation of the middle ear mucosa. 2000). C. Shriberg. Sonies. Preiksaitis. Rosenbeck.. S. Kramer. CA: Singular Publishing Group.g. Gaithersburg. Low socioeconomic status. or abnormal mobility are present (Stool et al. The literature addressing the hypothesis that early recurrent OME poses a threat to children’s speech and language development is large and contentious (for reviews. The prevalence of OME in young children is remarkably high. J. and the validity of parental judgments concerning the frequency or duration of episodes of OME is poor even when repeated feedback is provided (Anteunis et al. K. In addition. A.. and amount of exposure to other children were associated with an increased prevalence of OME during the first 2 years of life (Paradise et al. Robins. Substantive methodological di¤erences may account for much of the disparity in findings. (1992)..g. (1997). A. R624–R630. et al. J. with the method by which OME is diagnosed in di¤erent studies being critically important. Peters et al. Friel-Patti. E. 1997).. A.).. to determine whether indicators of e¤usion such as bulging. J. K. Shriberg. Logemann.. C. Coyle. Deglutition and its disorders.. Several recent studies have shown that after controlling for socioeconomic confounds. in a prospective epidemiologic study of 2253 children enrolled by age 2 months. no e¤ects. S. 1999). Behavioral management for oropharyngeal dysphagia. Friel-Patti.. (1997) reported that nearly 80% of children had at least one episode of OME by 12 months of age. Dysphagia..6% between 12 and 24 months. Smith. Robbins. Sullivan. more than 90% had an episode by age 24 months. and in children from less privileged backgrounds than in their more privileged counterparts (Paradise et al. sometimes within the same study. 2000). No accepted standard metric for speech delay or disorder currently exists..4% between 2 and 12 months of age. 120. 1996a). 1986). thresholds from 0 to 50 dB are not uncommon (Bess. or liquid. J. J. 1994. bubbling. and 16. (1996).. Roberts. E. J.. Bluestone and Klein. A. Dysphagia. 1996a).. 474–478. 93–98. after any necessary removal of cerumen. D. male sex. 11. A.. Otolaryngology–Head and Neck Surgery... Behavioral symptoms such as irritability are neither sensitive nor specific to the condition. Robbins. 1998. and Schulze-Delrieu. E. because a substantial percentage of apparently healthy and symptom-free children are found to have OME on otoscopic assessment (Bluestone and Klein. Lundy. see Stool et al. (1999). E. The SWAL-QOL outcomes tool for oropharyngeal dysphagia in adults: II. 1997). 2000). Finally... K. Although hearing thresholds for the majority of children with MEE fall between 21 and 30 dB (mild to moderate degrees of impairment). retraction. Folia Phoniatrica et Logopedica. Bricker. The hypothesis that OME poses a threat to speech or language development is typically linked to the assumption that e¤usion causes conductive hearing loss. Colangelo. Paradise et al.g. resulting from an infectious process (Scheidt and Kavanagh. it is important that OME be documented prospectively rather than via retrospective reports or chart reviews. The mean cumulative percentage of days with MEE was 20. which prevents children from perceiving and processing speech input in the usual fashion (e. C. Lazarus.. Chignell.. American Journal of Physiology.. 1997. (2000). MD: Aspen. L. Roberts et al. although the Speech Disorders Classification System developed by .. A second important di¤erence among studies of OME and speech development is the extent to which hearing levels are documented. (Ed. A penetration-aspiration scale. As noted earlier. OME has been reported to result in adverse e¤ects. 199–212. the presence of e¤usion is a poor predictor of hearing loss. D. L. Hearing thresholds must be measured directly to determine whether OME has e¤ects on development independent of its variable e¤ects on hearing (e. J.. et al. Flipsen.

Dollaghan.. (1996b). pp. and Manni. Campbell.. the question of whether OME may contribute independently to outcome when it occurs in conjunction with other risk factors or health conditions (e. Pediatric otolaryngology (3rd ed. et al. Engel. Colborn. D. 388–582). (1988) found no correlation between OME and number of consonant errors or phonological processes on a single-word test of articulation at ages 3. Stool. B. Feldman. Although the best available current evidence suggests that OME itself does not represent a significant risk to speech development in otherwise healthy children.). during which their MEE persisted (Paradise et al. M. D. 75–82.. (2000) likewise found no relationship between cumulative duration of MEE and scores on the Percentage of Consonants Correct–Revised measure (PCC-R. E. In J.. 1. J. atelectasis. 7. M. Philadelphia: Saunders. and M. D. E. children with persistent and substantial MEE who were randomly assigned to undergo prompt tympanostomy tube placement had no better PCC-R scores at age 3 than children who underwent tube placement after a delay of 6–9 months. J. Colborn. 1119–1130. J. Audiometric approaches used in the identification of middle ear disease in children. Bluestone. J.). reliable assessments of both medical and sociodemographic risk factors. Bess. Methods of examination: Clinical examination. C. 1993) in 241 sociodemographically diverse children at age 3 years. —Christine Dollaghan and Thomas Campbell References Anteunis. Shriberg. Paradise. K. J. In C.. Casby. speech sound production. E. (1997) represents an important advance toward meeting this need.. L. et al. By contrast with these negative findings concerning the impact of OME. D. (2000). (1997). W. 1998. T. and Klein. Bernard. Smith.. Language. See also otitis media: effects on children’s language. A. K. several studies in which hearing was documented showed poorer speech outcomes for children with elevated hearing thresholds. Rockette. (2000). American Journal of Speech-Language Pathology.. (2001). Otitis media and language development: A meta-analysis. L. C. C. J. Rvachew et al. Paradise et al. M. Bluestone. J. Roberts et al. (1996a). had a significantly increased risk of scoring more than 1. Further. 2001). et al. (1986). T. 150–164). the results of structural equation modeling suggested that hearing loss did not operate directly to lower speech performance. MD: York Press. E. 5. C. F. 1179–1187. Bernard. A longitudinal study of the validity of parental reporting in the detection of otitis media and related hearing impairment in infancy. H. 1. Paradise et al... Bernard. defined as average thresholds b20 dB (HL) during one evaluation between 6 and 18 months of age. In a longitudinal study of 55 low-SES children. F. O.. Additional investigations that include prospective otoscopic diagnosis of OME. valid. Kenna (Eds. 1999). Parkton. L.. Pediatrics. 2000) remains open. 105. Bluestone. 38. (2001) reported that PCC-R scores from children with even more persistent MEE from 2 to 36 months of age did not di¤er significantly from those of children with the less persistent levels of e¤usion reported by Paradise et al..136 Part II: Speech Shriberg et al.. Feldman. J. A. C. Campbell. the e¤ects of OME on speech have been sought on a wide range of articulatory and phonological measures.. et al.. frequent and independent assessments of hearing. Wallace et al. (2000) reported that children with hearing loss. not all of which are known to be predictive of eventual speech outcome (e. given that increased risk was not found across all speech metrics and that confidence intervals for risk estimates were wide. and eustachian tube dysfunction. Philadelphia: Saunders.g. E¤ect of early or delayed insertion of tympanostomy tubes for persistent otitis media on developmental outcomes at the age of three years. 344. Otitis media and child development (pp.). Paradise.. 2001). and a multifactorial analytic strategy will be needed to answer this question.. A.. S. and cognition in threeyear-old children in relation to otitis media in their first three years of life. In a sample of 70 middle to upper middle class 3-year-olds who received otoscopic evaluations every 6 weeks and hearing evaluations every 6 months between 6 and 18 months of age. Flipsen... only one significant speech di¤erence was found. Shriberg. J. K. the literature on early recurrent otitis media and speech development suggests converging evidence that OME in and of itself has a negligible relationship to early speech development. Kenna (Eds. In addition. T. When these cautions are borne in mind. 1996. (1999). 70–82). in which the group with more OME paradoxically obtained higher intelligibility scores than the group with fewer bouts of OME... and M. M. Hendriks. Instead. D.. et al. but rather was mediated significantly by language performance. D. Audiology. Otitis media in 2253 Pittsburgh-area infants: Prevalence and . S. D. B. F.. providing another indication of the need for multifactorial approaches to identifying the factors and pathways involved in normal and abnormal speech development.. F. et al. Kavanagh (Ed. Pediatric otolaryngology (3rd ed. C. Kurs-Lasky. L. Friel-Patti. (2000) examined ten speech measures derived from spontaneous speech samples obtained from 70 otherwise healthy.. S. Colborn. 10. G. J. Dollaghan. A. S.. Paradise. or 8 years.. note the need for some caution in interpreting these findings. and Klein. Bluestone. E.3 standard deviations below the sample mean on several percentage-consonants-correct metrics. Roberts et al. 4.. Shriberg. J. Otitis media. Friel-Patti. New England Journal of Medicine. 6. Shriberg et al. These findings of little or no relationship between OME and speech development mirror those of several recent reports showing negligible associations between early OME and later oral and written language performance (Peters et al. H. middle to upper middle class 3-year-olds who were classified according to the number of episodes of OME from 6 to 18 months of age. In C. H. M. Stool. 1997. S. Shriberg. A. vol. J.g. J. vol. Casby.. 65–80. H.. Several prospective investigations have shown little or no relationship between cumulative duration of otitis media (documented otoscopically) and measures of speech production in otherwise healthy children. B. pp. (2001).. O.

C. Teele. R. A preliminary account of the e¤ects of otitis media on 15-month-olds’ categorization and some implications for early language learning. S. R. E. D. F. H. E.. Burchinal. 1995).. J. 39. and Schilder. and the Greater Boston Otitis Media Study Group. W. S.. Katcher. Kertoy.... swallowing. W. (1997). 74. K. (1984). Rvachew. and first half of the seventh decades of life (Casper and Colton. It is estimated that there are 50. most of which arise from prolonged smoking or a combination of tobacco use and alcohol consumption. Brookes.. When a total laryngectomy is performed. the larynx contains the vocal folds for production of voice for speech... B. Hooper. Journal of Speech and Hearing Research. The Surveillance. Rockville. W.. 105–140. Lewis. Roush. J. 53. The primary disadvantages of total laryngectomy are the loss of the vocal folds that produce voice for speech and the need for a permanent tracheostomy for breathing. E. and Rosner. sore throat. and educational considerations. July). (2000). Schwartz. extensive. (1986). 43. L. 282–287. E.000 new cases of laryngeal cancer are diagnosed each year in the United States.... and Ruben. 12 (AHCPR Publication No. J. 40. Flipsen. (1999). Pediatrics. L. Otitis media in young children: Medical. 27–35. Journal of Speech and Hearing Disorders. Koch. O.). 105.. Flipsen. M. O. D. Gravel. and audible breathing (National Cancer Institute. 17. 357–378. Language. Berg. B. Chase. earache.. and Henderson.. develop- . (Eds. Scheidt. A. Shriberg. B. H. Developmental and Behavioral Pediatrics.. Journal of Speech.. (1997)... A. L. 9. Journal of Speech and Hearing Research. (1997). H. R. Journal of Speech.. (1994. F. Williams. (1990). M. but persistent hoarseness is common. D. Friel-Patti. et al.. B.. J. Pediatrics. Before the introduction of the extended partial laryngectomy. the patient loses his or her voice and must breathe through an opening created in the neck called a tracheostoma. L. The impact of early onset otitis media on babbling and early language development. 467–475. reading and spelling. S. Menyuk. Shriberg. (1997). L. Language. M. a lump in the throat. and Wilson. and language and cognitive outcomes at 2 years. W. and Brown. Shriberg. and Hearing Research. (1993). sixth.. Peters. and Kavanagh. P. W. D. and deeply invasive (Pearson. A. The contribution of risk factors to the e¤ect of early otitis media with e¤usion on later language. a lump in the neck. Otitis media with e¤usion in young children: Clinical practice guideline No.. G. 1998).. J. and Vernon-Feagans. D. Otitis media and child development (pp. Grievink. H.. C.. 100–120. 346–354. (1996). communication style of primary caregivers. speech. A. S. Wallace. the larynx serves as a valve during swallowing to prevent food and liquids from entering the airway and lungs. I. Roberts.. Journal of Applied Developmental Psychology. 94-0622). S. A... Total laryngectomy is usually performed to remove advanced cancers of the larynx. MD: York Press. J. and Hearing Research.. Four new speech and prosody-voice measures for genetics research and other studies in developmental phonological disorders. and speechlanguage outcomes: A preliminary structural equation model.. J. Journal of Speech. 1998). L. C. D.. et al. E. and language at age 7 years. 1998). (2000). R. 79–99. A. 416–424. 723–740. 33. (1988). 102. M. S.. Klein. 43. L. (1998). Roberts. D. Stool. In J.. Otitis media.. F. and Green. Developmental Medicine and Child Neurology. L. MD: Agency for Health Care Policy and Research. early and intermediate laryngeal cancers can be cured with conservation operations that preserve voice.. xv–xvii). Infant daycare and otitis media: Multiple influences on children’s later development. 685–694. M. P. L. M. school achievement. F. Journal of the Acoustical Society of America. A. Klein. 2000). Symptoms of laryngeal cancer vary. Friel-Patti. Journal of Speech. L. Otitis media. M. McSweeny. Zeisel. di‰culty breathing. 1998). P.). P. M. Otitis media in infancy and intellectual ability. Laryngectomy Total laryngectomy is a surgical procedure to remove the larynx. and Henderson. where it is commonly referred to as the Adam’s apple.. F. J. van den Bercken.. Risk for speech disorder associated with early recurrent otitis media with e¤usion: Two retrospective studies. R. total laryngectomy is a proven technique to control disease. and total laryngectomy is performed only in cases of very advanced cancers that are bilateral. Common terminology for conditions of the middle ear.. with a male-female ratio approximately 4 to 1 (American Cancer Society.000 laryngectomees (laryngectomized people) living in the United States today. Additionally. Journal of Infectious Diseases. depending on the exact site of the disease. F. Slawinski. J. and Hearing Research. van Bon. and language skills of 2 year olds: A preliminary report. E.. Kwiatkowski. Wallace. Located in the neck. patients with cancer of the larynx were treated primarily with total laryngectomy (Weber. Parkton. Pediatrics. L. About 10. Radiation therapy is often administered before or Further Readings Creps. R. the caregiving environment. As a treatment of laryngeal cancer. J. O. 21. Kavanagh (Ed. C. J. Burchinal.Laryngectomy risk factors during the first two years of life. (2000). Neebe. Rosner. C. and Finitzo. D. L. M. Today. 318–333. Language. Berman. S. 508–518. I.. Epidemiology and End Results (SEER) program of the National Cancer Institute (Ries et al. Austin.. A. E. Language. J. S. (1990). et al. T. 188–194. Teele.. and Hearing Research. 2000) reports that laryngeal cancer rates rise sharply in the fifth. Shriberg. The typical person diagnosed with cancer of the larynx is a 60-year-old man who is a heavy smoker with moderate to heavy alcohol intake (Casper and Colton. F. Thielke. The Speech Disorders Classification System (SDCS): Extensions and lifespan reference data. Roberts. 40. di‰culty swallowing. coughing. Otitis media with e¤usion during the first three years of life and development of speech and language. J. fluctuant hearing loss. G. Otitis media. Baltimore: Paul H.. S. Other signs include lowered pitch. Laryngeal cancers account for less than 1% of all cancers. Otitis media in early childhood and its relationship to later phonological development... 162. 31–39. and nasal breathing.. Language learning in a prospective study of otitis media with e¤usion in the first two years of life. 137 mental. Roberts. K. 36. Footo.

This silent speech is commonly referred to as ‘‘mouthing words’’ or ‘‘whispering’’.and moisture-exchanging filters over their tracheostoma to replicate the functions of nasal and oral breathing (Grolman and Schouwenberg. can be an e¤ective method of communicating after laryngectomy. The esophageal speaker requires no special equipment or devices. and quality of life (Weber. Immediately or soon after surgery. There are nonspeech methods of communicating that can be used immediately after total laryngectomy. First the laryngectomee pumps or sucks air into the esophagus. unlike a normal whisper. 1874). laryngectomized persons experience other changes. gesturing with pantomimes that are universally recognizable. a speech pathologist meets with the patient and family before the operation to provide information on basic anatomy and physiology of normal breathing. weighing the issues of survival. radiation therapy alone and sometimes in combination with chemotherapy has proved to be curative treatment for laryngeal cancer. In this circumstance it may be possible to use an oral artificial larynx with a plastic tube to place the tone directly into the mouth. and how these will change after removal of the larynx (Keith. yet a person who uses an artificial larynx well can produce intelligible speech in practically all communication situations. and they may wear heat. A person with laryngeal cancer and the family members have many questions about survival. typing on portable keyboards or speech-generating devices. and Rademaker. Unless the tongue is surgically altered or extensive pharyngeal or esophageal reconstruction beyond total laryngectomy is performed. 1997). A common fear of the laryngectomee is that he or she will never be able to speak without vocal folds. and the speaker’s hands are not monopolized during conversation.138 Part II: Speech after total laryngectomy. and many people can use one of these instruments as early as a day or two after surgery. Speech with an artificial larynx. but without voice. depending on the site and stage of the disease (Chyle. many do not attain a level of fluent speech su‰cient for all communicative situations. A radiation oncologist is a physician consulted for opinions about radiation and chemotherapy approaches to management. preservation of function. Usually the device is pressed against the neck or under the chin at a location where it produces the best sound. insu‰cient loudness and a speaking rate that is usually slower than before laryngectomy are common concerns of esophageal speakers. Besides voicelessness. home. followed by immediate sound production for speech. commonly known as ‘‘burp speech. pointing to letters or words or pictures on a speech or communication board. Controversy and research continue over nonsurgical versus surgical intervention or a combination of these for advanced laryngeal cancer. and the person articulates this ‘‘voice’’ into speech. If the neck is too swollen after surgery or the skin is hard as a result of radiation therapy. An otolaryngologist is the physician who usually diagnoses cancer of the larynx and provides information about possible surgical interventions. There is no concern for aspiration of food and liquids into the lungs after total laryngectomy. Although some become excellent esophageal speakers. Additionally. Since the nasal and oral tracts filter the air as well as provide moisture and warmth in normal breathing. In addition. 1995). also known as an electrolarynx. There are several methods of alaryngeal (without a larynx) speech. also known as esophageal speech. and using life-line emergency telephone monitoring systems. A significant disadvantage of esophageal speech is that it takes a relatively long time to learn to produce voice that is adequate for everyday speech purposes. and recreational activities they participated in prior to the laryngectomy. Speech with an artificial larynx has a sound quality that is mechanical. after a period of recovery and rehabilitation. the tone of the artificial larynx may not be conducted into the throat su‰ciently for production of speech. 1998). For this method. . The e¤ectiveness of the technique is variable and depends largely on the laryngectomee’s ability to precisely articulate speech movements and the ability of others to recognize or ‘‘read’’ them. swallowing. because the respiratory and digestive tracts are completely separated and no longer share the pharynx as a common tract. treatment options. 1998). Pauloski. air from the lungs does not move through the mouth after a laryngectomy. laryngectomees often require an environment with increased humidity. Sound or ‘‘voice’’ is generated as the air trapped in the upper esophagus moves back up through the narrow junction of the pharynx and esophagus known as the PE segment. the patient is informed that. most laryngectomized people return to the same vocational. A key to producing successful esophageal speech is getting air into the esophagus consistently and e‰ciently. Esophageal speech has distinct advantages over other alaryngeal speech techniques. however. and with a few modifications. These include writing on paper or on a slate. and speaking. If the patient decides to have a total laryngectomy. Most modern instruments are battery powered and produce a mechanical tone. Also. using e-mail. A laryngectomized person may be able to learn to use esophageal voice. Artificial larynges have been used since the first recorded laryngectomy in 1873 (Billroth and Gussenbauer. where it is articulated into speech. and the long-term consequences and outcomes of various treatments. most laryngectomees return to a normal diet and have few complaints about swallowing other than that it may require additional e¤ort (Logemann.’’ the person learns to use the esophagus (food tube) to produce voice. Then the voice is articulated into speech by the tongue and lips. Most laryngectomized people require training by a speech pathologist to use an artificial larynx optimally. a laryngec- tomized person can make speech movements with the tongue and lips as before the surgery. 1998). None of these methods of communicating is as e‰cient or as personal as one’s own speech. including over the telephone.

Hamaker (Eds. Hamaker (Eds. and ongoing costs of prosthesis-related supplies. The International Association of Laryngectomees and the American Cancer Society provide services to laryngectomized persons. and R. C. There are disadvantages associated with tracheoesophageal puncture. C. may be required (Ho¤man and McCulloch.). D. C. D. commonly known as Botox.). and grief as others with life-threatening illnesses. is the gold standard against which all other methods should be compared (Stone. Cited by R. A. Others maintain that esophageal speech. See also alaryngeal voice and speech rehabilitation. Tracheoesophageal voice restoration following total laryngectomy (pp. DC: Author. CA: Singular Publishing Group.. 1998). or special valve..). and R. Murry (Eds. D. rehabilitation. Head and neck cancer: Organ preservation. R. 1–8).). 1998). loss. I. In E. T. and distribute educational materials on topics of interest. laryngectomized persons may benefit from referral to other professionals and resources for psychological. Tracheoesophageal voice restoration following total laryngectomy (pp. fluent speech can be achieved soon after placement of a voice prosthesis. Surgical management of pharyngeal constrictor muscle hypertonicity. 2001). Toxicity of primary radiotherapy for early stage cancers of the larynx. TX: Pro-Ed. which were thought to delay or interfere with the learning of esophageal speech (Lauder. ¨ Billroth. D. W. depression. injection of botulinum neurotoxin. Keith and F. phrasing. Most believe any form of speech after laryngectomy is acceptable and should be encouraged. (1998). It does not generate voice itself. laryngectomees and speech pathologists have felt strongly about one form of alaryngeal speech being superior to others.Laryngectomy 139 Tracheoesophageal puncture with a voice prosthesis is another method of alaryngeal voice production (Singer and Blom. function. and rehabilitation (pp. and McCulloch. A. Today some think tracheoesophageal speech is superior because many laryngectomees are able to speak fluently and fairly naturally with this method only a few weeks after surgery. Usually a catheter is placed in the opening and a prosthesis is placed a few days later. (1995). rate. stress. and financial concerns. CA: Singular/Thomson Learning. and Colton. Looking forward: A guidebook for the laryngectomee (3rd ed. CA: Singular Publishing Group. Chyle. with no reliance on a prosthesis or other devices. When the person exhales and the tracheostoma is covered with a thumb. Shanks in Historical highlights: Laryngectomee rehabilitation.. P. Darley (Eds. CA: Singular Publishing Group. L. Blom. newly laryngectomized persons were discouraged from using artificial larynges. Blom. through the prosthesis. 1–48). since speaking is a fundamental and essential part of being human. 1968). (1998). H. Singer. 33–39). . CA: Singular Publishing Group. 109–121). F. They sponsor peer support groups. nutritional. Ho¤man. Hamaker. or myotomy of the pharyngeal constrictor muscles may be considered (Hamaker and Chessman. fear. 17. 343–356. Casper. In E. Expenses associated with tracheoesophageal puncture include those for initial training in the use and maintenance of the prosthesis with a speech pathologist and subsequent clinical visits for modification or replacement of the voice prosthesis. and a silicone tube with a one-way valve—a voice prosthesis— is placed in the puncture site. M. L. In T.. C. Singer. E. provide speech therapy. People who undergo total laryngectomy experience the same emotions of shock. or if it requires considerable e¤ort to produce. Keith and J. Botulinum neurotoxin for tracheoesophageal voice failure. Archiv fur die Klinische Chirurgie. (1998). Blom. 83–87). and specialized products and equipment for laryngectomized persons. Tracheoesophageal voice restoration following total laryngectomy (pp. The laryngectomee may dislike using a thumb or finger to cover the tracheostoma when speaking. Along with regular medical follow-up to monitor for possible recurrence of cancer and to review all the body systems. H. 19–21).). Keith. V. the speech characteristics of pitch and loudness. C. L. R. finger. Thomas References American Cancer Society. 1998). Robbins and T. M. San Diego. and R. C. In E. (1998). I. In E. (1874). M. R. If the PE segment is hypertonic and the tracheoesophageal voice is not satisfactorily fluent for conversation. San Diego. In the 1960s. into the upper esophagus. air from the lungs moves up the trachea. marital. Blom. such as cardiopulmonary resuscitation for neck breathers. and timing more closely resemble the laryngectomee’s presurgical speech qualities than can be achieved with other forms of alaryngeal speech. The opening is a tract through the posterior wall of the trachea and the anterior wall of the esophagus. Uber die erste durch Th. and Cheesman. K. (1998). L. CA: Singular Publishing Group. I. A speech pathologist specially trained in tracheoesophageal voice restoration measures the length of the tract between the trachea and the esophagus. Cancer facts and figures 2000. Grolman.. and Gussenbauer. Evolution of tracheoesophageal voice prosthesis. (2000). Historically. Hamaker (Eds. In R. San Diego. Lewin et al. Hamaker (Eds. During the surgery to remove the larynx or at a later time. M. Blom. For many laryngectomees. Laryngectomee rehabilitation (pp.).). and through the PE segment to produce voice. C. Clinical manual for laryngectomy and head/neck cancer rehabilitation (2nd ed. and Schouwenberg. Billroth am Menschen ausgefuhrte Kehlkopf Ex¨ tirpation und die Anwendung eines kunstlichen Kehlkopes.. New York: Thieme. T. Singer. D. I. and R. the surgeon makes an opening (puncture) just inside and inferior to the superior edge of the tracheostoma. T. San Diego. M. Postlaryngectomy airway humidification and air filtration. Blom. Tracheoesophageal voice restoration following total laryngectomy (pp.). Austin. 1980. San Diego. (1998). and use of a tracheostoma valve for handsfree speaking may not be possible. Washington. 1998. smoking cessation. —Jack E. D. San Diego. The prosthesis is nonpermanent and must be replaced periodically. Because lung air is used to produce voice with a tracheoesophageal puncture. C. Singer. J.

K. the most common known cause of inherited mental retardation (Down syndrome is more common but is not inherited). 1997) indicate abnormalities in articulatory development. et al. F. with males exhibiting more severe e¤ects. L. Shanks. (1994). The clinician’s guide to alaryngeal speech therapy. This hypothesis has two major flaws: first. and Stone. Hankey. TX: Pro-Ed. Ries. Oral communication after laryngectomy. B. M. 147–157. S. Singer. W.).. A.). (1998). J. The majority of research on children with mental retardation has involved children with Down syndrome (or trisomy 21). the prevalence of mental retardation in the noninstitutionalized population of the United States is 7. S. Toronto: Somerville House Books. Further experience with Botox injection for tracheoesophageal speech failure. Keith. E. J. (1998).. CA: Singular Publishing Group. K. in part. Help employ laryngectomized persons. and Laryngology. E. Bishop-Leone. and has a profound e¤ect on a child’s ability to learn to talk. Miller. TX: Pro-Ed. Murry (Eds. 1973–1997. Bethesda. Pearson. they undoubtedly influence speech-motor development and thus the articulatory and phonatory abilities of children with Down syndrome. and the presence of a narrow. CA: Singular Publishing Group. (1980). 33. Pauloski. with levels lower than would be expected. Surgical options in laryngeal cancer. M. R. 2001). This disorder is characterized by deficits in social . 23. Robbins and T. A. Autism is a developmental disorder with prevalence estimates ranging from two to five per 10. W. A. G. Head and neck cancer: Organ preservation. Kosary.73 per thousand. A handbook for the laryngectomee (4th ed.. Oklahoma State University. has an estimated prevalence of approximately one per 1250 in males and one per 2500 in females. J. (1983). M. (1995). Head and Neck. and rehabilitation (pp. to di¤erences in the structure and function of the oralmotor systems of boys with fragile X syndrome.). (Eds. Foundations of voice and speech rehabilitation following laryngeal cancer. R. Boston: Butterworth-Heinemann. San Diego. H. weak facial muscles. and Thomas. S. 89. This syndrome is the most common genetic cause of mental retardation. and the presence of atypical rate and rhythm. 11. 37–44). P. 33–36).. and general hypotonicity. These abnormalities may be attributed. C. I. R. 59–71).. Murry (Eds. J.. within a single type of mental retardation. patterns of language development vary across types of mental retardation. the number increases to 8. the presence of a high palatal vault and a larger than normal tongue in relation to the oral cavity. CA: Singular Publishing Group.). C. C. prosody.). L. Lewin. E. disfluncies. (1998). and second. Speech and swallowing rehabilitation for head and neck cancer patients. Bethesda. E. Austin. In T. J. including excessive drooling. Mental retardation is associated with limitations in learning and in the ability to communicate. and rehabilitation (pp. D. and Rademaker. Although the precise e¤ect of these di¤erences is di‰cult to determine. and rehabilitation (pp. higharched palate. In T. Advanced laryngeal cancer: Defining the issues. Journal of Speech and Hearing Disorders. Alaryngeal speech rehabilitation: For clinicians by clinicians (2nd ed. Stone. children with fragile X syndrome have a high incidence of otitis media and intermittent hearing loss. I. Mental Retardation and Speech in Children Mental retardation is defined by the American Association on Mental Retardation as significantly subaverage intellectual functions with related limitations in social and behavioral skills.. M. E. B. occurring in approximately one out of every 800 births. Graham. (Eds. 1988). Oncology.).140 Part II: Speech Lauder. function. Fragile X syndrome. Because Down syndrome is identifiable at birth. Robbins and T. and Rosenbaum. According to the most recent estimates (Larson et al. (1968). H. What you need to know about cancer of the larynx (NIH Publication No. Logemann.. D. Eisner. E. (1998).. Weber. and Diaz. MD: Author. 95-1568). (1997). These features include di¤erences in the vocal cords. 529–533.. S. Like their peers with Down syndrome.). J.. Salmon. Forman. P. and Blom. Rosenbaum. and Mount. National Cancer Institute. An endoscopic technique for restoration of voice after laryngectomy.. A. researchers have been able to trace developmental patterns from the first months of life. L. An additional factor a¤ecting the speech of children with Down syndrome is fluctuating hearing loss associated with otitis media and middle ear pathologies. R. Annals of Otology. 651–659. The development of speech and language is severely a¤ected in children with Down syndrome.8 people per thousand. 456–460. (2000). OK: National Clearinghouse of Rehabilitation Disorders. B. The laryngectomee and the artificial larynx. Stillwater. Children with Down syndrome di¤er from the normal population in respect to a variety of anatomical and physiological features that may a¤ect speech production. Little research has been done on the speech of young children with fragile X syndrome. MD: National Cancer Institute. San Diego... Further Readings Doyle. there is considerable heterogeneity.. Austin. Murry (Eds.000 (3 : 1 males). (1995). Head and neck cancer: Organ preservation. At one time it was believed that the language acquisition of all persons with mental retardation represented a slow-motion version of normal language development. R. Cancer supportive care: A comprehensive guide for patients and their families. B. hypotonia involving the oral-facial muscles. Robbins and T.). (Eds. (2001). Rhinology.. and voice. Available reports on older children (Abbeduto and Hagerman. (1998). San Diego. (1997). CA: Singular Publishing Group. In T. E. given mental age (Miller. function. Head and neck cancer: Organ preservation.. if institutionalized individuals are included in the prevalence rates. San Diego. Clegg. SEER cancer statistics review. Speech intelligibility is compromised throughout the life span because of problems with articulation. function. A.

abnormal voice quality. The magnitude of the delay cannot be easily predicted from the degree of retardation. 1997. The foundations for speech development are laid in the first year of life. the other 50% exhibit delays in acquiring language. Mervis and Bertrand. 1980) to programs aimed at modifying parent-to-child speech in order to provide optimal input in the face of delayed language acquisition. Whereas nonretarded children have a vocabulary of 250 words at 24 months. and unusual voice quality. 1997). 1994). delays in the acquisition of speech and language may serve as the first indication of a cognitive delay (except for Down syndrome. linguistic skills appear to be relatively normal (Bellugi. Cholmain. 1997). a genetic disorder that includes mental retardation. and typically developing. —Carol Stoel-Gammon . with a few reports of word use in the second year of life for a few children with Down syndrome but the majority showing first words appearing between 30 and 60 months. Lai. and Wang. a¤ricates. Research suggests great variability among children in this domain. it is important to assess hearing and oral-motor function. In contrast. and play. assessment typically adheres to traditional practices in speech-language pathology.000 live births. This dissociation of language and cognition underscores the importance of examining the relationship between mental retardation and speech in a variety of mentally retarded populations. also pose di‰culties for children with mental retardation. occurring in one in 25. There is some indication that children with fragile X syndrome also su¤er from low levels of intelligibility (Abbeduto and Hagerman. Phonemes that are later-acquired in normal populations. revealed a greater number and variety of error types in the children with Down syndrome (Dodd. these ‘‘canonical’’ babbles are similar or even identical to the forms used in first words. which may be quite protracted for some children. words are ‘‘simplified’’ in terms of their structure: consonant clusters are reduced to single consonants. communication. the emergence of words is often delayed among infants with mental retardation. is that their speech is hard to understand (Kumin. two out of three children with autism are mentally retarded (Pennington and Bennetto. Infants with retardation begin to produce canonical babble within the normal time frame or with minor delays. a normed articulation test) and by analyzing samples of conversational speech to determine intelligibility and overall speech characteristics. assessment is initially based on unstructured observations and parental report. Speech production is characterized by echolalia and abnormal prosody (see autism). Down syndrome. social communication skills in the prelinguistic period are atypical. In general. If language is slow to emerge. Moreover. which generally appear around age 6–7 months. Parents may be the first to raise concerns about atypical patterns of development. and pediatricians and social workers should be aware of the link between linguistic and cognitive development. with the parents. Some reports suggest that the phonologies of children with Williams syndrome may be relatively adultlike by the (chronological) age of 8. the prelinguistic vocalizations are like those of nonretarded infants. About 50% of autistic children fail to develop spoken language. 1994). and liquids. More formal assessments are done in two ways: by means of standardized tests that focus on the individual sounds and structures of a predetermined set of words (i. non-Down syndrome with mental retardation. 1998). thus. mental retardation. using therapy techniques similar to those for children with phonological delay or disorder. acquisition patterns for children with mental retardation are similar to those documented for nonretarded children (Rondal and Edwards. Parents report low levels of intelligibility through adolescence as a result of speech sound errors. In terms of phonemic development.Mental Retardation and Speech in Children 141 interaction. is relatively rare. rate of speech. Once mental retardation has been confirmed. although not to the same extent as children with Down syndrome do. 1997). with the emergence of nonmeaningful vocal types that serve as precursors for the production of words and phrases.e. See also communication skills of people with down syndrome. individuals with Down syndrome. 1989. even when they have a mental age of 8. Of particular importance is the production of consonant-vowel syllables. Phonetically. correct pronunciation of all phonemes is achieved by the age of 8 years. Williams syndrome. In some cases. comparisons of phonological development in three populations matched for mental age. Recommendations for the treatment of speech deficits in children with mental retardation range from intervention directed toward underlying causes such as hearing loss and deficits in speech-motor skills (Yarter. Most phonological interventions focus on increasing the phonetic repertoire and reducing the number of errors. such as [baba]. prelinguistic vocal development of infants with mental retardation resembles that of their nonretarded peers in terms of types of vocalizations and schedule for emergence. and consonants at the ends of words may be omitted. 1997). particularly those with Down syndrome (Stoel-Gammon. exhibit many articulation errors. disfluencies. this milestone is not reached until the age of 4–6 years for most children with Down syndrome. in spite of marked impairments in cognition. 1976). For many children with mental retardation. unstressed syllables are deleted. vocabulary growth is relatively slow. The di¤erence is recognition of the sound-meaning relationships that are the basis for words.. once words appear. the production [mama] may be a nonmeaningful babble at 8 months and a word at 14 months. Although in phonetic form. as well as in the clinic (Dodd and Leahy. Despite the nearly normal onset of canonical babble. Moreover. One of the most striking aspects of Williams syndrome is that. A persistent problem in children with Down syndrome. In the early stages. Among nonretarded children acquiring English. therapy may occur at home. In the prelinguistic period. which is easily diagnosed at birth). primarily fricatives. however.

The developmental asynchrony of language development in children with down syndrome. Mental Retardation and Developmental Disabilities Research Reviews. J. developmental speech production deficits have been categorized as either phonological or DAS. (1976). and phonology (Levelt. (2001). Larson. Cholmain. C. 167–198). Adamson and M. L. C. Phonological development in Down syndrome. H. basic movement patterns observed in babbling are linked to emerging intents and words (de Boysson-Bardis and Vihman. A comparison of the phonological systems of mental age matched normal. and I. Hodapp. London: Whurr. 1999). and Hagerman.. Lee. S.. 2000. recent empirical evidence suggests that a wider range of children (e. (1997). Pennington. 334–342. B. Baltimore: Paul H. Language models include categories such as concepts. UK: Cambridge University Press. British Journal of Disorders of Communication. Mental Retardation and Developmental Disabilities Research Reviews. Burack. How- Motor Speech Involvement in Children Motor speech involvement of unknown origin is a relatively new diagnostic category that is applied when children’s speech production deficits are predominantly linked to sensorimotor planning. emphasis is placed on those that are at least partially motor in origin. those with specific language impairment [SLI] or inconsistent speech errors) may exhibit deficits that are influenced by motor variables and. Usually. A. This category is . and E. in these cases. Sensory feedback is also a necessary component of motor systems (A. Levelt. 75–106). 3. broader than and encompasses that of developmental apraxia of speech (DAS). P. and Anderson. Working on phonology with young children with Down syndrome.. or praxis. Stoel-Gammon. Leudar (Eds. Language and Hearing. 1999). Prevalence of mental retardation and developmental disabilities: Estimates from the 1994/1995 National Health Interview Survey Disability Supplements. Motor systems are discussed in the very di¤erent terms of cortical inputs to pattern generators in the brainstem. programming. B. Kumin. Although the underlying causes of motor speech involvement are unclear. M. R. and Wang. 11. and Meyer. Dodd. Classically. (1980). Go¤man. which refers specifically to impaired planning. speech motor and language domains codevelop and mutually influence one another across development. Anderson. U.. speech production models are not explicit about the nature of the linkages. 3. Toward a neuropsychology of mental retardation. B. and Marquardt..)..142 Part II: Speech References Abbeduto. and Stark. and Edwards. Language and communication in fragile X syndrome. Hill. Journal of Clinical Speech and Language Studies. S. (1998). 106. Rondal. severely abnormal and Down’s syndrome children. Language. Developmental relations between cognition and language: Evidence from Williams syndrome. and Leahy. American Journal on Mental Retardation. Jakielski. 2001). most notably in common brain mechanisms in the lateral perisylvian cortex. the relations between language and motor levels in later periods of development have not been specified. (1998). 1991. A. 1. 49–61. (1994). London: Chapman and Hall. The psychobiology of Down syndrome (pp.).. 1995). it is extreme and persistent in disordered children. Handbook of mental retardation and development (pp. 80–114). However. Language and communication in mentally handicapped people (pp. may be classified as motor speech involved. 3. semantics. 1. Communication and language acquisition: Discoveries from atypical development (pp. L. imitation and repetition may not aid performance (Bradford and Dodd. Language in mental retardation. L. (1997). Lakin. Speech and language programs for the Down’s population. Kwak. F. 1999). At this level. and neural systems in Williams syndrome. Smith. However. In late infancy. Although it is established that motor and language domains both show a protracted developmental time course. 2000). G. it is apparent how language and motor levels constrain one another. Zigler (Eds. Lai. 300–306. In L. J. and Meyer. 1996). Conti-Ramsden. (1997). 78. Seminars in Speech. K. or execution (Caruso and Strand. Roelofs. Brookes. syntax.. N. In J. Nadel (Ed. Cambridge. J. In L. Phonological disorders and mental handicap. Miller. F. D. and Bertrand. Yarter. 307–313. 33–56). When the deficit involves movement planning. R. Z. even across multiple productions of the same word (Davis. Roelofs. J.).. Although variability is observed in speech motor (A.g. Mental Retardation and Developmental Disabilities Research Reviews. B. MA: MIT Press. J. Cambridge. communication. Romski (Eds.).. Variability. Mervis. C. A. The general view is that increasingly complex linguistic structures are linked to increasingly complex movements in the course of development. 1998) and phonetic output of young children who are normally developing. In M. variability is discussed as a phonetic error type. J. J. 313– 322.. (1994).. A large range of speech and language characteristics have been reported in children diagnosed with motor speech disorders. Neurophysiological findings support the interaction of cognitive and motor development. Beveridge. H. N. there is general evidence that motor and cognitive deficits often co-occur (Diamond. The disorder occurs in the absence of obvious neuromotor causes and often includes concomitant language deficits. (1997).. In the following summary. Dodd. (1989). Motor speech deficits occur when movement variables interfere with the acquisition of speech and language production. P. which in turn provide inputs to motor neuron pools for the generation of muscle activity. Children with motor speech disorders have been reported to produce highly variable errors. L. 231–252. 27–42. Smith and Go¤man. 1998). Apparently. Perceptual and Motor Skills. 14–35. B. Bellugi. B. the neocerebellum. and Bennetto. (1997). and the dorsolateral prefrontal cortex (Diamond. C. Intelligibility of speech in children with Down syndrome in natural settings: Parents’ perspective.

Moore. Overall. Gibbon (1999) has provided direct evidence that children with speech deficits contact the entire palate with the tongue. such as kicking and banging objects) (e. 2000). The earliest consonant-vowel structure seen in babbling is hypothesized to consist of jaw oscillation without independent control of the lips and tongue (MacNeilage and Davis. Go¤man (1999) reported that children with a diagnosis of SLI. 1996). Syllable shapes may also be influenced by motor factors. Vowel production requires highly specified movements of the tongue and jaw (Pollock and Hall. Major approaches to intervention have focused on motor programming (Hall. it is clear that intervention approaches for these children need to incorporate motor as well as language components. 2001). DAS (Bradford and Dodd. kinematic analysis of lip and jaw movement reveals that children with SLI show movement output that is less stable than that of their normally developing peers. even when producing an accurate phonetic segment (Go¤man. More complex syllable structures probably require increased movement control. 1987). Kent and Forner. Children with motor speech disorders display particular deficits in prosodic aspects of speech. Jordan. these errors may have origins in movement planning and implementation. A lack of di¤erentiated and coordinated movement leads to a collapsing of phonetic distinctions. Jordan. Aram. Prosodic Movement Organization and Sequencing. However. 2001). such as the homing movement for final consonant production (Kent.g. motor variables account for many aspects of the developmental sequence frequently reported in speech. Hence. Liquids. Although the emphasis has been on DAS. As they develop. For example. Jakielski. which is used to convey word and sentence meaning as well as a¤ect. 1991).Motor Speech Involvement in Children 143 ever. Kent (1992) suggests that early-developing stop consonants such as [b] and [d] are produced with rapid. were poor at producing large and small movements sequentially across di¤erent stress contexts. Rhythmicity is thought to have origins in prelinguistic babbling (and. 1993) and tactile-kinesthetic and rhythmic (Square. not just the anterior region. Duration. Phonetic Movement Organization and Sequencing. both within and across articulatory. 1994) deficits. and Robin. Thelen and Smith. and Robin. 1994). Rhythmicity underlies the prosodic structure of speech. It follows that segmental and syllabic inventories are reduced for children with motor speech deficits (Davis. 1993). the control of movement for the production of stress is a frequently cited deficit in children with motor speech disorders. and Marquardt. as proposed by Kent (1992). supporting the intimate . 1980). Jordan. In the clinical literature. both phonological and motor factors may contribute. Deficits in planning and implementing spatially and temporally organized movements may influence the acquisition of stable phonological units (Hall. perhaps. who also demonstrated speech production and morphological errors. 1987. A decreased speech rate provides the child with time to process.. these children had di‰culty producing small movements corresponding to unstressed syllables. children produce increasingly di¤erentiated speech movements. and Robin. in early stereotypic movements. peg moving. One major aspect of motor development that has been emphasized in motor speech disorders is rhythmicity. but it may also negatively influence speech motor performance. gesture imitation) performance are below expected levels in children with variable speech errors. An additional error type that may also be related to timing is poor movement coordination across speech subsystems. 1992). In children with motor speech involvement. general neuromotor status has long been implicated as contributing to even relatively subtle speech and language deficits (Morris and Klein.and language-impaired children. Consonant sounds that are earlydeveloping and that are most frequently seen in the phonetic inventories of children with motor speech deficits make relatively few demands on the motor system (Hall. these approaches could be tailored to more general motor speech deficits. 1997) found that a significant proportion of children diagnosed with DAS demonstrated errors characterized by even or misplaced stress in their spontaneous speech. laryngeal. Empirical studies have provided evidence that aspects of gross and fine motor (e. Thus.g. Such data indicate that motor control of di¤erentiated tongue movements has not developed in these children. an understanding of speech motor contributions to the acquisition of speech and language is in its infancy. 1993). in their production of alveolar consonants. 1999). which require highly controlled tongue movements. Jordan. and implement movement (Hall. Smith. are learned quite late in the developmental process. 1998). Shriberg and his colleagues (Shriberg. and Kwiatkowski. Such timing deficits in articulatory and laryngeal coordination may lead to voicing and nasality errors. Using electropalatography. ballistic movements. Although e‰cacy studies are scarce. Fricatives require fine force control and are acquired later. 1999. and many diagnosed with SLI (Bishop and Edmundson. Such findings suggest that many speech production disorders include a general motor component. and respiratory subsystems (Gibbon. General Motor Development. and Robin. in the problematic weak-strong prosodic sequence. 1993) as well as increased error rates on longer and more complex utterances. 1993).. Hill. In a study using direct measures of lip and jaw movement during the production of di¤erent stress patterns. plan. Overall. Increased movement durations are a hallmark of immature motor systems (B. the slow implementation of movement may lead to decreased performance on a nonlinguistic diadochokinetic task (Crary. As is apparent. several investigators have proposed techniques for the treatment of motor speech disorders in children. L. Vowel and consonant errors may be considered in reference to articulatory complexity. Hierarchical language organization has also been emphasized. 1978.

A. J. Moore. L. and Stark. A. A. (1991). (1999). Physiologic development of speech production. 91–101. (2000). and Steeve. new methods of recording respiratory. T. (1999). 40–43). Speech motor control in normal and disordered speech (pp. Menn. CA: Academic Press. and Kwiatkowski. Peters. 44–56. CA: Singular Publishing Group. and Hearing Research. 36. Thelen.. and Strand. and articulatory behaviors of infants and young children during the production of meaningful linguistic activity should provide crucial data for understanding how language and motor components of development interact across normal and disordered development. Hodge. E. (1995). 6. Hulstijn. 77–101. MA: MIT Press. (2000). and Hall. 37–67. and Klein. Timonium. Undi¤erentiated lingual gestures in children with articulation/phonological disorders. A. Science. J. (1987). Pre-feeding skills. S. W. T. L. P. S. Stability and patterning of speech movement sequences in children and adults. M. (2001). Adaptation to language: Evidence from babbling and first words in four languages. Austin. and Klee. Journal of Phonetics. Jakielski. A. 25– 45. (1993). An analysis of vowel misarticulations of five children with developmental apraxia of speech. Robbins.. In C. D. J. A dynamic systems approach to the development of cognition and action. F. D. (2000). (1987). Gibbon. M. R. Intrinsic dynamics and mechanosensory modulation of non-nutritive sucking in human infants. CA: Singular Publishing Group.. L. L. Journal of Speech. M. —Lisa Go¤man References Bishop. Phonological development: Models. S. M. Science. D. Dodd. Higashikawa. Developmental motor speech disorders. D. Developmental apraxia of speech: Determiners of di¤erential diagnosis. and Smith. P. TX: Psychological Corp. and Barlow. 42. (1991). (1995).. MD: York Press.. 527–531. and Hearing Research. New York: Thieme. C. Child Development. D. Clinical Linguistics and Phonetics. 157–168. Pollock. B. Finan. Developmental apraxia of speech: III. links between linguistic and movement variables (Velleman and Strand. R. Smith. San Antonio. (1998). Movement patterns in spoken language. Go¤man.). See also developmental apraxia of speech. Green. Close interaction of motor development and cognitive development and of the cerebellum and prefrontal cortex.. 87–99. A. Language. L. E. (1995). A. Speech segment durations in sentence recitations by children and adults. F. (1987). S. A. (2001). K. Shriberg.. M. 18–30. and Vihman. A. J. and C. On the origin of internal structure of word forms. P.). C. A. 442– 459. B.). R. (1994). AZ: Therapy Skill Builders. Language. In B. 16. J. V. 151–161. L. Language. (1999). L. D. Speech motor development. Assessment of children with developmental apraxia of speech: A rationale. Jordan. 22. A. P. Child phonology: Characteristics. 272–277. Journal of Speech. E. 41. and Marquardt. (1999). Clinical management of motor speech disorders in children.. Davis.. A. (2000). M. R. The biology of phonological development. A theory of lexical access in speech production. M. R. Bernthal and N. and Stemberger.. C. Stoel-Gammon (Eds. Nijmegen. 42.. B. 1499–1517. Crary. E. Specific language impairment as a maturational lag: Evidence from longitudinal data on language and motor development. M. and intervention with special populations. Hall. 313–337. and Dodd. A.. L.. Aram. 65–90). Journal of Speech and Hearing Research.. research. Bankson (Eds. assessment. Seminars in Speech and Language. A. In J.. The Verbal Motor Production Assessment for Children. 1–75. Caruso. Developmental Medicine and Child Neurology. 4.. de Boysson-Bardis. 288. B. Behavioral and Brain Sciences. laryngeal. Netherlands: Uitgeverij Vantilt. (1996).. 29. B. Kent. Morris.. P. Diamond. A. E... 12. and Davis. San Diego. Handbook of phonological development from the perspective of constraint-based nonlinear phonology. Journal of Speech. Clinics in Communication Disorders. B. and Go¤man. K.). 71. Journal of Communication Disorders. and P. B. Further. 382–397. . 181–197. (1998). International Journal of Language and Communication Disorders. Language. B. New York: Thieme. 52. Smith. Treatment approaches for developmental apraxia of speech. Journal of Speech. Journal of Phonetics. Smith.. L. San Diego.. San Diego. Language. New models of speech and language development are needed that integrate motor and language variables in a way that is consistent with recent neurophysiological and behavioral evidence. Di¤erential diagnosis and treatment of children with speech disorder. Journal of Speech. and Hearing Research. J.144 Part II: Speech Levelt. Maasen. L. (1994). Kent. (1978). K. S. 67. (1997). van Lieshout (Eds. and Meyer. A. and Robin. Temporal aspects of English speech production: A developmental perspective. J. Such tools should also help answer questions about appropriate interventions for children whose deficits are influenced by atypical motor control processes. P. D. (1998). Locke. D. 239–255. 207–224. 10. and Strand. E. MacNeilage. (1999). and Forner. M. Square. 52. 5. Ferguson. Non-specific nature of specific language impairment: A review of the literature with regard to concomitant motor impairments. 149–171. W. implications (pp. M. D. Language. Roelofs. Go¤man. and Hearing Research. Early Human Development.. 43. M. 297–318. M. and Square. Further Readings Bernhardt. (1992). Kent. 1994). Hayden. Do all speech-disordered children have motor deficits? Clinical Linguistics and Phonetics. Hill. TX: Pro-Ed. The physiologic development of speech motor control: Lip and jaw coordination. L. Bradford. Moore. Prosodic influences on speech production in children with specific language impairment and speech deficits. R. (1998). W. H. (1994).. 288. Tucson. 8.. M.. (1980). (1993). 40. Clinical Linguistics and Phonetics.. Developmental apraxia of speech: Theory and clinical practice. A subtype marked by inappropriate stress. 449–450. Clinical assessment of oropharyngeal motor development in young children.. 4. and Edmundson. and Hearing Research. L. Developmental verbal dyspraxia. H. Velleman. F. Cambridge. (Eds. L. A.

The hypothesis is that mutism due to apraxia reflects a profound failure of motor programming. Descriptive and theoretical markers. Strand. the literature can be a bit of a muddle. 1997) and to the drive or will to speak. (1997). Recent data suggest that the critical areas are the portions of the medial frontal lobes immediately anterior to the supplementary motor area and portions of the anterior cingulate gyrus above the most anterior body of the corpus callosum. motor. Bilateral and occasionally unilateral left or right anterior cerebral artery occlusion with involvement of the anterior cingulate gyrus or supplementary motor area is frequently implicated (Nicolai. Certain types of transcortical motor aphasia (Alexander. (1999). and Hearing Research. Each of these definitions has strengths. Journal of Speech. M. Aram. Lesions of the globus pallidus. 145 Mutism. 1995). Du¤y defines mutism traditionally as ‘‘the absence of speech’’ (1995. 1999). 1997). including degenerative diseases such as Creutzfeldt-Jacob disease (Otto et al.. may be associated with complete absence of spontaneous speech. parietal. 16. J.. It usually accompanies other signs. Therefore. L. with preservation of brainstem function (Kinney et al. Immediately after stroke. A reasonably traditional review of the syndromes and conditions of which mutism is a frequent part and traditional and emerging explanations for mutism’s appearance are o¤ered here. Akinetic Mutism. Variability revisited: An acoustic.Mutism. these patients are reasonably fluent during picture description. Speech movements are impossible because of upper and lower motor neuron . However. D. the mutism is thought to signal an apraxia of phonation. These regions appear to be involved in gating intention (plans of action) (Picard and Strick. but in rare cases it appears in isolation. Seminars in Speech and Language. Mutism in Aphasia. 40. D. aerodynamic. Metrical analysis of speech in children with suspected developmental apraxia of speech. but none dominates the literature. E. olivopontocerebellar atrophy. or by a mix of syndrome and medical etiology (Lebrun. The literature is also challenging because of the mutism population’s heterogeneity. slowly progressive anarthria (Broussolle et al. 1992). Neurogenic Shriberg. and Tavy. 126–139. van Putten. Journal of Speech. 1998). and occipital junction involvement in which the patient is speechless but moving. despite pain or threat. Treatment of motor speech disorders in children.. and execution. 111). Statholpoulos. A. 42. (1995). L. Definition. Patients with severe anomia. Developmental apraxia of speech: I. and at least some cognitive integrity and a normal level of arousal. Neurogenic Mutism is speechlessness. and Shriberg. most particularly the adynamic aphasia of Luria (1970). 273–285. including intention. and respiratory kinematic comparison of children and adults during speech. by syndrome. 1989). Gelabert-Gonzalez and Fernandez-Villa (2001) require ‘‘unimpaired consciousness’’ (p. and progressive supranuclear palsy (Nath et al. Mutism in Dysarthria. 2001). most often in relation to thalamic lesions. Mutism can be the final stage of dysarthria (anarthria) in degenerative diseases such as amyotrophic lateral sclerosis. thalamus. and Hearing Research. Mutism can be a feature of severe global aphasia. a profound apraxia of speech (called aphemia and by a variety of other names in the world’s literature) can cause mutism. by etiology. Shy-Drager syndrome.. Velleman. Language. Traditionally. Lebrun (1990) requires normal or relatively preserved comprehension. 1996).. Von Cramon (1981) adds the inability to produce nonverbal utterances. This last approach guides the organization of the following discussion. 1444–1460. Benson. but they can repeat. (1995). that alters what Schi¤ and Plum (2000) posit to be a series of corticostriatopallidal-thalamocortical (CSPTC) loops... Parkinson’s disease. Du¤y. D. Language. S. Damage to any of the putative processes critical to speech. It can be neurologic or behavioral. 282). and other subcortical structures can also result in AM. 2001). striatonigral degeneration. 1995). may initially exhibit no capacity for spontaneous language and little for naming. most critically the thalamus. T. One response to this heterogeneity has been to classify mutism according to relatively homogeneous subtypes. and Stuss. Neurogenic mutism is a sign and can result from many developmental or acquired nervous system diseases and conditions. 1990. E. The designation abulic state may be a synonym (Du¤y. Cohen et al. as can primary progressive apraxia of speech. The cause may be any nervous system–altering condition. In the acute stage of stroke. as are apallic state and coma vigil. Mutism in Apraxia. Journal of Phonetics. and this syndrome likely reflects a prelinguistic disorder involving defective spontaneous engagement of concept representations (Gold et al. 1994). as well as linguistic and prelinguistic processes have been invoked to explain mutism’s appearance. 23. Schi¤ and Plum (2000) advocate for a companion syndrome of ‘‘hyperkinetic mutism’’ resulting most frequently from bilateral temporal.. which reflects extensive damage to all cerebral structures. CSPTC loops are critical to triggering or initiating vocalization (Mega and Cohenour. groupings of mute patients have been organized according to the putative pathophysiology (Turkstra and Bayles. and Kwiatkowski. 1996.. Persons with AM often are silent. p. AM is to be di¤erentiated from persistent vegetative state. 67–80. motor programming. Akinetic mutism (AM) is a syndrome of speechlessness and general akinesia that exists in the context of residual sensory. All levels of the neuroaxis from the brainstem to the cortex have been implicated.

(1997).. Tommasi. Journal of Clinical Neurophysiology.. Bathgate. Dikkes. Traumatic aphasia: Its syndromes.. (1966). R. Slowly progressive anarthria with late anterior opercular syndrome: A variant of frontal cortical atrophy syndromes. M. G. (2000). Cerebellar mutism with subsequent dysarthria in an adult: Case report. Summary. Mutism in Traumatic Brain Injury. 57. 524–528. et al. Varma... Luria. Tarbell.. Journal of Neurology. Paris: Mouton. When cognitive processes are absent or severely degraded. F. S. T. L. destruction. 1469–1475.. A. 342–353. van Putten. 124–126. (2001). M. 254–259.. P. Journal of the Neurological Sciences. (1999). and supplementary motor area causes impaired triggering of vocalization (Gelabert-Gonzalez and Fernandez-Villa. M. N. Zerr. R. and Posner. or chronic sign of damage. called temporary mutism followed by dysarthria (TMFD) (Orefice et al. Gold. Cinotti. Acta Neurologica Scandinavica. for example. et al. Transient muteness followed by dysarthria in patients with pontomesencephalic stroke. —John C. and Tavy. D. 44–58.. Scott. BIPLEDs in akinetic mutism caused by bilateral anterior cerebral artery infarction. R. Broussole. M. R. Kinney. Mutism Post Surgery.. Si¤ert et al. S. .. 48. 53.. Lees. J. 144. J. Relatively recently. (1997). including corticobasal degeneration. Poussaint. 41. and Psychiatry. as an early. 17. the frontal lobes and their connections to subcortical and brainstem structures are the most critical. Y. (2000).. L. (1999). and speech processes.. Neuropsychiatry. The prevalence of progressive supranuclear palsy (Steele-RichardsonOlszewski syndrome) in the UK.. Speech depends on myriad general and specific cognitive. B. speech does not occur. Morris. A. Benson. and Plum. N. (1994). G. and Strick. and Behavioral Neurology. A. Y.. D. R.. Posterior fossa syndrome. Wood. (2001). It is hypothesized that disruption of connections between the cerebellum. Mutism... 2000). (1989).. Adair. Von Cramon (1981) called it the ‘‘traumatic midbrain syndrome. K. D. 438–452. and Poser.. linguistic. and Yuan. Pollack. (2001). Gonzalez-Rothi. Journal of Neuro-Oncology. N. R.. J. A.. J.. Korein. is common. Pontomesencephalic stroke is one cause. (1998). I. Frontal lobes and language. Akinetic mutism: Disconnection of frontal-subcortical circuits. 367–378. but not inevitable. Fragassi.. S. and Fernandez-Villa. Motor areas of the medial wall: A review of their location and functional activation. J. 111–114.. 1999) or mutism and subsequent dysarthria syndrome (MSD) (Dunwoody. psychology and treatment. Neurological dysfunction associated with postoperative cerebellar mutism. Laurent. St. 75–81. S. 112. Mutism. (1990). N. Ben-Shlomo. Bazin. Diagnosis of stupor and coma. 37. Cohen. G. 124. Mega. Bakchine. Lebrun. cerebrovascular dementia.. Behavior in frontotemporal dementia. F. late. J. Nicolai. has been described.. S. Brain and Language. and Neary. 1966) and the syndrome of bilateral infarction of opercular motor cortex. A. D. A. H. C. and linguistic processes. and Goode. U. and management. J. F. and Stuss. 411–432. K. S. Neuropathological findings in the brain of Karen Ann Quinlan: The role of the thalamus in the persistent vegetative state. J. Jenkins. E. R. A. Louis: Mosby.. (2001). New England Journal of Medicine. M. Jacobs. Motor speech disorders: Substrates. N. and Grossi. Mutism may also occur after callosotomy (Sussman et al. Z. Philadelphia: Davis. Mutism after posterior fossa surgery: Review of the literature. British Journal of Neurosurgery. Rosenbek References Alexander. 103. Nath. Otto. Its occurrence in the late stages of these conditions is predictable. Adynamic aphasia: A transcortical motor aphasia with defective semantic strategy formation. 2001). H.. The role of arousal and ‘‘gating’’ systems in the neurology of impaired consciousness.. Y. D. di¤erential diagnosis. (1996). Alsago¤. 9. Lantsch. Blackshaw... A. Brain and Language. International Review of Neurobiology. J. L.. 1438–1449. H.. A. 804) within the pontomesencephalic area. B. thalamus.. 1983).. Gelabert-Gonzalez. Cognitive changes may hasten the mutism in some of these degenerative diseases. (1996).. M. L.. R. F. Picard. S. L.146 Part II: Speech Alzheimer’s disease and vascular dementia. C. F.. et al. I.. Plum. Neurology. therefore. C.. and Yuan.. Akinetic mutism as a classification criterion for the diagnosis of Creutzfeldt-Jakob disease. Y. So-called cerebellar mutism can result from posterior fossa surgery. LaValley. M. Riedmann. Moser. Dunwoody. Thomson. and most frequently and perhaps earliest in frontotemporal dementia (Bathgate et al. 656–691... 10.. T. Schi¤. It can also occur in other corticosubcortical degenerative diseases. M.. Lanzillo. based on the hierarchical organization of cognitive. (1970). Si¤ert. M. Neurosurgery. Du¤y.. 6. regardless of type. D.. The Hague. Impairments of attention after cingulotomy. Often mutism is followed by a period of whispered speech in this population. 161–163. Cerebral Cortex. J. 1726–1728. W. and Cohenour. 11.. (1997). 1997).. Castellano. perhaps because of damage to frontal lobe structures and the cingulate gyrus. However.. to these mechanisms. C. H. Cerebrovascular Diseases.. R. 103. Weidehaas. 2001). Nadeau. 64. M. Neuropsychology. R. Alsago¤.. D. J. and Heilman. Anarthric mutism can be present at onset and chronically in locked-in syndrome (Plum and Posner. 819–824. 374–393. P. 1997. J.’’ He speculated that the mechanism is ‘‘temporary inhibition of neural activity within the brain stem vocalization center’’ (p. (1997). W. and Wilkinson. Brain.. E. Mutism has been reported in Alzheimer’s disease. Panigrahy. B. (1995). Kaplan. Snowden. 21. Orefice. D. Mutism can occur after neurosurgery (Pollack. Mutism in Dementia. C. Mutism is frequent in traumatic brain injury. motor.. These processes are widely distributed in the nervous system.. P. a syndrome beginning with mutism and evolving to dysarthria. M. Clinical Neurophysiology. Clinical Neurology and Neurosurgery. London: Whurr. A. D. A. J.. J. Goumnerova..

lisping. and O’Connor. M. a lips-apart posture persists. Whitaker and H. ASHA. J. Gustafson. Davidson. J. C. Aram. Van der Nerwe. Stahl. Caccuri. Richardson. K. N. L. 57. p. Further Readings Bannur.. Archives of Neurology. Tumor type and size are high risk factors for the syndrome of ‘‘cerebellar’’ mutism and subsequent dysarthria. Orofacial myofunctional disorders are characterized by abnormal fronting of the tongue during speech or swallowing.. Linguistic performance in the short term following cerebral commissurotomy. McNeil (Ed. 66. A. D. For example. M. G. D. (1998). R. mouth. R. 98. 138–144.. The clinical and pathological spectrum of Steele-RichardsonOlszewski syndrome (progressive supranuclear palsy): A reappraisal. Neurology. Neurosurgery. 759–770. Passant. and Geschwind. Bravo. D. The clinical picture of frontotemporal dementia: Diagnosis and follow-up. P. excessive lip licking. E. Orofacial Myofunctional Disorders in Children Orofacial myology is the scientific and clinical knowledge related to the structure and function of the muscles of the mouth and face (orofacial muscles) (American Speech-Language-Hearing Association [ASHA]. 273–290. 1998). Brun. R. J. 22).. Lavenu. et al. Mutism as a consequence of callosotomy.. Turkstra. Archives of Physical Medicine and Rehabilitation. and grinding (Van Norman. The corticobasal degeneration syndrome overlaps progressive aphasia and frontotemporal dementia. New York: Academic Press. D. Videla. E... Dementia and Geriatric Cognitive Disorders. and Perez. H. L. 55. (1999).. Mulder. (2000). M. or when the tongue is at rest. Neurology. J. 697–698. 1993. Bilateral infarction in the territory of the anterior cerebral arteries. Orofacial myofunctional disorders may be due to a familial genetic pattern that determines the size of the mouth.. Journal of Neurosurgery. Bogen. the arrangement and number of teeth.. and Bayles. (1985). development. Cairns. and orthodontic intervention (Umberger and Van Reenen. N... I. A. With orofacial myofunctional disorders. Annual Review of Neuroscience. W. Post operative supplementary motor area syndrome: Clinical features and outcome. 22). 10. 416–418. M. Brain. Perspectives in neurolinguistics and psycholinguistics (vol.. Acquired mutism: Physiopathy and assessment. Speech and brain mechanisms. British Journal of Neurosurgery. Thumb sucking. L.). may change the shape of a child’s upper and lower jaw and teeth. de Bruin. 204–210. This exaggerated tongue fronting is also called a tongue thrust or a tongue thrust swallow and may contribute to malocclusion. 101. (1964). NJ: Princeton University Press. J.. which is a ‘‘lips-apart resting posture or the inability to achieve a lips-together resting posture without muscle strain’’ (ASHA. 19. 289– 317. (1984). 333–359. 14. requiring speech. The open-mouth breathing pattern may persist even after medical treatment for the blocked airway. A. D. Archives of Neurology. Catsman-Berrevoets. Pennybacker. In M. Archives of Neurology. H. 801–805. R. Acta Neurologica Scandinavica. Environmental factors such as allergies may also lead to orofacial myofunctional disorders.. ASHA defines an orofacial myofunctional disorder as ‘‘any pattern involving oral and/or orofacial musculature that interferes with normal growth. E. O. 199–208. Paz y Geuze. A.. E..). R. Transient opercular syndrome: A manifestation of uncontrolled epileptic activity. During normal development. Journal of Neurology. H. (1941). and Psychiatry. A. and Mimouni. and Lequin. Muteness of cerebellar origin. V.... 1993. Neurosurgery. 1993). 335–338. Akinetic mutism with an epidermoid cyst of III ventricle. and Lees.. and Olszewski. A. J. Rekate. H. A theoretical framework for the characterization of pathological speech sensorimotor control. for example. von Cramon. Akinetic mutism: A report of three cases. 755–757. 1368–1375. 59... Gur. E.. F. K. or face muscles (Hanson and Barrett. Kertesz. Ure.. R. Journal of Neurology. the tongue moves forward in an exaggerated way and may protrude between the upper and lower teeth during speech. C. F. R. (1999). 118. Pasquier. R. 10. Other environmental causes of orofacial myofunctional disorders may be excessive thumb or finger sucking. E. and Munoz. Paquier. In H. D. Journal of Neurology. A. (1997).. .. (1981). Gur. 64. et al. J. and Guillaume. Englund. 1983. R. C. 42. P.. A. or at rest.. (2000). an open mouth posture may result from blocked nasal airways due to allergies or enlarged tonsils and adenoids. 73. New York: Thieme. and Welch. U. Martinez-Lage. and Ratcheson.. or function of structures. 1997). Clinical management of sensorimotor speech disorders. 193–224). M. Penfield. or calls attention to itself ’’ (ASHA. Clinical and neuropathological criteria for frontotemporal dementia. Daniel. The supplementary motor area of the cerebral cortex. (2000). Traumatic mutism and the subsequent reorganization of speech functions. B. or both (Young and Vogel. Oldfield. A.. and Whitteridge.. Neary.. pp. Giudice. Anterior opercular cortex lesions cause dissociated lower cranial nerve palsies and anarthria but no aphasia: Foix-Chavney-Marie syndrome and ‘‘automatic voluntary dissociation’’ revisited. (1995). F. L.. P. Grubb. A. 439–444. J. (1959). Penfield. Damasio. p.. and Roberts. F. 147 Weller. 514–519. Mann. N. A. Whitaker (Eds. M. Brain. Ollari. 127–147. (1994). C. (1999). Faccio. M. J. S. the lips are slightly separated in children. W. J.. (1976). Van Dongen. dental.. Lebert. 52. C. With orofacial myofunctional disorders. The forward tongue posture typically diminishes as the child grows and matures.. U. (1951). Acta Neurologica Scandinavica. A tongue thrust type of swallow is normal for infants. (1992).Orofacial Myofunctional Disorders in Children Sussman.. Steele. V. L. Princeton. 2.. Orofacial myofunctional disorders may also be due to lip incompetence. Romero. 7. H. Neuropsychologia.. G. 1997.. 10–14. (1983). Hahn. M. The neural basis of language. Minagar. Progressive supranuclear palsy. 1988). tongue. J.. H. and the strength of the lip. 1989). S. 67. 886–888. W. B. and Rajshekhar. (1993). and David.. Van Norman. 240. and Psychiatry. D. 1995. F. swallowing. Shuper.. teeth clenching.

    Case history Review of medical/clinical health history and status (including any structural or neurological abnormalities) Observation of orofacial myofunctional patterns Instrumental diagnostic procedures Structural assessment. An orofacial myofunctional assessment is typically prompted by referral or a failed speech screening for a child older than 4 years of age. with a focus on speech correction as well as exercises to treat tongue posture and swallowing patterns. th for s. social. liquids. speech articulation testing. 1991). and l. Assessment is conducted to diagnose normal and abnormal parameters of oral myofunctional patterns (ASHA. p. A physician needs to verify that an airway obstruction is not causing the tongue thrust. may be causally related to orofacial myofunctional disorders. Paul-Brown and Clausen. 1989. The assessment information is used to develop appropriate treatment plans for individuals who The expected outcome of treatment is to improve or correct the patient’s orofacial myofunctional swallowing and speech patterns. including observation of the face. Nature of atypical oral-facial patterns and their relationship to speech. Oral myofunctional treatment is e¤ective in modifying tongue and lip posture and movement and in improving dental occlusion and a dental open bite or overbite (Christensen and Hanson. 2002). However. or lip incompetence that result from orofacial myofunctional disorders. 1997). A combination treatment approach. aerodynamic measures) Speech may be una¤ected by orofacial myofunctional disorders (Khinda and Grewal. development. Speech-language pathologists evaluate speech sound errors resulting from orofacial myofunctional disorders. 1997). Establishing normal swallowing patterns. including the following: 1. appears to be the optimal way to improve speech and tongue thrust (Umberger and Johnston. and j. 1997. teeth. Orofacial myofunctional treatment may be conducted concurrently with speech treatment. and facial appearance . Treatment strategies may include modification of handling and swallowing of solids. this kind of tongue pressure may interfere with the normal process of tooth eruption. 1991. may also need to be eliminated or reduced before speech and swallowing treatments are initiated. such as thumb and finger sucking or lip biting. hard palate. Some speech and swallowing treatment techniques include      Increasing awareness of mouth and facial muscles. dentition. a team of professionals. using interdisciplinary approaches 3. education. and the timing of treatment in relation to orthodontia. jaw. 1981. 1997). Pedrazzi. Typically. Van Norman. speech. lips. zh. 69). ch. The length of treatment varies according to the severity of the disorder. Completing an individualized oral muscle exercise program to improve muscle strength and coordination. Benkert. and saliva (ASHA. sh. The value of early treatment is emphasized in the literature (Pedrazzi. emotional.g. Before speech and swallowing treatment is initiated. 1997). medical treatment may be necessary if the airway is blocked due to enlarged tonsils and adenoids or allergies. as in ‘‘thun’’ for ‘‘sun’’) or sound distortions may occur. Lip exercises may be successful in treating an open-mouth posture (ASHA. An orthodontist may be involved when the tongue pressure interferes with alignment of the teeth and jaw. 92). speech disorders.g. and function 2. ASHA has identified the basic content areas to be covered in university curricula to promote competency in the assessment and treatment of orofacial myofunctional disorders (ASHA. Green and Green. The dentist focuses on the e¤ect of pressure of the tongue against the gums. Assessment should be based on orofacial myofunctional abilities and education. p. 1997. 1989). p. Treatment strategies may include alternation of tongue and lip resting postures and muscle retraining exercises (ASHA. 1999). soft palate.. orthodontist. Establishing normal speech articulation. d.148 Part II: Speech The severity of the problem depends on how long the habit is maintained. Sound substitutions (e. 69). 1999). tongue. including a dentist. speechlanguage pathologists need to have the appropriate training. and speech-language pathologist. airway competency. 1997. 1997. and dental occlusion. called speech misarticulations. p. and experience to practice in the area of orofacial myofunctional disorders (ASHA. The sounds most commonly a¤ected by orofacial myofunctional disorders include s. Excessive and persistent oral habits. Oral-facial-pharyngeal structure. is involved in the assessment and treatment of children with orofacial myofunctional disorders (Benkert. the age and maturity of the patient. An orofacial myofunctional assessment by a speech-language pathologist typically includes the following procedures (ASHA.. As with all other assessment and treatment processes. 1989. Speechlanguage pathologists assess and treat swallowing disorders. 1997. Interrelationships among oral-vegetative functions and adaptations. vocation. Typically 14–20 sessions or more may occur over a period of 3 months to a year (ASHA. n. and medical status. some speech sound errors. Increasing awareness of mouth and tongue postures. 54):   are identified with orofacial myofunctional disorders. A weak tongue tip may result in di‰culties producing the sounds t. health. as well as lip incompetence and swallowing disorders (ASHA. 1999. and pharynx Perceptual and instrumental measures to assess oral and nasal airway functions as they pertain to orofacial myofunctional patterns and/or speech production (e. physician. ASHA. z. 1997).

(1997). and orofacial myology. G. 92–94.. Green. M.Orofacial Myofunctional Disorders in Children 149 4. J. Chapko. J. 22. .. 213–222. July/August). and observation and participation in the evaluation and treatment of patients with orofacial myofunctional disorders 6. M. L. D. A. M. (2000). S.. International Journal of Orofacial Myology. D. M. Report: Ad hoc Committee on Labial-Lingual Posturing Function. (1995). M. (1997). and Perez. Romero. M. ASHA. language. J. 23. and Butcher. MD: Author. P. and Dassel.. 16... 22. 334–340. European Journal of Orthodontics. 83. Cayley. Electropalatographic and cephalometric assessment of tongue function in open and non-open bite subjects. R. 31. V. Australian Orthodontic Journal. Journal of Speech and Hearing Disorders. The e‰ciency of oral myofunctional and coarticulation therapy. P.. and Hanson. Thumb sucking management: A review. and orofacial myofunctional disorders. 7. (1999). International Journal of Orofacial Myology. P. 8. Rockville. 46. Khinda. E. Journal of Clinical Pediatric Dentistry. contributing. 10). M.asha. P. R. 41–45. The role of the speech-language pathologist in management of oral myofunctional disorders. (1983). A. 160–167. 207–210. and Green. Relationship of tonguethrust swallowing and anterior open bite with articulation disorders: A clinical study. A. American Speech-Language-Hearing Association. (1997). 25. Scope of practice in speech-language pathology. 35(Suppl. and Hanson. 1993). 14. Treating the open bite.. Christensen. W. Tongue thrust and the stability of overjet correction. (1981). P. (1998). MD: Author. and Barrett. Young. Rationale and procedures for assessment of oral myofunctional patterns. Van Norman. 92(2). An investigation of the e‰cacy of oral myofunctional therapy precursor to articulation therapy for pre-first grade children. Springfield. American Journal of Orthodontics. R. F. References American Speech-Language-Hearing Association. (2002). (1997). 463–474. The interrelationship of wind instrument technic. L. E. 39–44. A. and the International Association of Orofacial Myology (www. The tasks required include the following:          Understanding dentofacial patterns and applied physiology pertinent to orofacial myology Understanding factors causing.. G.iaom. R. IL: Charles C Thomas. W. American Speech-Language-Hearing Association.. (1993).. International Journal of Orofacial Myology. Journal of Speech and Hearing Disorders. Andrianopoulos. (1988). Tindall. 160–165. (1999). Bravo. N. and Hanson. November).. 14–33. and treatment recommendations. Shapiro. 17(2). G. A. Fundamentals of orofacial myology. Mouth breathing in allergic children: Its relationship to dentofacial development. 5). F. Cayley. Pedrazzi. R. Collaborative approach for identifying and treating speech. Paul-Brown. 23. Sampson. and Van Reenen. G. K. and Grewal. The use of cueing and positive practice in the treatment of tongue thrust Further Readings Alexander. ASHA. A. International Journal of Orofacial Myology. K. 2001) Further information on oral myofunction and oral myofunctional disorders is available from ASHA’s Special Interest Division on Speech Science and Orofacial Disorders (www. An investigation of the e‰cacy of oral myofunctional therapy as a precursor to articulation therapy for pre-first grade children. Sampson.. and Johnston. and Butcher. Preferred practice patterns for the profession of speech-language pathology. or related to orofacial myology Understanding basic orthodontic concepts Understanding interrelationships between speech and orofacial myofunctional disorders Demonstrating competence in comprehensive assessment procedures and in identifying factors a¤ecting prognosis Demonstrating competence in selecting an appropriate. American Speech-Language-Hearing Association. Digit sucking: A review of the literature. D. S. 23–33. The e¤ectiveness of orofacial myofunctional therapy in improving dental occlusion. 21. Rockville. (1999. criterion-based treatment plan Demonstrating a clinical environment appropriate to the provision of professional services Demonstrating appropriate documentation of all clinical services Demonstrating professional conduct within the scope of practice for speech-language pathology (ASHA. (2000). Genioglossis muscle electrical activity and associated arch dim changes in simple tongue thrust swallow pattern.. 33(Suppl.. 3–9. Umberger.. American Speech-Language-Hearing Association. L. 21–23. Orofacial myofunctional disorders: Knowledge and skills. V. 5–16. and Clausen. Angle Orthodontist. Relevant theories such as those involving oral-motor control and dental malocclusion 5. Alpha Omegan. A. individualized. K.. V. Journal of Indian Society of Pedodontia and Preventive Dentistry. H. 35–46. (1989. 73–77. 22. M. International Journal of Orofacial Myology. MD: Author. clinical observations. Umberger. Application of current instrumental technologies to document clinical processes and phenomena associated with orofacial myofunctional disorders 7. Bresolin.. L. S... (2001). (1983). M. Journal of Clinical Pediatric Dentistry.. Electropalatographic and cephalometric assessment of myofunctional therapy bite subjects. (1997). 57. Journal of Behavior Therapy and Experimental Psychiatry. 21.. S. Open bite due to lip sucking: A case report. American Speech-Language-Hearing Association. (1991). S. orthodontic treatment. M. Hanson. ASHA. A. (1997). 18–29. M. Code of ethics. 46. (1987). Shapiro.. R. Treatment options A Joint Committee of ASHA and the International Association of Orofacial Myology has also delineated the knowledge and skills needed to evaluate and treat persons with orofacial myofunctional disorders (ASHA. (1981). 121–135. and Sudha. —Diane Paul-Brown Benkert. Tindall. Journal of General Orthodontia. Rockville. M. and Vogel. 33–39.

1999). Tongue thrust and malocclusion. Hanson. Treatment for the young child. and Snow (2001) illustrates special symbols for intonation. (1995). 4–7. L. J. 2003). R. (1997). These symbols consist of capital letters to represent major sound classes. which are shown in a typical vowel quadrangle. R. 12(1). V. Descriptions and examples can be found in Ball. Kokubyo Gakkai Zasshi. Gommerman. G. and Andrianopoulos.150 Part II: Speech Dworkin. Relatively little attention has been paid to the transcription of vowels in children’s speech (see. 14. Shriberg and Kent. Pedrazzi. Correction of tongue-thrust swallowing habits. Some new computers now come equipped with ‘‘Unicode’’ phonetic symbols. 33–39. F. 14.. that is. as are numerous diacritics. Martin. (1985). (1993). International Journal of Orofacial Myology. and Sessle. The symbols that are most commonly used are those of the International Phonetic Alphabet (IPA). 21. 9–18. Their goal was to provide a di¤erent symbol for each unique sound. R. J. G. M. Hanson.g. Although extensive. Even less attention has been paid to the transcription of suprasegmentals or prosodic features. Examples of relevant IPA and extIPA symbols appear in Powell (2001). (1982). and Wertzner. E. S. Pierce. 8. 1973. 2001). some child/clinical phonologists have proposed additional symbols and diacritics (e.. B. E. L. Current issues in orofacial myology. The IPA has undergone several revisions since its inception but remains essentially unchanged. Orthodontic perspectives on orofacial myofunctional therapy. Wasson. 14(1). however. 17(2). as in [su]. Orofacial myofunctional disorders: Guidelines for assessment and treatment. F. 9– 22.. such as for denasalized and unaspirated sounds. training materials and phonetic fonts can be downloaded from the Internet. L. 22. L. Age and articulation characteristics: A survey of patient records on 100 patients referred for ‘‘tongue thrust therapy’’ January 1990–June 1996. 8. Journal of General Orthodontics.. Khinda.. 193–207. V. such as Ladefoged (2001) and Wells and House (1995). 45. (1999). manner of articulation. are listed separately. the elongated s is used for the voiceless palatoalveolar fricative. C. 29. 17(2). M.. M. 64. American Journal of Orthodontics.. When transcribing child or disordered speech. Phonetic Transcription of Children’s Speech Phonetic transcription entails using special symbols to create a precise written record of an individual’s speech. 2001. In addition. 32–33. K. M.. (1988).. 11(3). Nevia. Treating the open bite. J. N. R. International Journal of Orthodontics. 27–32. symbols for pulmonic consonants are organized according to place of articulation. an unidentifiable voiceless fricative can be transcribed with a capital F and a small under-ring for voicelessness (e. (1988). because [s] and [S ] are phonemically distinct in some languages. Tongue thrust: Attitudes and practices of speech pathologists and orthodontists. L. (1991). (1996). S. H. open-bite. 49–55.. Thus.. For example. Thus. Journal of the Indian Society of Pedodontics and Preventive Dentistry. E¤ects of oral myofunctional therapy on swallowing and sibilant production. M. International Journal of Oral Myology. B. E¤ects of form and function on swallowing and the developing dentition. and Peachey. Pierce. Hanson. Umberger. L. A study on improving tongue functions of open-bite children mixed dentition period: Modifications of a removable habit-breaker appliance and their sonographic analysis. as well as many diacritics. J. fast or slow speech). Stoel-Gammon. the IPA does not capture all of the variations that have been observed in children’s speech.. F. The most recent version of the complete IPA chart can be found in the Handbook of the International Phonetic Association (IPA. 8–19. Symbols for suprasegmentals. 27–29. It also includes symbols for transcribing connected speech (e. and voicing. Ladefoged. as in [Su]). 1999) as well as in a number of phonetics books (e. (1989). Mason.. 63–82. (1973). P.. G. Pollock and Berni. ‘‘cover symbols’’ may be used. such as labiodental and interdental plosives. and Tench (1996) and Powell (2001). first developed in the 1880s by European phoneticians. For this reason. such as [s] " for a dentalized [s].g.. Weld. In such cases. 33–39. and Cohen.. 277–282. M. International Journal of Orofacial Myology.g. Rahilly. The role of the cerebral cortex in swallowing. H. Dysphagia.. 1986. Small. modified with appropriate diacritics. it is sometimes impossible to identify the exact nature of a segment. (1988). International Journal of Orofacial Myology. such as English. they are represented di¤erently in the phonetic alphabet. 2001). and articulatory proficiency. . and Van Rennen. International Journal of Orofacial Myology.g. Edwards. J. 5–16. to differentiate it from the voiceless alveolar fricative. M. The extended IPA (extIPA) was adopted by the International Clinical Phonetics and Linguistics Association (ICPLA) Executive Committee in 1994 to assist in and standardize the transcription of atypical speech (e. International Journal of Orofacial Myology. L. are also provided. 22. Illustrations of the sounds of the IPA are available through various sources. The extIPA includes symbols for sounds that do not occur in ‘‘natural’’ languages. (2001). Relationship of tonguethrust swallowing and anterior open bite with articulation disorders: A clinical study. International Journal of Orofacial Myology. (1980). sequences of quiet speech.g. 1990). Bush et al. A protocol for oral myofunctional assessment: For application with children. and Culatta. and Grewel. Hanson. Saito. International Journal of Oral Myology. Journal of Clinical Orthodontics. M. Tongue strength: Its relationship to tongue thrusting. such as length and tone. Nonpulmonic consonants. 195–202. (1996). as are vowels. 68. to achieve a one-to-one correspondence between sound and symbol. and Hodge. M. S. In the familiar consonant chart. as well as ways to mark features such as silent articulation. Journal of Speech and Hearing Disorders. J. B. 5–13. such as clicks and ejectives. Duckworth et al.

which often include diacritics. between [p¼] and [b]. This could be frustrating for a child who is already making a subtle (but incorrect) contrast. 1991).g. free of distractions (see Stoel-Gammon. or distortions. Stoel-Gammon (2001) suggests using diacritics only when they provide additional information. A narrow transcription more accurately represents actual pronunciation. necessitating transcription of entire utterances. A broad transcription is generally adequate to capture error patterns that involve deletion. Errors were classified as substitutions. and only the substitutions were transcribed. For instance. as well as those that involve substitutions of one sound class for another. using minimal pairs such as pea and bee. and it should take place in a quiet environment. If a speech-language pathologist is going to expend the time and energy necessary to complete a phonological analysis that is maximally useful. The clinician might then decide to work on initial voicing. Although this makes the transcription process more e‰cient..) To facilitate whole word transcription. Stoel-Gammon (2001) suggests measuring agreement of features (place or manner) rather than identity of segments. For example. 1986). Shriberg and Kwiatkowski. [p¼]. Moreover.. although impractical in some settings. Khan and Lewis. unreleased final stops). /trvk/) ahead of time and modifying them ‘‘on line’’ for a tentative live transcription that can be verified or refined by reviewing a tape of the session. as in [p h aI ] for pie. the transcription on which it is based must be as accurate and reliable as possible. a narrow transcription is crucial. (In fact. Such stops can easily be mistaken for the corresponding voiced stops and erroneously transcribed as [b]. Ideally. Therefore. 1980. such as Hodson (1980) and Louko and Edwards (2001). the testing session should be audio. if a vowel is nasalized in the absence of a nasal consonant. if a child fails to aspirate initial voiceless stops. for example. and [bi ] (bean). If no detail is included in a transcription. recommend writing out broad transcriptions of target words (e. basic IPA symbols are su‰cient for some clinical purposes.or video-recorded on high-quality tapes and using the best equipment available. [t¼]. 2001). and so on. How narrow a transcription needs to be in any given situation depends on factors such as the purpose of the transcription. is an excellent way to derive a transcription and to sharpen one’s skills. if a client’s consonant repertoire is a subset of the standard inventory. the unaspirated stops should be transcribed with the appropriate (extIPA) diacritic (e. [d]. Unless the vowels are transcribed narrowly. such as final consonant deletion or cluster reduction. as in [p¼i] for pea). vowel lengthening (if voiced obstruents are deleted) or nasalization (if nasal consonants are deleted). as in /paI/ or /tElPfon/.g. Sometimes it is desirable to assess the reliability of a transcription. omissions. Phonetic transcription became increasingly important for speech-language pathologists with the widespread acceptance of phonological assessment procedures in the 1980s and 1990s. the skill of the transcriber. however. Alternative methods of assessing transcription agreement may sometimes be appropriate. 1984). 1996.. most phonological assessment procedures require whole word transcription (e. Shriberg and Lof. the analyst may miss important distinctions. the transcriber relistens to a portion of the sample at some later time and compares the two transcriptions on a soundby-sound basis. with aspiration on the initial voiceless stop. are customarily written in slashes (virgules). Goldman and Fristoe. whether correct or incorrect. or if inappropriate nasalization is observed. determining a percent of ‘‘point-topoint’’ agreement. In order to describe patterns in children’s speech. 1969) did not require much transcription. This involves two or more people transcribing a sample at the same time. such as assimilation (as in [gvk] for truck). Louko and Edwards (2001) provide suggestions for counteracting the negative e¤ects of such expectation.. then listening together to resolve disagreements. for example. One way to enhance the accuracy of a transcription is to transcribe with a partner or to find a colleague who is willing to provide input on di‰cult items. Traditional articulation tests (e. For instance. or a young child’s rendition of star as [t¼aU ] or fish as [FIs]. To give another example.g. However. it can also lead the transcriber to mishear sounds or to ‘‘hear’’ sounds that are not there (Oller and Eilers. The same procedure may be used for determining interjudge reliability. and the amount of time available. As Powell (2001) points out. for instance. which capture only the basic segments. it is advisable to do some transcribing on-line.g. a child who is deleting final consonants may retain some features of the deleted consonants as ‘‘marking’’ on the preceding vowel. Reliability rates for children’s speech vary greatly. such as between [bi] ~ (beet). Because some sounds are di‰cult to transcribe accurately from an audiotape (e. use continuous speech samples. 1975). and Ho¤man.g. the analyst may miss potentially important aspects of the production. as in the preceding example. 1980. Kwiatkowski. the nasalization would not need to be transcribed. such as gliding of liquids or stopping of fricatives. in assessing the phonetic inventories of young children. if a vowel is nasalized preceding a nasal consonant.. People who spend long hours transcribing children’s speech often look forward to the day when accurate . depending on factors such as the type of sample (connected speech or single words) and how narrow the transcription is. Hodson. For intrajudge reliability. so that phonological processes involving more than one segment. with reliability rates being higher for broad transcription (see Cucchiarini. some clinical phonologists.Phonetic Transcription of Children’s Speech 151 Broad or ‘‘phonemic’’ transcriptions. [bi:] (bead ). are written in square brackets. except that a second listener’s judgments are compared with those of the first transcriber. ‘‘Transcription by consensus’’ (Shriberg. it is necessary to transcribe their errors. not when they represent adultlike use of sounds. working independently. can be more easily discerned. ‘‘Narrow’’ or ‘‘close’’ transcriptions. no narrow transcription was involved.

In T. Rahilly. J. S. M. H. Ball.). and Kent. Shriberg. L. 53–73.. and Ball. Small. J. 42–52.. (1987).... J. Stanford University. L. J.. L. Louko. UK: Cambridge University Press. (1993). Therefore.. M. Oller. and House. D. 10. 20.. (Eds. Bronstein. Edwards. L. 95–98. Luckau. (1993). M. H. L. IL: Interstate Printers and Publishers. Boston: Allyn and Bacon. The extIPA chart. Goldman. Shriberg. 131–155. C. I. A. Ball. C. Snow. On specifying a system for transcribing consonants in child language. Topics in Language Disorders. Macken. 24. Code.. New Orleans. Stoel. Collecting and transcribing speech samples: Enhancing phonological analysis. London: Whurr.). A procedure for phonetic transcription by consensus.. Further Readings Amorosa. (1994). Although computer programs may be developed to make transcription more objective and time-e‰cient. UK: Blackwell. (1999). Cucchiarini. Principles of phonetics. A. M. W. MN: American Guidance Service. Topics in Language Disorders. and Hutton. 281–287. and Berni. (2003). Journal of the International Phonetic Association. (1996). 1–11.. Conference papers on American English and the International Phonetic Alphabet. J.). Suprasegmentals. J.. Louko. 21(4). Journal of Communication Disorders. H. Journal of Speech and Hearing Research..). LA: ICPLA. UK: Blackwell. (1996). (2001). and Tench. and Lewis. London: Department of Phonetics and Linguistics. (1994). University College London. L. 27. Natural process analysis. Phonetica. 21. Non-segmental aspects of disordered speech: Developments in transcription. 21(4). Clinical Linguistics and Phonetics. P. AL: University of Alabama Press. J. M. (1991). San Diego. J. The sounds of the International Phonetic Alphabet. I. and Harding. Pathologies of speech and language: Contributions of clinical phonetics and linguistics (pp. Laver. Needham Heights. Transcribing phonetic detail in the speech of unintelligible children: A comparison of procedures. and Peterson. 35–38. (2001). (2001).. K.. Ladefoged.. R. (1996). (1996). computer transcription will become a reality. Topics in Language Disorders. L. G. Powell (Ed. Wells. —Mary Louise Edwards References Ball. I. 5. Characteristics of atypical speech currently not included in the Extension to the IPA. (1986). P.. (1994). D. D. (1984). MN: American Guidance Service. Clinical Linguistics and Phonetics. Allen. M. San Francisco: Carousel House. and Hazelett. MA: Allyn and Bacon.).. New York: Wiley. 157–161. Oxford. Cambridge. C.). A. P. Applied Phonetics: The Sounds of American English (2nd ed. D. J. Acoustic and auditory phonetics. Vowels and consonants: An introduction to the sounds of languages. Edwards. and Keck. and Edwards. Cambridge. M. U. J. J. Phonetics: A practical guide for students. J. J. CA: Singular Publishing Group. Extensions to the International Phonetic Alphabet for the transcription of atypical speech. M.. British Journal of Disorders of Communication. N. von Benda. 21(4). Introduction to applied phonetics: Laboratory workbook. A course in phonetics (4th ed. UK: Cambridge University Press. Reliability studies in broad and narrow phonetic transcription. Vieregge. Stanford. J. 225–279. Circle Pines. C. Khan. Duckworth. 21. D. E. M. (1990). J. M. Topics in Language Disorders. S. 288–304. Ladefoged.. L. Khan-Lewis phonological analysis. 8. CA. Shriberg. Ladefoged. A note on describing types of nasality. L. K. Hodson. and Kwiatkowski. Clinical phonetics (3rd ed. Kwiatkowski. and Eilers. Brown. Issues in collecting and transcribing speech samples.. 24. 10. Stoel-Gammon.). (1991). Bernhardt. (1980). and Fristoe. J. G. and Edwards. Clinical Linguistics and Phonetics. A.. TX: Harcourt College Publishers. Hardcastle. Journal of the International Phonetic Association. Clinical Linguistics and Phonetics. Assessing transcription agreement: Methodological aspects. Oxford. 21. Committee on Linguistics. L. Ball. The phonetic transcription of disordered speech. W. and Thoonen. K. (2001). M. 456–465. M. D. (1985). Phonetics: The science of speech production (2nd ed. Maassen. J. L. The Assessment of Phonological Processes. D. G.. MA: Allyn and Bacon. W. Unpublished manuscript. C. Clinical Linguistics and Phonetics.152 Part II: Speech Shriberg.. O¤erninga. C. M. 67–83. 273–280. B. Lehiste. Needham Heights. A. Phonetic expectation and transcription validity. (1999). (1970).. Boston: Little. and Lof. and Maddieson. Transcription of vowels. Phonetics for children’s misarticulations. M. D. MA: MIT Press. Mackay. speechlanguage pathologists will continue to engage in the transcription process because of what can be learned through carefully listening to and trying to capture the subtleties of a person’s speech. (2001). L. Compton. Tuscaloosa. San Diego.. Rahilly. Powell. Phonetic transcription of disordered speech. L.). (1986). 12–21. R. Bush. J. Topics in Language Disorders. (1975). (1997). (Ed. M. Recent developments in the transcription of non-normal speech. T. Danville.. Transcription of pathological speech in children by means of extIPA: Agreement and relevance. B. CA: Singular Publishing Group. (1997). L. 37–43). P. 31. Goldman-Fristoe Test of Articulation. D. (2001). Transcription of suprasegmentals... J. 4. Circle Pines. 22–41. The sounds of the world’s languages. Handbook of the International Phonetic Association: A guide to the use of the International Phonetic Alphabet. M. (1980). and Ball. Pollock. Johnson. E. R. (1996). (2001). 23. UK: Blackwell... International Clinical Phonetics and Linguistics Association Executive Committee. (1969). P. and Ho¤man. (1995). . (1980). Grunwell. M. J. (1973). phonetic transcription is likely to remain an essential skill for anyone engaged in assessing and remediating speech sound disorders.. International Phonetic Association. (1988). Fort Worth. 59–78. Phonetics for speech pathology (2nd ed. Edwards.. K. Cambridge. Topics in Language Disorders. N. B.. (2001). Transcribing the speech of young children. T. Oxford.

Bird.html SIL International home page http://www. some examiners might view them as equal.html http://www. (1996). (1999).. however. 1980) and that phonological awareness can be enhanced by direct instruction (see Blachman et al. Severity Considerations.utoronto. Chicago: University of Illinois Press. Shriberg. Pathologies of speech and language: Advances in clinical phonetics and linguistics (pp. Groenen (Eds..arts. have reported that phonological impairments alone do not have as great an impact on literacy as language impairments do. and Trost-Ste¤en. A growing body of evidence indicates that young children with severe EPI go on to experience problems in literacy. Excercises in phonetic transcription: A programmed workbook (2nd If. Typically such children produce final morphemes as they learn the phonological pattern of word-final consonants.sil. as well as phonological awareness. if two children have 16 errors on the same test. who tested children first in kindergarten and again 1 year later. ExtIPA transcriptions of consonants and vowels spoken by dyspractic children: Agreement and validity. and McFadden (1998) provided classroombased phonological awareness treatment (15 minutes twice a week) to 16 children with speech and/or language disorders (8 in a preschool class and 8 in a prekindergarten class).uk/IPA/ipa. . Bishop. A. Woburn. W. Although there have been numerous studies reporting the results of phonological awareness treatment. and writing.. http://hctv. in fact.arts. E. Bishop and Adams.gla. A fourth term. and Maassen. London: Whurr. 153 are children with expressive phonological impairments (EPIs) (Webster and Plante. includes phonological production. Clarke-Klein and Hodson (1995) obtained similar results for spelling. C. K. and ultimately literacy.g. with multisyllabic words) than their peers with typical reading abilities (Catts. one child evidences a lisp for all sibilants and the other has 16 omissions. found that expressive phonology (measured by a multisyllabic word and nonword production task) and phonological awareness scores in kindergarten accounted for significant amounts of variance in first-grade reading. have a severe phonological impairment with intact receptive language abilities...). 1994). whereas phonological awareness includes syllables and intrasyllabic units (onset and rime).html Phonological Awareness Intervention for Children with Expressive Phonological Impairments Phonological awareness refers to an individual’s awareness of the sound structure of a language. These three terms are generally considered comparable in meaning. word retrieval. Phonological results from another line of research indicate that individuals with reading disabilities evidence more phonological production di‰culties (e. however. A possible explanation for this discrepancy may be the level of EPI severity in the participants in their studies. W. the impact on intelligibility will be vastly di¤erent. The small-group sessions focused on rhyming during the first semester and on phoneme On-line Resources International Phonetic Association (IPA) home page http://www2. (1989). L. verbal working memory. R. Pullum. P. Hinke. As well. Results from a number of studies indicate that phonological awareness skills are highly correlated with reading success (see Stanovich. Relationship Between Expressive Phonological Impairment (EPI) and Phonological Awareness. and Freeman (1995) found that the children who had severe EPI experienced greater di‰culty with phonological awareness tasks than their ability-matched peers. Clinical Linguistics and Phonetics.chass. Larivee and Catts (1999). Gillam.html http://www. Not all speech sound errors are equal. and Ladusaw. G. refers only to phonemes. 171–189. Some scientists prefer using the terms phonological sensitivity or metaphonology rather than phonological awareness. phonemic Awareness Intervention for Children with Expressive Phonological Impairments Paden. the child with extensive omissions might be identified as having a language impairment because of the omission of final consonants (which would a¤ect the production of word-final morphemes on an expressive language measure).). B.gla. Phonological Awareness Treatment Studies for Children with VowelsandConsonants IPA Fonts http://www2. A procedure to select and train persons for narrow phonetic transcription by consensus. 1990. The Phonetic Representation of Disordered Speech: Final report.g. except that metaphonology implies that the awareness is at a more conscious level.. For example. Some highly unintelligible children who are considered to have a language impairment may. 1992). 1993).humnet. A common practice in the articulation/phonology literature is to report the number of errors on an articulation test. Among the individuals who have been identified most consistently as being ‘‘at risk’’ for failure to develop appropriate phonological awareness skills. spelling. 275–284). London: King’s Fund. In B.).org IPA learning materials http://www2.. PRDS.sil. only a few investigators have focused on children with phonological or language impairments. Several investigators (e. however.arts. (1987). even when the tasks did not require a verbal response. (1983). the most encompassing of these related terms. Maassen and P. Phonetic symbol guide (2nd ed. 1986). MA: Butterworth-Heinemann. Vieregge.ucla. van Kleeck.

Twenty-three children participated in an experimental ‘‘integrated’’ treatment program. however. Children are taught to represent the sounds in one. Moreover. and voicing aspects of the sounds in their phonological system.g. and the other consisted of 30 phonologically normal children. and one targeted final consonants. Single subject case study results indicated that the children improved on both phonological production and phonological awareness tasks (sentence and phoneme segmentation).g. using Elkonin cards (Ball and Blachman. medial. and Halle (1999) provided individual treatment to four preschool children with EPI for 6–9 months that focused on both feature awareness and production for three phonological patterns that the children lacked. 1963). The bottom half has the appropriate number of boxes for the phonemes needed for the word. The children in the first group did not receive direct production treatment for EPI during the course of the study. In phase 2. Two additional groups served as controls. Initially blank tiles or blocks are used. children progress from the concept/sound (not speech) level to the phoneme level to the word level. up). manner. The results of this investigation lend support to the contention that it is important to incorporate phonological awareness tasks into treatment sessions for children with EPI. Children in the treatment groups. Children are taught to say each word slowly and to move one manipulative for each sound into the boxes from left to right. Both of the children targeting velars also evidenced concomitant gains in production and awareness. and sometimes medial sounds. For the remaining targets. which was based on a ‘‘Whole Language’’ model. there was a slight tendency for the two variables (phonological awareness and production) to move in similar directions. a). or three-phoneme (e.. Harbers. Three targeted strident singletons.g. two targeted velars. Blending tasks com- ... The investigators used a combination of the Metaphon (Howell and Dean. Minimal pairs are used extensively during phase 1. All of the children continued participating in their regular classroom literacy instruction. Activities included (a) picture Bingo and oddity games for rhyme awareness. The top half of the paper has a picture of a word. Typically the child is given four pictures and is to identify the one that does not match the others in some aspect (e.. Learning to blend phonological segments to make words is another important task and one that is extremely di‰cult for some children. The phonological awareness treatment focused on the development of skills at the phonemic level and integrated phonological awareness activities with grapheme-phoneme correspondence training. 1991. or final position). 1991) treatment approaches.g. the progression is from word level to sentence level.g. (c) phoneme segmentation. (b) identification of initial and final sounds. Gillon (2000) conducted a phonological awareness treatment study in New Zealand that involved 91 children with ‘‘spoken language impairment’’ between the ages of 5 and 7 years. 1998) has a component that specifically addresses teaching the articulatory characteristics of phonemes to all children with reading disabilities. Information on changes in expressive phonology or language was not provided by the investigators. One treatment group of 15 children who received ‘‘minimal’’ intervention. when children learn about where a sound is located in a word (initial.. but inconsistencies occurred. (d) phoneme blending. cat) words by using manipulatives. Improvement in the production of /s/ clusters coincided with gains in recognizing /s/ cluster features for two of the four children targeting /s/ clusters. Howell and Dean (1994) used their Metaphon program to provide both phonological awareness and production treatment for 13 preschool children with EPI in Scotland. This task requires matching and oddity awareness skills.’’ Categorization also is used for individual sounds (e.. rhyme) and thus is the ‘‘odd one out. In phase 1 of this program. The second group participated in phonemeoriented sessions for the same amount of time. All four children targeted /s/ clusters. When children are taught how a sound is produced and how it feels. however. Another phonological awareness activity that is widely used both for assessment and for segmentation practice is categorization. adapted from Elkonin. many activities that are commonly used in treatment sessions have phonological awareness components. they develop awareness about word positions. The children attended between 11 and 34 30-minute sessions weekly. and (e) linking speech to print. the children also made greater gains in phonological production than children in the other groups with EPI.154 Part II: Speech awareness during the second semester. Tiles with graphemes are incorporated after the child demonstrates recognition of the sounds for the letters.(e. Additional stimulus items for children’s individual speech sound errors were integrated into some of the activities.g. even when there are no phonological production problems. Available tasks range in di‰culty from simple ‘‘yes-no’’ judgments regarding whether two words rhyme to complex phonological manipulation activities (e. they develop awareness about place.(e. two targeted liquids. Paden. Children in the first treatment group received two 60-minute sessions per week until a total of 20 hours of intervention had been completed. Moreover. made markedly greater gains on phonemic awareness tasks than children in the nontreatment group. One phonological awareness activity that has proved to be particularly e¤ective is the ‘‘Say-It-And-Move-It’’ task. Moreover. 1994) and Cycles (Hodson and Paden. A second group of 23 children received traditional speechsound treatment. Enhancing Phonological Awareness Skills. The children in this group made significantly greater gains in phonological awareness and reading scores than the children in the other groups. two. initial consonants). The treatment groups and a nontreatment comparison group all made substantial gains in rhyming. pig Latin. One phonological awareness treatment program (Lindamood and Lindamood. spoonerisms).

E. L. I. T. 6. H. Educational psychology in the USSR (pp. (1995). 176–182. and body and coda. B.). Phonemic awareness in young children: A classroom curriculum.). American Journal of Speech-Language Pathology. H. D. 839–849. and speech (LiPS). N. 504–508. and Tangel. and Freeman... Foorman. W. 446–462. Simon (Eds. Language and reading disabilities. (Ed. Webster. Howell. take away /t/ from note/.. H. KS. and McFadden. —Barbara Hodson and Kathy Strattman References Ball. and Dunham. E. Gillon. C. H.. Clarke-Klein. M. Wichita. 49–66. (1998). leaving no). (Eds. American Journal of Speech-Language Pathology. B. 23. Simon and J. and reading. Phonological manipulation in ‘‘pattern’’ songs (e. Does phoneme awareness training in kindergarten make a di¤erence in early word recognition and developmental spelling? Reading Research Quarterly. Language. and Adams. B. (2001). Brookes. 6. P. Strattman.g.. and Blachman.. Larrivee. 7. Toward an interactive compensatory model of individual di¤erences in the development of reading fluency. (1998). Predictors of second graders’ reading and spelling scores. M. Bishop. B..g. P. and Hearing Services in Schools. (1963). S.. Speech. (1999). G. enhancing phonological awareness skills appears to serve a dual purpose for children with expressive phonological impairments.). Harbers. J. Ball. and reading retardation. Hodson. A. G. 30. Rosner.g. B. Badian. (1994).. Lundberg. (1995). R. Early reading achievement in children with expressive phonological disorders. M. ‘‘Apples and Bananas’’) seems to be an extremely enjoyable task for very young children and can help them be more aware of sounds and word structures. (1986). 165–179). W. and Hearing Services in Schools. Austin. E. Baltimore: Paul H. and Simon. and Dean. A study of classroom-based phonological awareness training for preschoolers with speech and/or language disorders. E¤ects of phonological impairment on word.. 31. Bishop. (2000)... (1991). In B. A. London: Whurr. Blachman.g. can plus dee. (1993). and phoneme segmentation and reading. . (2001). 50–60. Journal of Speech and Hearing Research. Kindergarten teachers develop phonemic awareness in low-income. MA: Allyn and Bacon. 126–141.. Journal of Learning Disabilities. Moreover. Austin. 32–71. Journal of Child Psychology and Psychiatry. 216–226. 384–392. Wichita State University. The auditory analysis test. elision task.g. 4. Speech. Not all phonemes are created equal: The e¤ects of linguistic manipulations on phonological awareness tasks. C. B.. H. Ball. V. and Tangle. T. 65–76. (1998).. D. D. Catts. (1990). Rosner and Simon. TX: Pro-Ed.. (1971). Chafouleas.. V. 1–18. Treating phonological disorders in children (2nd ed. (1991). The child says the word (e. Speech. H. J. Thus. S.). (Ed. and Kamhi. Implications for Best Practices. Elkonin.. Language. and Hodson. 38. onset and rime. D. and Plante. Journal of Psychoeducational Assessment.. and Olsen. K. ice plus cream) followed by blending syllables (e. (1993). R. Catts. A phonologically based analysis of misspellings by third graders with disordered-phonology histories. Paden. after part of the word is removed (e. Mahwah. (2000). says the new word (cow). Road to the code.. J. 16. T. A. H. P. cowboy). and Beeler. W. Prediction and prevention of reading failure. as shee plus p) should precede blending individual phonemes (e. 31.. Further Readings Adams. it seems prudent to incorporate activities to enhance phonological awareness skills while they are receiving treatment for phonological production. (1999). E.. NJ: Erlbaum. D. Children who are most successful performing phoneme manipulation tasks such as spoonerisms typically are the best decoders (Strattman.. it is important to begin with the larger segments (e. syllable. (1992). Black..g... E. Bird. Targeting intelligible speech (2nd ed.. M. and Catts. The psychology of mastering the elements of reading.. R.). R. and Paden. After a child demonstrates success at the larger unit levels. B.. 1027–1050.. IL: LinguiSystems. Phonological awareness and literacy development in children with expressive phonological impairments. Another task that has been found to be highly correlated with success in reading is deletion (e. Unpublished doctoral dissertation. Blachman. 19. Needham Heights. Foundations of reading acquisition and dyslexia. VanAuken. Journal of Speech and Hearing Research. Brookes. U. Baltimore: York Press. B. (1994). van Kleeck.. A prospective study of the relationship between specific language impairment. (1980). Gillam. individual phonemes are deleted (e. Phonological awareness and production: Changes during intervention. and Hearing Services in Schools. 118–128. sh plus ee plus p). Because children with EPI appear to be at risk for the development of normal reading and writing skills even after they no longer have intelligibility issues. Does it make a di¤erence? Reading and Writing: An Interdisciplinary Journal. phonological disorders. Language. M. Catts. As with blending. 8. Blending intrasyllabic units (e. K. compound words).g. Blachman. D. (1999). London: Routledge. S.. Baltimore: Paul H. The Lindamood Phoneme Sequencing program for reading.. E. J. 38. 948–958. Speech production/phonological deficits in reading-disordered children. Stanovich.g. W. The task that consistently has accounted for the greatest amount of variance in predicting decoding success is manipulation. as sh plus eep. T.g. W. P. and Lindamood. Journal of Speech and Hearing Research. results from Gillon’s (2000) study indicate that enhancing phonological awareness skills leads to improvement in phonological production. Lindamood. The relationship between speech-language impairments and reading disabilities. T. B.. Sounds abound: Listening. E.).g. 1971). 2001). Catts. and Halle.. 26. candy). K. East Moline.Phonological Awareness Intervention for Children with Expressive Phonological Impairments 155 monly start at the word level with compound words (e. (1997). D.. Reading Research Quarterly. J. and then. 19. inner-city classrooms. rhyming. Black. boy).. The e‰cacy of phonological awareness intervention for children with spoken language impairment. Journal of Learning Disabilities. TX: Pro-Ed. spelling. (2000)..

The residual errors of the first group are thought to reflect environmental influences. the expected developmental period for speech sound acquisition ends at approximately 9 years of age.. Progress in understanding reading. while nonenvironmental causal factors such as genetic transmission are thought to be responsible for the phonological errors of the second group. Shriberg. From phonology to metaphonology: Issues. Sound linkage: An integrated programme for overcoming reading di‰culties. thus encompassing birth through the early school years. (2000). 1997). Ohde and Sharf (1992) provide excellent descriptions of the acoustic and physiologic parameters of common distortion errors. B. Generally. Some productions were judged to be minor distortions.. (2000). Identification and intervention. J. such productions are either permanent or temporary manifestations of inappropriate allophonic representation and/or the sensorimotor control of articulatory accuracy. Smit et al. E. O. 1998). The sounds abound program. Development of phonological sensitivity in 2. 1980. Clinical distortions are potential targets for treatment and have been categorized by prevalence into common and uncommon types. 5-year-old children. J. and intervention [special issue]. New York: Guilford Press. Shriberg and Kwiatkowski. fluency. The most common and uncommon types are listed in Figure 1. (2002). Children’s speech and literacy di‰culties: Vol.. C. Hatcher. (2001). C. Stanovich. individuals in whom a speech delay was diagnosed at some time during the developmental period and those who were not so diagnosed). Individuals with residual errors can be further classified into subgroups of those with a history of speech delay and those without a history of speech delay (i. London: Whurr. Some individuals with developmental phonological disorders acquire normal speech. Washington. Burns. and Wells. assessing. It has been hypothesized that distortions reflect incorrect allophonic rules or sensorimotor processing limitations. East Moline. 429–444. (1998). Sound e¤ects: Activities for developing phonological awareness. Anthony.156 Part II: Speech Cunningham. however. despite having received treatment for the phonological disorder (Shriberg et al. Preventing reading di‰culties in young children. Explicit vs. Dyslexia. or psychosocial processes (Bernthal and Bankson. B. P. B. Lonigan.). Residual Shriberg (1994) has conceptualized developmental phonological disorders as speech disorders that originate during the developmental period. Spector. P. Mahwah.. (1994). M. (Eds. (2001). /l/. while others were designated as clinically significant. A basic guide to understanding. Hulme. Stackhouse.. 1993) of the expected allophones of a particular phoneme.). B.). That is. and a¤ricates. and Wells. (1999). Moats. and Joshi. It is postulated that the two groups di¤er with respect to causal factors. Journal of Experimental Child Psychology. NJ: Erlbaum. J. M... 1990. 23. It has been suggested that children initially delete and substitute sounds and then produce distortions of sounds such as /r/. Children’s speech and literacy di‰culties: A psycholinguistic framework. Reading and spelling: Development and disorders. 1998). Burgess. In sum. Shriberg (1993) also noted such di¤erences in his study of children with developmental phonological disorders. Baltimore: Paul H. DC: National Academy Press. (Ed. Speech to print. L. (1990). 1988). 2. Hodson... assessment. fricatives. J. IL: LinguiSystems. and Gri‰n. C. (1990) conducted a large-scale investigation of speech sound acquisition and reported that the distortion errors noted in the speech of their older test subjects varied with respect to judged clinical impact or severity. B. (1998).. London: Whurr. Stackhouse. Timonium. 14. implicit instruction in phonological awareness. 1997). and Podhajski. WI: Thinking Publications. (1998). Brookes. Torgesen. Nonclinical distortions are thought to reflect dialect or other factors such as speechmotor constraints and are not targeted for therapy. 90. residual errors constitute . 1994). Distortions are variant productions that do not fall within the perceptual boundaries of a specific target phoneme (Danilo¤. Seminars in Speech and Language. The most common residual errors include distortions of the sound classes of liquids. while others continue to exhibit a phonological disorder throughout the life span. Lencher. T. 294–311. Children with developmental phonological disorders are heterogeneous and exhibit a range in the severity of their phonological disorders. (1994).). Topics in Language Disorders. (Ed. cognitive-linguistic functions. Snow. 1998). M. Most residual errors have been identified as distortions (Smit et al.. it is posited that children who exhibit phonological disorders di¤er with regard to the etiology and severity of the disorder and include both preschool and school-age children (Deputy and Weston. and the brain. but causal origins may be related to genetic or environmental di¤erences (Shriberg. TX: Pro-Ed. In most cases the cause of such disorders cannot be attributed to significant involvement of a child’s speech or hearing processes. and Stephens.. (1997). K.e. In most cases. and teaching phonological awareness. Journal of Educational Psychology. C. J. and Pascoe. A. Wells.).. (Eds. 1994. Stackhouse. (1998). 27–42. Bernthal and Bankson. MD: York Press. Phonological Errors. Wolf. R. London: Whurr.. Residual phonological errors are a subtype of developmental phonological disorders that persist beyond the expected period of speech-sound development or normalization (Shriberg. They are present in the speech of older school-age children and adults. Austin. (2000). investigative study has not supported this hypothesis as a generality in children who normalize their phonological skills with treatment (Shriberg and Kwiatkowski. and Mathes. 50. From phonological therapy to phonological awareness.. and Barker. Eau Claire. P. He classified the errors into nonclinical and clinical distortion types. S. and /s/ when normalizing sound production. Uncommon distortion errors include errors such as weak or imprecise consonant production and di‰culty maintaining nasal and voicing features. (Eds.

L. Ruscello. K. Boston: Allyn and Bacon.Phonological Errors. and Toth (1995) identified two older children with residual /r/ errors who had received traditional long-term phonological treatment without success. E¤ect of lisping on audience evaluation of male speakers. A. Language. R... Wilcox. but research indicates that normal speakers react negatively to persons with even minor residual errors (Mowrer.. N. 347–363. and Doolan. Ruscello. and Weston. Bernthal. Baltimore: Williams and Wilkins. Ruscello. and Crampin. W. Hardcastle. 36. Shuster. (1998). 1998). (1993). Mowrer. J. (2000). specially designed treatments are necessary to facilitate remediation of residual errors. D. residual errors are minor in terms of severity and do not interfere with intelligibility. Phonology: Assessment and intervention applications in speech pathology. Lateralization of voiced/voiceless sibilant fricatives or a¤ricates 4. In summary. R. Four new speech and prosody-voice measures for genetics research and other studies in developmental phonological disorders. D. Language. N. M. but normal speakers do react negatively to such minor speech variations. J. A framework for di¤erential diagnosis of developmental phonologic disorders. J. Widening access to electropalatography for children with persistent sound system disorders. (1995a). 334–339. Deputy. and Toth. Ruscello (Eds. J. (1994). Di¤erent forms of sensory information other than auditory input have been provided to assist the individual in developing appropriate target productions. M. The actual number of clients in the respective categories is unknown. D. Ruscello by Shriberg (1993). D. —Dennis M. Journal of Speech and Hearing Research. Articulatory and phonological impairments: A clinical focus. 140–148. A. . Journal of Speech and Hearing Disorders. (1978). D. but survey data of school practitioners reported by Ruscello (1995a) indicate that a subgroup of clients do not improve with traditional treatment methods. 1995. Danilo¤. (1995b). References minor involvement of phonological production and do not have a significant impact on intelligibility. P. E. J. Journal of Communication Disorders.). Derhotacized /r/. P. D. Common and uncommon distortion errors as reported cated that the two subjects were able to acquire correct production of the former residual error. L. some individuals do not (Dagenais. Generally. 8. but it is thought that there are substantial numbers of individuals with such a phonological disorder. J. F. 1995b. P. and Hearing Research. 279–302. Stewart. Ruscello. (1990). J. E. Visual feedback in treatment of residual phonological disorders.). Attitudes of fourth and sixth graders toward peers with mild articulation disorders.. American Journal of Speech-Language Pathology. Di¤erential diagnosis in speech-language pathology (pp. Speech and Hearing Services in Schools. 41. Imprecise articulation of consonants and vowels 3. 1991). Shuster. Articulation and phonological disorders (4th ed.. Dagenais. Journal of Speech. (1999). /E/. S. which are sound variations that are not within the phonetic boundaries of the intended target sound. 22. New York: Merrill. N. Gibbon et al. 105–140. Inability to maintain oral/nasal contrasts 4. The treatment approaches are based on motor learning or cognitive-linguistic concepts (Lowe. principles from biofeedback and speech physiology have been incorporated into treatments (Dagenais. 43. 1989. Wahl. In some cases. Electropalatography in the treatment of articulation/phonological disorders. Gibbon. An acoustic-articulatory description of children’s defective /s/ productions. 1978. The respondents did not list the types of sound errors. M. /F/ 3. J. (1998). and Doolan.. 331–353. Crowe Hall. 113–158). Treatment for persons with residual errors is generally carried out using approaches that have been used with younger children. 319–334. 28. but the error sounds reported are in agreement with the residual errors identified by both Shriberg (1993) and Smit et al. 2000). Labialized /l/ or /r/ Uncommon Distortion Errors 1. B. 1995. Journal of Communication Disorders.. (1998). Dentalization of voiced/voiceless sibilant fricatives or a¤ricates 2. (1995). W. Boston: Allyn and Bacon. 28. 303–330. and Stephens. I. however. An exact estimate of children and adults with residual errors is unknown. Journal of Communication Disorders. In B. in most cases a motor learning approach is utilized (Gierut. Silverman and Paulus. A biofeedback treatment utilizing real-time spectrography was implemented for both subjects. 1994. Although most individuals normalize their residual errors with intervention. S85–S100. Velarized /l/ or /r/ 5. Ohde. Crowe Hall. Lowe. Ruscello. Residual 157 Common Distortion Errors 1. and Bankson. and the results indiBauman-Waengler. Gierut. Journal of Communication Disorders.. Weak consonant productions 2. M. Respondents indicated that children either were unable to achieve correct production of an error sound or achieved correct production but were unable to incorporate the sound into spontaneous speech. (1991). Wahl. 13. residual errors are a distinct subtype of developmental phonological errors that are present in the speech of older children and adults who are beyond the period of normal sound acquisition. 1999). (1980). For example. R. 28. Speech appliances in the treatment of phonological disorders. J. Philips and D. Phonetic analysis of normal and abnormal speech... (1992). Treatment e‰cacy: Functional phonological disorders in children. and Sharf. Most residual errors are described as distortions. Boston: Butterworth-Heinemann. Di‰culty in maintaining correct voicing contrasts Figure 1. Bauman-Waengler. Shriberg. F.. A. 1995).

Edwards (Eds. F. E. D. Smit. P. A clinical profile.g. Intelligibility can be decreased further by co-occurring dialect di¤erences in prosodic or nonsegmental (rhythmic and vocal pitch) features (Tarone. As a result of litigation. and McSweeny. 105–132). 1991). (1994). (1995). (1982). O. M. San Diego. Yet AAVE is not an open-syllable dialect. This mandate has created challenges for clinical practices. and Hearing Services in Schools. (1999). 20. Lewis. Weismer. 219–221.. and Bernthal. African Americans are racially.. and Paulus. 4. B. this > /dIs/). Yoder (Eds. 38–53. (1990). A. 42. L. A. M. Austin. 1993). E. D. In both dialects. L. 53. 40. Bleile. and Toth. American Journal of Speech-Language Pathology. Acoustic characteristics of /s/ in adolescents. In N.. coupled with known grammatical. W. D. Journal of Speech and Hearing Research. Speech. Shriberg. Stockman. the continuing physical and social segregation of African Americans has sustained large AAVE communities.). Not all learn AAVE. D. but their use in words di¤ers (Wolfram. J. Shriberg. J. unstressed syllables (e. This discussion considers only those African Americans with an indigenous slave history in the United States and ancestral ties to Subsaharan Africa. 42. 1975. respectively). D. D. Articulation assessment. Others are absent as single sounds (e. L. Ruscello... (1994)... Developmental phonological disorders: I. A diagnostic classification system. St. 1996b). and McSweeny. M. (1995). 663–677. (1989). P. ethnically. Phonology: Clinical Issues in Serving Speakers of African-American Vernacular English Word pronunciation is an overt speech characteristic that readily identifies dialect di¤erences among normal speakers even when other aspects of their spoken language do not. Shriberg. L. the vowel and consonant sounds are the same (with a few exceptions). J. and hearing (pp. L. W. 1986). legislation. 779–798. and D.. L. Consider just the number of grammatical and phonological di¤erences between SE and AAVE in the following example: SE: AAVE: They are not fixing to ask for the They not finna ask for the the ar nat fIksIn tu aesk fOr thP deI na fInP 0ks fv dP car car kaF ka: / / / / . Language. Shriberg.. and Mason. L. Lass. (1999). L. These broadly predictable AAVE pronunciation patterns di¤er enough from SE to compromise its intelligibility for unfamiliar listeners. and pragmatic ones. fixing to > finna.. Freilinger. and Kwiatkowski. McReynolds. Language. away > /-weI/) in any position may be absent. D. 37. This dialect is labeled in various ways but is referred to here as African American Vernacular English (AAVE).).. Flipsen.. and Bird. a populous ethnic minority group. L. Nonprestige social dialects in particular were viewed simply as disordered speech. Shriberg. L. The native English spoken today is rooted partly in a pidgin-creole origin. 4. best clinical practice now requires speech clinicians to regard social dialect di¤erences in defining speech norms for clinical service delivery. Language. J.. The Iowa articulation norms project and its Nebraska replication. I. Shriberg. Journal of Speech and Hearing Disorders. Five subtypes of developmental phonological disorders. particularly in southern states. The use of visual feedback to elicit correct /r/. Philadelphia: Saunders. and multiple words may be merged phonetically (e. Phonological disorders: I.. Journal of Speech. (1981). 1100–1126. language. (1991). One clinical issue is how to identify AAVE speakers.. N.. Since slavery was abolished.. J. and social changes beginning in the 1960s. L. D. J. man) or in consonant clusters (test > /tEs/). A follow-up study of children with phonologic disorders of unknown origin.. The dialects di¤er in their distributions of word-final consonants. (1997). 236–242. Final consonants are variably absent in predictable or rule-governed ways.g. the density of use varies. Journal of Speech and Hearing Research. (1997). Journal of Speech and Hearing Disorders. 226–241.. D.. and among those who do. Shuster. and Hearing Research. H. semantic.. Language. Word-initial single and clustered consonants in AAVE typically match those in SE except for interdental fricatives (e. J.. B. 572–590). Karlsson. Ruscello. Clinics in Communication Disorders. K. Journal of Speech and Hearing Disorders. 1461–1481. 34. Dejarnette and Holland. Some final consonants in AAVE are replaced (cf. D. Peer reactions to teenagers who substitute /w/ for /r/. Hodson and M. Gaithersburg. Tomblin. Prevalence of speech delay in 6-year-old children and comorbidity with language impairment. Perspectives in Applied Phonology (pp..158 Part II: Speech Shriberg. and Hearing Research. Although regional pronunciation di¤erences in the United States were recognized historically. A case in point is the native English dialect spoken by many African Americans. Louis. In multisyllabic words. G. CA: Singular Publishing Group. Bernthal. bath and bathe > /f/ and /v/.. H. 47. Northern. Contemporary AAVE pronunciation is both like and unlike Standard English (SE)... and Hearing Research. 37–44. Further Readings Bankson. and Kwiatkowski. J. The speech disorders classification system (SDCS): Extensions and lifespan reference data. J. J. L. L. Manual of articulation and phonological disorders. V.g. Speech. J. 1994) or when a consonant is an alveolar as opposed to a labial or velar stop (Stockman. E. 55. 723–740. Journal of Speech. School-aged children with phonologic disorders: Coexistence with other speech/language disorders. and Wilson. J. Journal of Speech. K. They are more likely to be absent or reduced in clusters when the following word or syllable begins with another consonant rather than a vowel (Wolfram. (1988). B. suppose to > sposta) to function as separate words. 144–155. L. ask > /s/). Silverman. McSweeny.g. 1994. D. and Kwiatkowski. MD: Aspen. N. A. depending on grammatical and semantic factors (VaughnCooke. Developmental phonological disorders: One or many? In B. J. Shriberg.g.. and linguistically diverse. L.. social dialects were not. Hand. L. G. Consonants may also be reordered in some words (e.

Wolfram (1994) suggested that these three error categories provide a heuristic for scaling the severity of the pronunciation di‰culty and selecting targets for treatment. 1981. One remediates atypical speech relative to a client’s native dialect. Arensberg. such as bath/b0T/ > /b0t/ or /b0s/. or when the pronunciation patterns for a child and caregiver are compared on the same test words (Terrell. if observed at an age when developmental errors are not expected. Cole and Taylor.g. and Rosa. For abnormal speakers. e. final consonant deletion. For both client populations. This means that the pronunciation of bath/b0T/ as /baf/ should not be targeted for change. especially if known causes of disordered speech— hearing loss. which penalize AAVE speakers even more. 1976. is targeted.g. In contrast. they favor the sampling of abutting consonant sequences (e. They a¤ect which patterns are targeted and how change is facilitated. or an actual higher prevalence of speech disorders as a result of economic poverty and its associated risks for development in all areas. But a deviation from this expected pronunciation. Which features to target in therapy and how to model the input become issues. (2) selection of stimuli (e. interdental fricative substitutions) or quantitatively (Type III error.Phonology: Clinical Issues in Serving Speakers of African-American Vernacular English 159 Enough is known about the complex perceptual judgments of speech intelligibility to predict that the more work listeners have to do to figure out what is being said. Errors on shared features (Type I) should be targeted first in treatment. AAVE speakers with disorders can di¤er from their nondisordered peers on speech sounds that are like SE (Type I error. They di¤er from typically developing community peers in both the frequency and patterning of speech sound error. for speakers with abnormal pronunciation. because most clinicians do not speak AAVE. and interdental fricative substitutions) to those commonly observed among immature or disordered SE speakers. 1994).g.. bath > /baT/ and /b0f/).. just as bilingual speakers switch languages. They typically provide no contexts for sampling AAVE’s variable pronunciation rules. the goal is to eradicate and replace existing patterns that decrease intelligible speech in the native dialect. Besides the production practice. brain damage. Misdiagnosing normal AAVE speakers as abnormal is encouraged further by the similarity of their typical pronunciation patterns (e.. Correct or target productions are judged relative to SE. Clinicians must know a lot about the dialect to defend a diagnosis.g. 1992). Haynes and Moran. However. 1996). 1989). Wolfram (1994) reminded us that AAVE and SE share many of the same target features (e. tests of isolated word pronunciation are not entirely useful. Identifying atypical AAVE speakers can be di‰cult. However. Taylor and Peters. e. they make more errors than their predominantly white. 1993. second language acquisition principles are relevant. 1992). 1989).. service delivery requires contrastive analysis of the two dialects and attention to sociocultural issues that a¤ect code switching. 1996a. They are likely to impair intelligibility . 1991.g. 1999). Therefore it is unknown whether the overrepresentation of African Americans in clinical caseloads is due to practitioner ignorance. AAVE should be targeted. e. bus fish). 1996b).. 1976. 1992). An additive approach assumes that speakers can learn to switch SE and AAVE codes as the communicative situation demands. word-initial single and clustered consonants). Despite the assessment challenges. Simmons. given their tendency to delete final consonants that precede other consonants as opposed to vowels (Stockman. the service delivery goals do di¤er for these two populations. They can also di¤er on sounds that are not like SE either qualitatively (Type II error. These issues have encouraged the use of criterion-referenced evaluations of spontaneous speech samples for assessment (see Stockman. This means that a speaker’s bidialectal repertoire includes both the SE and AAVE pronunciation of ‘‘bath’’ (cf. Meeting these two di¤erent service goals requires attention to some issues that are not the same. Two service delivery tracks are within the scope of practice for speech clinicians. as in the case of final consonant absence. the more likely is speech to be judged as unclear. 1988. games and objects) for therapy activities. if it conforms to the client’s target dialect. 1986). However. e¤ective service delivery requires clinician sensitivity to cultural factors that impact (1) verbal and nonverbal interactions with clients. 1983). This is true whether the clinical and nonclinical groups are distinguished by the judgments of community informants. and (3) scheduling of sessions (Seymour.. 1990). the service delivery goal for normal AAVE speakers is to expand rather than eradicate the existing linguistic repertoire (Taylor. 1988. age-matched peers (Ratusnik and Koenigsknecht. or speech-language clinicians (Stockman and Settle. as is often the case. They also may resist modeling a low social prestige dialect because of negative social attitudes towards it.. 1986). In contrast. 1981. and Schraeder et al. it is readily agreed that some AAVE speakers do have genuine phonological/articulatory disorders (Seymour and Seymour. which can cross word boundaries. test bias. 1968) do elicit paired word combinations. 1990). 1992). But most clinicians (95%) are not African American and have little exposure to AAVE (Campbell and Taylor.g. The accuracy in identifying articulation/phonological disorders improves when test scores are adjusted for dialect di¤erences (Cole and Taylor. most word-initial consonants). Wilcox. cluster reduction. The other one expands the pronunciation patterns of normal speakers who want to speak SE when AAVE is judged to be socially or professionally handicapping (Terrell and Terrell. Seymour and Seymour. Although standardized deep tests of articulation (McDonald. typically developing AfricanAmerican speakers make fewer errors on standardized articulation tests as they get older (Ratusnik and Koenigsknecht. and so on—are absent. other classroom teachers (Washington and Craig.. Still. even when nonstandard dialect use is not penalized. Simmons. For typical AAVE speakers learning SE. such as Head Start teachers (Bleile and Wallach.g. 1986. Proctor. more frequent final consonant absence in abutting consonant sequences). and they do so beyond the age expected for developmental errors (Haynes and Moran.

Indiana University. The Screening Deep Test of Articulation. (1986). 46. Articulatory patterns would not be modified if they di¤ered from the clinician’s SE-modeled pattern but matched expected AAVE patterns. Stockman References Bleile. 207–245). The promises and pitfalls of language sample analysis as an assessment tool for linguistic minority children. November). Fluharty Preschool and Language Screening Test: Analysis of construct validity. M. Lowe (Ed. 42. M. Legitimizing social dialects like AAVE in the United States has required researchers and clinicians to (1) broaden the reference point for normalcy and (2) explore alternative strategies for identifying service needs and modifying word pronunciation. Seymour. GA. Parent-child comparative analysis: A criterion-referenced method for the nondiscriminatory assessment of a child who spoke a relatively uncommon dialect of English. J. 20. O. (1996). Stockman. (1975). Language. November). 76. In D. (1986). In O. Speech. and Taylor. and Craig. 54–62. Unpublished master’s thesis.. (1992). F.. W. Cole.. Phonology and cultural diversity. Language variety in the South (pp. 400–406. Applications in speech pathology (pp. (1992). Pollock. The issues singled out in this entry are not unique to phonological/articulatory problems. Child phonology: Characteristics. Language. A sociolinguistic investigation of the speech of African-American preschoolers. Journal of Speech and Hearing Disorders. (1994). Terrell. Bankson (Eds. McDonald. Black English and Standard American English contrasts in consonantal development for four. Bernthal and N. H. J.). Language. K. such as stop replacement of interdental fricatives (cf. (1996b). and Rosa. D.). 27– 29. 23. 276–280. Taylor. Lexical di¤usion: Evidence from a decreolizing variety of Black English. J. O. and Holland. Aspects of intonation in Black English. this /dIs/ > /bIs/). S. Vaughn-Cooke. Taylor (Ed. Campbell. (1991.. Poster presented at the annual convention of the American Speech-Language-Hearing Association. Language. 27. O. Baltimore: Paul H.. 203–207. 675–689. Stockman. (1992). 23. and Taylor. African-American preschoolers with communication impairments. I. 48. A. CA: College-Hill Press. Taylor. 168–174. S. and Hearing Services in Schools. and intervention with special populations (pp. However. (1983). Variable word initial and medial consonant relationships in children’s speech sound articulation. Battle (Ed. Perceptual and Motor Skills. CA: College-Hill Press. (1993). O. (1986). they may turn up more often in clinical work. Ratusnik. (1999). Quinn. Distinguishing between phonological difference and disorder in children who speak African-American English. Treatment of communication disorders in culturally and linguistically diverse populations (pp. (1989).). F. and Settle. Pittsburgh. and Terrell. ASHA. E¤ects of speaking Black English on employment opportunities. 8. 199–206. Moran. Seymour. Atlanta. Taylor (Ed. Brookes. New York: Thieme. 161–166. assessment. Haynes. (1988). Perceptual and Motor Skills. W. Kamhi. Influence of age on black preschoolers’ nonstandard performance of certain phonological and grammatical forms.. or quantitative (Type III) errors. Initial consonants in young black children’s conversational speech. E. 3.. Performance of working-class African-American children on three tests of articulation. Stockman. A cross-sectional developmental study of final consonant production in southern black children from preschool through third grade. language disorders in african-american children. Speech. American Journal of Speech-Language Pathology. M. American Journal of Speech-Language Pathology. Speech. In O. Washington. 153–178). K. J. Terrell. K.. (1992). 24..). Language. Tuscaloosa: University of Alabama Press. In O. Montgomery and G. See also dialect speakers. The nature of communication disorders in culturally and linguistically diverse populations (pp. L. and Koenigsknecht. M. Simmons. I. and Hearing Services in Schools. G. GA. (1981). E. (1990). —Ida J. Wilcox. 95–200. (1968). 53.). H. Speech. 227–244).. San Diego. and Hearing Services in Schools. Baltimore: Williams and Wilkins. and Moran. Arensberg. CA: College-Hill Press. and Peters. 34–42. assessment and intervention. and Hearing Services in Schools. American Speech. 157–180). H.). Stockman. Bailey (Eds. Phonology: Assessment and intervention. 212–238). P. Authentic assessment as an approach to preschool speechlanguage screening. R. (1993). Atlanta. Speech. In J. 163–176. (1994). and Seymour. (1976).. Wolfram.. Language.. 171–176. C. and Wallach. PA: Stanwix House. Articulation test performances of low-income. In M.). H. Dejarnette. and Hearing Services in Schools. I. Harris (Eds.. and Miller. given their typically higher frequency of occurrence relative to other domains of spoken language in all groups. even more than the smaller sets of qualitative (Type II) errors. dialect versus disorder.160 Part II: Speech English. Bloomington. 25. W. (1996a). I. In A. Voice and voice disorders. San Diego. Stockman. L.and five-year-old children. (1991. 1. Treatment of communication disorders in culturally and linguistically diverse populations (pp. (1986). C. O.). Schraeder. Poster presented at the annual convention of the American Speech-Language-Hearing Association. Speech. D.. Tarone.. Phonological development and disorders in African American children. Proctor. Boston: Andover. Final consonant deletion in African American children speaking Black English: A closer look. 153–178). Communication development and disorders in African American children: Research. and J. 21. The phonology of a sociocultural variety: The case of African American vernacular English. Stockman. (1993). I. P. AAVE features should be targeted for treatment only when pronunciation patterns di¤er from AAVE norms. Clinical principles for language intervention for language disorders among nonstandard speakers of . Constraints on final consonant deletion in Black English. Howard Journal of Communication. 29–36. Speech and language disorders in blacks. Teaching English as a second dialect. I. San Diego. S. ASHA certified speechlanguage pathologists: Perceived competency levels with selected skills. and Hearing Services in Schools. In R. Communication disorders in multicultural populations (pp. Taylor (Ed. such as final consonant deletion in more than the allowable context number and types. 111–130). Journal of Speech and Hearing Disorders. 355–366.

Children’s articulation of medial consonant clusters: Implications for syllabification. Both of these lines of work are briefly discussed here. (1976).. D. R. Despite this reorientation. This interest has taken different faces over the years as researchers and clinicians have focused on various aspects of the relationship between communicative impairment and psychological and social di‰culties. (1973). 24. 56. Atlanta. Battle.. (1998). Structure of African American vernacular English. as manifestations of underlying psychological dysfunction (e.. In R. Boston: Allyn and Bacon. San Diego. Ohio State University. Journal of Communication Disorders. Goldman-Fristoe Test of Articulation. Fasold and D. N. (University Microfilms No. New York: Routledge. Philadelphia: University of Pennysylvania Press. Newman. S. Teaching Standard English in the inner city. (1981). G. The Hague: Mouton. G. Clinical management of communication disorders in culturally diverse children (pp.). P. P. L. and Huntley. E. Fudala. Fasold. 12–32..Psychosocial Problems Associated with Communicative Disorders 161 Further Readings Bailey. Circle Pines.g.and English-speaking children. Schi¤ren (Eds. (1998).). Analysis of selected prosodic features in the speech of black and white children. Co-occurrence of Disorders. J. Communication disorders in multicultural populations. Mowrer. The first is the frequent co-occurrence of speech and language impairment and socioemotional problems..). Are black and white vernaculars diverging? American Speech. however.. N. such as stuttering. Austin. Luelsdor¤. (1983). Poster presented at the national convention of the American Speech-Language-Hearing Association. Baugh. San Diego. J. The implementation of a phonological change: The case for re-syllabification in Black English. (1975). Illustrative of these findings is the work of Baker and Cantwell (1987). Coleman (Ed. Phonological patterns in the conversational speech of African-American Children. Wolfram. language. Craighead. W. Dissertation Abstracts International. Seymour. R. These researchers performed psychiatric evaluations on 600 consecutive patients seen at a community speech. (1998). (1989). Malden. MA: Blackwell Publishers. L. New York: Random House. R. TX: University of Texas Press. Black English: Its history and usage in the United States.. Columbus. W. F. Travis. Vaughn-Cooke.g. Rickford. Tull. CA: College-Hill Press. L. voice. Fasold. GA. W. Nature of communication disorders in culturally and linguistically diverse populations. J. J. CA: College-Hill Press. American Speech. Mufwene. 173–196). (1989). In N. The relation between black and white speech in the South. and Ralabate. Weddington. In T. some investigators approached specific communicative disorders.). M. Secord (Eds. (1987). (1972). Numerous investigators have reported a high level of co-occurrence between communicative disorders and socioemotional problems. The literature is both extensive and wide-ranging. Seymour.. (1972). language impairment). Newman. DC: Center for Applied Linguistics. G. and Schilling-Estes. I. and much of it focuses on specific types of impairment (e. Green. (1986). R. O. E.). In S.). 234A. MN: American Guidance Service.. and Stephenson. This high level of co-occurrence has been observed in various groups of children. Arizona Articulation Proficiency Scale (2nd ed. A segmental phonology of Black English. and Debose. T. Black street speech: Its history. that are of particular interest. A great deal of research has been directed toward exploring this relationship as well as toward determining what mechanisms might underlie this comorbidity. peer relations. (1970). B. (1974). OH: Merrill. A comparative analysis of phonological acquisition of consonants in the speech of 2 1/2to 6-year-old Xhosa. C. and J. (Ed. S. socioemotional status). Amsterdam: John Benjamins. A. F. and hearing clinic. 139–148.). 139–164. stuttering. (1999). L. 163–189. W. B. 301–332). There are two general areas of study. For example. including both those with a primary diagnosis of speech and language impairment and those with a primary diagnosis of psychiatric impairment or behavior disorder. (2000). P. Baugh (Eds. The acquisition of a phonologic feature of Black English. Van Keulen. and Burger. R. D. W. M. Speech. 5. there is still considerable interest in the psychosocial aspects of communicative disorders.. AAC7714537) Vaughn-Cooke. and Craighead. (1991). language. Myers-Jennings. American English: Dialects and variation. A second area of interest concerns the long-term outcomes of communicative problems across various areas of psychosocial development (e. Boston: Butterworth-Heinemann. Children were divided into three subgroups of communication problems: speech (children with disorders of articulation. and .. A. Phonological disorders in culturally diverse populations. (1985). (Ed. Stockman. Taylor.. Phonological characteristics of African American Vernacular English. learning and the African American child. 185–204. Labov. C. R.. Taylor. Goldman. P. Washington. More recent approaches have moved away from considering psychiatric dysfunction as the basis for most speech and language impairment (an exception is alexithymia). C. W. Current issues in linguistic theory: Language change and variation (pp. O. Assessment of articulatory and phonological disorders. Bailey. Boston: Allyn and Bacon. H.g. 18. Clinical Linguistics and Phonetics. 38(01). Unpublished dissertation. Psychosocial Problems Associated with Communicative Disorders Individuals who study communicative disorders have long been interested in the psychosocial di‰culties associated with these problems. (1991). Structural variability in phonological development: Final nasals in vernacular Black English. Dillard.. J. Language and Speech. (1986). and W. 62. (1986). W. Treatment of communication disorders in culturally and linguistically diverse populations. H. Assessment and remediation of articulatory and phonological disorders. relatively early in the development of the profession of speech-language pathology. Los Angeles: Western Psychological Services. 1957). and Shuy. E. J. (1981). and Fristoe. Columbus. Wolfram. Language in the inner city. structure and survival.

generalizations across individuals with di¤erent types of speech impairment must be made with caution. Long-Term Consequences. 2001). It is clear that speech and language skills play a critical role in social interaction and that children who have di‰culty communicating are likely to have di‰culty interacting with others. These researchers followed children with speech impairment and language impairment and their typical controls longitudinally over a 14-year period (Beitchman et al. 21. severity of language impairment. Further clarification is needed to determine how these areas of development interact to produce social outcomes. is not as straightforward as might initially be thought.g. (2000) reported that reading disability is a key mediating factor predicting whether children with language impairment demonstrate behavioral di‰culties. Of particular interest is the relationship between social competence. 23–24 years of age. Several researchers have speculated on the basis for this high level of co-occurrence between communication and socioemotional disorders.. and di‰culty establishing friendships. neurodevelopmental status) accounts for both types of problems. Records. approximately 50% were diagnosed as having a psychiatric disorder. The two groups had converged over the years. At age 5. (2) impaired communicative skills result in academic problems.’’ the unique psychosocial di‰culties associated with such disorders may be masked . it would appear that children with speech di‰culties achieve better psychosocial outcomes than children with language difficulties (see also Toppelberg and Shapiro. and Wilson (1996) proposed several potential relationships. Additionally. solitary active withdrawal). such as stuttering.. was not related to severity of withdrawal. in part or in whole. At age 14 years and at age 19 years. a broader deficit underlies both the language delay and the social impairments’’ (p. The young men with language impairment showed a high incidence of social di‰culties. in large group design studies where individuals are categorized together under the general heading of ‘‘speech. Children with speech impairment tend to have more favorable longterm outcomes. Although this may generally be the case. More specific evaluation revealed that these di¤erences were based on particular types of withdrawal (reticence. 573). ‘‘as in autism. Fujiki et al. For example. socioemotional status was closely linked to status at age 5. One approach to this problem has been to investigate various child factors that may contribute to developmental risk. including the following: (1) impaired communicative skills lead to socioemotional impairment. Of these children. however. One group was identified with autism and the other with language impairment.162 Part II: Speech fluency). Further research is needed to clarify the relationship between speech and language ability and socioemotional status. Most still lived with their parents and had unstable employment histories in manual or unskilled jobs. such as employment or social relationships. Howlin et al. Given some of the data cited above. (2000) concluded that in language impairment. A related line of work has focused on the long-term psychosocial and sociobehavioral consequences of speech and language impairment. who had first been evaluated at 7–8 years of age. differences were not observed with respect to satisfaction in relation to specific aspects of life. language (children with problems in language expression. socioeconomic status) explain. Howlin. at least as measured by a formal test of language. Tomblin et al.. Brownlie. communicative competence. Aram and Hall (1989) stated that children with language impairment have frequently been found to have high rates of persistent social and behavioral problems. The groups did not significantly di¤er on reported personal happiness or life satisfaction. Neither childhood language ability nor current language ability predicted social functioning in adulthood. consistent with much of the existing literature. At age 12. These problems were categorized into two general groups of behavior disorder and emotional disorder. limited social contacts. Thus. The way in which various components of behavior interact. however. the group with language impairment showed fewer social and behavioral problems than the group with autism. the relationship between communicative problems and socioemotional di‰culties. but also have relatively low incidence rates. and di¤erences between the two were not qualitative. For example. which in turn lead to behavioral problems. For example. Tomblin. and Rutter (2000) reported a bleaker picture.6 years) with specific language impairment and 29 controls. including problems with social interaction. Children in the group with speech impairment did not di¤er from the controls. At follow-up. The work of Beitchman and colleagues provides one example of a research program examining long-term psychosocial outcomes of individuals with communicative impairment. Mawhood. They reexamined two groups of young men. (3) other variables (e. and what factors may exacerbate or moderate socioemotional status. A few studies have examined the long-term psychosocial outcomes of individuals with speech and/or language impairment as they enter adulthood. Beitchman. In summarizing numerous studies looking at the outcomes of communication disorders. individuals in the group with language impairment had significantly higher rates of psychiatric involvement than the control group.g. Further. are likely to have important psychosocial implications. and pragmatics). and (4) an underlying factor (e. the children in the group with speech impairment and the group with language impairment had a higher rate of behavioral problems than the control group. 2000). and socioemotional functioning. For example. comprehension. (1999) found that children with language impairment were more withdrawn and less sociable than their typical peers. Some types of speech problems. and Freese (1992) examined quality of life in a group of 29 young adults (mean age. and a speech and language group (children with a mixture of problems).

M. Longitudinal follow-up of children with preschool communication disorders: Treatment implications. Curtiss. N. D.. B... II. and clinical perspectives. and Shapiro.. J. H. Journal of the American Academy of Child and Adolescent Psychiatry. 487–494. H. Ferguson. L. Comparison of well. Beitchman... (1997).. W. Roberts (Eds. and Rutter. Buckwalter. J.. H. Prevalence of psychiatric disorders in children with speech and language disorders.. A. 193–196. D. Language. and R. 1992). and Cantwell. and Tannock. and Hart. In summary. —Martin Fujiki and Bonnie Brinton atric outcome.. G. Beitchman..Psychosocial Problems Associated with Communicative Disorders 163 by the psychosocial profiles associated with more commonly occurring communication problems. however. generalizations must be made with caution. D. and clinical perspectives (pp. Brownlie. (1996). 22. Language. and Lancee.... 916–946). C. S. B. and selfappraisal interact in complex ways to produce psychosocial outcomes in children with cleft lip and palate. A prospective psychiatric follow-up of children with speech/language disorders. R. New York: Cambridge University Press. T. Individual studies. M. Walker and M. Konstantareas. P. B.. 75–82. It should also be noted that speech impairments may vary from having no outward manifestations aside from those involved in talking to relatively severe physical or cognitive deficits. H. In L. Journal of the American Academy of Child and Adolescent Psychiatry. J. L. Fujiki. Johnson. and Nation. Speech may also vary considerably. H. and language impairment among second-grade children. B. Records. 41. emotionally disordered. Clegg. Journal of the American Academy of Child and Adolescent Psychiatry. (1996). C.. B. and Eliason. 487– 501. There is also evidence that children with language impairment have more psychosocial di‰culties than children with speech impairment. School Psychology Review. Thus. and psychiatric outcomes. Wilson. These children may have articulation problems and hypernasality secondary to specific physical anomalies. and Freese. emotional. Baker. A. It must be remembered. M. Given the accumulated evidence. 25. Baker. Konstantareas. 26. 1997).. learning. and Tallal. to various degrees.. Young. 39. J.. that speech problems di¤er by type of impairment. J. Brief report: Cleft lip and palate: Longitudinal behavior and relationships of cleft conditions to behavior and achievement. and Patel. M. 493–514). Beitchman. B. J.. 44–53. Tannock (Eds. Toppelberg. biological.. H. Nair. Walters. Richman. H. (1986). P. Tomblin.. (1989)... B. and Hearing Services in Schools. P. 35. O. Travis. Inglis. Long-term consistency in speech/language profiles: II. Wilson. there is good reason to believe that parents. and Cantwell. Language disorders: A 10-year research update review. Zhang. Journal of the American Academy of Child Psychiatry... 27. Cohen. 537–552). it is clear that individuals with communicative disorders often have di‰culty with aspects of psychosocial behavior and that these problems can have long-term implications. (1987). Beitchman. Brinton. 30. E. 15. and behavior disorders: Developmental. D. C. Tomblin. In J. X. 143–152. Withdrawn and sociable behavior of children with specific language impairment. A.. (1982). 41. Behavioral. Beitchman. J. H. The unspeakable feelings of people with special reference to stuttering. E.. Linguistic impairment to psychiatric disorder: Pathways to outcome. M. R. C. L. social development and language impairment. M. degree of disfigurement. and behavior disorders: Developmental. (1996). pp. Cohen. Handbook of speech pathology (pp. A. 183–195. Ekelman. J.. Journal of the American Academy of Child and Adolescent Psychiatry.. Richman. These physical anomalies may be resolved. (1987). P. learning behavioral disturbances in childhood: A References Aram. and Catts. J. D. B. New York: Cambridge University Press. B. P. (1999)..). M.. M. L. The association of reading disability.... 40. 113–126. 1. (1992). learning. Atkinson. 18. E. Preschoolers with language disorders: 10 years later. et al. E. severity. Psychiatric disorder in children with di¤erent types of communication disorders. L.. and social outcomes. biological. 528–535. and other variables. (2001). however. Journal of Child Psychology and Psychiatry and Allied Disciplines.. Beitchman. R. H. 546–553. L. Morgan. P. P. Journal of Speech and Hearing Research. New York: Wiley. E. Journal of Pediatric Psychology. The quality of life of young adults with histories of specific language impairment. (2000). It appears that factors such as family support. Disorders of communication: Developmental language disorders and cleft palate. (1993). N. and clinicians working with children with speech and language impairment should give serious consideration to psychosocial status in planning a comprehensive intervention program. A. Journal of Communication Disorders. Mawhood.. Language.). L. (1984). behavioral disorders. Benasich. No specific personality type has been associated with children with cleft palate (Richman and Eliason. T. Illustrative of the complexity even within a specific category of speech impairment are children with cleft lip and palate. Journal of the American Academy of Child Adolescent Psychiatry. Social... (2000). and Millard. N. 475–482. P. and Wilson. Language. (1957). C. Handbook of clinical child psychology (2nd ed. See also poverty: effects on language. N. Further Readings Aram. M. New York: Appleton-Century-Crofts. educators.. and Cantwell. B. Journal of Child Psychology and Psychiatry. (1992). Austism and developmental receptive language disorder: A follow-up comparison in early adult life. Travis (Ed. J.. Fourteen-year follow-up of speech/language-impaired and control children: Psychi- . 561–578. (2000). J. behavioural. C. Speech. and Hall. Baker.). 26. The impact of associated problems on the psychosocial development of children with di¤ering types of communicative impairment is di‰cult to summarize briefly. with surgery. American Journal of Speech-Language Pathology. 232–244. have found these children to exhibit higher than expected rates of both internalizing and externalizing behavior (Richman and Millard. and behaviorally disordered children with linguistic problems. E. L. 815–825. L. M. In C. M. Adlaf. Howlin. Brownlie.

Journal of Child Psychology and Psychiatry and Allied Disciplines. and automated interfacing with alternative response mode systems. 744–760. 35. Journal of Speech. Journal of Child Psychology and Psychiatry and Allied Disciplines. 547–559. C. social cognitive processing. which are then converted to profiles or derived scores of interest (Long. Speech and Language Disorders in Children: Computer-Based Approaches Computers can be used e¤ectively in the assessment of children’s speech and language. Language. 803–811. 1992) can be used to supplement the clinician’s perceptions of phonological contrasts (Masterson. and Amorosa. N. Long. and some provide tools that reduce and simplify the time-consuming process of transcribing samples (Long. 38. M. (2000). M. their use in clinical settings remains limited.. Long. Journal of Child Psychology and Psychiatry. Clinical significance of childhood communication disorders: Perspectives from a longitudinal study. measures of jitter and shimmer can be recorded. 257–264. Cohen. N. These programs allow researchers and clinicians to perform complex. Noterdaeme. the system identifies related skills that need testing. Paul. L. Cochrane... 1999). Incorporation of some principles from artificial intelligence also makes the future of computers in assessment exciting. (1999).. Of particular promise are the computerized tests that adapt to a specific client’s profile. 8. 585–594. 1999.. Fourteen year followup of children with and without speech/language impairments: Speech/language stability and outcomes. 643–655. (1998). for unclear reasons. 32. Journal of Child Psychology and Psychiatry and Allied Disciplines. For the evaluation of a client suspected of having a fluency disorder. such as speaking or even pointing. L. and McGue. They provide instant analysis of a wide range of phonological and linguistic measures. Mawhood. Journal of Child Neurology. M. N.. Green. L. and Wasowicz (2001) developed a tool for spelling assessment that employs complex algorithms for parsing spelling words into target orthographic structures and then aligning a student’s spelling with the appropriate correct forms. Long. D. (1992). H. Appraisal and coping in adults with cleft lip: Associations with well-being and social anxiety. et al. (1999). 1114–1125. P. 42. Im. Computers can also be used to administer or score a formal test (Cochran and Masterson. and Kellogg. Johnson. Long and Channell. Howlin. A. B. J. Hallowell (1999) discusses the use of instrumentation for detecting and measuring eye movements for the purpose of comprehension assessment. 1999). Masterson and Bernhardt. For example... The type of task or specific items that are administered can be automatically determined by a client’s ongoing performance (e. 1999. such as phonological awareness or morphological knowledge. B. and behavioral characteristics of psychiatrically disturbed children with previously identified and unsuspected language impairments. Menna. This exciting tool allows the clinician to evaluate comprehen- sion in a client for whom traditional response modes. Based on the type of misspellings exhibited by each individual student. tracking of response latency. Hallowell and Katz. Autism and developmental receptive language disorder: A comparative follow-up in early adult life. 2. Computerized language and phonological sample analysis (CL/PSA) has been in use since the 1980s (Evans and Miller. Evaluation of emotional and behavioral problems in language impaired children using the Child Behavior Checklist. A. 1999). Vallance. however. recent software developments allow the clinician to gather measures of both the number and type of speech disfluencies and to document signs of e¤ort. 1999. R. and Rutter. 1997) do not support this conjecture.. data from recent surveys (McRay and Fitch. Despite the power of CL/PSA programs. Many of the CL/PSA programs also include comparison databases of language samples from both typical and clinical populations (Evans and Miller. A 28-year follow-up of adults with a history of moderate phonological disorder: Linguistic and personality results.. the potential for such instruments is quite high. Cantwell. since most . 1999. (1996). 1999a). Computer-based scoring systems allow the input of raw scores. H. L... Cognitive and language outcomes. The value of such programs is inversely related to the ease of obtaining the derived scores by hand. M.. That is. 1996. and Horodezky. stimuli are presented in a manner that is contingent on the individual’s prior responses (Letz. and Woodard. along with perceptual judgments about a client’s pitch and intensity perturbations (Case. J. Language. 71–77. S. If the translation of raw scores to derived scores is tedious and time-consuming. 1999). It is possible that funding for software and hardware is insu‰cient. 6. Young. P. Felsenfeld. L. and Hearing Research.. I. struggle. Escobar. This system makes possible a comprehensive description of a student’s spelling abilities that would otherwise be prohibitive because of the time required to perform the analyses by hand and administer the individualized follow-ups. or disruption of airflow and phonation (Bakker. For example. are not possible.. 853–864. (1997). P. Journal of the American Academy of Child and Adolescent Psychiatry. and Buder. M. 2001). and Slade. (1988). Although few computerized tests are currently available. 39... Hallowell and Katz (1999) point out that computerized test administration could allow tighter standardization of administration conditions and procedures. Acoustic analyses (Kent and Read. 485–503. Beitchman. Biofeedback instrumentation allows the clinician to obtain relatively objective measures of certain aspects of speech production. 1998). I..164 Part II: Speech longitudinal perspective. Practitioner review: Developmental language disorder: A clinical update. Temperament in late talkers.. Barwick. R. European Child and Adolescent Psychiatry. which makes individualized assessment more feasible than ever. Wilson.g. 1995. Apel.. 1999). and Baker. indepth analyses that would likely be impossible without the technology. Atkinson. 2001). Masterson and Oller. D. Broen. (1999). British Journal of Medical Psychology. Rapin. clinicians might find the software tools worth their investment in time and money. 41. Masterson. 1996). ASHA. V. A. Journal of Speech and Hearing Research. 72. M.

As with any tool. Optimal writing involves more than a simple. 1999. students will still need specific training in the optimal use of the technology. 271–280. P. Technical solutions for quantitative and qualitative assessments of speech fluency. Lack of use is more likely related to insu‰cient familiarity with many of the measures derived from language sample analysis and failure to recognize the benefits of these measures for treatment planning (Cochran and Masterson. and Nelson. J. (1999a). 7. the focus must remain on the target linguistic structures rather than the toys or activities that are used to elicit or model productions. and it is likely that speech-language pathologists will capitalize on this trend. Seminars in Speech and Language. Seminars in Speech and Language. including an appreciation of their limitations. the Speech Enhancer. clinicians can choose one of several software packages that allow access and display of multimedia stimuli on the basis of phonological characteristics (Masterson and Rvachew. and Rosenbek. Not using a computer in language assessment/intervention: In defense of the reluctant clinician. K. K. 2002). such as the palatometer. Computers add a new twist to an old standard in phonological treatment. . J. Language.. If a clinician can do an activity just as well without a computer. Case. and Wood. See also aphasia treatment: computer-aided rehabilitation. clinicians will likely turn to the computer if they are convinced that the tasks themselves are worth it. MD: Author. and spelling can be so challenging for students with language disorders that it interferes with text construction. Omnibus Survey Results: 1997 edition. (1999). Journal of Medical Speech-Language Pathology. it is unlikely that she or he will go to the expense in terms of time and money to invest in the computer tool. computers o¤er reasonable compensatory strategies for older. Cochran.. Students who employ speech recognition software to construct written texts will need focused instruction regarding the di¤erences between the styles of spoken and written language. and Masterson. In an e¤ort to address this problem. school-age students with language-learning disabilities (Wood and Masterson. 20. One particularly promising technology. Computer software for use in speech and language intervention has progressed significantly from the early versions. Currently. Technology applications in intervention for preschool-age children with language disorders. Seminars in Speech and Language. L. Seminars in Speech and Language. provide clients with critical feedback for sound production when tactile or kinesthetic feedback has not been su‰cient. 203– 218. and perhaps someday they will free writers with language disorders from the burden of text entry. computer programs can be used to provide objective feedback regarding the frequency of stutterings. Long established the Computerized Profiling Website (http:// www. In addition to therapeutic benefits. Bakker. K. S. Rockville. Cochran and Nelson (1999) cite literature that confirms what many clinicians knew intuitively: software that allows the child to be in control and to independently explore based on personal interests is more beneficial than computer programs based on the drill-and-practice model. Apel. J. (1995). but a potential source of motivation as well. (1999). (1999b). Speech recognition systems continue to improve. 1999b). (1999). Cariski and Rosenbek (1999) collected data from a single subject and found that intelligibility scores were higher when using the Speech Enhancer than when using a high-fidelity amplifier. for those tasks that cannot be done as well or even at all. which were based primarily on a drill-andpractice format. Instead of having to sort and carry numerous picture cards from one treatment session to the next. Similarly. Cariski. 260–262. Cochran. For example. New technologies. 315–322.computerizedprofiling. as long as students have been su‰ciently trained in the optimal use of these tools. 20. 169–184. direct translation of spoken language to written form. speech recognition technology remains limited in recognition accuracy for students with language disorders (Wetzel. (1997). which requires choices regarding spelling. Technology in the assessment of voice disorder. The authors suggested that their results supported the notion that the device did indeed do more than simply amplify the speech output. 20. The e¤ectiveness of the Speech Enhancer. 1999). Fitch and McRay.. Masterson. Clinicians can visit the web site and obtain free versions of this CL/ PSA software as well as instructional materials regarding its use and application. 1997). Finally. incorporates real-time processing of an individual’s speech production and selectively boosts energy only in those frequencies necessary for maximum intelligibility. word processors with text-to-speech capabilities allow students to check their own work by listening to as well as reading their text. Masterson References American Speech-Language-Hearing Association. which might be considered less confrontational than feedback provided by the clinician (Bakker. L. The decision to use computers in both assessment and treatment activities will continue to be based on the clinician’s judgment as to the added value of the technology application. The percentage of school-age children who use the Internet on a daily basis for social as well as academic purposes continues to increase. Even when accuracy improves to an acceptable level. 26. 185–196. Speech. —Julie J. Improvements in multimedia capacities and an appreciation for maximally e¤ective designs have resulted in a proliferation of software packages that can be e¤ectively used in language intervention with young children. 1996). 1995. Clinical technologies for the reduction of stuttering and enhancement of speech fluency. Bakker. On the other hand. the Internet provides not only a context for language intervention. D. and Hearing Services in Schools. Spell and grammar checkers can be helpful. in 1999.Speech and Language Disorders in Children: Computer-Based Approaches 165 respondents do report owning and using computers for other purposes. 20.

101–116. Implementing computerized language sample analysis in the public school. R. Friel-Patti. (1999). Rolland. Nelson. 180–188. TX: Psychological Corporation. K. NJ: Erlbaum.. W. (1992).0) (MS-DOS) [Computer program]. J. New and emerging technologies: Going where we’ve never gone before. and Masterson. Journal of SpeechLanguage Pathology. (1994). C. Case Western Reserve University. 68–86. ASHA. Waisman Center on Mental Retardation and Human Development. R. J. J. Masterson. FL: Psychological Assessment Resources. Green.. Farrall. Wilkinson. Seminars in Speech and Language.. Matesich. and Hearing Services in Schools. Freiberg. Masterson. K. 273–293). pp.. 281–295. 29. Spelling Evaluation for Language and Literacy (SPELL) [computer software]. a computerized administration of the Carrow-Woolfolk Test for Auditory Comprehension of Language. (1992). and Chapman. (1999). In K. Wide Range Achievement Test 3 (WRAT3) Scoring Program [Computer software]. M. Wynne. 134–136. (2001). and Parsons. (1999). Masterson.. 20. Masterson.. 20. and Miller. C.. 41. Seminars in Speech and Language. L. Madison. L. and Mergner. (1996). J. Development of a computer-based battery designed to screen adults for neuropsychological impairment... Technological applications in the treatment of acquired neurogenic communication and swallowing disorders in adults. 133–148. (1999). Language. and Thibodeau... J. and Wasowicz. Long. Speech-recognizing computers: A writtencommunication tool for students with learning disabilities? Journal of Learning Disabilities. Language. AZ: Sunset Software. H. Kent. 20. L. B. 10. and writing in children with languagelearning disabilities: New paradigms for research and practice (pp. F. R. Speech. H. MN: Author. 18. NJ: Erlbaum. A new way of looking at auditory linguistic comprehension. S. Long. The CHILDES project: Computational tools for analyzing talk. (1992).. Current oculomotor research: Physiological and psychological aspects (pp. CA: Singular Publishing Group. S. (1999).. and Rvachew. (1999). W. Hallowell. and Wood. Rockville. 16–20. (1999).). 33–48. PICApad PC [Computer software]. . (1993). W. 10. Masterson.. Seminars in Speech and Language. G. MS-DOS) [Computer program]. 287–291). and Hearing Services in Schools. J. Technological applications in the assessment of acquired neurogenic communication and swallowing disorders in adults. J. and Woodard. A. 378–406). 117–132. Language. Technology applications in the assessment of children’s language. C. L. Further Readings American Guidance Service. Bernthal and N. J. J. (1997). J. (1998). Australian Journal of Human Communication Disorders.. J. (1996). E. Jamieson. Integrating technology into school programs. S. (2001). 180– 188. Remediation of speech production errors with sound identification training. Tye-Murray. Woodcock. L. 28. Seminars in Speech and Language. L. J. R. and Reeves. and Channell. 1. Systematic analysis of language transcripts (SALT) (Version 4. J.). 203–215.. A comparison of a traditional test format vs. J. R.. (1992). Miller. H. (1996). K. Itasca. Speaking. (1992). B... and Bernhardt. M. D. J. B. and McRay. 243–254. Mahwah.. (in press). Neurotoxicology and Teratology.166 Part II: Speech Case. 37. B. and Channell. Seminars in Speech and Language. and Hearing Services in Schools. and Hearing Services in Schools. Linking software and hardware applications to what we know about literacy development. L. MD: Aspen Press. (1999). Integrating technology into school programs. PPVT-III ASSIST [Computer software]. 19. N. S. Instrumentation in clinical phonology. Wood. 20. R. 28. R. and Buder. Masterson. H. Computerized Articulation and Phonology Evaluation System (CAPES) [computer software]. Long. J. 371–380. and Oller. Apel.. Long. 10. (1999). L. J. Bankson (Eds. American Journal of Audiology.. B. S. and Channell. B.. J. Speech. DesBarres.. Seminars in Speech and Language.). A survey of computer use of public school speech-language pathologists. Odessa. Journal of Speech-Language Pathology and Audiology.. (1998). W. 251–269. Wetzel. L. (1996). Masterson. (2001).-B. Rvachew. B. (1999).. Evanston. J. Fitch. Porch. 20. S. E. Topics in Language Disorders. 20. C. R. NJ: Prentice-Hall. 20. 20. Accuracy of four language analysis procedures performed automatically.). Woodcock Scoring and Interpretive Program [Computer software]. and Hallowell. Apel. Training analogical reasoning skills in children with language disorders. Articulation and phonological disorders (4th ed.. The acoustic analysis of speech. C. J.. Long. Hallowell. B. L. G. Kuster. Use of technology in phonological assessment: Evaluation of early meaningful speech and prelinguistic vocalizations. Topics in language disorders. OH: Department of Communication Sciences. M. M. Learning to spell: Implications for assessment and intervention. L. J. American Journal of Speech-Language Pathology.. L. Laser videodisc technology in the aural rehabilitation setting: Good news for people with severe and profound hearing impairments. Language. and Fitch. Deubel. 53–61... Evans. 201–210.. L. (1998). L. Katz.. WI: Language Analysis Laboratory. and Katz. IL: Riverside. R. B. (1998). and Rvachew. 233–250. S. McRay. Speech. and Read.. K. Journal of Speech and Hearing Research. S. 16. 40– 47. reading. J. 8. Accuracy of four language analysis procedures performed automatically... (2002). Speech. T. Language sample analysis in the 21st century. (Eds.. University of Wisconsin. In J. 347–357. (1997). C. 33–36. 20. New York: Plenum Press. C. (1998). L. 30. In Becker. Fey. J. Seminars in Speech and Language. 365–370. Computerized Profiling (CP) (Version 9. J. S. L.. Scottsdale. J. and Katz. Letz. Cleveland. C. 27. R. (1999). Masterson. H.0. Englewood Cli¤s.. Using microcomputer technology to advance assessment and intervention for children with language disorders. San Diego. Miller. Butler and E. S. S. Dollaghan (Ed. and Crede. D. Silliman (Eds.. Speech perception training can facilitate sound production learning. and Perrey. (1999).. K. IL: Learning by Design. Use of technology in phonological intervention. (1997). Mahwah. San Antonio. Circle Pines. R. (2001). and Stierwalt. J. Seminars in Speech and Language. (1999). and McRay. J. Technology in the treatment of voice disorders. MacWhinney. Case studies of children using Fast ForWord. Masterson. 149–167. Fitch. American Journal of Speech-Language Pathology. W. American Journal of Speech-Language Pathology.. J. 219–232. The use of technology to facilitate language skills in school-age children. and Masterson. 134–136.

S. and physicians. including consulting with priests. and Korea). Micronesia. Laos. 1985). Cultural tendencies of AsianPacific Americans may be quite di¤erent from those of individuals born and raised in a Western culture. India. Languages. Attitudes Toward Disability and Treatment Methods. A person needs to endure hardships and persevere. and therefore share many similarities. and their English is influenced by various dialects and languages. or South Asia (India. New Zealand. including New Guinean. By the year 2020. 1994). A person is unique and individualistic. and how parents Table 1. childrearing practices. All over the world. including Khmer. There are di¤erences in how parents respond to their children’s language. The Asian-Pacific island cultures.000 in the United States. Table 1 provides a sampling of these di¤erences. Pacific Asia is divided into the following regions: East Asia (China. or spirits.Speech and Language Issues in Children from Asian-Pacific Backgrounds 167 Speech and Language Issues in Children from Asian-Pacific Backgrounds Asian-Pacific Americans originate from Pacific Asia or are descendants of Asian-Pacific island immigrants. for example. 2002). Cultural Di¤erences Between Asian-Pacific Americans and Western Groups Eastern Tendencies A person is not autonomous. including attitudes toward disability and treatment. Taiwan. However. healers. unique. Vietnamese. clansmen. and Tagalog. A person needs to feel good about self. In general. Qi-Gong specialists. Many Asian countries do not have medical records or cumulative school records. Southeast Asia (Philippines. Yao. caution should be taken not to overgeneralize this information in relation to a particular client or family. Dravidian. shamans. and special. Review all pertinent documents and background information.4 million. A person needs to be humble. Ilocano. population. A person is oriented toward harmony. A person makes rational choices. such as an imbalance in inner forces. and Hmong. elders. and Australia). herbalists. Oral reports are sometimes unreliable. hot or cold forces. In general. including Japanese and Korean (Ma. including Thai. A person is responsible for own actions and takes the consequences. China. Melanesia. Malaysia. Pregnancy and delivery records . Western Tendencies A person is autonomous. gods. Bangladesh. (4) Papuan. Disabilities may be explained by a variety of spiritual or cultural beliefs. Japan. (3) Austro-Asiatic. A person needs to self-reflect. Indo-Aryan. The following information is presented to provide an understanding of Asian-Pacific Americans in order to assist speech-language pathologists and audiologists in providing services to these culturally and linguistically diverse populations. Vietnam. Some believe disability is caused by karma (fate) or a curse. Singapore. languages. however. there are 15 major languages in India from four language families. the Indian subcontinent. observe. A person is di¤erent. A person is a partner in the community where people are mutually responsible for behaviors and consequences. including Chamorro. A person is part of society. surgical intervention is viewed as invasive and harmful. and (5) Altaic. resulting in guilt and shame. AsianAmerican children in U. Pakistan. 1990. Recommended Assessment Procedures The following assessment guidelines are often referred to as the RIOT (review. Pakistan. Van Kleeck. However. and Cantonese. Eastern cultures may view a disabling condition as the result of wrongdoing of the individual’s ancestors.477. Mandarin. 1995). Thailand). Malaysia. The recent Asian influx represents a diverse group from Southeast Asia. have interacted with and influenced each other for many generations. improve. AsianPacific Americans are the fastest-growing segment of the U. Indonesia. The hundreds of di¤erent languages and dialects that are spoken in East and Southeast Asia and the Pacific islands can be classified into five major families: (1) Malayo-Polynesian (Austronesian). Sri Lanka). Recommended assessment procedures and intervention strategies are provided. A person needs to maintain relationships and have constraints. people use di¤erent methods to treat illnesses and diseases. Among the Hmong. or fright. Additionally. demons. Asian-Pacific populations speak many languages. interview. and the Pacific islands (Polynesia. Numbering 10. socioeconomic and individual di¤erences must always be considered. A person is active in decision making. Childrearing practices and expectations of children vary widely from culture to culture (Westby. bad wind. What constitutes a disability depends on the values of the cultural group.8% of the nation’s population and 10% of California’s population (Population Reference Bureau. and culture. Indonesia. A cultural informant or an interpreter is generally needed to obtain this information because of the lack of English language proficiency of the parents or guardians. Cambodia. AustroAsiatic. Asian-Pacific Americans are extremely diverse in all aspects of life. schools will total about 4. Cultural Tendencies. 1995.S. test) protocol (Cheng. who interacts with children. 2001). A person needs to toot own horn. and families encourage children to initiate and continue a verbal interaction. They are adapted here for AsianPacific American populations: 1. spoiled foods. and other Pacific Rim areas. (2) Sino-Tibetan. and master skills. and Tibeto-Burman (Shekar and Hegde. representing 3. Childrearing Practices.

such as looking down when the teacher approaches Use of Asian-language-influenced English. problems of acculturation. the client’s frame of reference. letting them think through a problem and waiting for them to make the decision to participate in the treatment program. Interview questions are available from multiple sources (Cheng. using activities that are culturally and socially relevant. Alternative strategies should be o¤ered when clients or caregivers are reluctant to accept the treatment program recommended by the speech-language pathologist or audiologist. Langdon and Saenz. 1990. Expect frustration and possible misunderstanding. Interact with the client. The clinician needs information regarding whether or not the client is proficient in the home language. Clinicians need to be doubly careful and not interpret these di¤erences as deficient. In addition to traditional intervention techniques of modeling and expansion. Observe interactions at school. 1996):    Make no assumptions about what students know or do not know. such as speaking softly to persons in authority. Interview teachers. and the American educational system. and other informants and work with them to collect data regarding the client and the home environment. and undesirable. as well as historical and comparative data on the client’s language development. and experiences. Intervention activities and materials can be selected based on the client’s family and cultural background. Test the client using informal and dynamic assessment procedures in both the school language and the home language. and the ways the family spends time together are some areas for investigation. 2.168 Part II: Speech  might not have been kept. the understanding of social rules. confusion regarding one’s sense of identity relating to culture. Other individuals can be e¤ective in sharing their personal stories about their experiences with therapy. The clinician should be patient with the clients. and ideology between Asian students. Anticipate their needs and greatest challenges. and family. Asian-Pacific American children may be fluent in English but use the discourse styles of their home culture. 1991. 2002. contrasting influences from home and the classroom. Intervention should be constructed based on what is most productive for promoting communication and should incorporate the client’s personal and cultural experiences. The family’s home language. language. Use the portfolio approach by keeping records of the client’s performance over time. Direct observation of social behavior with multiple participants allows the evaluator to observe the ways members of di¤erent cultures view their environment and organize their behavior within it. the patterns of language usage. and histories of the Asian-Pacific population. such as a frown signaling concentration rather than displeasure Short responses Use of a soft-spoken voice Taking few risks These are just a few examples of the observed behaviors that may be misinterpreted. religions. society. This cognitive-ecological-functional model takes into account the fact that clients often behave differently in di¤erent settings (Cheng. Following are some suggestions to create an optimal language learning environment and to reduce di‰cult communication (Cheng. The clients or caregivers may also be asked to talk with other Asian-Pacific Americans who have experiences with treatment programs. The family can provide valuable information about the communicative competence of the client at home and in the community. both in and outside the classroom. its proficiency in di¤erent languages. 1996). Questions should focus on obtaining information on how the client functions in his or her natural environment in relation to age peers who have had the same or similar exposure to their home language or to English. 3. These di‰culties can include the background of traditions. Salient and relevant features of the client’s culture should be highlighted to enhance and empower the client. Seeking assistance from community leaders and social service providers may also be necessary to convince the clients of the importance of therapy or recommended programs. Sociol and psychological di‰culties arise in the conflict of culture. family members. and the implications of receiving special education services. which may appear impolite. especially if the birth was a home birth or in a refugee camp. speech-language pathologists can include activities such as those discussed by Cheng (1989). aberrant. such as the deletion of plural and past tense    Delay or hesitation in response Frequent topic shifts and poor topic maintenance Confused facial expressions. their parents. . and avoiding close physical contact. 1999):        Lack of participation and lack of volunteering information Di¤erent nonverbal messages Embarrassment over praise Di¤erent greeting rituals. looking down or away. and at home. The discourse styles in e¤ect in American homes and schools may di¤er from those that are practiced in Asian classrooms. Behaviors that can be easily misunderstood include the following (Cheng. 1991). Observe the client over time in multiple contexts with multiple communication partners. 4. Inviting them to special classes or speech and language sessions is a useful way to provide the needed information. disordered. peers. being sensitive to his or her needs to create meaning based on what is perceived as important. What clinicians learn from the assessment should be integrated into their intervention strategies. Surface analysis of linguistic and pragmatic functions is not su‰cient to determine the communicative competence of children and might even misguide the decision-making process. the definition of disability. There are many challenges professionals face in working with the Asian-Pacific American populations.

Paper presented at the Israeli Speech and Hearing Association International Symposium on Bilingualism. W. and Saenz. Of course. On-line. Journal of Child Communicative Disorders.krysstal. 3. Integrating language and learning for inclusion. A. Cheng.zompist. London: Bergin and Garvey. CA: Academic Communication Associates. 9–21. (1989). L. (1991). Dutt (Ed. Population Reference Bureau. needle. CA: Singular Publishing Group. and Hegde. In L. Cheng. Assessing Asian language performance: Guidelines for evaluating LEP students. —Li-Rong Lilly Cheng Cheng. I. Ma. Beyond bilingualism: A quest for communicative competence. Southeast Asia: Realm of contrast. 67–68. Boulder. Instrumental  169   Encourage students to join social activities such as student government. C. Journal of Childhood Communication Disorders. Clinicians need to be creative and sensitive in their intervention to provide comfortable. and personal history of the individual lays a solid foundation to further explore the client’s strengths and weaknesses. Ethnographic interviewing: Asking the right questions to the right people in the right way. Topics in Language Disorders. (1995. WI). (1990). L. morphology. (1994). Israel.html http://www. Speech articulation proper is deemed here to begin with the movement of muscles required to produce aerodynamic changes resulting in the flow of an airstream (see Laver. This area has been investigated using electromyography (EMG). Instrumental The instrumental analysis of speech can be approached through the three main stages of the speech chain: articulatory. Cultural diversity. 1–14.). Language Assessment and Intervention with Multicultural Students: A Guide for Speech-Language-Hearing Professionals. CA: Academic Communication Associates. as language is a social tool and should be used for fulfilling multiple social needs and requirements. M. using culturally unique experiences as topics for discussions) and conducting social/pragmatic activities (Cheng. N. J. Gentil and Moore. home language. Ball and Rahilly. Communication disorders in multicultural populations. Some publishers that have developed materials for use with Asian-Pacific American populations include Academic Communications Associates (Oceanside. Nurture bicultural/multicultural identity. T. (1996). The bilingual language-delayed child: Diagnosis and intervention with the older school-age bilingual child. L. Washington. E. Haifa. Providing speech-language and hearing services to Asian-Pacific Americans is challenging. 1997). July).. culture. (1996). H. 13. L. K. (1999). (1995). clubs. 1989). American Journal of SpeechLanguage Pathology. Facilitate the transition into mainstream culture through such activities as role-playing (preparing scripts for commonly occurring activities. 13.). Park and M. L. Shekar. L. . Introduce multicultural elements not only in phonology. Communication Skill Builders (Tucson. In C. L. and enriching services for all clients.S. and hooked wire) are used to gather data on electrical activity within target muscles. In A. Newbury House (Rowley. Boston. (2001).Speech Assessment. Asian and Pacific American cultures. Oceanside. Cheng. Cheng (Ed. and languages. and these data are matched with a simultaneously recorded speech signal (Stone. productive. C. DC: U. L. AZ). and ritualized patterns. culture. L. India: Its people. 1996. The results of assessment should take into consideration the cultural and pragmatic variables of the individual. 1994. and auditory phonetics. L. CA). The goals of intervention must include the enhancement of appropriate language and communication behaviors. Bureau of the Census. MA: Butterworth-Heinemann. but also in pragmatics. Assessment procedures need to be guided by the general principles of being fair to the culture and http://www. Service delivery to Asian/Pacific LEP children: A cross-cultural framework. Thinking Publications (Eau Claire. Battle (Ed. CO: Westview Press. Sociocultural adjustment of ChineseAmerican students. L. Chi (Eds. Oceanside. MA). This technique has been used to examine both normal and disordered speech. (1985). AsianAmerican education. L. Westby. C. Preassessment information on the language.travlang. Potential bias in training parents as conversational partners with their children who have delays in language development. In D. 9. Cheng. and literacy. Intervention can be extremely rewarding when culturally relevant and appropriate approaches are used. Van Kleeck. On-line Resources http://www.. Cheng. Topics in Language Disorders. and organizations to increase their exposure to di¤erent types of discourse. 113–119. The identification of communicative disorders in Asian-Pacific students. the neurological aspects of both speech production and perception can be studied through the use of brain imaging techniques. electrodes of di¤erent types (surface. L. 16. 1999).).html Speech Assessment.). semantics. San Diego. L. In this way the timing of muscle activity in relation to di¤erent aspects of speech can be investigated. This entry reviews the instrumentation used to assess the articulatory and acoustic phases. such as a birthday party and a Thanksgiving celebration. In EMG. L. muscle movements also occur throughout articulation. (2002). and syntax. Langdon. Areas studied include References Cheng. Auditory phonetic techniques are covered elsewhere in this volume. 101–111. (1990). Although speech planning in the brain (neurophonetics) lies outside the traditional tripartite speech acoustic. L.

and certain acquired neurological problems. The velotrace is an instrument designed to indicate directly the height of the velum (see Bell-Berti et al. 1997). orbicularis oris inferior (OOI). however. as stroboscopic endoscopy allows the viewer to see individual movements of the folds (see Abberton and Fourcin. where a variety of phonation types may be implemented. as part of the device must be inserted into the nasal cavity to sit on the roof of the velum. tongue. and generally also a microphone to record the speech signal. Both approaches have been used in the investigation of normal and disordered voice.. 1993). Hardcastle and Gibbon the respiratory and laryngeal muscles. This technology is often coupled to a stroboscopic light source. Most important here is the placement of the individual articulators. Endoscopy. Indirect investigation of vocal fold activity is undertaken with electroglottography (EGG). 1996) consists of a wire band placed around the subject’s chest that measures changes in cross-sectional area during inhalation and exhalation. The velotrace is invasive. for example.) movements of the folds. Figure 1 shows EMG traces from a patient with Friedreich’s ataxia. a rigid or flexible endoscope connected to a camera is used to view the Figure 2. Aerodynamic activity in speech is studied through aerometry. The study of laryngeal activity (more particularly. A variety of devices have been used to measure speech aerodynamics (Zajac and Yates. Trace adapted from a Kay Elemetrics nasometer showing normal and hypernasal versions of ‘‘eighteen.170 Part II: Speech Figure 1. This technique allows vocal fold movement to be extrapolated from measuring the varying electrical resistance across the larynx. Abberton and Fourcin. Many systems have employed an airtight mask that is placed over the subject’s face and attached to a pneumotachograph. anterior belly of the digastric (ABD). also termed electrolaryngography (see Stone. airflow from the lungs passes through the larynx. Velic action and associated di¤erences in oral and nasal airflow (and hence in nasal resonance) can also be measured directly or indirectly. and various disorders. of vocal fold activity) can be direct or indirect. see Stone. In direct study. If the focus of attention is lung volume changes. and soft palate. The mask contains sensors to measure pressure changes and airflow at the nose and mouth. 1997). The next step in the speech production chain is the articulation of sounds. Averaged integrated EMG signals for the mentalis muscle (MENT). This is an airtight box that houses the subject. two external microphones to measure airflow di¤erences. In normal pulmonic egressive speech. nineteen. while nasometric devices of varying sophistication measure oral versus nasal airflow (see Zajac and Yates. and the depressor labii inferior (DLI) for a patient with Frie` dreich’s ataxia uttering /epapap/. is invasive. (Courtesy of Michele Gentil.’’ . Nasometers measure indirectly using. orbicularis oris superior (OOS). twenty. against which the airflow can be plotted. 1997). then a plethysmograph may be employed. Figure 2 shows a trace from the Kay Elemetrics nasometer of hypernasal speech. and electropalatography (EPG) has proved to be a vital development in this area of study. including disorders of voice and fluency. muscle groups in the lips. and any changes to the air pressure within the box (caused by changes in the subject’s lung volume) are recorded. and use of a rigid endoscope precludes normal speech. 1996. 1997). A simpler plethysmograph (the respitrace.

frequency. 1997). and x-ray microbeam imaging. Reliable analysis depends on good recordings (see Tatham and Morton. which can be used to construct an image of the tissue involved. Instrumental 171 Figure 3. which uses low doses of radiation to give clear pictures of the vocal tract. which provides good frequency resolution but poor time resolution. The final imaging technique to be considered is magnetic resonance imaging (MRI). This palate has a large number of electrodes embedded in it (from 62 to 96. If a brief radio pulse is introduced at the same frequency as the precessing. 1996. As with x-ray microbeam imaging. Reading EPG3 system stylized palate diagram (left) showing misarticulated /s/ with wide channel.. A thin acrylic artificial palate is made to fit the subject. 1997). the protons are moved out of alignment and then back again. (1997) describe this technique. they emit weak radio signals. This field causes hydrogen protons (abundant in human tissue) to align but also to precess. In this technique the subject is placed within alternating magnetic fields generated by transmitter coils in a helmet assembly. creating an electromagnetic field. Farmer. the alveolar region).Speech Assessment. Ball and Grone. and the resultant tongue-palate contact patterns can be shown on a computer screen. depending on the system employed) to cover important areas for speech (e. giving good time resolution but poor frequency resolution. EPG has been used to study normal speech and a wide range of disordered speech patterns. amplitude. When the tongue touches these electrodes. Figure 4 shows ultrasound diagrams for two vowels and two consonants. in which the movements of pellets attached to relevant points of the tongue and palate are tracked. This allows the technique to be used both for research and for feedback in therapy. Kay Palatometer stylized system palate diagram (right) showing target /s/ articulated at the postalveolar region. The electrodes are normally sampled 100 times per second.. a waveform displays amplitude versus time. a narrow-band spectrogram shows frequency versus time using a narrowband pass filter (around 29 Hz). among them videofluorography. These . For example. Because of the dangers of radiation. The oldest of these tech¨ niques is x-radiography. 1991. and intensity aspects of a speech signal (see Baken and Danilo¤. alternative imaging techniques have been sought. the tracked points can be used to infer the shape and movements of articulators within the vocal tract. tongue tip. MRI can provide good images of the vocal tract but currently not at su‰cient frequency to allow analysis of continuous speech. Small receiver coils are placed at articulatorily important sites (e. mapping of the tongue (from below) is possible. tongue body).g. Because ultrasound waves do not travel through the air. which uses the time taken for sound waves to bounce o¤ a structure and return to a receiver to map structures in the vocal tract. As they realign. Electromagnetic articulography (EMA) is another tracking technique. Among these is ultrasound. Speech analysis research has generally concentrated on wideband spectrograms and spectral envelopes. All of these imaging techniques have been used to study aspects of both normal and disordered speech. a wideband spectrogram displays frequency versus time using a wideband pass filter (around 200– 300 Hz). Other ways of examining articulation (and indeed a whole range of speech-related activity) can be subsumed under the overall heading of speech imaging (see Stone. Spectrographic analysis packages currently allow users to analyze temporal. and the patterns are displayed in real time. A variety of di¤erent x-ray techniques have been used in speech research. The imager surrounds a subject with electromagnets. 1997). Figure 3 shows tongue-palate contact patterns in a stylized way for two di¤erent EPG systems. but mapping of tongue–palate distances is not. and spectral envelopes show frequency versus intensity at a point in time (produced either by fast Fourier transform or linear predictive coding).g. or wobble. they fire. as the palate cannot be mapped through the air space of the oral cavity. Acoustic analyses via sound spectrography are now easily undertaken with a range of software programs on personal computers as well as on dedicated hardwaresoftware configurations such as the Kay Elemetrics Sonagraph. The movements of the receiver coils through the alternating magnetic fields are measured and recorded by computer.

’’ (Courtesy of Joan Rahilly.) . Wideband spectrogram of a disfluent speaker producing ‘‘(provin)cial t(owns). Ultrasound images of two vowels and two consonants. (Courtesy of Maureen Stone.) Figure 5.172 Part II: Speech Figure 4.

Electro-magnetic midsagittal articulometer (EMMA) systems for transducing speech articulatory movements. R. Papers in speech communication: Speech production. Gracco. (1991). (1998).. Ball and C.). and Fourcin. MRI-based speech production study using a synchronized sampling method. 28.). (Eds. Journal of Communication Disorders. Recording and displaying speech. Tatham. London: Whurr.). W. 19. aphasia. 92.. Videostroboscopy of the larynx. Ball References Abberton.).). apraxia and dysarthria. Stone. Ball. M. Introduction to sound (3rd ed. 251–266. and Danilo¤.. D.. Imaging techniques for the investigation of normal and disordered speech production. Hardcastle.). Electrolaryngography. J. F. (Eds. (1995).. (1999). Perkell. (1997). NY: Acoustical Society of America. Readings in clinical spectrography of speech. (1996). I. Code (Eds. J... and Laver.. MA: MIT Press. Segment duration can easily be measured from spectrograms in modern analysis packages.. 1–21). D. Kent. (1994). 303–329. Instrumental 173 both show formant frequencies (bands of high intensity at certain frequency levels). Journal of Speech and Hearing Research. acoustics and perception of speech (3rd ed. Hardcastle. Principles of phonetics. R. Ball and C. UK: Blackwell. Physiology of speech production. (Eds. (1994). Speaks..Speech Assessment. D. 149–193). NY: Acoustical Society of America. R. CA: Singular Publishing Group. Gibbon. In M. London: Whurr. (1976). Stone. S. K. M. 20. (1993). Code (Eds. Figure 5 shows a wideband spectrogram of disfluent speech. R.. M. Code (Eds. V. —Martin J. J. Journal of Phonetics.. M. Speech aerodynamics. Oxford. The rise and fall of the soft palate: The velotrace. London: Arnold. while plosives can be noted from the lack of acoustic activity during the closure stage and the coarticulatory e¤ects on the formants of neighboring sounds. and Nicolaidis. Principles of experimental phonetics (pp. Woodbury. Lieberman. Code (Eds. . D. Westbury. W. Acoustic phonetics. Ball and C. N. Ball and C.. L. Measurement of airflow in speech. Atal. J. Ball and C. Woodbury. London: Whurr.. Imaging techniques. 155–176.. and the speech of the hearingimpaired. (1992). C. F. D. M. Woodbury. St. R. (2001).. (1992). M. (1997). In M. and Stone. Garabieta. Three-dimensional tongue surface shapes of English consonants and vowels.). J.). M. D. (1997). and Read. (1997). Instrumental clinical phonetics (pp. London: Whurr. Gentil. 375–379.. London: Whurr. (1991). (1977). EPG data reduction methods and their implications for studies of lingual coarticulation. and Bless. Journal of the Acoustical Society of America. 3078–3096.. M. 107–120. K. C. W. Fricatives are distinguishable from the boundaries of the broad areas of frequency seen clearly on a spectrogram. In M. J. 1–10. Papers in speech communication: Speech processing. The significance and measurement of head position during speech production experiments using the x-ray microbeam system.. Louis: Mosby. and Miller. 20. (2000). Lass (Ed. (1991). Matthies. In M. J. Kent. Phonetics: The science of speech. Farmer.. In N. J. 93. child speech disorders. (1999). CA: Singular Publishing Group. M. F. Nakamura. EMG analysis of speech production of patients with Friedreich disease. Masaki. Principles of experimental phonetics. Cambridge. San Diego. K. Y.). and Lundberg. J. The handbook of phonetic sciences. fluency. A.). Ball. Honda. Code (Eds. Hardcastle. and Yates. and Rahilly. Journal of the Acoustical Society of America.. Electropalatography and its clinical applications.).. P. London: Whurr. Papers in speech communication: Speech perception. Journal of the Acoustical Society of America. R. J. (1993). Rothenburg. R. Louis: Mosby.. E.). Code (Eds. In M. Rothenburg. Clinical Linguistics and Phonetics. J. Journal of the Acoustical Society of America.). Laver. 13–24.. M. 64–86). Ball. Harris. Miller. (Eds. Speech: A special code.. Various pitch extraction algorithms are provided for the investigation of intonation. (1991).). and Jackson. M. and Atal.. Clinical measurement of speech and voice (2nd ed. 89. Ball.. J. A. Methods in clinical phonetics. Y. and Moore. and Lowry. and Raphael. Farmer (1997) provides an extensive review of acoustic analysis work in a range of disorders: voice.. (1996). K. Instrumental clinical phonetics (pp. Svirsky. Instrumentation for the study of speech physiology. San Diego.. Borden. Hardcastle. MA: MIT Press. W. Philadelphia: Lippincott Williams and Wilkins. ¨ Ball and C. (2001). M.). 4. Gentil. 22–63). M. St. CA: Singular Publishing Group. Instrumental clinical phonetics. Speech science primer: Physiology. 87. Lass. Instrumental clinical phonetics (pp. In M. Ross. Baken. I. J. Kent. 87–118). and Orliko¤. M. J. M. B. and Kent. UK: Cambridge University Press. Dagenais. J. Zajac.. Krakow. M.. (1991). B. Cambridge. M... (2002). (1996). A multichannel electroglottograph. A. D. The acoustic analysis of speech. 495–524). Jr. B. (1999). R... Baken. Fujimoto. M. London: Whurr. R. which are useful in the identification of and discrimination between vowels and other sonorants. London: Academic Press. J. 194–227). Bell-Berti. A three-dimensional model of tongue movement based on ultrasound and x-ray microbeam data. A. (1997). Code (Eds.. Journal of the Acoustical Society of Japan. et al. Cambridge.. (1991). 36–43. G. (1990). Advances in Speech-Language Pathology. Stevens. J. O. 6. In M. and Morton. 2416A. Instrumental clinical phonetics (pp.. Further Readings Atal. Electromyography. Journal of the Acoustical Society of America. and Grone. and Gibbon. 2207–2217. (1990).).. (1997). Electropalatography in the treatment of articulation/phonological disorders. J. London: Whurr. J. Stone. (1997). 119–148). 3. CA: Singular Publishing Group. Tiede. B. Instrumental clinical phonetics (pp. (pp. H. Instrumental clinical phonetics (pp. Cohen. M. Shimada. San Diego.. 99. Journal of Voice. W.. (1996). J. London: Whurr. Miller. K. Spectrography. 1782–1791. C. (1977). Ball and C. (Ed. and Horiguchi. NY: Acoustical Society of America. Hirano. San Diego. S.

Asymmetries in the distribution of sounds may be further indicative of systematic rule-governed alternations in sound production (Kenstowicz. Phonemes are used to signal meaning di¤erences in a language. then. for example ‘‘pat’’ and ‘‘bat’’ or ‘‘cap’’ and ‘‘cab. the phonetic inventory may be quite large despite errors of production.’’ Alternations are typically sampled by adding either a prefix or su‰x to a base word in order to change the context in which a sound occurs. 1985). and final. these gaps would be characterized as a type of phonotactic constraint (Dinnsen. There are two general types of rule-governed change: allophonic variation and neutralization. whereas the implied property Y is unmarked and predictably easier to learn. Children’s phonetic inventories reflect the range of individual variability expected in development. These same methods are also well-suited to the study of language development. A phonetic inventory comprises all sounds produced or used by a child. Thus. An example is /t/ produced as aspirated in word-initial position ‘‘tap. the contrast between phonemes is no longer apparent at the phonetic (surface) level. In addition to examining these properties. there is a one-to-many mapping between phoneme and phones in allophonic variation. The Distribution of Sounds. including the phone tree methodology (Ferguson and Farwell. initial.’’ Here. but the phonetic characteristics of the output di¤er predictably by word position. a¤ricates. for example. As with segmental structure. or population of study. and Neumann. 1994). Rule-Governed Alternations. the nonoccurrence of these sound classes in children’s speech parallels markedness. there is a many-to-one mapping between phonemes and phone.174 Part II: Speech Speech Assessment in Children: Descriptive Linguistic Methods Descriptive linguistic methods have long been used in the analysis of fully developed primary languages. Phonemes are conventionally determined by the occurrence of minimal pairs. age.’’ and as unreleased in word-final position ‘‘it. Markedness defines lawful relationships among sound categories that have been found to hold universally across languages of the world.’’ In each case. these would be said to function as phonemes in the di¤erentiation of meaning. therefore. sounds may be used in all word positions. In the acquisition literature. For children with speech sound disorders. A minimal pair is defined as two words identical except for one sound. The Phonemic Inventory. Descriptive methods are a preferred analytic tool because they are designed to gather evidence that reveals the hallmark and defining characteristics of a sound system. 1997). In linguistic terminology. the phonemic inventory is generally smaller than the phonetic inventory (Gierut. In development. In development. particularly the analysis of children’s speech sound systems. The implying property X is taken to be marked. but not vice versa. From a linguistic perspective. descriptive linguistic methods may evaluate prosodic levels of structure by examining units larger than the sound. restrictions on the distribution of sounds correspond to markedness. 1984). The Phonetic Inventory. or they may be limited to certain contexts. For children. complementary methods have been designed to further depict developmental variation. independent of theoretical orientation. Consequently. One type of markedness is implicational in nature. Distribution refers to where sounds (phones or phonemes) occur in words and is determined by examining context. the consonants /p/ and /b/ are the only point of di¤erence in each pair of words. Allophonic variation occurs when a single phoneme has multiple corresponding phonetic outputs that vary by context. As such. As with the phonemic inventory.’’ as flap in intervocalic position ‘‘bitter. For children with speech sound disorders. 1975) and the typology of phonetic complexity (Dinnsen. In children. Kehoe and Stoel-Gammon. the conventional criterion for determining the phonetic status of sounds is a two-time occurrence independent of the target or context. regardless of whether those sounds are correct relative to the intended (adult) target. Gaps in the phonemic repertoire often a¤ect the sound classes of fricatives. these four properties define the most basic elements of a sound system at a segmental level of structure. and liquids. Rule-governed alternations occur when morphologically related words are produced in di¤erent ways. phonemic gaps in the inventory correspond to more marked (di‰cult) structures of lan- guage. The defining properties of descriptive linguistic analyses of children’s sound systems are discussed in this article. such as permissible syllable types and combinations and the overlay of primary and secondary stress on these in ´ the formation of words and phrases (Lleo and Prinz. the target sound is /t/. and may consist of sounds that do not occur in the ambient language. 1984). 1994). intervocalic. nontarget allophonic variation and neutralization have been observed and parallel the rules of fully developed languages of the world (Camarata and Gandour. the emergence of target-appropriate morphophonemics occurs later in language development. 1996. with children having a tendency toward unmarked as opposed to marked structure. such that the occurrence of property X in a language implies property Y. 1992). An example is /t/ and /d/ both produced as flap in intervocalic position ‘‘writer’’ and ‘‘rider. For children. that is. and is presumably more di‰cult to acquire. whereas fricatives and liquids commonly occur postvocalically but not word-initially (Smith. Simmerman. any sound produced twice is included in a child’s phonetic repertoire (StoelGammon.’’ In neutralization. ‘‘electric’’ but ‘‘electricity. 1973). Neutralization occurs when two or more phonemes are merged into one phonetic output in a well-defined context. obstruent stops commonly occur word-initially but not postvocalically. Together. children typically use unmarked pro- .

. Phonology in generative grammar. For children with speech sound disorders. ´ Lleo. D. A number of theories have been advanced to account for the fundamental properties of sound systems. Ritchie and T. Stoel-Gammon (Eds. syllable shape processes. Handbook of child language acquisition (pp. Cambridge. Fey. and Cortese. M. 1999). J. Elbert. A. the relationship between perception and production in speech sound development. Kenstowicz. and to descriptively label these patterns as phonological processes. including autosegmental. implications (pp. (1984). Ferguson. Journal of Speech and Hearing Disorders. Phonemic structures of delayed phonological systems. underspecification. In C.. 495–508). The Speech Production-Perception Task is one clinical technique that establishes a child’s ability to perceptually di¤erentiate target sounds from their corresponding substitutes (Locke. N. and C. 12. and G. Journal of Speech and Hearing Research. S. D. 1995). (1991). Language. and other processes. metrical. D. they are considered external (not primary) evidence in conventional linguistic analyses of sound systems (Anderson. (1989). H. A... On describing idiosyncratic phonologic systems. Language. Cambridge. Relational analyses establish a one-to-one correspondence between a child’s errored outputs and intended target sounds. and Prinz. Journal of Child Language. Bhatia (Eds. involving di¤erent manners or places of production than the target. Chomsky. Language. C. C. and Cortese. These challenges have been handled in di¤erent ways by different linguistic theories. B. 23. 1991). and feature geometry frameworks (Goldsmith. and. implications (pp. use. Weismer (Eds. 113–144. Gierut. MD: American Speech-Language-Hearing Association. Camarata. (1992). In W. M. Menn. because these skills lie outside the domain of phonology in particular and language in general. such as reversals in the sequencing of sounds or articulatory di¤erences in sound production such as lisping. optimality theory (Prince and Smolensky. B. On the nature. Words and sounds in early language acquisition: English initial consonants in the first fifty words. A. 1997). 23. Kehoe. C. nonlinear phonology. Klein. they have served to outline a well-defined set of research issues about children’s speech sound development that as of yet remain unresolved.). (1992). R. Central questions bear on the nature of children’s mental (internal) representation of sound. Finally. there are other methods of analysis that may be relevant to a comprehensive characterization of the sound system (Fey. function. Why phonology isn’t natural. A. Supplementary clinical methods have also been designed to evaluate perceptual or metalinguistic skills. Stoel-Gammon (Eds. B. and C. Lederer. Consonant clusters in child phonology and the directionality of syllable structure assignment. Variation in developing and fully developed phonologies. L. 291–316. and acquisition of child language. but at the core. Four main categories of phonological processes characterize children’s commonly occurring developmental errors (Ingram. (1984). research. Speech and Hearing Services in Schools. Phonological disability in children. 493–539. (1994). In M. Menn. S. 73. (1996).. 1992). (1999). Other metalinguistic procedures employ categorization tasks that evaluate a child’s judgment of the similarity of target sounds and their substitutes (Klein. Phonological development: Models. see speech sound disorders in children: description and classification). (1992). Although these methods may have clinical utility in isolating the source of breakdown and in designing appropriate intervention for a child’s speech disorder. MA: Blackwell. (Ed... research. (1994). 33–54). 1992. MA: Blackwell. Lederer. 419–439. These analyses are intended to capture the patterns of a child’s errors. C. 225–232. Articulation and phonology: Inextricable constructs in speech pathology. 49.). Rockville. Journal of Child Language.). and Stoel-Gammon. with preferences for open syllables and trochaic (strong-weak) stress assignment. including standard generative and natural frameworks. 51. 262–266. 191–210). L. E. Gierut References Anderson. Acquisition data present unique challenges for linguistic theory because of the inherent variability within and across children’s sound systems within and across points in time (Chomsky. Phonological theory and the misarticulating child (pp. 1981). and organization of sounds in a speaker’s mental lexicon. Ingram. Timonium. assimilatory processes.). Linguistic Inquiry. London: Cole and Whurr. including those pertinent to children with speech sound disorders.). Leonard. The handbook of phonological theory. Dinnsen. 5–17). and the contribution of innateness and maturation to language acquisition. most recently. and Farwell. A. J. one of the most central aspects of a descriptive linguistic analysis of a sound system is the interpretation or theoretical account of the data. E. D. The acquisition of prosodic structure: An investigation of current accounts of children’s prosodic development. 1989).. Among the most recognized frameworks are linear phonology. A. Methods and empirical issues in analyzing functional misarticulation. A. H. (1997). —Judith A. 31–56. J. C. and Gandour. E. In C. M. A. Each relies on a unique set of assumptions about the structure. S. J. (1995). 34. L. New York: Academic Press. (1981). These categories are substitution processes. . and Neumann. Dinnsen. L. M. M. H. (1975). Children’s knowledge of auditory/articulatory correspondences: Phonologic and metaphonologic.Speech Assessment in Children: Descriptive Linguistic Methods 175 sodic structure. Ferguson. Ferguson. as these skills may a¤ect a child’s knowledge of the ambient sound system. MD: York Press. Children with speech sound errors are likely to use other unusual phonological processes and to persist in their use of these processes for longer durations than are typical (Leonard. involving sounds produced more alike in a word than in the target. Phonological development: Models. Dinnsen. 559–564. 21. involving di¤erent canonical (consonant-vowel) shapes than the target. Timonium. MD: York Press. Models of phonological development and children with phonological disorders. Simmerman. Any formal theory of language must account for the facts of acquisition. Goldsmith. 1980).

Individual variation and its relevance to a theory of phonological acquisition. Gierut. Bernhardt. Vihman. L. 1482–1498. The lower airways consist of the trachea. Oral communication in children occurs in tandem with growth and maturation of the structures of the speech apparatus. Journal of Speech and Hearing Disorders. J. H. 269–276. Macken. San Diego. D..). Edwards. (1985). 123–143.. A. (1981). 11–29. The growth of phonemic and lexical patterns in infant speech. The acquisition of phonology: A case study. A. R. (2001). MacNamara (Ed. (1983). A. Phonological assessment of child speech. Speech and Hearing Services in Schools. P. 14. 419–432. and articulatory subsystems of the speech apparatus are at risk for pathological changes a¤ecting the development of speech. Dinnsen (Ed. Nonlinear phonology: Introduction and clinical application. D. in fact. M. Speech Development in Infants and Young Children with a Tracheostomy A tracheostomy is a permanent opening of the trachea to outside air. Phonetics and phonology: Vol. (1998). and Stoel-Gammon. Kent. The respiratory subsystem of the speech apparatus comprises the lower airways. 42. CA: Singular Publishing Group. Journal of Linguistics. A. 47–78). In particular. J. McGregor. L. Haas. 1993). C. Goad. A functional analysis of phonological knowledge and generalization learning in misarticulating children. Gerken. 37. the procedure is invaluable for acute and long-term airway management (Fry et al.. Schwartz. 72. Phonological acquisition and change. D. 45. The new phonologies: Developments in clinical linguistics. New York: Academic Press. In D. Smith. Cambridge. UK: Cambridge University Press. 28.. The underspecification of coronals: Evidence from language acquisition and performance errors. 2: The Special Status of Coronals (pp. CA: College-Hill Press. Gandour. J. J. N. B. Phonological development: The origins of language in the child.. San Diego. 1604–1610. Gierut. Journal of Communication Disorders. 239–246. Phonetic inventories. B. laryngeal. A. Netherlands: Mouton. Kiparsky. (1999).000 infants and children per year who need a tracheostomy.). Chin. (1973). (1968). and the lungs. C. diaphragm. D. Ingram. Feature geometry in disordered phonologies. 708–726. J.. (1983). Journal of Speech and Hearing Research.. 30. 15–24 months: A longitudinal study. and Gierut. Clinical Linguistics and Phonetics. J. The nondeviant nature of deviant phonological systems. 1989). (1991). Language. CA: Academic Press. The Hague. Language. 281–292. J. 505–512. and Stampe. and Ball. and abdominal structures. Some clinically novel procedures. The study of natural phonology. J. M. When a tracheostomy or mechanical ventilation is used over a long period. (1991). Journal of Speech and Hearing Research. UK: NFER-Nelson..). A.176 Part II: Speech Locke. J. Grunwell. J. the right and left mainstem bronchi. and Stemberger. some findings. D. (1977). M. H. (1980). 462–479. S. Clinical applications of recent advances in phonological theory. (1987). (1987). Cambridge. Language. (1963). (1996). Procedures for the phonological analysis of children’s language. (1992). (1999). W. 5. and Schwartz. K. L. Neuromuscular or biomechanical di‰culties resulting from altered patterns of growth or structural problems can negatively a¤ect the development of oral communication. (Ed. aphasia and phonological universals. 1985). Journal of Child Language. 596–603. Child language. Prunet (Eds. D. The inference of speech perception in the phonologically disordered child: Part II. H. Journal of Speech. Language. Optimality: From neural networks to universal grammar. Journal of Speech. Optimality theory in phonological acquisition.). The primary reason for performing a surgical tracheostomy is for long-term airway management in cases of chronic upper airway obstruction or central or obstructive sleep apnea. San Diego. Further Readings Barlow. Current approaches to phonological theory (pp. Language Learning and Thought (pp. and Smolensky. Journal of Speech and Hearing Research. Clinical forum: Recent advances in phonological theory and treatment. Bernhardt. Phonological analysis of a case of dyslalia. and Hearing Research. R. G. Language. 275. B. R. Barlow. (1980). New York: Academic Press. A. P. P. the impact on communication and feeding behavior can be significant. (1997). and Hearing Research.. Although the mortality associated with a chronic tracheostomy in young children is twice that in adults. M. G. 683–712. Syllable onsets: Clusters and adjuncts in acquisition. and Hearing Services in Schools. 19. Windsor. L.. M. It most often requires a surgical procedure for closure. (1979). (1985).. 35. In C. C. (Eds.. Language. Donegan. (1943). 16. Elbert. Stemberger.-F. In J. and di¤ers in shape and bio- . R. On the acquisition of phonology. Prosodic structure in young children’s language production. (1992). A. Most of the estimated 900–2. Bloomington: Indiana University Press. (1994). 23.. 32. rib cage. Science. and Dinnsen. or both for a month or more are. less than a year old (Singer et al. 28. the respiratory. K. 126–173). 445–468. Prince. Jakobson.). Baltimore: University Park Press. (1981).. and Dinnsen. J. Locke. 329–337. The child’s lexical representation: The ‘‘puzzle-puddle-pickle’’ evidence.. (1996). A.. Stoel-Gammon. 14. Speech. and Ingram. L. Phonology: Applications in communicative disorders. (1997). Journal of Speech and Hearing Disorders. L. 1–17. V. Paradis and J. P. A. Journal of Speech and Hearing Research. P. D. The use of assisted ventilation for more than 1 month in the first year of life has been considered to constitute a chronic tracheostomy (Bleile. their use. M. Velten. J. 225–297. P. MA: Blackwell. San Diego. or to provide long-term mechanical ventilatory support. Handbook of phonological development from the perspective of constraintbased non-linear phonology. The tracheobronchial tree is much smaller in children than in adults. 42. CA: Academic Press. Converging evidence for underlying phonological representations in a child who misarticulates. a ventilator. 181–199). and Menn. and Stoel-Gammon. and Shriberg.

Speech Development in Infants and Young Children with a Tracheostomy


mechanics as well. The trachea in young children has been described as the size of a soda straw, and is highly malleable (Fry et al., 1985). The infant tracheal diameter is approximately 0.5 cm, whereas adult tracheal diameters are 1.5–2.5 cm. C-shaped cartilage rings joined by connective tissue help to keep the trachea from collapsing against the flow of air during breathing. Because the membranes of the infant trachea are soft and fragile, there is a risk of tracheal compromise secondary to a tracheostomy. Complications may include reactive granulation at the site of cannula, edema and scaring, chronic irritation of the tracheal lumen, and tracheal collapse as a result of increased negative pressure pulling air through a compromised structure (Fry et al., 1985). During the first several years of life, significant changes occur in the structure and mechanics of the respiratory system. The airways increase in radius and length and the lungs increase in size and weight. The thoracic cavity enlarges and changes in shape, and overall chest wall compliance decreases with upright posture. Airway resistance decreases, and pleural pressure becomes more subatmospheric (Beckerman, Brouillette, and Hunt, 1992). Tidal volume, inspiratory capacity, vital capacity, and minute ventilation increase with age. Besides providing phonation, the larynx, along with the epiglottis and soft palate, protects the lower airway. The infant larynx is located high in the neck, close to the base of the tongue. The thyroid cartilage is located directly below the hyoid bone, whereas the cricoid cartilage is the lowest part of the laryngeal structure. Because of its location and size, the infant larynx, like the trachea, is susceptible to trauma during airway management procedures. The laryngeal structures become less susceptible to injury as they change shape and descend during the first year of life. The articulatory subsystem, composed of the pharynx, mouth, and nose, also undergoes significant changes in growth and function during infancy and early childhood. The pharynx plays a critical role in both respiration and swallowing. The infant pharynx lacks a rigid framework and can collapse if external suction is applied within the airway. If the airway-maintaining muscles are weak or paralyzed, normal negative pressures associated with inspiratory e¤orts also can cause airway collapse at the level of the pharynx (Thach, 1992). Movement of the pharyngeal walls, elevation of the soft palate, and elevation of posterior portion of the tongue are important maneuvers for achieving velopharyngeal closure. The infant tongue is proportionately larger in relation to mouth size than the adult’s; thus, tongue retraction can cause upper airway blockage and respiratory distress. Various craniofacial abnormalities may result in structural or neurological situations that require airway management interventions, including tracheostomy. The decision to use long-term airway maintenance in the form of a tracheostomy requires consideration of many factors. Even the type of incision can make a difference in overall outcome for the infant or young child (Fry et al., 1985). Other information is needed to select

the appropriate tracheostomy tube. Driver (2000) has compiled a list of the critical factors in tracheostomy tube selection. These factors include the child’s respiratory requirements, age and weight, tracheal diameter, distance from the tracheal opening to the carina, and anatomical features of the neck for selection of a neck plate or flange. In addition, decisions must be made regarding whether or not there should be an inner cannula, the flexibility of the cannula, whether or not there should be a cu¤ (an air-inflatable outer bladder used to create a seal against the outer wall of the tracheal tube and trachea), and what external adapters might be used (Driver, 2000). Tracheostomy tubes are selected primarily on the basis of the ventilatory needs of the infant or young child. Tracheostomy tubes will be larger in diameter and may have a cu¤ in the event the child needs high ventilator pressures with frequent suctioning. However, because of a young child’s susceptibility to trauma of the speech apparatus, it is optimal to have a smaller-diameter, flexible tube without a cu¤. When a smaller tube is s