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Applied Anatomy& Physiology forSpeech–LanguagePathology &

Audiology



Donald R. Fuller, Ph.D., CCC-SLP, ASHA FellowProfessor of Communication DisordersDepartment of Communication DisordersEastern Washington UniversitySpokane, WA

Jane T. Pimentel, Ph.D., CCC-SLP Associate Professor of Communication DisordersDepartment of Communication DisordersEastern Washington UniversitySpokane, WA

Barbara M. Peregoy, Au.D., CCC-ASenior Lecturer in Communication DisordersDepartment of Communication DisordersEastern Washington University

Spokane, WA

Applied Anatomy& Physiology forSpeech–LanguagePathology &

Audiology



Acquisitions Editor: Peter SabatiniProduct Manager: Paula C. WilliamsMarketing Manager: Allison PowellDesigner: Teresa MallonCompositor: Aptara, Inc.

Copyright © 2012 Lippincott Williams & Wilkins, a Wolters Kluwer business

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All rights reserved. This book is protected by copyright. No part of this book may be reproduced or trans-mitted in any form or by any means, including as photocopies or scanned-in or other electronic copies,or utilized by any information storage and retrieval system without written permission from the copyrightowner, except for brief quotations embodied in critical articles and reviews. Materials appearing in thisbook prepared by individuals as part of their ofcial duties as U.S. government employees are not coveredby the above-mentioned copyright. To request permission, please contact Lippincott Williams & Wilkins atTwo Commerce Square, 2001 Market Street, Philadelphia, PA 19103, via e-mail at [email protected] ,or via Web site at lww.com (products and services).

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Library of Congress Cataloging-in-Publication Data

Fuller, Donald (Donald R.), author. Applied anatomy and physiology for speech-language pathology andaudiology / Donald Fuller, Ph.D., CCC-SLP, Jane Pimentel, Ph.D.,CCC-SLP, Barbara M. Peregoy, Au. D., CCC-A. p. ; cm. Includes bibliographical references and index. ISBN 978-0-7817-8837-3 (hardback : alkaline paper) 1. Communicative disorders—Pathophysiology. 2. Human anatomy.3. Human physiology. I. Pimentel, Jane, author. II. Peregoy, Barbara M.,author. III. Title.

[DNLM: 1. Language Disorders—physiopathology. 2. Hearing Disorders—physiopathology. 3. Nervous System—anatomy & histology.4. Respiratory System—anatomy & histology. 5. Speech—physiology.6. Speech-Language Pathology—methods. WL 340.2] RC423.F824 2010 616.85 5—dc22 2010044328

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Care has been taken to conrm the accuracy of the information present and to describe generally acceptedpractices. However, the authors, editors, and publisher are not responsible for errors or omissions or forany consequences from application of the information in this book and make no warranty, expressed orimplied, with respect to the currency, completeness, or accuracy of the contents of the publication. Applica-tion of this information in a particular situation remains the professional responsibility of the practitio-ner; the clinical treatments described and recommended may not be considered absolute and universalrecommendations.

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To my wife, Zhe Qu (“Joyce”), and our daughter, Ersi Nie (“Sisi”), two intellectuallysuperior women who understand the importance of life-long learning; and to our younger children—Destiny, Richard, and Aidan—may the love of learning be just asimportant to them. Finally, to my mother, Hannah Louise Bridges, and father, RoyFuller, Sr., both now deceased, who instilled within me the need to never stop learning.

Donald R. Fuller

To my husband, Paul, for his limitless patience and support and to my late mother,Ramona, for her incredible enthusiasm for my professional pursuits.

Jane T. Pimentel

To my husband, Bob, for his patience and for encouraging me to continue when I wantedto quit; to my sons, Stephen and William, for understanding when I told them, “I can’tright now, I have a deadline”; and to my big brother, Steve, for teaching me by examplethat life’s challenges are “do-able” even if you just pick your way down the mountain.

Barbara M. Peregoy



vii

REVIEWERS

Jillian G. Barrett, Ph.D., CCC-A, FAAA Private PracticeDanville, California

James Feuerstein, Ph.D., CCC-A, FAAA Professor of Audiology Department of Communication Sciences &

DisordersNazareth CollegeRochester, New York

Eric W. Healy, Ph.D.

Associate ProfessorDepartment of Speech and HearingScience

The Ohio State University Columbus, Ohio

Rajinder Koul, Ph.D., CCC-SLPProfessor and Chair, Associate Dean

(Research)Department of Speech, Language, and Hear-

ing SciencesTexas Tech University Health Sciences CenterLubbock, Texas

Thomas Littman, Ph.D., CCC-A AudiologistFactoria Hearing CenterBellevue, Washington

Beverly Miller, M.A., CCC-SLP Assistant ProfessorDepartment of Communication DisordersMarshall University

Huntington, West Virginia

Amy T. Neel, Ph.D., CCC-SLP Associate ProfessorDepartment of Speech and Hearing

SciencesUniversity of New Mexico Albuquerque, New Mexico

Shawn L. Nissen, Ph.D., CCC-SLP Associate ProfessorDepartment of Communication DisordersBrigham Young University Provo, Utah

Sarah Poissant, Ph.D., CCC-A Associate ProfessorDepartment of Communication DisordersUniversity of Massachusetts Amherst, Massachusetts

Tracie Rice, Au.D., CCC-A Clinical DirectorDepartment of Communication

Sciences and Disorders Western Carolina University Cullowhee, North Carolina

Howard Rothman, Ph.D.Professor EmeritusUniversity of FloridaGainesville, Florida

CONTRIBUTOR Charles L. Madison, Ph.D., CCC-SLPProfessorDepartment of Speech and Hearing Sciences Washington State University Spokane, Washington



“Why do we need to know all of this anatomy?”It’s a question for the ages. Every instructor who has ever taught anatomy and phys-

iology of the speech and hearing mechanism has heard that question at least once—ifnot several times—in his or her career. Too often, and for various reasons, anatomyand physiology is taught separately from the disorders in the typical communica-tion disorders curriculum. For those of us who are “purists,” there is a belief that thefoundational courses for the profession should be taught before the applied coursesare introduced. This is reinforced by the classication of anatomy and physiologyas one of the “basic human communication processes.” The assumption for many isthat applied coursework is not appropriate until the underlying basic processes areunderstood. For others, the logistical nightmare of trying to coordinate anatomy andphysiology with the disorders within a 3-, 4-, or even 5-credit course has precluded the

introduction of applied information with the information pertaining to anatomy andphysiology. The problem is exacerbated by the fact that the most commonly used text-books on anatomy and physiology of the speech and hearing mechanism provide verylittle, if any, applied information. Other than the occasional “clinical application” boxor short paragraph, one would be hard pressed to nd any substantive informationabout how anatomy and physiology is used clinically to govern the decision-makingprocess regarding diagnosis or potential intervention strategies.

The reality is that for whatever reason we choose not to integrate anatomy and physi-ology with their clinical relevance, students are not provided the “big picture.” At least while they are taking the course, most students do not fully comprehend how anatomyand physiology ts into this big picture. Most of us try to provide clinically relevantexamples while we are teaching the course, but too often, the few examples we provide

are simply not enough. The industrious student may take the initiative and seek out thatinformation independently. Most students, however, wait until they take the appliedcourses and hope that at that point they will begin to see the big picture. From thesestudents who no doubt make up the majority, those often said words are uttered:

“Why do we need to know all of this anatomy?”Throughout the many years we have taught anatomy and physiology of speech

and hearing, we must have heard that question a thousand times. Even in light of ourattempts to provide clinically relevant examples to illustrate the importance of under-standing the anatomy and physiology, that question kept rearing its ugly head. Weare happy to report that the vast majority of students who have taken an anatomycourse under us went on to make the connection later in their studies. However, we

have always had the nagging feeling that students needed to make that connectionmuch sooner in their undergraduate careers.

We have never been overly enamored with the textbooks in anatomy and physiologythat have been published over the years. Some of them were too technical or advancedfor the typical undergraduate student, bogging the student down in detail after detailto the point that comprehension was minimal. Other textbooks were too simplistic, notproviding enough detail to be meaningful to the student. With the exception of one ortwo, most textbooks provided very little in the way of ancillary materials. All of themprovided too little information about the clinical relevance of anatomy and physiol-ogy. The more and more we taught anatomy and physiology over the years, the more we thought about what we would like to see in an anatomy textbook: a good balance

PREFACE

ix



x PREFACE

in terms of the complexity of the information provided; ancillary materials to assist thestudent in further understanding the material; and most importantly, a good, healthydose of applied clinical information to assist the student in making the critical connec-tion between anatomy/physiology and its clinical application. Such a textbook, and acourse built around it, would hopefully eliminate the need for students to ask:

“Why do we need to know all of this anatomy?”Enter the American Speech-Language-Hearing Association (ASHA). When ASHA

introduced its new standards for certication in January 2005, we saw it as an opportu-nity. With the new certication standards being knowledge- and skills-based as opposedto course-based, we realized that professional programs were freed from counting aca-demic credits in various areas such as basic human communication processes, pro-fessional courses, etc. Instead, programs could concentrate on ensuring that studentsacquire certain knowledge and skills outcomes. Such a shift in focus allows professionalprograms to redesign their curricula to meet knowledge and skills outcomes insteadof counting academic credits. Other than the general requirement that graduates have75 semester hours credit of coursework in the profession (with 36 of those credits beingearned at the graduate level), there are no longer specic academic credit requirements. An obvious benet of this is that the need to separate the anatomy and physiology from

the clinical application no longer exists. Both could be taught in parallel since profes-sional programs are no longer required to “bean count” the academic credits.This textbook represents the culmination of the ideas we have had for the last 20

years. First, a conscious attempt was made to present the anatomy and physiology ofspeech and hearing in a manner that is not too complex, but also not too simplistic.The critical information is here. The terminology is here. The detail is also here. The writing style is what possibly separates this textbook from the other texts available onthe market. An attempt was made to write in a style that invites the reader on a tour ofanatomy and physiology.

Second, ancillary materials are available to assist the student in understanding theanatomy and physiology and also to assist the instructor in presenting the material.In our opinion, the artwork (both drawings and photographs) in this textbook is supe-rior by comparison with the artwork in other textbooks on the market. Case studies,clinical “tie-in” boxes, a large glossary, references to research, study questions, andterminology “hint” boxes are used liberally to assist the reader’s comprehension. Acompanion Web site is also available; this includes a library of images and other peda-gogical materials to further reinforce the concepts learned. This textbook is possiblythe rst one in our profession to link the information contained within to the perti-nent knowledge outcomes of ASHA’s certication standards (see the section Address-ing Knowledge and Skills [KASA] Outcomes later).

Third, and most importantly, this textbook includes chapters on pathology and itsrelationship to anatomy and physiology. Each major part of this book (articulatory/resonance system, auditory/vestibular system, nervous system, phonatory system,and respiratory system) consists of two chapters. The rst chapter in each unit providesthe relevant information pertaining to anatomy and physiology. The second chapterin each unit provides an in-depth discussion of pathology and its relationship to theanatomy and physiology. Although these chapters do not provide an exhaustive list ofall the possible pathologies, sufcient detail is provided about a large number of organicand nonorganic disorders to allow the student to see the big picture. This textbook isorganized in such a manner that it can be used in a stand-alone anatomy and physiologycourse or as the primary text in a combined undergraduate anatomy/pathology course.

Speaking of the organization of this textbook, one may note that it differs from theother anatomy textbooks. After an introductory section on terminology and basicconcepts, most other textbooks present the anatomy and physiology in the following



PREFACE xi

order: respiratory system, phonatory system, articulatory/resonance system, nervoussystem, and auditory system. This textbook organizes the anatomy/physiology infor-mation in a slightly altered sequence: nervous system, respiratory system, phonatorysystem, articulatory/resonance system, and nally the auditory/vestibular system.The rationale for this sequence is that since the nervous system underlies all otherprocesses in speech and hearing, it should be presented rst. It should be presentedrst also because information presented in later chapters (e.g., physiology of muscles)

is dependent upon the student’s understanding of the neurological bases. Once thestudent has been introduced to the nervous system, the traditional sequence of respi-ration, phonation, and articulation/resonance is presented. As a somewhat indepen-dent system, the auditory/vestibular system is presented last.

We have told our students over the years, “If you understand the anatomy andphysiology, you’re more than half-way to understanding the pathology.” Many of thesestudents have come back to us years later and afrmed that observation. These sameformer students have almost invariably mentioned that it would have been more help-ful had they made that connection earlier in their academic careers. Hopefully, thistextbook represents a successful attempt to align the basic science of anatomy andphysiology with the applied art and science of communication disorders. We will knowthat this attempt was successful if we no longer hear students ask:

“Why do we need to know all of this anatomy?”

Additional Resources

Applied Anatomy and Physiology for Speech–Language Pathology and Audiology includes additional resources for both instructors and students that are available onthe book’s companion Web site at http://thePoint.lww.com/Fuller .

INSTRUCTOR RESOURCES

Approved adopting instructors will be given access to the following additionalresources:

• Test bank • Answers to Part Questions that are within the textbook • Image bank to assist in creating Powerpoint slides• Acland Human Anatomy videos related to speech and hearing

STUDENT RESOURCES

• Interactive student quiz bank • Animations on the workings of anatomical and physiological structures of the

body as they relate to speech and hearing • Acland Human Anatomy videos related to speech and hearing

In addition, purchasers of the textbook can access the searchable Full Text On-line bygoing to the Applied Anatomy and Physiology for Speech–Language Pathology and Audiol-ogy Web site at http://thePoint.lww.com/Fuller . See the inside front cover of this textbookfor more details, including the passcode you will need to gain access to the Web site.

Donald R. FullerJane T. Pimentel

Barbara M. Peregoy February 2011

http://thepoint.lww.com/Fuller






xiii

ADDRESSING KNOWLEDGEAND SKILLS (KASA) OUTCOMES

This textbook may be the rst of its kind to indicate which knowledge outcomes of theKnowledge and Skills Acquisition (KASA ) form are addressed through the content found within its pages. On January 1, 2005, the American Speech-Language-Hearing Asso-ciation (ASHA) revised its certication standards. These are standards every studentmust meet to earn the Certicate of Clinical Competence (CCC). The old standards were based upon the student taking certain courses in specic domains. For example,the Basic Human Communication Sciences domain required that the student earn 15semester credit hours in such courses as anatomy and physiology of speech and hear-ing; phonetics; speech and language development; and speech and hearing science.The new standards are no longer primarily based upon the student earning a set num-ber of academic credits but instead are primarily competency-based. Now, the studentmust demonstrate competence in certain knowledge and skills.

Table P-1 indicates the KASA knowledge outcomes that are addressed in this text-book. Up to 25 knowledge outcomes may be addressed by this textbook, depending on

TABLE P-1

KASA KNOWLEDGE AND SKILLS OUTCOMES ADDRESSED BY THE CONTENT OF THIS TEXTBOOK

Addressed to Addressed inKnowledge Outcome What Extent? Chapter(s)

1. Biological basis of the basic human communication processes (III-B) 80% 2, 3, 6, 8, 10, 12 2. Neurological basis of the basic human communication 30% 2, 3, 4, 6, 8, 10, 12 processes (III-B) 3. Acoustic basis of the basic human communication processes (III-B) 20% 8, 10, 12 4. Psychological basis of the basic human communication processes (III-B) 10% 4

5. Developmental and life span bases of the basic human communication 20% 4, 8, 13 processes (III-B)

6. Linguistic basis of the basic human communication processes (III-B) 10% 4 7. Biological basis of swallowing processes (III-B) 80% 8, 10 8. Neurological basis of swallowing processes (III-B) 30% 4

9. Etiologies of articulation disorders (III-C) 10% 1110. Characteristics of articulation disorders (III-C) 10% 1111. Etiologies of uency disorders (III-C) 10% 5, 9, 1112. Characteristics of uency disorders (III-C) 10% 5, 9, 1113. Etiologies of voice and resonance disorders (III-C) 20% 914. Characteristics of voice and resonance disorders (III-C) 20% 9

15. Etiologies of receptive and expressive language disorders (III-C) 10% 5, 1316. Characteristics of receptive and expressive language disorders (III-C) 10% 517. Etiologies of hearing disorders (III-C) 80% SLP/50% Aud. 1318. Characteristics of hearing disorders (III-C) 60% SLP/30% Aud. 1319. Etiologies of swallowing disorders (III-C) 10% 5, 9, 1120. Characteristics of swallowing disorders (III-C) 10% 5, 9, 1121. Etiologies of cognitive aspects of communication (III-C) 10% 522. Characteristics of cognitive aspects of communication (III-C) 10% 523. Prevention of voice and resonance disorders (III-D) 10% 924. Prevention of hearing disorders (III-D) 50% SLP/10% Aud. 1325. Prevention related to the cognitive aspects of communication (III-D) 10% 5



xiv ADDRESSING KNOWLEDGE AND SKILLS (KASA) OUTCOMES

how the textbook is used. It should be noted that the items in this table are numberedconsecutively from 1 to 25; these numerals were arbitrarily assigned by the authors ofthis textbook solely for the purpose of organization and reference, and do not corre-spond to any numbering system developed by ASHA.

The reader will note right away that a horizontal line separates the rst eightknowledge outcomes from the remaining outcomes. If this textbook is used as theprimary source of information for a stand-alone course in anatomy and physiology of

the speech and hearing mechanism, then only knowledge outcomes 1 through 8 areapplicable. However, if this textbook is used as the primary source of information in acourse having greater content than simply anatomy and physiology (e.g., the anatomyand physiology are presented within a larger course on organic speech, language, andhearing disorders), all 25 knowledge outcomes are applicable.

Table P-1 also provides information as to the relative extent a particular knowl-edge outcome is being addressed. It should be emphasized that these are relative percentages based upon the expected amount of information that would be providedin an anatomy and physiology and/or an organic disorders course and the amountof information that would be provided elsewhere in a typical communication dis-orders curriculum. To illustrate, the relative extent to which a stand-alone anatomyand physiology course would address the biological basis of the basic human com-munication processes (outcome 1) has been estimated at 80%. In other words, one would expect that approximately 80% of the information provided within a typicalcommunication disorders curriculum related to outcome 1 would come from a basic,stand-alone course in anatomy and physiology of the speech and hearing mechanism.The remaining 20% is typically addressed in disorders courses, where a review of theanatomy and physiology may be provided as part of the course. For outcomes 17, 18,and 24, relative percentages are provided separately for speech–language pathologyand audiology majors. For example, this textbook provides approximately 80% of theinformation in a typical communication disorders curriculum related to etiologies ofhearing disorders for speech–language pathology majors, but only 50% of the sameinformation for audiology majors because they’d more likely receive more extensive

information in other courses within their major. Once again, it should be emphasizedthat these are relative percentages. The actual extent to which this textbook addressesthe knowledge outcomes in Table P-1 will likely differ from academic program to aca-demic program. It is up to the individual program to determine that extent.

Finally, Table P-1 indicates the chapter or chapters in which the individual knowl-edge outcomes are addressed. This column is provided as a means of cross-referencingthe content of the textbook to the specic knowledge outcomes. The reader will notethat in some instances the chapter number has been boldfaced in the table. Chapternumbers that are boldfaced provide the greatest amount of information relative to theknowledge outcome in question. When no chapter number is boldfaced for a corre-sponding KASA outcome, the information provided in this textbook for that outcomeshould be considered minimal. Relative percentages are provided in Table P-1 to guide

academic programs as they determine how the KASA outcomes are to be addressed within their own unique curriculum.



xv

CONTENTS

Reviewers and Contributor vii

Preface ix

Addressing Knowledge and Skills (KASA) Outcomes xiii

PART 1Terminology, Nomenclature, and Basic Concepts, 1

CHAPTER 1 An Overview of this Textbook .................................................................................

CHAPTER 2 Understanding Orientation and Nomenclature .....................................................

CHAPTER 3 The Structural Organization of Humans ...............................................................

PART 1 SUMMARY...................................................................................................PART 1 REVIEW QUESTIONS .................................................................................

PART 2Anatomy, Physiology, and Pathology of the Nervous System, 35

CHAPTER 4 Anatomy and Physiology of the Nervous System ...................................................

CHAPTER 5 Pathologies Associated with the Nervous System...................................................

PART 2 SUMMARY ...................................................................................................

PART 2 REVIEW QUESTIONS ..................................................................................

PART 3Anatomy, Physiology, and Pathology of the Respiratory System, 109

CHAPTER 6 Anatomy and Physiology of the Respiratory System ............................................1

CHAPTER 7 Pathologies Associated with the Respiratory System ............................................14

PART 3 SUMMARY...................................................................................................


PART4Anatomy, Physiology, and Pathology of the Phonatory System, 161

CHAPTER 8 Anatomy and Physiology of the Phonatory System ...............................................1

CHAPTER 9 Pathologies Associated with the Phonatory System ..............................................1CHARLES L. MADISON

PART 4 SUMMARY...................................................................................................




xvi CONTENTS

PART 5Anatomy, Physiology, and Pathology of the Articulatory/Resonance System, 215

CHAPTER 10 Anatomy and Physiology of the Articulatory/Resonance System ....................217

CHAPTER 11 Pathologies Associated with the Articulatory/Resonance System ...................269

PART 5 SUMMARY....................................................................................................

PART 5 REVIEW QUESTIONS ...................................................................................

PART 6Anatomy, Physiology, and Pathology of the Auditory/Vestibular System, 295

CHAPTER 12 Anatomy and Physiology of the Auditory/Vestibular System .............................297

CHAPTER 13 Pathologies Associated with the Auditory/Vestibular System .............................327

PART 6 SUMMARY....................................................................................................

PART 6 REVIEW QUESTIONS ...................................................................................

Appendix Terms and Afxes to Assist You in Learning the Meanings of Anatomical and Physiological Words........................................................................

TERMS AND PREFIXES USED TO DESCRIBE MOVEMENT ...........................................35

TERMS AND AFFIXES USED TO DENOTE ANATOMICAL STRUCTURESOR THEIR PARTS........................................................................................................

TERMS AND PREFIXES USED TO DESCRIBE COLOR, FORM,GENERAL LOCATION, RELATIVE SIZE, OR SHAPE ........................................................3

TERMS AND AFFIXES USED IN REFERENCE TO BONES, CARTILAGES,CAVITIES, MEMBRANES, OR SPACES.............................................................................

TERMS AND AFFIXES USED IN REFERENCE TO THE NERVOUS SYSTEM ..............358

TERMS AND PREFIXES USED IN REFERENCE TO THEAUDITORY/VESTIBULAR SYSTEM................................................................................

MISCELLANEOUS TERMS AND AFFIXES USED IN ANATOMY,PHYSIOLOGY, AND PATHOLOGY ...............................................................................

Glossary 363

References 395

Index 401



Terminology,Nomenclature, and Basic Concepts

PART 1



3

“Why do we have to learn all of this anatomy andphysiology?”

It is a question for the ages. Speech–language pathol-ogy and audiology students have asked this questionpractically since the beginning of the professions. Although many come to appreciate the relationshipbetween speech perception and production and the

concomitant anatomy and physiology, there often-times seems to be a disconnect between the two formost clinicians in training. It is not until much later intheir education that the link is solidied in the mindsof these future professionals.

The answer is simple, yet complex at the same time.To understand what may be pathological, one mustrst know what is “normal” or “typical.” Many of theso-called organic disorders of speech, language, andhearing have an etiology that points toward aberra-tions in the anatomy and/or physiology of the speechor hearing mechanism. An anatomical or physiologi-cal etiology will likely provide the clinician with cluesas to the expected signs and symptoms associated with a given disorder, and may also indicate whatcourse of intervention to take.

The complexity of the answer lies in the complex-ity of the human body. There are literally hundreds ofanatomical structures (e.g., bones, cartilages, muscles,organs, and nerves) involved in the speech perceptionand production processes. Likewise, many laws, prin-ciples, and theories of physical science are involvedin the physiology of speech and hearing. The pros-

pect of learning all of the terminology and conceptsrelated to speech perception and production can beoverwhelming to many students. However, the learn-ing process can seem more manageable (and formany students downright fun!) if one understandsthat there is actually a method to the madness. Moreinformation will be provided about this method in alater section of this chapter.

The authors of this textbook have a combined experi-ence in anatomy and physiology reaching into decades.

CHAPTER 1

An Overview of this Textbook

Hundreds of students have passed through our classesin anatomy and physiology of speech and hearing. Although we have used clinical examples to somedegree in our classes, most of the class time involved thepresentation of anatomical and physiological conceptsand nomenclature. We suspect this is true for most aca-demic programs in communication disorders.

Because of this, many students simply cannot see

a clear relationship between anatomy and physiologyand disorders of speech and hearing. The anticipationis that students will come to understand the relation-ship when coursework in the disorders is taken. Theproblem with this is that by the time most students takethe disorders courses, they have forgotten the anatomyand physiology because a solid link was never estab-lished early on. This textbook attempts to alleviate thisproblem by offering not only the concepts and nomen-clature associated with the anatomy and physiology ofthe speech and hearing mechanism but also in-depthinformation about a variety of disorders of speech andhearing so that you can understand the link betweenthe two early in your educational experience.

A Quick Tour of this Textbook

Traditionally, speech perception and production havebeen described according to several components:articulatory/resonance, auditory/vestibular, neural, pho-natory, and respiratory. This textbook will not deviatefrom organizing the anatomy and physiology of speech

and hearing according to this well-established scheme.However, we refer to each of these components as a sys-tem . By denition, a system is a group of independentbut interrelated elements comprising a unied whole.The processes of articulation/resonance, hearing, pho-nation, and respiration are indeed anatomically inde-pendent from each other, but they are also composedof interrelated elements that come together for a spe-cic purpose—that purpose being speech perceptionand production. Although the nervous system is not



4 PART 1 TERMINOLOGY, NOMENCLATURE, AND BASIC CONCEPTS

involved mechanically in speech perception and pro-duction in the way the other systems are, without thenervous system the processes of speech perception andproduction would not be possible. We view the nervoussystem as the overriding system that coordinates andcontrols all other systems.

Because we refer to these components of speech

perception and production as systems , you shouldnot confuse them with the systems that comprisethe human body. Depending on the anatomist, thehuman body may be organized into as few as nine andas many as twelve body systems. Some of these bodysystems include the circulatory (or vascular) system,digestive system, muscular system, nervous system,reproductive system, respiratory system, and skel-etal system. As Table 1-1 illustrates, the systems thatare mechanically involved in speech perception andproduction (i.e., the articulatory/resonance, audi-tory/vestibular, phonatory, and respiratory systems)are in turn composed of structures from several bodysystems. Right away, you may note that the muscu-lar, nervous, skeletal, and vascular body systems areall components of every system that is mechanicallyrelated to speech perception and production. Usingthe auditory/vestibular system to illustrate, the con-tribution of the muscular system comes in the formof several muscles such as the stapedius and tensortympani muscles. The nervous system contributes by way of the vestibulocochlear nerve and the auditorypathway. The skeletal system is represented by bones

(e.g., the ossicles: malleus, incus, and stapes) andcartilages (e.g., the ear canal and pinna). Finally, thevascular system contributes several arteries and veinsto the auditory/vestibular system to provide nutrientsand to take away waste products.

It is interesting to note that not only is respirationconsidered a body system but is also considered a sys-tem of speech production. Dened as a body system,the respiratory system typically includes only thetrachea, bronchial tree, and lungs. When viewed as asystem of speech production, respiration also drawsupon the muscular, nervous, skeletal, and vascular

systems. This points up the fact that when one refersto body systems, one is generally referring to an ana-tomical organization of the human body. It becomesapparent that when one considers the physiology ofthe human body, the body systems overlap consider-ably. Therefore, although this textbook will describethe articulatory/resonance, auditory/vestibular, ner-vous, phonatory, and respiratory systems in terms oftheir anatomy, these systems of speech perceptionand production are organized primarily according totheir physiological function .

TABLE 1-1

THE SYSTEMS OF COMMUNICATION ANDTHE HUMAN BODY SYSTEMS (WITH EXAMPLESIN ITALICS) THAT COMPRISE THEM

Communication System Human Body Systems

Speech Perception Auditory system Muscular system

Stapedius muscle; tensortympani muscle

Nervous system Facial nerve;

vestibulocochlearnerve

Skeletal system Temporal bone of the

skull Vascular system Anterior inferior

cerebellar artery Speech Production

Respiratory system Muscular system Diaphragm; external intercostals Nervous system Phrenic nerve Respiratory system Lungs Skeletal system Cervical, thoracic,

lumbar vertebrae;ribs

Vascular system Pulmonary artery Phonatory system Muscular system Cricothyroid; posterior

cricoarytenoid Nervous system Recurrent laryngeal

nerve Skeletal system Hyoid bone Vascular system Inferior laryngeal

artery Articulatory/resonance

system Digestive system Oral cavity; pharynx

Muscular system Levator veli palatini;palatoglossus

Nervous system Mandibular branch

of the trigeminalnerve

Skeletal system Ethmoid; mandible;

vomer Vascular system Lingual artery



CHAPTER 1 AN OVERVIEW OF THIS TEXTBOOK 5

Although this textbook will not deviate from theestablished organizational scheme of articulatory/res-onance, auditory/vestibular, nervous, phonatory, andrespiratory systems, these systems of speech percep-tion and production will be presented in a slightly dif-ferent order than they typically appear in most anatomytextbooks. Traditionally, the nervous system tends to be

presented after the three systems of speech production(respiration, phonation, and articulation/resonance).However, we feel that since the nervous system coor-dinates and controls all of the other systems of speechperception and production, it should be presented rst.Therefore, the nervous system is presented in this text-book in Part II. Following the nervous system will bethe three systems involved in speech production. PartIII will present the respiratory system, Part IV will pres-ent the phonatory system, and Part V will present thearticulatory and resonance systems. Finally, the audi-tory/vestibular system will be presented last, in Part VI.It should be noted that although the auditory system isof primary interest to speech perception, informationabout the vestibular system is also provided becausethe audiologist or speech–language pathologist is verylikely to encounter patients who exhibit disturbancesin balance and equilibrium.

Part I consists of three chapters. The purpose of thepresent chapter is to orient you to the general organiza-tion and intended use of this textbook. Chapter 2 pro-vides basic information to orient you to the anatomicalposition; planes of reference; terminology describing

spatial relationships between and among structures;and other nomenclature related to anatomy, physiol-ogy, and pathology. Chapter 3 provides you with basicinformation concerning the organization of the humanorganism: cells, tissues, organs, and systems. Uponcompletion of the rst part, you will have the basicbuilding blocks to assist in understanding the informa-tion presented in the remaining parts. For the remain-ing parts of this textbook, not only will anatomy andphysiology be presented but information about therelationship between anatomy and physiology andmany disorders of speech, language, and hearing will

also be presented. For Parts II through VI, the anatomyand physiology of each of the ve systems mentionedearlier will be presented rst in a stand-alone chapter(Chapters 4, 6, 8, 10, and 12). Following each chapter onanatomy and physiology, a separate chapter will includeinformation relative to certain disorders affecting thosesystems (Chapters 5, 7, 9, 11, and 13). It is hoped thattaken together, the two chapters within each part willprovide you with that elusive link between anatomyand physiology and the disorders that may occur whenabnormal structures or conditions exist.

A Quick Overview of SpeechPerception and Production

As mentioned previously in this chapter, the processesof speech perception and production are quite com-plex, enlisting the participation of literally hundreds

of anatomical structures such as bones, cartilages,muscles, organs, and nerves. In addition, the vari-ous anatomical parts are bound together by differenttypes of connective tissue such as fascia, ligaments,membranes, and tendons. In general, the various sys-tems involved in speech perception and productionrequire that you know the entire human body exceptfor the upper and lower extremities (i.e., arms, legs,hands, feet, ngers, and toes).

To illustrate, speech perception involves the audi-tory and nervous systems. Acoustic energy in the formof sound waves (whether speech or environmen-tal sounds) are collected by the pinna and directedinto the ear canal. At the terminus of the ear canalresides the tympanic membrane (eardrum), whichconverts the acoustic energy into mechanical energy.The mechanical energy is then transmitted throughthe middle ear cavity by way of the ossicular chain(the malleus, incus, and stapes). To protect the innerear from being excessively driven, the acoustic reexmay enter the picture. This reex is accomplishedthrough the contraction of muscles. As mechanicalenergy is transmitted through the middle ear, the sta-

pes acts upon the oval window of the cochlea, whichis in the inner ear. Housed within a chamber of thecochlea is the essential organ of hearing (the organof Corti) that contains uid and is also surroundedby two other chambers lled with uid. The rock-ing action of the stapes causes the uid inside thesechambers to vibrate. Vibration of the uid within thecochlea sets up a receptor potential from the organ ofCorti. Sensory nerve impulses then travel to bers ofthe cochlear portion of cranial nerve VIII (the vestib-ulocochlear or auditory nerve), where the impulsesare then relayed through the auditory pathway. The

auditory pathway includes portions of the lower brainstem, upper brainstem (i.e., the midbrain), and cere-bral cortex. It is at the cerebral cortex where soundis nally perceived and interpreted. Separate fromthe acoustic and vestibular functions of the hearingmechanism, the Eustachian tube assists in regulat-ing air pressure within the middle ear cavity. Whenair pressure within the middle ear cavity becomesnegative in relation to atmospheric pressure, theEustachian tube opens to equalize pressure. This isaccomplished in part through muscle contraction.




In total, a very large number of anatomical structuresmake up the auditory/vestibular system. These includebones, cartilages, ligaments, membranes, muscles,neurons, organs, and tendons.

By the same token, the process of speech produc-tion is equally complex. This process requires coordi-nated activity of the nervous, respiratory, phonatory,

and articulatory/resonance systems. To an extent, theauditory system is also involved, as it is used by indi-viduals who can hear as a means of acquiring speechand language. Further, once speech and languagehave been acquired, the auditory system is used bypersons with normal hearing to monitor their ownspeech.

Proper timing of the events that make up speechproduction is essential. Neural impulses will regulatethe various aspects of speech production such as res-piration, phonation, and articulation/resonance, and will also provide the brain with sensory informationrelated to tactile and kinesthetic feedback during thespeech production process. Respiration will serve asthe energy source for speech production. Expired air will be used to set the vocal folds into vibration toproduce voicing. Neural impulses will cause certainmuscles to contract, thereby resulting in respiration.The process of inhalation—whether for the purposeof speech production or not—is always active; thatis, muscle contraction is always necessary to effectthis process. On the other hand, normal exhalationis passive (i.e., no muscle contraction), while exha-

lation for vocal activity is typically active. Once thevocal folds are adducted (i.e., brought together or“closed”) by muscles of the larynx, the air trappedbelow the closed vocal folds must be pressurized byactive muscle action in the abdomen and thorax. Thevocal folds must also be abducted (i.e., separatedor “opened”) for the production of voiceless speechsounds and to replenish air during vocal activity.The abductor muscles of the larynx are needed forthis action. In turn, neural impulses are needed tocontract the abductor and adductor muscles of thelarynx.

Upon adduction of the vocal folds, exhaled air com-ing up from the lungs gets trapped below the vocalfolds, creating air pressure (referred to as subglotticpressure). Subglottic pressure will eventually force anopening between the vocal folds, setting them intovibration as the air passes through (a process referredto as phonation). During phonation, only a buzz-ing sound is produced. This buzzing sound is thenshaped and molded (i.e., articulated and resonated)as it proceeds up through the pharynx and into theoral and/or nasal cavities. When oral speech sounds

are produced, the soft palate will raise and seal offthe nasal cavity from the oral cavity so that all of theresonating sound passes through the oral cavity andout through the lips. When the nasal speech sounds(i.e., /m/, /n/, and / /) are produced, the soft palate will lower, creating an opening between the oral andnasal cavities so that part of the vocal tone can reso-

nate within the nasal cavity. Action of the soft pal-ate is mediated through muscle activity. The tongueis the primary structure involved in articulation andresonance. All vowel sounds and most of the conso-nant sounds of English are created by placement and/or movement of the tongue. The tongue consists ofmuscle tissue. For some speech sounds, there may berounding of the lips (e.g., the /w/ sound). Shaping ofthe lips is accomplished by muscle action. Once again,muscle activity is accomplished via neural impulsesfrom the nervous system.

The entire speech production mechanism is over-laid either upon or within the skeletal system. Forexample, the thoracic region is primarily associated with respiration and consists of the ribs, sternum,and thoracic vertebrae of the spinal column. In addi-tion, the bones of the pectoral (i.e., shoulder) andpelvic (i.e., hip) girdles serve as a point of attachmentfor many of the muscles involved in respiration. Thetrachea (a structure made of cartilage) and the lungs(which are organs) are also involved in the respiratoryprocess.

In terms of the phonatory system, the primary struc-

ture is the larynx, which is composed of a series of car-tilages interconnected by membranes and ligaments.The hyoid bone serves as the superior attachmentfor the larynx as well as the skeletal base for many ofthe muscles of the tongue. The pharynx, soft palate,and tongue consist of connective tissue, muscles, andmucous membrane. Many of the bones of the skullserve as points of attachment for muscles involved inarticulation and resonance. The bones of the craniumhouse the brain.

In all, it should be apparent to you that a study ofthe anatomy and physiology of speech and hearing

will require extensive knowledge of the human bodyand its components. In the parts that follow, each ofthe various systems (nervous, respiratory, phonatory,articulatory/resonance, and auditory/vestibular) willbe provided in greater detail. You will learn the vari-ous components that make up each of the systems(e.g., bones, cartilages, muscles, organs, and nerves)and will also gain knowledge of the normal physiol-ogy of the various systems individually, as well as thephysiology of the various systems collectively as theyare used for the purpose of speech perception and



CHAPTER 1 AN OVERVIEW OF THIS TEXTBOOK 7

production. However, before engaging in the studyof the various systems involved in speech perceptionand production, you should have a solid understand-ing of the basic terminology and concepts that areused in the study of anatomy, physiology, and pathol-ogy. The remaining chapters of this part provide you

with a basic foundation of terminology and conceptsrelated to anatomy, physiology, and pathology so thatlearning of the various systems will be facilitated. Wenow turn our attention specically to the nomencla-ture of anatomy, physiology, and pathology.



9

Knowledge Outcomes for ASHA Certication for Chapter 2• Demonstrate knowledge of the biological basis of the basic human communication

processes (III-B)• Demonstrate knowledge of the neurological basis of the basic human communication

processes (III-B)

Learning Objectives• You will be able to recite the denitions of biology, anatomy, physiology, and pathology.• You will describe the anatomical position, planes of reference, and spatial terminology

used to denote the position and orientation of anatomical structures of interest to speechperception and production.

• You will determine the meaning of unfamiliar terminology by analyzing the meaning of the rootand any afxes that may be attached.

CHAPTER 2

Understanding Orientation and Nomenclature

Basic Concepts, Terminology,and NomenclatureANATOMY, PHYSIOLOGY, AND PATHOLOGY

Anatomy and physiology are both branches of biology . You may recall from a high school biological sciencecourse that biology is the scientic study of livingorganisms. A living organism is anything that exhibitsthe properties of life, including but not limited to:

• Cell structure —the cell is the basic unit of theorganism, and in many organisms can create morecomplex structures like tissues and organs.

• Metabolism —the organism captures energy tobe used to maintain itself.• Reproduction —the production of offspring to

perpetuate the species.• Mutation —random changes in the structure or

composition of the organism.• Death— eventually, the organism will die.

Living organisms can range from single-celledcreatures (e.g., bacteria) to more complex structuressuch as plants and animals. The human being, of

course, is a complex animal, and therefore is a livingorganism.

Anatomy and physiology both fall under theumbrella of biology. Anatomy is the scientic studyof the structure and organization of living organisms.The term comes from the Greek words “anatomia” and“anatemnein,” meaning to cut up or cut open. Yearsago, in order to study the structure and organizationof the human body it would have had to have beendissected. Since not too many human beings want tobe cut up so that someone else can study them, ana-tomical studies were accomplished through the useof cadavers (an acronym of the Latin phrase “ ca roda ta ver mibus,” which translated means “esh given

to worms”), deceased human bodies that have beendonated to science for the purpose of study. Althoughcadavers are still used today to study the anatomi-cal structure of the human body, modern technologysuch as positron emission tomography allows us tostudy these structures without dissecting the body.The advantage of imaging technology is that anatomycan be studied on living human beings.

Physiology is the study of the functions of livingorganisms and their parts. Physiology cannot be stud-ied using a cadaver since a deceased organism does




not function. Instead, physiology must be studied byusing a living human being, by using an animal thatis similar in structure to a human being, or by using amodel of the particular anatomical part of interest tothe scientist. Taken together, anatomy and physiologyare biological sciences that examine the living organ-ism in terms of its parts and the functions of those

parts and of the organism as a whole.Pathology is the scientic study of the nature ofdiseases and of the structural and functional changesthat are imposed upon the living organism as a result.In other words, pathology is concerned with conditionsor processes that are outside the realm of typical ornormal, whether the aberration is associated withanatomical structure or physiological function. Oneshould note that a good understanding of pathologyand its effect on the organism cannot be fully realizeduntil the individual has an equally good understandingof the anatomy and physiology of the organism.

ORIENTATION TO THE HUMAN BODY

The Anatomical Position

To understand the human body and the spatial rela-tionships among the various bones, cartilages, muscles,organs, nerves, and other structures, one must have ageneral point of reference. In the study of anatomy, thispoint of reference is known as the anatomical posi-tion. You should always remember that the anatomi-cal position is in reference to the body being observed

(whether a living human or a cadaver), not the observer.For illustrative purposes, a cadaver will be the bodybeing observed. Thus, when one refers to the left sideof the body, it is the left side of the cadaver’s body. If thecadaver is facing the observer, its left side will be on theright side to the observer. If you always remember thatspatial terminology is used in reference to the cadaver, you will have little difculty in understanding the termi-nology associated with positioning and orientation.

The anatomical position is illustrated in Figure 2-1.Note that the body being observed is standing upright,facing the observer, with its eyes straight ahead, armsat its side with the palms of the hands and toes of thefeet facing forward. All of the terminology that will beused in this textbook, including terms associated withplanes of reference and spatial orientation, will be inreference to the anatomical position.

Planes of Reference

The internal structures of the human body can beviewed from several different perspectives. For example,one can look at a particular organ from any angle, or

the organ can be dissected in a horizontal, vertical, orother plane. When anatomical structures are photo-graphed or drawn, it is important to note the plane ofreference in which the structure is being presented.

An anatomical structure may look quite differentdepending on its plane of reference. As you view thephotographs and drawings in this textbook (and inother media as well), it is important that the gurecaption be read and the plane of reference be noted.

There are three planes of reference that will beused throughout this textbook; these are illustrated inFigure 2-2 and dened in Table 2-1. These planes ofreference include coronal, sagittal, and transverse. Thecoronal plane of reference is a vertical plane that sep-arates the body or body part into anterior (front) andposterior (back) sections. It is called the coronal plane

in reference to the coronal suture, a suture of the skullimmediately above the forehead, running from templeto temple and separating the frontal bone of the skullfrom the parietal bones. This plane of reference is alsosometimes referred to as the frontal plane.

The sagittal plane is also a vertically oriented planeof reference, although the orientation is a bit differ-ent than the coronal plane. In the case of the sagittalplane, the body or body part is separated into a leftand a right portion. This plane is named in referenceto the sagittal suture that runs lengthwise down the

LeftRight

Figure 2-1 The anatomical position used as the general pointof reference for describing the spatial orientation of the variousparts of the body. (Reprinted with permission from Cohen, B.J.(2008). Memmler’s the human body in health and disease (11th ed.).Baltimore: Lippincott Williams & Wilkins.)



CHAPTER 2 UNDERSTANDING ORIENTATION AND NOMENCLATURE 11

The terms and afxes in Table 2-1 are presented inalphabetic order. However, one should note that manyof the terms describing spatial position or orientationcome in pairs, in which the two terms have oppositemeanings. These include:

• Anterior/posterior (i.e., front/back)• Caudal/cranial or rostral (i.e., closer to the tail/

closer to the head)• Central/peripheral (i.e., located centrally/located

in the periphery)• Contra-/ipsi- (i.e., opposite side/same side)• Deep/superficial (i.e., away from the body

surface/toward the body surface)• Distal/proximal (i.e., away from the point of

origin/toward the point of origin)• Dorsal/ventral (i.e., toward the back/toward the

belly)

• Ecto-/endo- (i.e., outer/inner)• External/internal (i.e., outside/inside)• Extra-/intra- (i.e., outside/inside)• Extrinsic/intrinsic (i.e., coming from the outside/

coming from within)• Inferior/superior (i.e., below/above)• Infra-/supra- (i.e., below/above)• Lateral/medial (i.e., toward the side/toward the

middle)• Post-/pre- (i.e., after/before)• Prone/supine (i.e., face down/face up)

It should also be noted that Table 2-1 contains sev-eral prexes. These are placed at the beginning of root words to indicate direction, position, or spatial ori-entation. For example, take the prexes “infra-” and“supra-.” When placed in front of the root word hyoid, they literally mean “below the hyoid” and “above thehyoid,” respectively. In Chapter 8, you will be presentedthe anatomy and physiology of the phonatory system.In that chapter, a discussion will center on the extrin-sic muscles of the larynx (note the term extrinsic here,

which is dened in Table 2-1 as “external or comingfrom the outside”). Muscles of the larynx are classiedas either intrinsic or extrinsic. The extrinsic muscles aresubdivided into suprahyoid and infrahyoid muscles. Allof these muscles make an attachment to the hyoid bone(hence the root word hyoid ). The suprahyoid musclescome from anatomical structures located above thehyoid bone, whereas infrahyoid muscles come fromanatomical structures located below the hyoid.

As a second example, consider the prexes “pre-”and “post-.” When used in conjunction with the term

center of the top of the skull, where the two parietalbones articulate with each other. If one were to dividethe body or a body part right down the middle sothat there is a left and right portion of relatively equalsize, this is referred to as the midsagittal plane. Theterm parasagittal is often used in reference to anysection that is parallel to the midsagittal plane.

Finally, the transverse plane is a horizontal plane ofreference that separates the body or body part into anupper and a lower portion. When a magician performsthe trick where the assistant lies down in a box and

is supposedly cut in half, essentially the assistant isbeing divided in a transverse plane. It should be notedthat in neuroanatomy, the term horizontal plane isused more often than transverse plane.

Other Terminology Associatedwith Spatial Orientation

Now that the anatomical position and planes ofreference have been established, your attention isdirected toward more specic terminology that isassociated with the spatial relationships that exist

between and among the various structures of thebody. Although not an exhaustive list, Table 2-1 pro-vides a “survival list” of terms that will help youunderstand the relationships various body parts haveto each other. Figure 2-3 also illustrates some of themore commonly used terms to describe spatial posi-tion and orientation. It is imperative that you becomecomfortable using these terms. Learning these termsis half the battle when it comes to understanding therelationships between and among the various ana-tomical structures of the human body.

Transverse(horizontal)

plane

Sagittalplane

Frontal(coronal)

plane

Figure 2-2 The planes of reference used to indicate the angle atwhich the observer is viewing the anatomy. (Reprinted with permis-sion from Cohen, B.J. (2008). Memmler’s the human body in health anddisease (11th ed.). Baltimore: Lippincott Williams & Wilkins.)




TABLE 2-1

TERMS AND PREFIXES USED TO DESCRIBE PLANES OF REFERENCE AND SPATIAL RELATIONSHIPS

Term Denition

Ante- Situated before or in front of Anterior One structure is situated closer to the front of the body than another structure; sometimes the

term ventral is used; opposite of posterior Anteroposterior Situated in an anterior-to-posterior (front-to-back) plane Anti- Situated against or on the opposite sideBilateral Pertaining to both sides of the body or an anatomical structureCaudal One structure is situated closer to the tail than another structure; opposite of

cranial and rostral Central Pertaining to the center, or composing the primary part; opposite of peripheral Contra- Pertaining to the opposite side; opposite of ipsi-Coronal Vertical plane of reference that divides the body or a structure into an anterior and a posterior

part; also known as the frontal planeCranial One structure is situated closer to the head than another structure; used synonymously with

rostral ; opposite of caudal Deep One structure is situated further away from the body surface than another structure; opposite

of supercial

Distal Situated away from the center of the body or from the point of origin; opposite of proximal Disto- Pertaining to distal Dorsal Pertaining to the back; opposite of ventral Dorsi- Toward the dorsal (back) directionEcto- Outer or on the outside; opposite of endo-Endo- Inner or on the inside; within; opposite of ecto-Ento- Inner or withinEpi- Situated upon, following, or subsequent toExternal Situated on the outside; one structure is situated to the outside of another structure; opposite

of internal Extra- Situated to the outside; opposite of intra-Extrinsic External or coming from the outside; opposite of intrinsic Frontal Situated in front of or relating to the anterior part of the body; also used synonymously with

coronal as a plane of referenceHypo- Situated below; used sometimes instead of sub- or infra-Inferior Situated below or in a downward direction; opposite of superior Infra- Situated below; used sometimes instead of sub- or hypo- ; opposite of supra-Inter- Situated betweenInternal Situated on the inside; one structure is situated to the inside of another structure; opposite

of external Intra- Situated within or inside; opposite of extra-Intrinsic Internal or completely within; opposite of extrinsic Ipsi- Pertaining to the same side; opposite of contra-Lateral Situated to the side or farther from the midsagittal plane; opposite of medial Longitudinal Situated lengthwise or in the direction of the axis of the body or any of its partsMedial Situated toward the middle or center, or closer to the midsagittal plane;

opposite of lateral Mes-, Mesio-, Meso- Situated in the middle; intermediateMesial Toward the median or midsagittal planeMet-, Meta- After, behind, or hindmost; see also post-Midsagittal Vertical plane of reference through the midline of the body, dividing the body into left and right

halvesOblique Situated in a slanting or diagonal directionPalmar Pertaining to the palm of the hand




A METHOD TO THE MADNESS

At the beginning of this chapter, it was mentioned thatalthough the prospect of learning all of the anatomyand physiology of speech and hearing may cause anxi-ety on your part, there is a method to the madness thatcan make the learning process much easier than it rstappears. There is no getting around it; to become a com-petent clinician you must learn the anatomy and physi-ology of speech perception and production. In part, this will involve committing a huge body of terminology to

memory. How can one be expected to remember thevast nomenclature associated with anatomy and physi-ology? If you take each individual term and attempt tocommit it to memory without really thinking about whatthe term really means, then the process of memorizingthe vast amount of terminology will indeed be nearlyimpossible. However, if you analyze each term by con-sidering the root and any afxes that may be attached,the learning process can be a lot less taxing.

In addition to the terminology presented in Table2-1, you are referred to the appendix at the end of this

central and in reference to gyri (convolutions of thecerebrum), these terms denote two very importantgyri of the brain. The precentral gyrus is the primarymotor area and the postcentral gyrus is the primarysomatosensory area. In this example, the root wordcentral is in reference to the central sulcus, a narrowtrough that separates the frontal lobe from the pari-etal lobe. The precentral gyrus is located immediatelyanterior to the central sulcus, whereas the postcentralgyrus is located immediately posterior to the centralsulcus.

In the chapters that follow, the position of a par-ticular body part may be described in reference to itsspatial relationship to another body part. As you readthese chapters and attempt to make sense of the anat-omy, it is important to note the spatial terminologythat is being used. These are not trivial terms. To thecontrary, these terms allow you to pinpoint the exactlocation or orientation of a body part. You cannot havea complete understanding of anatomy without know-ing where the various parts are located, especially inreference to other body parts.

TABLE 2-1

TERMS AND PREFIXES USED TO DESCRIBE PLANES OF REFERENCE AND SPATIAL RELATIONSHIPS (Continued)

Term Denition

Para- Adjacent, alongside, or nearPeri- Around, about, or nearPeripheral Pertaining to the periphery, or composing the secondary part; opposite of central Plantar Pertaining to the sole of the footPost- After, behind, or posterior to; see also meta- ; opposite of pre-Posterior One structure is situated closer to the back of the body than another structure; sometimes the

term dorsal is used; opposite of anterior Pre- Before, in front of, or anterior to; opposite of post-Prone Body lying face down; opposite of supine Proximal Situated toward the center of the body or close to the point of origin; opposite of distal Rectus Straight, usually in a longitudinal directionRetro- Situated behind or in a backward directionRostral One structure is situated closer to the head than another structure; used synonymously with

cranial ; opposite of caudal Sagittal Vertical plane of reference that divides the body or a structure into a left and a right partSub- Situated beneathSupercial One structure is situated closer to the body surface than another structure; opposite of deep Superior Situated above or in an upward direction; opposite of inferior Supine Body lying face up; opposite of prone Supra- Situated above; used sometimes instead of epi- ; opposite of infra-Transverse Horizontal plane of reference that divides the body or a structure into upper and lower partsUnilateral Pertaining to one side of the body or an anatomical structure Ventral Pertaining to the front or belly; opposite of dorsal Version Deviation of a body part from its normal axis




book. The appendix contains seven tables that presentterms and afxes that are used extensively in describ-ing the anatomy, physiology, and pathology of thespeech and hearing mechanisms. Although you wouldcertainly be in a better position if you committed tomemory the vocabulary and afxes found within thesetables, the tables are provided primarily as a referencefor you as you encounter the vast nomenclature ofanatomy and physiology throughout the remainder ofthis textbook. Many of the terms and afxes presentedin the appendix will also be included in the individualchapters that follow. It is hoped that by presenting theterminology numerous times throughout the book, you will be more likely to learn the nomenclature.

How to Use the Appendix

As mentioned above, the appendix is organized intoseven tables. Each table presents vocabulary andafxes that are related in terms of what they describe.These include:

• Table A-1: Terms and afxes associated withmovement

• Table A-2: Terms and afxes associated with ana-tomical structures or their parts

• Table A-3: Terms and afxes associated with color,form, general location, relative size, or shape

• Table A-4: Terms and afxes associated withbones, cartilages, cavities, membranes, or spaces

• Table A-5: Terms and afxes associated with thenervous system

• Table A-6: Terms and afxes associated with theauditory/vestibular system

• Table A-7: Miscellaneous terms and afxes usedin anatomy, physiology, and pathology

With the exception of Table A-1 (which providesdenitions only), the tables in the appendix providedenitions of the terms and afxes as well as an exam-ple of the use of each term or afx. The paragraphsthat follow also provide more detailed information

Medial

Lateral

Proximal

Distal

R o s t r al

or

c r ani al

C a u d al

Anterior

Posterior

V e n t r a l

D o r s

a l

A B

Hyoidbone

Thyroid cartilage

Cricoidcartilage

Superior

Inferior

Splenius capitis

Levator scapulae

Trapezius

D

C

Trachea

Figure 2-3 An illustration of the more commonly used terms for describing spatial position and orientation. A . Distal vs. proximal; lateralvs. medial; rostral (cranial) vs. caudal. B. Anterior vs. posterior; dorsal vs. ventral. C . Superior vs. inferior (note that the hyoid bone and thyroidcartilage are superior to the cricoid cartilage, and the trachea is inferior to the cricoid). D . Deep vs. supercial (note that the levator scapu-lae and splenius capitis are deep to the trapezius). ( A and B: Modied with permission from Cohen, B.J. (2008). Memmler’s the human bodyin health and disease (11th ed.). Baltimore: Lippincott Williams & Wilkins. C : Reprinted with permission from Cohen, B.J. (2008). Memmler’sthe human body in health and disease (11th ed.). Baltimore: Lippincott Williams & Wilkins. D : Reprinted with permission from Scheuman, D.W.(2006). The balanced body: A guide to deep tissue and neuromuscular therapy (3rd ed.). Baltimore: Lippincott Williams & Wilkins.)




What does sternocleidomastoid mean? By knowing theterminology in Table A-2, you can determine that it is amuscle that has three attachments. “Sterno-” refers tothe sternum, “-cleido-” refers to the clavicle, and mas-toid refers to the mastoid process, which is the roundedpart of the base of the skull right behind the ear. There-fore, the sternocleidomastoid is a muscle that attaches

to the sternum, clavicle, and mastoid process.Table A-3 provides terms and prexes associated with general location, size, shape, color, or generalform. For example, the serratus posterior superiormuscle can be found in the upper part ( superior ) of theback ( posterior ) and has a jagged or sawtooth ( serratus )appearance. In Chapter 8, while learning about thecricoid cartilage (one of the cartilages of the larynx), you will encounter the term posterior quadrate lam-ina. From Table 2-1, you know that posterior refers tothe back. Table A-3 denes quadrate as something thatis somewhat square- or rectangular-shaped. Finally,according to Table A-4 lamina is a thin plate or atlayer of bone or cartilage. Taken together, you willcorrectly deduce that the posterior quadrate laminais the back plate of the cricoid cartilage that is somewhat square-shaped.

Table A-4 includes terms and afxes that are used inreference to bones, cartilages, membranes, or cavities.For example, “cerato-” refers to a horn of some sort. Thethyroid cartilage has two sets of cornua (horns) alongits posterior margin. The superior cornua articulate with the greater cornua of the hyoid bone. The infe-

rior cornua of the thyroid cartilage articulate with thecricoid cartilage, forming the cricothyroid joint. This joint is held in place by a series of ligaments knownas the ceratocricoid ligaments. The term ceratocricoidrefers to the two parts that make up the joint—theinferior cornua of the thyroid cartilage and the cricoidcartilage. Similarly, the mental symphysis refers to thefusion of the two halves of the mandible (jaw). Dur-ing fetal development, the two halves of the mandiblefuse to form a singular bone. The point where the twohalves meet is the mentum, which is the protrudingpart of the chin. A symphysis is a union of two struc-

tures, in this case the two halves of the mandible.Table A-5 provides terms and afxes associated

primarily with the nervous system, and Table A-6 pro-vides terms and prexes associated with the auditory/vestibular system. (It should be noted here that althoughthe respiratory, phonatory, and articulatory/resonancesystems have their own unique nomenclature, many ofthe terms and afxes provided in Table 2-1 in this chap-ter and Tables A-1 through A-4 in the appendix are alsoused to describe structures and functions pertaining tothese systems.)

as to how knowledge of these terms and afxes canassist you in developing a deeper understanding ofthe anatomy, physiology, and pathology of the speechand hearing mechanisms.

Table A-1 presents terms and prexes that are usedto describe movement. In terms of muscle activity,the terms extension and exion are used to denote

how muscle contraction affects the movement of thebody part being acted upon. The terms abduction and adduction are also very important. Although asingle anatomical structure can abduct or adduct,these terms are used most often to describe the move-ment of two structures. For example, humans havetwo vocal folds. When the vocal folds are abducted(moved away from midline), the glottis—a variable-sized aperture between the vocal folds—opens sothat air can ow in and out of the lungs. When thevocal folds are adducted (moved toward midline),they come together so that expired air can be used tovibrate them to produce voicing.

The terms depressor, levator, and tensor are alsoused to describe the action that occurs when musclescontract and act upon an anatomical structure. Theseterms are sometimes used as part of the name of amuscle, and therefore describe the action that partic-ular muscle makes. For example, the tensor tympanimuscle tenses the eardrum (tympanic membrane) bypulling inward on the malleus, to which the eardrumis attached. The depressor anguli oris is a muscle ofthe lips that pulls the corner of the mouth downward,

as in frowning. Finally, the levator veli palatini muscleelevates or raises the soft palate (i.e., the velum, whereaccording to Table A-2 the term veli palatini comes).

In reference to pathology, the prexes “hyper-” and“hypo-” are often used to describe movement disor-ders. For example, a hyperkinetic movement disordermeans that the patient exhibits involuntary, excessive,extraneous movements. By the same token, a patient with a hypokinetic movement disorder exhibits pau-city of movement (i.e., the movements tend to be dif-cult to initiate and are very slow).

Table A-2 provides terms and afxes whose mean-

ings are related to specic body parts. For example,upon rst encountering the omohyoid muscle, youmay scratch your head in wonder. However, if theterm was analyzed into its components “omo-” andhyoid, one would be able to discern very quickly thatthe omohyoid muscle runs from the shoulder area tothe hyoid bone. Similarly, by understanding the rootterms and afxes, one can readily understand that cra-nial nerve III, the oculomotor nerve, is responsible formovements of the eyeball (“oculo-” meaning eye, andmotor referring to activity resulting in movement).




In reference to the nervous system, the terms affer-ent and efferent are often used to describe nerves andnerve pathways. Afferent nerves are also known assensory nerves because the impulses originate in theperiphery (where the sense organs are located) andthen are sent toward the central nervous system forinterpretation. On the other hand, the impulses of

efferent (or motor) nerves originate in the central ner-vous system and then proceed to the various musclesand viscera located in the periphery. The purpose ofthese nerves is to effect movement.

Many of the structures of the brain have peculiarnames: caudate nucleus, corpus striatum, olives, andpyramids to name a few. Once again, by analyzingthese names you can remember something abouteach of them. Caudate means tail (see Table A-5 of theappendix). A nucleus is a collection of gray matter—nerve cell bodies. Therefore, the caudate nucleus is amass of gray matter that has a head and a long slendertail. Corpus means body. Striatum refers to a stripedappearance. The corpus striatum then is a series ofbodies deep within the brain that has a striped appear-ance. Finally, the olives (technically, the olivary com-plex) and pyramids can be seen on the ventral surfaceof the medulla oblongata. They each get their namefrom their general shape. To carry this thought out abit further, when one encounters the term pyramidalmotor tract, one should not be alarmed. The astuteobserver will note that another term for motor is effer-ent. The pyramidal motor tract is a tract of efferent

nerve bers that passes through the pyramids on the way to the spinal cord, which is immediately below themedulla oblongata. In fact, the pyramidal motor tractis the primary motor tract, as opposed to the extrapy-ramidal motor tract, which is a secondary motor tract whose nerve bers also pass down to the spinal cord,but do not make a stop at the pyramids along the way.Remember from Table 2-1, “extra-” means situated tothe outside, so extrapyramidal means “situated to theoutside of the pyramids.”

In regard to the auditory/vestibular system (seeTable A-6), terms and prexes can also be analyzed to

provide meaning to the nomenclature. For example,incudostapedial refers to the incus and stapes, andin fact, the incudostapedial joint is formed by thearticulation of the incus with the stapes. As anotherexample, a pathological condition of the middle ear,otitis media, can easily be remembered if the termis analyzed into its individual parts: “ot-” means ear;“itis-” means inammation; and media refers to themiddle. Therefore, otitis media is an inammation ofthe middle ear cavity.

The last table in the appendix (Table A-7) providesa list of miscellaneous terms and affixes that canalso be used to assist you in retaining the nomen-clature of anatomy, physiology, and pathology. Although many of the terms and affixes in this tableare pertinent to anatomy and physiology, a largenumber of them are used in reference to pathology.

Once again, the terms and affixes presented in thistable can be considered a “survival set” of vocabu-lary for you. For example, a tracheotomy is a proce-dure in which an incision is made in the anterior wall of the trachea through the outer neck to assistthe patient in breathing (usually due to some typeof upper airway obstruction). You know from Table A-2 that “tracheo-” refers to the trachea or windpipe.Table A-7 shows that “-otomy” means an operationinvolving cutting. As a second example, Table A-7provides the definition for malacia (a softening orloss of consistency of tissues or organs). From Table A-4, you can see that “chondro-” is a prefix mean-ing cartilage. Therefore, chondromalacia is a patho-logical condition in which a cartilage is too soft orunderdeveloped.

As a final word, it should be noted that the termspresented in Table 2-1 of this chapter and Tables A-1through A-7 in the appendix are not an exhaustivelist but are presented as a starter set for you. You areencouraged to consult a dictionary when an unfa-miliar term is encountered. Pay particular attentionto the root and any affixes that may be attached.

Clues often exist to assist you in learning thenomenclature. Also, it should be emphasized thatmany of the terms presented in this chapter wereplaced in a particular table because of the primary context in which the term is used. There are manyterms and affixes in these tables that could just as well be presented in another table. For example, theprefixes “ary-,” “crico-,” and “thyro-” were all placedin Table A-2 because they refer to specific parts ofthe human body (i.e., the arytenoid cartilages, cri-coid cartilage, and thyroid cartilage, respectively).However, all of them could just as easily have been

placed in Table A-4 because they are associated with cartilages. You are discouraged from relyingtoo heavily on how these terms and affixes are orga-nized in the tables. Instead, your focus should besimply on the terminology.

It should be readily apparent from all of theseexamples that the process of learning anatomy, phys-iology, and pathology is not as difficult as one mayfirst imagine. Learning anatomy and physiologyshould not be an exercise in rote memorization of




the meaning of the unfamiliar term may very wellpresent itself.

Now that you have an understanding of the basicnomenclature in terms of the anatomical position,planes of reference, spatial terminology, and morespecic vocabulary related to anatomy, physiology,and pathology, it is time to turn your attention to the

structural organization of human beings.

terms. Instead, by focusing more on the meaningsof a relatively small, finite set of terms and affixes, you have nearly the entire world of anatomy, physi-ology, and pathology within grasp. As you proceedthrough the remaining chapters of this textbookand encounter terminology that is unfamiliar to you, the last thing you should do is panic. Step back,

think of the meanings of the root and affixes, and



19

Knowledge Outcomes for ASHA Certication for Chapter 3• Demonstrate knowledge of the biological basis of the basic human communication processes

(III-B)• Demonstrate knowledge of the neurological basis of the basic human communication

processes (III-B)• Demonstrate knowledge of the biological basis of swallowing processes (III-B)

Learning Objectives• You will dene cell types and organelles.• You will describe the four tissue types and subclassications.• You will discuss the organ systems most pertinent for speech and swallow function.

CHAPTER 3

The Structural Organization of Humans

MEDICAL TERM PART BOXTERM MEANING EXAMPLE

-arthrodial joint di arthrodial

bi- two or double bi polar

cellular related to a cell intra cellular movement

chondrium related to cartilage peri chondrium

cyto- pertaining to a cell cyto plasm

endo- toward the interior endo mysium

epi- upon or above epi mysium

extra- outside of extra cellular

inter- between inter cellular

intra- within intra cellularmeatus an opening external auditory meatus

meso- middle or intermediate meso thelial tissue

micro- small size micro tubule

-mysium pertaining to muscle peri mysium

os bone os sicles

-osteum pertaining to bone peri osteum




TERM MEANING EXAMPLE

peri- around peri mysium

-plasm cellular substance cyto plasm

proto- rst proto plasm

uni- one or single uni polar

The complexity of human communication is largely what sets human beings apart from other vertebratespecies. Thought, language, and speech are all nec-essary for effective verbal communication. Speech,our primary mode of expressive communication, isthe sequential production of sounds to represent ourthoughts resulting in a comprehensible auditory sig-nal for a listener to perceive. Furthermore, the abilityto produce speech relies on the coordination of mul-tiple speech processes: respiration, phonation, andarticulation /resonance. In order to better understandthese speech processes, they can be broken downby reducing them to their structural makeup. Forexample, the process of respiration relies on the tho-racic skeletal framework of the ribcage and vertebralcolumn upon which the muscles attach to enact themovement necessary to breathe for speech. In addi-tion, each speech process includes organs, such aslungs, and each organ has a predominant tissue type.Tissues are dened by their cellular makeup. Thus,the cell is our most basic component of life.

Cells

There are more than 100 trillion cells in the humanbody. Some cells live the life span of the body such asthose in the central nervous system; some live a mod-erate amount of time such as blood cells, and somecells are continuously dying and being replaced such asthose that comprise the epithelium—otherwise knownas skin.

A cell possesses ve characteristics, making it a liv-

ing organism. These characteristics are (1) irritability,(2) growth, (3) spontaneous movement, (4) metabo-lism, and (5) reproduction. Irritability refers to thecell’s ability to respond to stimulation. A cell, in mostcases, goes through a life process of birth, develop-ment, and death; this is considered growth. Sponta-neous movement is characterized by movement thatoriginates and occurs within the cell; that is, intra-cellular movement. Metabolism refers to the cell’scapability to take in raw products, break down theseproducts, and utilize the “food” in the form of usable

energy to carry out its life support roles. Lastly, cellshave the ability to reproduce themselves.

Cells are formed out of protoplasm which is thebasic living substance that comprises all cells. Thisprotoplasm subdivides into the cell nucleus and thesurrounding cytoplasm , the uid outside the nucleus(see Figure 3-1). The outer membrane surroundingthe cell is referred to as the plasma membrane . It iscomposed of a double layer of molecules that exhib-its selective permeability ; that is, some materials areallowed to enter or exit the cell whereas other materi-als are prohibited. Essentially, the plasma membranecontrols the exchange of molecules and ions betweenthe cell and its external environment (i.e., extracellu-lar space). Further explanation and illustration of thisdouble-layered membrane is presented in Chapter 4.The nucleus is considered the “control center” of thecell. It is usually found toward the center of the celland is separated from other cellular material by thenuclear membrane. The nucleus contains the geneticmaterial of the cell in the form of threadlike structurestermed chromosomes, which are double strands ofdeoxyribonucleic acid. The most prominent structure within the nucleus is the nucleolus, the genetic con-trol center for ribosome synthesis.

Inside each cell are a number of structures calledorganelles (“cell organs”) found within the cytoplasm(see Figure 3-1). Each organelle performs a specictask necessary for the functioning and survival of thecell. For example, mitochondria provide energy andserve as a power source for the cell. The Golgi appa-ratus serves to store materials and is responsible forpackaging substances for intracellular transport. The

endoplasmic reticulum (granular or agranular) syn-thesizes, stores, and releases various substances suchas fatty acids, protein, and calcium. Lysosomes breakdown and digest bacterial and cellular debris thathave been ingested by the cell; they are considered the“garbage can” of the cell. Microtubules and microla-ments assist with cell movement as well as provide forintracellular transport of substances. Centrioles arefused sets of microtubules that participate in nuclearand cell division (i.e., reproduction). Refer to Table 3-1for further descriptions of these organelles.



CHAPTER 3 THE STRUCTURAL ORGANIZATION OF HUMANS 21

the production of mechanical forces, which producemovement. Connective tissue cells are specializedfor the formation and secretion of various types ofextracellular connecting and supporting elements—connecting, anchoring, and supporting structuresof the body. Nerve cells (i.e., neurons) are specializedfor the initiation and conduction of electrochemical

Cells can be classied into four types specializedfor specic functions: epithelial cells , muscle cells ,connective tissue cells, and nerve cells or neurons.Epithelial cells are specialized for the selective secre-tion and absorption of molecules and ions; they coversurfaces and form selective barriers. Muscle cells,synonymous with muscle bers, are specialized for

Cilia

Plasmamembrane

Cytoplasm

Nucleolus

Nucleus

Smooth endoplasmicreticulum (ER)

Nuclearmembrane

Golgi apparatus

Mitochondrion

Ribosomes

Vesicle

Rough

endoplasmicreticulum (ER)

Lysosome

Centrioles

Microtubule

Figure 3-1 A generic human cell illustrat-ing the plasma membrane, cilia, nucleus,and organelles found within the cytoplasm.(Reprinted with permission from Cohen, B.J.(2008). Memmler’s the human body in healthand disease (11th ed.). Baltimore: LippincottWilliams & Wilkins.)

TABLE 3-1

PARTS OF A TYPICAL CELL

Cell Part Function

Centrioles Assist in cell division, microtubule formationChromosomes Store and pass on genetic informationGolgi apparatus Stores and delivers various proteinsLysosomes Digest cell debris and bacteria

Microlaments Support cytoplasm, cell movementMicrotubules Provide cell framework and movement of parts of cellsMitochondria Produce energy for the cellNucleus Genetic control center via both deoxyribonucleic acid and ribosome synthesisPlasma membrane Surrounding barrier of a single cell; separates intracellular material from

extracellular material and dictates entry and exit of material from the cellRibosomes Synthesize protein as directed by genetic informationRough (granular) endoplasmic Protein production, stored and released reticulumSmooth (agranular) Stores and releases enzymes and calcium for muscle contraction endoplasmic reticulum




information traveling over distances; they are the basicfunctional unit of the nervous system. Aggregates ofcells form the four different tissue types. It is impor-tant for groups of cells to join and cooperate for thegood of the organism as a whole. Thus, groups of cellssimilar in structure, function, and embryonic originband together with varying amounts of extracellular

material to form tissues. An organization of these tissuetypes and subclassications is presented in Table 3-2.

TissuesEPITHELIAL TISSUE

Epithelial tissue refers to “tissue upon tissue”; thus,by denition this tissue lines the surface of the bodyand those passages communicating with the externalenvironment (e.g., the ear canal) and the cavities ofour body. Epithelium has very little extracellular mate-rial, so the cells lie adjacent to one another. This tissueis often described on the basis of cell shape and num-ber of cell layers. Epithelial cells can be at or plate-like (i.e., squamous), cube-shaped (i.e., cuboidal), oroblong (i.e., columnar). In addition, epithelial cellsmay have cilia (short, hairlike structures) protrudingfrom their surface to provide a transport mechanismto move materials over the surface of the cells (e.g.,respiratory tract). Tissue is made up of these differentcell shapes organized in one or more layers. Where

transport of material occurs, the cells are arranged inone layer; this is referred to as “simple.” Multiple celllayers are referred to as “stratied” or “compound.”Hence, the terms can be combined to describe bothcell shape and layers—for example, simple columnaror stratied squamous (see Figure 3-2).

Epithelial tissue can also be classied into threegroups based on location. Epithelial tissue proper istissue forming the skin (i.e., epidermis) and the inter-nal membranes continuous with the skin. This tissuecomprises various layers and shapes of cells that linethe digestive, respiratory, urinary, and reproductive

tracts and tubes. Endothelial tissue makes up the lin-ings of blood and lymph vessels. Simple squamouscells comprise this tissue because of the necessity tohave extremely smooth surfaces to reduce the possi-bility of fragmenting blood cells. It should be notedhere that arteries and veins also require elastic tis-sue (a type of connective tissue) and smooth muscle(a type of muscle tissue). Lastly, mesothelial tissue lines the internal body cavities. Mesothelial tissue isoften referred to as serous membrane because thecells secrete a serous uid or serum, which has a thin,

TABLE 3-2

TYPES OF TISSUES WITH SUBCLASSIFICATIONS

I. Epithelial tissue A. Shape 1. Squamous 2. Cuboidal 3. Columnar B. Number of cell layers 1. Simple 2. Stratied /compound C. Location 1. Epithelial tissue proper 2. Endothelial 3. Mesothelial a. Peritoneal b. Pleural c. Pericardial II. Connective tissue

A. Loose 1. Areolar 2. Adipose B. Dense 1. Tendons 2. White brous a. Ligaments b. Fascia C. Specialized 1. Cartilage a. Hyaline b. Fibrous (brocartilage)

c. Elastic (yellow) 2. Blood 3. Bone a. Compact b. Spongy III. Muscle tissue A. Striated/skeletal (voluntary) B. Smooth (involuntary) C. Cardiac (striated, involuntary) IV. Nervous tissue A. Neurons B. Glial cells

watery constitution. There are a total of four bodycavities that are lined with serous membrane (seeFigure 3-3). Three are located in the thorax: the peri-cardial cavity housing the heart and the two pleuralcavities housing each lung. The fourth cavity, in theabdomen, is the peritoneal cavity housing the viscera(i.e., abdominal organs). The pleural cavities will bediscussed in more detail in Chapter 6.




and adipose , which includes a number of fat-storingcells. Dense connective tissue is characterized byan abundance of tightly packed extracellular bers,either collagen or elastic. Collagen is a brous protein with great strength; therefore, these tissues are able totolerate high degrees of tension. Furthermore, thereare three types of dense connective tissues: tendons ,ligaments , and fascia . Tendons are tough, nonelasticcords that are associated with muscle as they attachmuscle to bone, muscle to cartilage, or muscle toanother muscle. Broad tendinous sheets are calledaponeuroses . Ligaments are also tough cords but, incontrast to tendons, they have an abundance of elas-tic bers and they join bone to bone, bone to carti-lage, or cartilage to cartilage; thus, they are a criticalpart of joints. Finally, fascia makes up brous tissueunderlying the skin or covers and separates muscleinto functional groups.

Cartilage and bone make up specialized connec-tive tissue; their hardness is imposed by solid or rigidextracellular substance. Cartilage is characterized byits rigidity, exibility, and varying amounts of elas-ticity depending on the type of cartilage. Cartilage isfurther subdivided into hyaline , elastic or brous .Hyaline cartilage is the most abundant type of carti-lage in the human body. It has a bluish-white trans-lucent appearance and is found primarily in places where strong support is needed with some exibil-ity as well. Hyaline makes up most of the embryonicskeleton, which later turns to bone. In regard to struc-

tures critical for speech production, hyaline carti-lage is found in the rib cage, the larynx, and the nose.Figure 3-4 illustrates the nasal septum; the most ante-rior part comprises hyaline cartilage. Elastic cartilageappears yellow and opaque and is extremely exible.This cartilage is the basis of the outer ear, comprisingthe pinna and the cartilaginous portion of the exter-nal auditory meatus (i.e., ear canal; see Figure 3-5).The epiglottis and small cartilages of the larynx (i.e.,corniculates and cuneiforms ) also comprise elasticcartilage. Fibrous cartilage has a coarse appearance

CONNECTIVE TISSUE

Tissues which combine or hold together structures,support the body, and aid in body maintenance arereferred to as connective tissues . In contrast to epi-thelial tissue, there are fewer cells making up connec-tive tissue but much more extracellular substance.

The extracellular components of connective tissue arecollectively called matrix . Matrix is formed by proteinbers such as collagen, nonprotein molecules such asground substance, and uid. Connective tissue canbe classied according to the make-up of its extracel-lular matrix as connective tissue proper or specializedconnective tissue (see Table 3-2).

Connective tissue proper is further classied intoloose or dense connective tissue. Loose connectivetissue lls spaces and is considered the “packingmaterial of the body.” Loosely packed bers are dis-tributed throughout the body to bind parts together.Just deep to the skin are two loose connective tissuetypes: areolar , which forms the “bed” for the skin,

ACB

Cilia

Figure 3-2 Examples of epithelial tissue of different shapes and layers. Note the close adjacency of the cells and the lack of extracel-lular material. A. Simple cuboidal. B. Stratied squamous. C. Pseudostratied ciliated columnar. (Reprinted with permission from Porth,C.M., & Matn, G. (2008). Pathophysiology: Concepts of altered health states (8th ed.). Philadelphia: Lippincott Williams & Wilkins.)

Pleural cavities

Pericardialcavity

Peritonealcavity

Figure 3-3 Body cavities. (Reprinted with permission fromNath, J.L. (2005). Using medical terminology: A practical approach. Baltimore: Lippincott Williams & Wilkins.)




as bers are arranged in thick parallel bundles. Thiscartilage is slightly compressible and can withstandgreat amounts of pressure; therefore, it is found inregions that support body weight such as the inter-vertebral discs (see Figure 3-6) and some joints of thebody such as the temporomandibular joint (which will be described more fully in Chapter 10).

Bone is a specialized connective tissue that pro-vides the framework for other tissues of the body.

Bone is unique in that the collagen and matrix areintermixed with minerals (i.e., calcium phosphateand calcium carbonate salts) that impart rigidity andhardness. Each bone has a dense, outer, compact layersurrounded by a brous membrane termed perios-teum . Each bone also has a porous, inner, spongylayer where bone marrow is found for the productionof red and white blood cells.

The adult, human skeleton has approximately206 bones, depending how they are counted, and isbroadly divided into the axial and appendicular skele-

ton (see Figure 3-7). The axial skeleton is most relevantto speech and hearing anatomy as it consists of theskull which includes the ossicles (bones of the middleear) and the facial bones, as well as the hyoid bone,the ribcage, and the vertebral column. The appendic-ular skeleton refers to the pectoral girdle (shoulder)and bones of the arms and hands (upper extremities)as well as the pelvic girdle (hip) and bones of the legsand feet (lower extremities). It should be noted thatboth the pectoral girdle and pelvic girdle are connec-tion points for muscles involved in breathing. These will be described more completely in Chapter 6.

Bones join other bones at joints, as do some car-tilages. These joints are held together by ligaments.Joints may be described on the basis of their anatomyor their function (see Table 3-3). Anatomically, brous joints are united by brous connective tissue. These joints are considered synarthrodial as they are onlyslightly movable or totally immovable. Cranial suturesthat join the bones of the cranium are one exampleof a class of brous joints that are immovable. Carti-laginous joints are considered amphiarthrodial oras joints that yield. These joints utilize either hyaline

Pinna

External canal

Cranial cavity

Bony portionof nasal septumCartilaginous

portion ofnasal septum

Hard palate Soft palateFigure 3-4 The nasal septum; the most anterior portioncomprises hyaline cartilage. (Reprinted with permission fromAnatomical Chart Company.)

Figure 3-5 The external ear; note that the pinna and externalear canal are made up of elastic cartilage. (Reprinted with permis-sion from Anatomical Chart Company.)

Vertebrae

Intervertebraldisc

Figure 3-6 A segment of the vertebral column; note that theintervertebral discs are made up of brous cartilage. (Reprintedwith permission from Anatomical Chart Company.)




or brocartilage to unite bone to bone. If hyaline is

the cartilage involved, the joint is referred to as a syn-chondrosis joint. An example of this type of joint per-tinent to speech is found within the ribcage between

Appendicular skeletonAxial skeleton

Figure 3-7 Adult, human skeleton with the axial skeleton high-lighted. (Reprinted with permission from Cohen, B.J. (2008). Mem-mler’s the human body in health and disease (11th ed.). Baltimore:Lippincott Williams & Wilkins.)

Manubrium

Clavicle

Rib

Costalsternal joint

Costalcartilage

Sternum

Manubriosternal joint

Figure 3-8 Anterior view of the ribcage illustrating the costal-sternal joint and the manubriosternal joint. (Modied with per-mission from Hendrickson, T. (2009). Massage and manual therapyfor orthopedic conditions (2nd ed.). Baltimore: Lippincott Williams

& Wilkins.)

TABLE 3-3

ANATOMICAL AND FUNCTIONAL TERMS FOR COMMON JOINTS SEEN IN THE ANATOMY OF THESPEECH AND HEARING MECHANISM WITH EXAMPLES

Functional Name Anatomical Name Example

Synarthrodial Fibrous Syndesmosis Stylohyoid syndesmosis

Sutures Coronal suture Gomphosis Dentoalveolar joint Amphiarthrodial Cartilaginous Synchondrosis Costosternal synchondrosis Symphysis Manubriosternal symphysisDiarthrodial Synovial Plane (gliding) Costovertebral joint Saddle Malleoincudal joint Hinge Genu (knee) Pivot Atlas (C1) and axis (C2) Ball-and-socket Humeral (shoulder) joint Ellipsoid (condyloid) Temporomandibular joint

the bony ribs and the sternum via the costal cartilages(see Figure 3-8). A synchondrosis joint allows for somemovement given the exibility inherent in hyaline car-tilage. This is imperative to breathing as the ribcagemust be able to expand in order to inhale and, con-versely, get smaller to exhale. The most common jointis the synovial joint that is considered diarthrodial , which means freely moving. The synovial joint is ana-tomically more complex than brous or cartilaginous

joints.The synovial joint itself is enclosed by a brouscapsule called the articular capsule that is lined by a




membrane called the synovial membrane. The syn-ovial membrane secretes synovial uid which (1)

lubricates the joint, (2) provides nourishment to thearticular cartilages (which are hyaline), and (3) pro-tects the joint from impact and friction. There are sixtypes of synovial joints which are classied accord-ing to the shape of their articulating surfaces: plane,saddle, hinge, pivot, ball-and-socket, and ellipsoid (orcondyloid). An example of a saddle joint, which allowsfor all types of movement except rotation, is the mal-leoincudal joint , which joins two of the ossicles in themiddle ear, the malleus and the incus (see Figure 3-9).Table 3-3 provides examples of amphiarthrodial, diar-throdial, and synarthrodial joints.

MUSCLE TISSUE

Muscle cells, which are also called muscle bers, cometogether to form muscle tissue. Muscle tissue has theimportant property of contractility—the ability tochange shape, becoming shorter and thicker thusenabling movement of bones and other structures.Muscle tissue is described in terms of its anatomy,being striated or nonstriated, and function, being vol-untary or involuntary. There are three types of mus-

cle tissues: cardiac, smooth, and striated or striped(see Figure 3-10). Cardiac muscle forms the walls ofthe heart and is responsible for pumping blood; it isunder involuntary control. Each cardiac muscle cellhas one nucleus, appears striated, and branches toconnect with adjacent cells. This branching is sig-nicant in regard to the type of communication thatoccurs between cardiac cells, allowing for continuousheart muscle contraction.

Smooth muscle forms the muscular portion of thevisceral organs (e.g., lower esophagus, stomach, intes-

tines) and is also found within blood vessels. Smoothmuscle controls the size, shape, and movements ofthese visceral organs. It is nonstriated and is underinvoluntary control (i.e., it contracts without the indi-vidual having conscious control over it).

Striated muscle tissue is also referred to as skeletalmuscle. Skeletal muscle is easiest to envision as it con-

nects to our skeletal framework and contraction resultsin body movement. Skeletal muscle can contract toabout one-half its original length. The larger the diam-eter of the muscle, the greater its strength. As the nameimplies, cells making up skeletal muscle tissue appearstriated and its function is under voluntary control.Skeletal muscle is the predominant type of muscleinvolved with speech production. Speech productionis, indeed, a voluntary behavior and is mediated by thecontraction and relaxation of skeletal muscles.

Skeletal muscle is attached to bone or cartilage andoccasionally inserts into another muscle (i.e., muscles

of the tongue) or to the epidermis (e.g., eyelids, lips).Muscle is attached via a tendon to the periosteum ofthe bone or the perichondrium of the cartilage. Mus-cle may also be attached via an aponeurosis (a broadtendinous sheet).

The microscopic structure of skeletal muscle is veryorganized with the help of connective tissue. Muscleconsists of bundles of muscle bers (recall that amuscle ber is a muscle cell). Each bundle is termeda fasciculus . Each muscle ber in the fasciculusis surrounded by a thin layer of delicate connective

Stapes

Malleus

Malleoincudal jointIncus

Figure 3-9 The three ossicles of the middle ear. The malleoin-cudal joint is a saddle joint, a type of synovial joint. (Reprintedwith permission from Anatomical Chart Company.)

Striatedmuscle tissue

Smoothmuscle tissue

Cardiacmuscle tissue

Figure 3-10 Three types of muscle tissues: cardiac, smooth, andstriated (skeletal). (Reprinted with permission from AnatomicalChart Company.)




Axons are also referred to as nerve bers. Nervebers are classied as Type A, Type B, or Type C basedon their diameter. Type A bers transfer informationmost rapidly, as they are large diameter, myelinatedaxons. Type B bers have a medium diameter andare slightly myelinated resulting in a slower speed ofinformation transfer as compared with Type A. Finally,

Type C bers are relatively slow as they are small indiameter and are nonmyelinated. Speech processesrely on Type A nerve bers for rapid sensory input tothe brain and for rapid motor impulses to the musclesof respiration, phonation, and articulation /resonance.

An example of Type A nerve bers is the motorneurons that inform muscles whether to contractand how much to contract; this occurs at the neu-romuscular junction . The neuromuscular junc-tion is the point of communication and informationtransfer between the terminal branches of an axonand the muscle bers it innervates. This junction isalso referred to as the myoneural junction as “myo-”refers to muscle and “neural” refers to the nerve ber.This point of information transfer between the nerveber and its muscle bers is a synapse. Synapses alsotake place between neurons but here the synapse isspecic to the neuron and the muscle. The terminalbranches from a single neuron synapse with manymuscle bers. A motor unit is one motor neuron andall the muscle bers it innervates.

Similar to muscle, nerves of the peripheral nervoussystem have an organization imposed by their con-

nective tissue coverings (see Figure 3-11). A delicateconnective tissue called endoneurium surroundsthe individual nerve bers (i.e., axons). These nervebers run in bundles called fascicles ; each fascicle isencased in perineurium . Fascicles, in turn, are bun-dled in groupings that form a nerve which is wrappedby epineurium . These connective tissue coveringsallow a peripheral nerve, such as the hypoglossalcranial nerve, to function as a unit with a specicresponsibility. For instance, the hypoglossal cranialnerve provides impulses to muscles of the tongue formovement.

Organs

Organs are the result of a combination of two ormore tissue types that come together to form a func-tional unit. A functional unit refers to tissues workingtogether to perform a specic function. Examples per-tinent to speech production and swallowing includethe lungs, which function to provide breath supportfor speech. The larynx is also an organ that provides

tissue called endomysium . Each fasciculus is, in turn,surrounded by a sheath of brous connective tissuecalled perimysium , which serves to separate groupsof muscle bers from each other to enable muscle tofunction as a unit. A group of fasciculi is encased in acoarser connective tissue called epimysium . Finally,the entire outer surface of each muscle is enclosed

with fascia, a dense connective tissue which is con-tinuous with the connective tissue of the tendons andperiosteum or perichondrium. Figure 3-11 illustratesthis organization.

NERVOUS TISSUE

Nervous tissue consists of nerve cells (i.e., neurons)and support cells called glial cells . This tissue is foundin the brain, spinal cord, and peripheral nervous sys-tem, and relays information to and from the head,neck, and body. Nervous tissue is specialized to trans-mit information across distances. This information ispassed on through both chemical (e.g., neurotrans-mitters ) and electrical (e.g., action potentials ) means.Neurons are composed of four parts—dendrites, cellbody (i.e., soma), axon, and terminal (see Figure 3-12).In general, the dendrites receive electrical signals andconduct them toward the cell body. The cell bodyhouses the nucleus and a number of organelles criti-cal to the function of the neuron. The axon projectsoff the cell body and is key in transmitting the elec-trical signal (i.e., impulse) in one direction, down the

axon toward the terminal. The terminal, if adequatelystimulated, then releases a chemical to carry the mes-sage to the next neuron in line. In the case of musclein the periphery, the neuron releases a chemical thatdirects the muscle to contract.

Neurons are classied according to number of pro-cesses (i.e., axons and dendrites), function, and speedof information transfer. Neurons with multiple den-drites and a single axon are called multipolar neurons ;these are the most commonly seen in illustrations ofneurons. The majority of the neurons in the brain aremultipolar, often having a motoric function. Those

with a single dendrite and a single axon are bipolarneurons and those with only a single axon emerg-ing from the cell body are unipolar neurons . Bipolarneurons are found in systems involved with specialsenses. For example, the cells of the sensory cochleaand the vestibular ganglia are bipolar. Unipolar neu-rons are found in the dorsal root ganglia next to thespinal cord. Neurons function in sensory, motor,or integrative (i.e., association neurons) capacities.Speed of transfer is dependent on the covering of theaxon (i.e., myelin) and the diameter of the axon.




Fascia

Fasciculus

Epimysium

Perimysium

Endomysium

Muscle fiber

A

B

Lower lip

Superiorlongitudinal muscle

Mandible

Nerve

Epineurium

Perineurium

Fasicle

Endoneurium Myelin sheath

Axon

C

Figure 3-11 A . Microscopic structure of striated muscle illustrating connective tissue coverings enlarged from a section of the supe-rior longitudinal tongue muscle. B . Tongue muscles. C . Microscopic structure of peripheral nerves illustrating connective tissue coveringsof the nerve innervating the superior longitudinal tongue muscle. ( A : Reprinted with permission from Moore, K.L., Agur, A.M., & Dalley, A, F.(2010). Essential clinical anatomy (4th ed.). Baltimore: Lippincott Williams & Wilkins. B: Reprinted with permission from Anatomical ChartCompany. C : Reprinted with permission from Moore, K.L, Agur, A.M., & Dalley, A.F. (2009). Clinically oriented anatomy (6th ed.). Baltimore:Lippincott Williams & Wilkins.)




Terminal

Soma

Axon

Dendrites

Figure 3-12 A single nervecell highlighting four key compo-nents. (Reprinted with permis-sion from Smeltzer, S.C., Bare,B.G., Hinkle, J., & Cheever, K.H.(2009). Brunner and Suddarth’stextbook of medical surgical nurs-ing (12th ed.). Philadelphia, PA:

Lippincott Williams & Wilkins.

airway protection during swallow and provides acritical sound source, that is, the voice. The tongueis an organ that provides movement necessary formastication (i.e., chewing) and for sound productionand resonation. An organ usually has a predominanttissue type. In the case of the tongue, muscle tissueis predominant, with supporting connective tis-

sue (e.g., the hyoid bone for attachment), vasculartissue (blood supply), and nervous tissue (e.g., motorneurons to innervate tongue muscles). In the case ofthe larynx, connective tissue (by way of the cartilagesthat comprise it) is the predominant tissue type.

Systems

Two or more organs combine to form a functionalunit called a system. There are 9 to 12 systems in thehuman body, depending on the anatomist. The mostimportant body systems for speech production and

swallowing function are the following six: circulatory(or vascular); digestive; muscular; nervous; respi-ratory; and skeletal (see Table 3-4). The circulatorysystem includes the blood vessels, the blood itself,and the cardiac muscle that comprises the heart.The skeletal system includes the human body’s bonyframework inclusive of cartilage and the connecting

elements of joints, ligaments, and tendons. The mus-cular system includes the striated muscle of the body, which attaches to the skeletal framework. The respira-tory system includes organs and structures of both theupper and lower respiratory airways. Thus, the nasaland oral cavities, the pharynx (throat), the larynx (asa passageway), the trachea, the bronchi and all theirbranches, and the lungs themselves are included.The digestive system is included for its pertinence inswallowing function; it includes again the oral cavity,the pharynx, the larynx (as a protective mechanism),the esophagus, and the lower digestive tract (e.g.,stomach, intestines). Structures of the oral cavity

TABLE 3-4

BODY SYSTEMS THAT HAVE A FUNCTION IN SPEECH PRODUCTION

System Major Organs and Tissues Primary Function Professional Relevance

Circulatory Heart, blood vessels, blood Provide oxygen and nutrients to Blood supply to the brain and (vascular) the body other parts of the speech

mechanismDigestive Lips, teeth, tongue, velum, Take in and process nutrients, Mediate articulation and pharynx, esophagus, eliminate byproducts resonance of the vocal tone stomach, intestinesMuscular Skeletal muscle Enact movements on the skeletal Movement for speech framework and maintain posture productionNervous Brain, spinal cord, peripheral Control and regulate internal Innervation of muscles and nerves, ganglia, sensory environment and interaction mucosa associated with receptors (sensory and motor) with the speech external environmentRespiratory Nasal passages, pharynx, Exchange of O 2 and CO 2 Power source for speech larynx, trachea, bronchi production and branches, lungsSkeletal Cartilages, bones, ligaments, Provide structure and support, Framework for the speech tendons, joints and to mediate movement production mechanism




(e.g., teeth, tongue, soft palate) are also involved inarticulation and resonance, and the larynx is the pri-mary organ of phonation.

Speech Processes

The mechanism for speech production requires thecoordinated effort of multiple systems functioningtogether to produce speech. As mentioned previously,these speech processes are respiration, phonation,and articulati ο n/resonance. Each process is sup-ported by the various organ systems just discussed.Each of these processes will be presented in detail inthe coming chapters. Following is a brief descriptionof each.

RESPIRATION

The respiratory system is necessary to provide thepower behind our speech signal (see Figure 3-13A).The breath we take in is converted to energy toproduce both the voiced and unvoiced sounds forspeech. Furthermore, control over our breath streaminuences pitch, loudness, and timing of our speech.Necessary to understanding the respiratory system isthe bony and cartilaginous framework of the ribcageincluding the ribs, the sternum, and the vertebral col-umn. Upon this framework are the muscles criticalfor expanding or contracting the size of the lungs for

inspiration and expiration, respectively. The anatomy

and physiology of the respiratory system is presentedin detail in Chapter 6.

PHONATION

The phonatory system provides the sound sourcefor voicing (see Figure 3-13B). All speech processes

interact but the interaction here between the respi-ratory and phonatory system is especially evident. Itis the power generated by the breath rising from therespiratory system along with the movement and theproperties of the muscles and connective tissues ofthe vocal folds that is responsible for producing voice.Necessary to understanding the function of the pho-natory system is the largely cartilaginous frameworkof the larynx along with the hyoid bone and the mus-cles and connecting structures that allow the larynx tofunction as a unit. The anatomy and physiology of thephonatory system is presented in detail in Chapter 8.

ARTICULATION /RESONANCE

The articulatory /resonance system modies thesound produced at the larynx into the sounds thatare heard and perceived as speech (see Figure 3-13C).This is done by changing the conguration of thevocal tract. The vocal tract includes the nasal and oralcavities and the pharynx. For example, resonance issignicantly affected when the back and upper part ofthe pharynx is opened to the nasal cavity. In this case,

the sounds produced have a nasal resonance to them;

A B C

Figure 3-13 Illustration of the three speech systems. A . Respiratory speech system. B . Phonatory speech system. C . Articulatory/resonance speech system. (Reprinted with permission from Cohen, B.J. (2008). Memmler’s the human body in health and disease (11th ed.).Baltimore: Lippincott Williams & Wilkins.)




such is the case for the sounds /m / , /n / , and / / . Neces-sary to understanding the function of the resonatorysystem is learning the bony framework of the cranialand facial bones (i.e., the skull) and the bony pro-cesses that project and serve as attachment points formuscle. In regard to resonance, many muscle groupsare involved including muscles of the pharynx, mus-

cles of the velum or soft palate, muscles of the tongue,and muscles of the mouth and cheeks.The articulatory system acts as both a sound

source and a resonator of sound. Articulation refersto movement; in this case, movement and placementof the articulators. The articulators include the lipsand tongue and their interaction with the hard palate,teeth, and velum. It is the process of articulation thatthe layperson commonly thinks of as speech. Whilecritical, articulation alone cannot produce speech.Consider an individual without a larynx as in the caseof someone who had laryngeal cancer (i.e., a larynge-ctomee). Without the power of the respiratory system(the individual with the laryngectomee must breathedirectly in and out of the trachea through an open-ing in the neck) and the voice source from the pho-natory system, effective speech cannot be produced. Again, knowledge of the bony framework of the skullis necessary to understanding the functioning of thissystem. In addition, many of the same muscle groupsinvolved in resonance are involved in articulation.These include muscles of the mouth and the tongue.Because of this overlap of anatomical structures the

processes of articulation and resonance are oftenconsidered together as is the case in this textbook.

The anatomy and physiology of the articulatory sys-tem is presented in detail in Chapter 10 along with theresonatory system.

Summary

In order for you to understand the systems involved with speech and swallowing these systems arereduced to the basic components of cells and tissues.Cells of a particular type come together to comprisetissues of the same name: epithelial, connective,muscle, and nervous. Each of these tissue types hassubclassications based on location and /or function.These tissues then come together to form an organ;an organ has a predominant tissue type with othertissues for support and life functioning. Finally, theorgans come together in functional groupings to formsystems. There are a number of these systems; thosemost pertinent to speech and swallowing are circu-latory (or vascular); digestive; muscular; nervous;respiratory; and skeletal systems. These systemsare called upon to support the processes of speech.Speech processes are also referred to as speech sys-tems. The process of respiration relies on the respira-tory system, the process of phonation relies on thephonatory system, the process of resonance relies onthe resonatory system, and the process of articula-tion relies on the articulatory system. These systemsare the focus of the three units of this textbook that

immediately follow the next unit on the nervoussystem.



PART 1 SUMMARYIn Chapter 2, you were presented the basic nomenclature associated with the studyof human anatomy, physiology, and pathology. First, a denition was provided for theanatomical position, the general point of reference for all terminology associated withspatial orientation and positioning. Second, you were exposed to the planes of refer-ence and more specic terminology associated with spatial relationships among thevarious body parts. Finally, as preparation for the remaining chapters of this textbook, you were provided with information pertaining to how you can understand unfamiliarterminology by analyzing specic terms into their roots and afxes.

In Chapter 3, you were provided basic information about the organization of thehuman organism. To understand the systems involved with speech and swallowing,these systems are reduced to the basic components of cells and tissues. Cells of aparticular type come together to comprise tissues of the same name: epithelial, con-nective, muscle, and nervous. Each of these tissue types has subclassications basedon location and/or function. These tissues then come together to form an organ; anorgan has a predominant tissue type with other tissues for support and life function-ing. Finally, the organs come together in functional groupings to form systems. There

are a number of these systems. Those most pertinent to speech and swallowing arecirculatory (or vascular); digestive; muscular; nervous; respiratory; and skeletal. Thesesystems are called upon to support the processes of speech. Speech processes are alsoreferred to as speech systems. The process of respiration relies on the respiratory sys-tem, the process of phonation relies on the phonatory system, the process of reso-nance relies on the resonatory system, and the process of articulation relies on thearticulatory system.

PART 1 REVIEW QUESTIONS 1. Refer back to Table 1-1 in Chapter 1. Describe specically how the body systems

on the right side of the table contribute to the systems of speech perception andproduction (i.e., auditory, articulation/resonance, phonation, and respiration) onthe left side of the table. In other words, name a few specic structures from eachof the body systems that can be found in each of the systems of speech percep-tion and production, other than the ones provided in the table as examples.

2. Without returning to Chapter 2, assume the anatomical position and describe itas accurately as possible.

3. Without returning to Chapter 2, name and describe as accurately as possible thethree planes of reference.

4. Use your knowledge of terminology to decipher the general meaning of each ofthe following terms.• Hypothalamus

• Epidural space • Pneumotachygraph • Laryngoplasty • Tympanosclerosis • Subclavius • Suprasternal notch • Cricotracheal ligament

32




• Chondro-osseous junction • Subglottic pressure

5. Describe the four tissue types discussed in Chapter 3 and give one specicexample of each.

6. Name the three types of muscle tissue. Of the three, which is involvedpredominantly in speech production? What does this indicate about theprocess of speech production?

7. Both muscle and nerves are organized by connective tissue coverings. List thenames for some of these coverings for both muscle and nerves using the prexesendo-, epi- and peri-. What do these prexes mean?

8. Indicate the speech system that is being described: • Speech sound production source for speech • Energy source for speech • Sound modier for speech • Voice source for speech • Source of speech reception and interpretation

9. With the limited information you’ve been provided up to this point, try to de-scribe one situation in which damage to any of the body systems (e.g., circulato-ry, digestive, muscular, nervous, respiratory, skeletal) may have a negative impacton speech perception or production.



PART 2Anatomy,Physiology, andPathology of the Nervous System



PART 2The Nerv ousSystem

Knowledge Outcomes for ASHA Certication for Chapter 4• Demonstrate knowledge of the neurological basis of the basic human communication

processes (III-B)• Demonstrate knowledge of the neurological basis of swallowing processes (III-B)

Learning Objectives• You will be able to outline nervous system organization.

• You will be able to explain the neurodevelopment of the central nervous system.• You will be able to list surface anatomy of the brain including gyri and sulci most pertinent to

speech, language, and hearing.• You will be able to describe the supporting systems of the central nervous system including

meninges, ventricles, cerebrospinal uid and blood supply.• You will be able to explain the basic microscopic nervous system anatomy and will demon-

strate preliminary understanding of neural function.

CHAPTER 4

Anatomy and Physiology of the Nervous System

AFFIX AND PART-WORD BOXTERM MEANING EXAMPLE

arachn- spider’s web arachn oid

brachium arm brachium of inferior colliculus

colliculus bump inferior colliculus

cortex outer “bark” or covering cerebral cortex

di- through di encephalon

dura hard, tough dura mater

-encephalon pertaining to the brain di encephalon

falx sickle-shaped falx cerebelli

fasciculus bundle dorsal fasciculus

glosso- tongue glosso pharyngeus

lemniscus ribbon lateral lemniscus

mes- middle mes encephalon

met- after met encephalon

myel- marrow myel encephalon

peduncle bridge cerebral peduncle

phagein to eat phag ocyte

37



38 PART 2 ANATOMY, PHYSIOLOGY, AND PATHOLOGY OF THE NERVOUS SYSTEM


pros- at pros encephalon

radiation fanning out auditory radiation s

rhomb- diamond shaped rhomb encephalon

sub- below sub cortical

tel- end tel encephalontrigone triangular ridge hypoglossal trigone

Clinical Teaser

Sisi, an elderly woman age 82, enjoyed a quiet evening withher spouse and retired to bed early. Sometime in the ear lyhours of the morning (around 2:00 AM), she awoke thinkingshe needed to use the bathroom. As she swung her legsover the edge of the bed she noticed her right leg seemedparticularly heavy. She attempted to assist her leg with herright arm but realized she could no longer move her rightarm. She laid back down and tried to go back to sleep inhopes that these symptoms would resolve. The symptomsdid not resolve and some time later, with some alarm, sheused her left arm to wake her husband. When she tried to

tell him what was happening, she found she could not speakalthough it seemed to her that her thoughts were quiteclear. Her husband immediately called 911 and the para-medics were on the scene as promptly as possible given

that they lived in a rural area of Washington. After initialassessment, Life Flight was called and Sisi was taken to anurban center for evaluation and treatment.

On admission to the emergency room, around 7:00AM, the physician conducted a basic neurology exam andsent her off for a computed tomography (CT) scan. Noevidence of hemorrhage was found, so the physician ad-ministered tissue plasminogen activator to break up whatwas inferred to be a clot or plug in the arterial circulation of

the brain. The neurologist diagnosed this at this ear ly stageas a thromboembolic stroke minimally involving the frontalcortex of the left cerebral hemisphere. Sisi was admitted to

the hospital for observation with referral to the speech– language pathologist for evaluation the following day. The speech–language pathologist conducted a briefspeech–language examination at bedside across all languagemodalities and speech functions. A cranial nerve exam re-vealed a right facial droop (cranial nerve VII—the facial )and a slight slurring of any speech she did have (cranialnerve XII—the hypoglossal ) with no other signicant cra-nial nerve involvement regarding speech production. Ver-bal output was limited to automatic speech (e.g., counting,reciting the days of the week) and vocalizations. Writtenoutput was extremely limited although she did attempt

to write her name albeit illegibly. Sisi’s writing was fur therconfounded by the fact that she is right-handed and shehad right hemiparesis of the upper (and lower) extremities.Auditory comprehension and reading comprehension weredetermined to be language strengths.

Note any terms or concepts in the above case study that are unfamiliar to you. As you read the rst chapterof this part, pay particular attention to the anatomy andphysiology pertinent to this case. We will return to thiscase at the conclusion of this part.

Introduction

The nervous system of a human is both simple in itsorganization and amazing in its complexity. In a simplemodel of speech production, we can see that the ner-vous system directs all the activity that occurs; it doesthis by both receiving information from the external (the world around us) and internal (our body) environments.This applies equally to swallowing. Without the nervoussystem, nothing happens. Understanding nervous sys-tem organization along with key terminology will assist you in mastering the basics of the neuroanatomy andneurophysiology of the human nervous system.

The central nervous system (CNS) is made up of thebrain and spinal cord and all the structures and spaces

within. The brain itself has over 100 billion neurons andhas been likened to the consistency of jello but is prob-ably more like tofu in substance (Firlik, 2006). The brainconstitutes about 2% of an individual’s weight, yet it is a

demanding oxygen consumer as it requires 20% of thebody’s blood supply. In fact, it could be argued that thefunctions of the rest of the body’s organs are devotedto keeping the brain alive (Goodman, 2003). In turn,the brain makes our reality conscious and allows us torespond in thought, planning, and action.

TERMINOLOGY

The importance of understanding critical terms in neu-roanatomy and neurophysiology cannot be stressedenough, as these terms form the foundation to build



CHAPTER 4 ANATOMY AND PHYSIOLOGY OF THE NERVOUS SYSTEM 39

upon and provide the critical information necessaryto apply reasoning to determine the location and func-tion of structures and systems. The terms presented inTable 4-1 provide a foundation for understanding theinformation presented in this chapter. You are stronglyencouraged to attend to these terms, as they will ariserepeatedly in this chapter.

ANATOMICAL ORIENTATION

In Chapter 2, you were introduced to anatomicaldirectional terms and planes or views of anatomy. Afew of these terms take on a different meaning whenreferring to the CNS. During development of the CNS,the front end of the encephalon (brain) undergoeselaboration and takes a sharp turn, which alters spa-tial orientation and thus the anatomical terms used torefer to the CNS above the spinal cord. As illustratedin Figure 4-1, above the diencephalon (central regionof the brain), the term rostral means toward the nose,caudal toward the back of the head, ventral towardthe jaw, and dorsal toward the top of the skull. Thisis a little different as compared with the spinal cordextending down the vertebral canal where rostralmeans toward the head, caudal toward the tail (e.g.,tail bone), ventral toward the belly, and dorsal towardthe back.

Directional terms can be combined in different ways to very specically describe a location. It maybe helpful to review the denitions of these termsin Chapter 2. The directional terms that may be

combined include medial, lateral, supercial, deep,and, as just discussed, dorsal, ventral, rostral, andcaudal. For example, consider the thalamus , whichis a mass of gray matter located in the center of thebrain. This mass of gray matter is comprised of a num-ber of nuclei. Many of these nuclei are named for theirlocation relative to the thalamus itself. For example,the nucleus responsible for acting as a relay station

for body sensations of pain, temperature, and touch isthe ventrolateral nucleus found on the bottom (ven-tral) side (lateral) of the thalamus.

Anatomical planes of reference are also worthyof a brief review, as these different planes are used

Caudal/ posterior

Rostral/ anterior

V e n t r a l

entra

l

D o r s a l

orsa

l

Posterior

Caudal/ inferior

Anterior

Dorsal/ superior

V e n t r a l

D o r s a l

Rostralostr lRostral

Diencephalon

Ventral

Figure 4-1 Illustration of the use of directional terms in regardto the central nervous system.

TABLE 4-1

NEUROSCIENCE TERMS, DEFINITIONS, AND EXAMPLE(S)

Terms Denition Example

Neuron Basic cell of the nervous system Multipolar neuronGlial cell Support cell of the nervous system Oligodendroglia Afferent Coming toward the CNS or a given structure Sensory spinal nervesEfferent Going away from the CNS or a given structure Motor spinal nervesTract Bundle of axons in the CNS Corticospinal tractNerve Bundle of axons in the PNS Facial cranial nerveNuclei Cluster of neuronal cell bodies in the CNS Caudate nucleusGanglia Cluster of neuronal cell bodies in the PNS Dorsal root gangliaGyrus Mound of cortical surface nervous tissue Postcentral gyrusSulcus Groove or depression between gyri Central sulcusCortical Pertaining to the outer surface of the brain Cerebral cortex Subcortical Deep to the cortex Subcortical nuclei (e.g., putamen)Gray matter General term for any collection of neuronal cell bodies Cerebral cortex in the CNS Basal ganglia White matter General term for any axonal bundle in the CNS Internal capsule Corpus callosum




Gray matter White matter

White matter

Cerebral cortex

Insula

IC, posteriorlimb

Thalamus

Caudal

Rostral

Cerebral cortex

Brainstem Cerebellum

Longitudinalfissure

Corpuscallosum

Gray matter

IC, Genu

IC, anteriorlimbBasal

nuclei

Cerebellum

CC,splenium

CC, body

CC, Genu

Septumpellucidum

CC, rostrum

Hypothalamus

Infundibulum

Pituitary gland

Thalamus

Midbrain

Pons

Medulla

A B

C

D

Figure 4-2 Different anatomical views and sections of the brain. ( A ) Lateral view of the left cerebral hemisphere. ( B) Coronal sectionillustrating gray and white matter. ( C ) Horizontal section illustrating gray and white matter (IC, internal capsule). ( D ) Midsagittal viewof the right cerebral hemisphere (CC, corpus callosum). ( A . Reprinted with permission from Bear, M.F., Connors, B.W., Paradiso, M.A.(2007). Neuroscience: Exploring the brain (3rd ed.). Baltimore, MD: Lippincott Williams & Wilkins. B . Reprinted with permission from Bear,M.F., Connors, B.W., Paradiso, M.A. (2007). Neuroscience: Exploring the brain (3rd ed.). Baltimore, MD: Lippincott Williams & Wilkins.C . Reprinted with permission from Premkumar, K. (2004). The massage connection anatomy and physiology. Baltimore, MD: LippincottWilliams & Wilkins. D . Reprinted with permission from Bear, M.F., Connors, B.W., Paradiso, M.A. (2007). Neuroscience: Exploring the brain (3rd ed.). Baltimore, MD: Lippincott Williams & Wilkins.)




repeatedly in the study of neuroanatomy. A coronal(frontal) section is perpendicular to midline and splitsa structure into front and back. A horizontal sectionis literally taken “across the horizon” resulting in topand bottom sections of the structure. A sagittal sec-tion is parallel to midline and splits a structure intoleft and right parts. Sagittal sections can be right at

midline (i.e., midsagittal) or off midline (i.e., parasag-ittal). Figure 4-2 illustrates a lateral view and a coro-nal, a horizontal, and a midsagittal section of the brain with various structures labeled for future reference inthe chapter. Each time you view a gure illustratingan anatomical plane, take the time to determine thespecic plane being viewed as well as gain your direc-tional bearings (e.g., where is rostral?) prior to locat-ing specic structures in the gure.

Neurodevelopment

There are four general stages of nervous systemgrowth: induction, proliferation, migration , and dif-ferentiation . The nervous system develops from ecto-dermal tissue (i.e., the outermost layer of the threegerm layers). This ectoderm changes around the 18thday of gestation through a critical event known asinduction. Induction refers to the interaction of ecto-derm with the underlying mesoderm causing a com-mitment of tissue to become neural tissue; this newtissue is termed neuroectoderm . Following induction,

the nerve cells increase their rate of production andproliferate. Nuclear movement of these cells occursvia migration where the cells travel from where theyoriginated to the region of the nervous system wherethey will end up. Differentiation refers to cell special-ization and the formation of the parts of the neuronand early synaptic patterns.

Once induction occurs, the development of thenervous system is rapid. At 21 days, a neural plate develops and, as this plate thickens via cell prolifera-tion, it folds upon itself and a neural tube is createdby 25 days growing rostrally and caudally like a zippergoing in both directions (see Figure 4-3). This neu-ral tube develops into all the neurons and glial cells

in the CNS. Pinched off from this neural tube is theneuroectoderm, now called the neural crest , that willdevelop into the neurons and glial cells comprisingthe peripheral nervous system (PNS).

Through this rapid period of growth, the CNS furtherdifferentiates into vesicles with spaces (i.e., lumen) sur-rounded by walls (nervous tissue). As illustrated in Figure4-3, by 28 days, three vesicles are formed: prosencepha-lon, mesencephalon , and rhombencephalon . Thesevesicles further differentiate 1 week later with the pros-encephalon dividing into the telencephalon and thediencephalon and the rhombencephalon further divid-ing into the metencephalon and the myelencephalon .The mesencephalon remains and the lumen becomesthe ventricular spaces discussed later in this chapter.

The spinal cord is also undergoing development,dividing into two plates (see Figure 4-4). The alarplate is found dorsally and develops into nervous tis-sue serving sensory purposes, whereas the basal plate is found ventrally and develops into nervous tissue formotor functions. A dividing point between these twoplates is the sulcus limitans ; lateral to the sulcus limi-tans is the area devoted to development of nervous

tissue supporting autonomic functions.

ORGANIZATION

The nervous system is divided into two parts, theCNS and the PNS as schematized in Figure 4-5. Thesetwo parts are separated by the meninges, which are

RostralProsencephalon

Mesencephalon

Rhombencephalon

Caudal

Telencephalon

Diencephalon

Optic discs

Mesencephalon

Rhombencephalon

A BFigure 4-3 Neurodevelopment of the central nervous system. ( A ) The three primary vesicles of theneural tube. ( B) The ve secondary vesicles of the neural tube that further develop into the structuresof the brain. The optic discs of the diencephalon develop into the retina of the eyes. (Reprinted withpermission from Bear, M.F., Connors, B.W., Paradiso, M.A. (2006). Neuroscience exploring the brain (3rd ed.).Baltimore, MD: Lippincott Williams & Wilkins.)




connective tissue coverings of the CNS. The PNS isconnected to the CNS via nerves: cranial nerves atthe brainstem and spinal nerves at the spinal cord.

These nerves take information to and from the CNS inregard to our head and neck (i.e., cranial nerves) andour body (i.e., spinal nerves).

The developed human brain has ve divisions: thetelencephalon, diencephalon, mesencephalon, met-encephalon, and myelencephalon. The organizational

owchart (see Figure 4-5) under each encephalon areashows the general brain structures for that region. Forexample, the telencephalon includes the left and right

cerebral hemispheres and all cortical and subcorticalstructures, that is, both gray and white matter. Thediencephalon is the thalamic region and the mesen-cephalon is composed of those structures making upthe midbrain. The metencephalon includes part of thebrainstem (i.e., pons) and the cerebellum, whereas

Whitematter

Centralcanal

Dorsal horn

Ventral horn

Graymatter

Alarplate

Sulcuslimitans

Basalplate

Dorsal

VentralFigure 4-4 Neurodevelopment of the spinal cord. The alar plate and the basal plate become sensoryand motor regions of the mature spinal cord. (Reprinted with permission from Bear, M.F., Connors,B.W., Paradiso, M.A. (2006). Neuroscience exploring the brain (3rd ed.). Baltimore, MD: LippincottWilliams & Wilkins.)

TelencephalonCerebral hemispheresLateral ventricles

DiencephalonThalamusThird ventricle

MesencephalonMidbrainCerebral aqueduct

MetencephalonPonsCerebellumFourth ventricle

MyelencephalonMedullaFourth ventricle

MeningesDura materArachnoidPia mater

CentralNervous System

PeripheralNervous System

Somaticnervous system

Visceral (autonomic)nervous system

Sympatheticnervous system

Parasympatheticnervous system

Figure 4-5 The organization of the nervous system. The meninges divide the central nervous system from theperipheral nervous system.




the myelencephalon is the most caudal portion of thebrain—the medulla oblongata. The medulla is con-tinuous with the spinal cord.

The spinal cord is necessary for the control of ourbody’s sensations and movements. The spinal cordis connected to the brain at the brainstem in theregion of the foramen magnum . The spinal cord is

organized into two axes: longitudinal and transverse(or segmental) axes. The longitudinal axis runs upand down the spinal cord carrying information viatracts. The segmental axis runs perpendicular to thelongitudinal axis at each segment of the spinal cordand receives or sends out information via the spinalnerves. The spinal cord is further organized by seg-ments that correspond to the sections of the verte-bral column: cervical, thoracic, lumbar, sacral, andcoccygeal.

The PNS is also further subdivided. The two com-ponents of the PNS are the visceral nervous system and the somatic nervous system . The visceral ner-vous system is considered involuntary and carriesinformation to organs, glands, and blood vesselsto regulate arousal and body functions; this is ourautonomic nervous system (ANS) , which is furthersubdivided into the sympathetic division and theparasympathetic division (see Figure 4-5). The ANScarries afferent information regarding visceral func-tion (e.g., oxygen content of blood) and sends efferent commands (e.g., secretion from glands). The sympa-thetic division expends energy during body responses

in stressful situations such as in ght or ight scenar-ios. The projections from this system arise from thethoracic and lumbar spinal cord. On the other hand,the parasympathetic nervous system conserves bodyenergy and works to maintain the internal balance ofour body systems (i.e., homeostasis ). Many projec-tions from the parasympathetic division arise fromthe brainstem as well as from the sacral region of thespinal cord. Thus, a number of the cranial nerves haveparasympathetic components; this will be returned tolater in the chapter. The neurons of the ANS, regard-less of division, are made up of a two-neuron chain.

The rst neuron has its cell body in the CNS (eitherspinal cord or brainstem) and is called the pregan-glionic neuron. The preganglionic neuron synapsesat the ganglia found in the PNS. The ganglia for thesympathetic division are quite near the spinal cord, whereas the parasympathetic division’s ganglia arelocated near the organ to be innervated.

The somatic nervous system has both motor andsensory functions carrying information to and fromskeletal muscle via the cranial nerves and the spinalnerves. The motor or efferent bers innervate the

skeletal muscles of the body; these include thoseresponsible for speech and hearing function. Thesensory or afferent bers transmit head, neck, andbody sensations for touch, pain, temperature, andbody position.

Why You Need to Know These sensory and motor systems work togetherto perform functions such as speech production. Although we may look at speech production asprimarily a result of motor movement (e.g., movingour tongue to shape sounds, moving our vocal foldsto produce voice), our brains must receive sensoryinformation to plan and produce speech. Exactlyhow body sensation contributes to speech produc-tion is not well understood. Minimally, it appearsthat sensory feedback regarding where articulatorystructures are (i.e., proprioception) is necessary for

optimal speech production. As an example, considerthe effects Novocain can have on your ability toclearly articulate following a dentist appointment.

Gross Anatomy

Gross anatomy refers to what can be identied withthe naked eye. In the case of the CNS, this gross anat-omy will include the surface features of the brainand spinal cord as well as the internal anatomy of

the same. The following section of the chapter pres-ents the gross anatomy most relevant to speech, lan-guage, and hearing function for the ve divisions ofthe CNS.

TELENCEPHALON

The telencephalon is made up of two symmetricalcerebral hemispheres, a right and a left. In each hemi-sphere are four lobes that correspond to the bonesof the skull. These are the frontal , parietal, temporal ,and occipital ; sometimes a fth lobe is named—the

limbic lobe (see Figure 4-6). Each lobe has surface fea-tures and outer “bark” (i.e., the cortex) and structuresdeep to the cortex including both gray and white mat-ter. The lobes are separated from one another on thesurface by grooves or sulci .

Most obvious upon inspection of the brain arethe grooves and mounds of the cortex. The corticalmounds are called gyri and the cortical grooves arereferred to as sulci (sulcus if singular) or, if they arelarge, ssures. Each of these gyri and sulci has a par-ticular name and is associated with one of the lobes




(see Table 4-2). For our purposes, those areas of thecortex most signicant to speech, language, andhearing are illustrated in Figures 4-6A and 4-6B andare presented here. The largest of these grooves isthe longitudinal ssure (refer back to Figure 4-2B), which divides the cerebrum into right and left halves:the right cerebral hemisphere and the left cerebralhemisphere. Furthermore, the longitudinal ssure isdeep extending all the way down to the corpus cal-losum (a major tract). Another prominent groove is

the central sulcus ; it divides the frontal lobe fromthe parietal lobe in each hemisphere. The precentralsulcus is found immediately anterior to the gyrus ofthe same name in the frontal lobe, whereas the post-central sulcus is found immediately posterior to thegyrus of the same name in the parietal lobe. The lat-eral sulcus (also known as the Sylvian ssure) is alsodeep, separating the frontal and parietal lobes fromthe temporal lobe. The temporal lobe is demarked with anatomically labeled sulci, the superior temporal

Post central gyrus

Parietal lobe

Heschl’s gyrus

Post central sulcus

Supramarginal gyrus

Occipital lobe

Parietal-occipitalsulcus

Angular gyrus

Occipital gyri

Cerebellum

Superior temporal gyrusSuperior temporal sulcus

Temporal lobe

Lateral fissure

Orbital gyrus

Inferior frontal gyrus

Middle frontal gyrus

Superior frontal gyrus

Frontal lobe

Central sulcus

Precentral sulcusPrecentral gyrus

Uncus/amygdala

Cingulate sulcus Cingulate gyrus

Callosal sulcus

Hippocampus

Parahippocampal gyrus

Lingual gyrus

Calcarine sulcus

Cuneus gyrus

A

B

Middle temporalsulcus

Figure 4-6 Two views of the cerebral cortex. ( A ) Lateral view of the left cerebral hemisphere illustrating the lobes ofthe brain and prominent sulci and gyri. ( B) Midsagittal view of the right cerebral hemisphere with the brainstem and cer-ebellum removed to reveal the limbic lobe and prominent sulci and gyri. (Reprinted with permission from Bear, M.F., Con-nors, B.W., Paradiso, M.A. (2006). Neuroscience exploring the brain (3rd ed.). Baltimore, MD: Lippincott Williams & Wilkins.)




sulcus is found toward the top and the middle tem-poral sulcus is found in the middle of the temporal

lobe. The most prominent sulcus of the occipital lobeis the calcarine sulcus , which is located centrally onthe medial aspect of the lobe (see Figure 4-6B). Theparietal lobe is separated from the occipital lobe bythe aptly named parietal–occipital sulcus. The lim-bic lobe also has prominent sulci. These are seenon a midsagittal view (see Figure 4-6B) and includethe callosal sulcus running the length of the corpuscallosum along its superior border and the cingu-late sulcus found superior to the gyrus of the samename.

Similar to sulci, particular gyri are found in the

lobes of the cerebral hemispheres; these also havenames (see Table 4-2). Processing of neural informa-tion occurs at the gyri for various functions, which will be elucidated later in the chapter. For now, theprimary focus is on the location of these various gyrias seen in Figure 4-6A. The precentral gyrus is themound of gray matter anterior to the central sulcusextending from the longitudinal ssure superiorly tothe lateral ssure inferiorly. The inferior frontal gyrus is located anterior to the inferior end of the precentralgyrus and the middle frontal gyrus is located anterior

to the precentral gyrus. These three gyri, found in thefrontal lobe, are involved with motor function. More

anterior areas of the frontal lobe are involved withcognitive processes (e.g., attention, memory, and rea-soning) and our personality. These areas include theorbital gyrus found immediately superior to our eyeorbits inside the cranium and the superior frontalgyrus located above the orbital gyrus; these two areastogether make up the bulk of the prefrontal cortexthat we will return to later.

The parietal lobe is responsible for the consciousreception and integration of various sensations.Immediately behind the central sulcus is the postcen-tral gyrus. Like the precentral gyrus, it extends from

the longitudinal ssure down to the lateral ssure.Two complex areas associated with the parietal lobecritical to language function are the supramarginalgyrus and the angular gyrus. The supramarginal gyrusis found superior to the posterior end of the lateral s-sure (see Figure 4-6A) with the angular gyrus inferiorto it.

The temporal lobe is critical for auditory func-tion and language comprehension. Heschl’s gyrusis found at the very superior aspect of the superiortemporal gyrus; this is the primary auditory cortex

TABLE 4-2

GYRI (WITH BRODMANN NUMBERS AND GENERAL FUNCTION) AND SULCI PERTINENT TO SPEECH,LANGUAGE, AND HEARING SPECIFIC TO EACH LOBE

Lobe Gyri Function Sulci

Frontal lobe Inferior frontal gyrus (44, 45) Expressive language Longitudinal ssure Precentral gyrus (4) Volitional movement Central sulcus Middle frontal gyrus (46) Motor planning Precentral sulcus

Orbital gyrus (11) Cognition Lateral ssure Superior frontal gyrus (10) CognitionParietal lobe Postcentral gyrus (3, 1, 2) Conscious sensation Longitudinal ssure Supramarginal gyrus (40) Language a Central sulcus Angular gyrus (39) Language a Postcentral sulcus Lateral ssureTemporal lobe Heschl’s gyrus (41) Audition Lateral ssure Superior gyrus (22) Receptive language Superior temporal sulcus Middle temporal sulcusOccipital lobe Cuneus gyrus (17, 18) Vision Longitudinal ssure Lingual gyrus (17) Vision Calcarine sulcus Occipital gyri (17, 18, 19) Visual recognition Parietal–occipital and association sulcus

Limbic lobe Cingulate gyrus (24, 23) Emotion Callosal sulcus Parahippocampal gyrus (28) Memory Cingulate sulcus Uncus (34) Emotion, fear, and

aggression

a Part of the multimodal association cortex integrating auditory, visual, and somatosensory inputs for language activities such as word retrieval, reading, and writing.




where signals from the cochleae in the inner ears endup. The remainder of the superior temporal gyrus isknown as Wernicke’s area, an area specic to languagecomprehension.

A midsagittal view of the occipital lobe revealsthe cuneus gyri and the lingual gyri surrounding thecalcarine ssure (see Figure 4-6B). The occipital gyri

make up the remainder of the lobe given the lateralview (see Figure 4-6A).

Finally, the limbic lobe has three gyri associated withit: the cingulate, the parahippocampal, and the uncus .The cingulate gyrus is large, surrounding the corpuscallosum at its anterior, superior, and posterior aspects.The parahippocampal gyrus is nearly continuous withthe cingulate gyrus at its posterior inferior site (seeFigure 4-6B). The parahippocampal gyrus continues

inferiorly and anteriorly on the medial aspect of thetemporal lobe. At its most anterior end, this gyrus foldsback on itself at a point called the uncus. Two impor-tant nuclei of the limbic system are deep to these gyri;the hippocampus is deep to the parahippocampalgyrus and the amygdala is deep to the uncus.

A part of the cerebral cortex hidden from externalview is the insular cortex. The insula can be viewed when portions of the frontal and temporal lobeare pulled away from each other as can be seen inFigure 4-7. Those cortical areas that overlie the insu-lar cortex are referred to as opercular regions associ-ated with the various lobes. Hence, there is a frontaloperculum , a temporal operculum, and a parietaloperculum.

At this point, we move from a presentation of theexternal anatomy of the telencephalon to the inter-nal anatomy which includes both nuclei and tracts.The most prominent subcortical nuclei are clusters ofgray matter collectively referred to as the basal gan-glia . Here is one of those instances when the use of“ganglia” is technically in error as we are referring toa collection of neuronal cell bodies deep to the tel-

encephalon (part of the CNS); thus, the appropriateterminology is nuclei. Indeed, it is more appropriateto refer to the basal ganglia as basal nuclei but old

Why You Need to Know The cerebral hemispheres are largely mirror imagesof one another with the same sulci and gyri; how-ever, functions differ across the hemispheres espe-cially in regard to the way the hemispheres processinformation. A good example of this is our auditoryprocessing. Auditory processing occurs in both theleft and right cerebral hemisphere temporal lobes(superior and middle temporal gyri) communi-cating with one another via the corpus callosum.In general, the left cerebral hemisphere processesspeech and language, whereas the right cerebralhemisphere processes speech prosody (e.g., melody,rate, and stress), environmental sounds, and certainmusical elements. For instance, Gazzaniga, Ivry,and Mangun (1998) found that when listening toa lyrical song, the perception of the words is a lefthemisphere function while perception of the song’smelody is a right hemisphere function. Of course,it is important to note that the hemispheres com-

municate with one another and share functions tosome extent.

Parietaloperculum

Temporal operculum

Frontal operculum

Insula

Figure 4-7 Lateral view of the rightcerebral hemisphere with the lateralssure opened to reveal the insularcortex. (Reprinted with permission fromBear, M.F., Connors, B.W., Paradiso, M.A.(2007). Neuroscience: Exploring the brain (3rd ed.). Baltimore, MD: LippincottWilliams & Wilkins.)




terminology dies hard. Nonetheless, the individualnuclei making up the telencephalic basal gangliaare the putamen , the globus pallidus , and the cau-date nucleus ; these are paired nuclei found in eachcerebral hemisphere. The putamen and the caudatenucleus together are collectively called the striatum .

Figure 4-8 shows these nuclei via a lateral transparentdrawing of the cerebral hemisphere. In neuroimagingstudies (e.g., CT scans or magnetic resonance imag-ing [MRI]) or gross dissections, the basal ganglia arebest viewed with coronal or horizontal slices becausethey are deep to the cerebral cortex (see Figures 4-2Band 4-2C). Two other prominent nuclei lie deep tothe temporal lobes and are part of the limbic system;these are the hippocampus and the amygdala; again,one in each hemisphere. The hippocampus is an out-growth of the medial wall of the temporal lobe, fold-ing back on itself and roughly resembling a seahorse

in shape; it is deep to the parahippocampal gyrus.The almond-shaped amygdala is found rostral to thehippocampus and deep to the uncus in the anteriormedial portion of the temporal lobe. These structuresof the basal ganglia and limbic system communicate with one another and/or other areas of the brain by way of tracts or bers.

Collectively, the white matter ber systems in thecerebral hemispheres are called medullary centers .The three medullary centers are commissural bertracts, projection ber tracts , and association ber

tracts . You will recall that tracts are bundles of axonsfound in the CNS; furthermore, these tracts connectnuclei with each other and provide a means of infor-mation transfer throughout the CNS. Commissuralber tracts connect the hemispheres of the brain andcan be roughly visualized as horizontal connections;there are three of these. The largest is the corpus cal-

losum, which is large enough to require labeling ofdistinct regions. From rostral to caudal, these are therostrum, genu, body, and splenium (refer back to Fig-ure 4-2D). Much smaller commissural tracts includethe anterior commissure found ventral to the rostrumof the corpus callosum and the hippocampal com-missure connecting the left hemisphere hippocam-pus with the right hemisphere hippocampus in thetemporal lobes.

Projection ber tracts establish connections betweenhigher and lower parts of the CNS and can be roughlyvisualized as vertical connections. The telencephalicprojection tract is the internal capsule . The internalcapsule carries motor and sensory information to andfrom the cerebral cortex as well as information travel-ing between the nuclei of the basal ganglia and thethalamus. It is an incredibly busy expressway of mul-tidirectional information ow with particular infor-mation traveling in specic lanes. As expected, thereare different areas of the internal capsule—the ante-rior limb, the genu, and the posterior limb (refer backto Figure 4-2C). Similar to the basal ganglia, areas ofthe internal capsule are usually viewed via coronal or

horizontal planes. Association ber tracts connect different corticalareas within the same hemisphere. These tracts canbe very short or very long. Notable examples of longassociation tracts are the arcuate fasciculus connect-ing the frontal lobe speech and language centers withthe temporal lobe language centers and the uncinatefasciculus connecting the orbital gyri of the frontallobe with the anterior region of the temporal lobe.

DIENCEPHALON

The diencephalon is found deep in the center of thebrain extending down to the ventral medial surface.The thalamus and all other anatomical regions with“thalamus” in their name are part of the diencepha-lon. This includes the epithalamus , subthalamus ,and hypothalamus . In addition, the mammillarybodies, part of the limbic system, are included here.The thalamus is often viewed on a midsagittal brainsection as can be seen in Figure 4-2D. Only one-half ofthe thalamus is seen in this view, as the thalamus hasa right and left half that correspond to the cerebral

Cleft forinternal capsule

Caudate nucleus,head

Putamen

Optic tractAmygdala

Thalamus

Caudatenucleus, tail

Figure 4-8 Transparent view of the left cerebral hemisphere toillustrate the location of the subcortical basal nuclei. (Reprintedwith permission from Bhatnagar, S.C. (2008). Neuroscience for thestudy of communicative disorders (3rd ed.). Baltimore, MD: Lippin-cott Williams & Wilkins.)




hemispheres. The halves are connected by the inter-thalamic adhesion (or massa intermedia). The thal-amus itself is made up of multiple nuclei comingtogether to form a gray mass that resembles a smallegg sitting in the center of the brain. Some of the moresignicant of these nuclei for speech, language, andhearing include the anterior nucleus, the ventrolat-eral nucleus, the ventroposterior medial nucleus, thelateral geniculate nucleus (LGN) , and the medialgeniculate nucleus (MGN) . Figure 4-9 illustrates thesethalamic nuclei and their connections to other areasof the nervous system; we will return to these laterin the discussion of brain function. The hypothala-

mus can also be viewed in Figure 4-2D and is ante-rior and ventral to the thalamus. The hypothalamus iscomposed of multiple nuclei and directly inuencesendocrine function via its attachment to the pituitarygland by way of the infundibulum (i.e., pituitary stalk;refer back to Figure 4-2D). Finally, the mamillary bod-ies, of which there are two, are seen supercially onthe ventral surface of the brain; a tract runs betweenthese bodies to the anterior nuclei of the thalamus.

METENCEPHALON (CEREBELLARCOMPONENT)

The cerebellum comprises part of the metencephalonand is posteriorly oriented in the cranium just ventralto the occipital lobes. The cerebellum resembles cau-liower when viewed from a midsagittal section witha nely convoluted cortex and intricate weaving ofinternal white matter (refer back to Figure 4-2D). Thecerebellum is divided into right and left lateral hemi-spheres complete with lobes, cortex, ssures, subcor-tical nuclei, and tracts (i.e., gray and white matter).The hemispheres are separated at midline by the

vermis , the central area of the cerebellar cortex. Thecerebellar hemispheres are divided into three lobes:the posterior lobe, the anterior lobe, and the oc-culonodular lobe . The primary ssure separates theanterior from the posterior lobe (see Figure 4-10). Theocculonodular lobe comprises the inferior aspect ofthe cerebellum with the nodular portion at midline(i.e., vermis) and the occular portion on the sides.The occulonodular lobe receives afferent informa-tion from the vestibular system and is important inassisting in controlling eye movements and posturaladjustments secondary to head position and gravity.

A set of deep cerebellar nuclei receives input and

sends output via the white matter. As seen in Fig-ure 4-11, the fastigial nucleus is found most medi-ally and the dentate nucleus is found most laterally,one in each hemisphere of the cerebellum. Betweenthese nuclei lie the emboliform nucleus and globosenucleus, collectively referred to as the interposednuclei.

Tracts travel in and out of the cerebellum by wayof the cerebellar peduncles (see Figure 4-12A). Thereare three pairs of cerebellar peduncles—the supe-rior, the middle, and the inferior—which connect tothe brainstem. Importantly, the cerebellum receives

much more neural information that it sends out (by aratio of approximately 40:1). This large ratio of inputto output relates directly to the function of the cer-ebellum. The cerebellum is responsible for analyzingand synthesizing large amounts of sensory informa-tion (input) and then, based on that synthesis, send-ing out neural impulses to adjust movements by wayof motor control centers. The vast majority of neuralinformation comes into the cerebellum through theinferior and middle cerebellar peduncles with thesuperior cerebellar peduncle reserved primarily for

Anteriornucleus

efferent:cingulate

gyrus

afferent:mamillary

bodies

Medial geniculate nucleus

afferent:from inferior

colliculus

efferent:to primaryauditorycortex

Lateralgeniculate

nucleus

efferent:to primary

visual cortex

afferent:from optic

tract

efferent:somatosensorycortex for face,

gustatory center

afferent:trigeminal

tracts

Ventral posteriormedial nucleus

Figure 4-9 The nuclei of thethalamus. Those nuclei discussed inthe chapter are labeled here alongwith their afferent input and efferentoutput. (Reprinted with permissionfrom Bhatnagar, S.C. (2008). Neurosci-ence for the study of communicativedisorders (3rd ed.). Baltimore, MD:Lippincott Williams & Wilkins.)




Leftcerebellar

hemisphere

Anterior lobe

Primary fissure

Posterior lobe

Vermis Rightcerebellarhemisphere

Midbrain

PosteriorlobePrimaryfissure

Anteriorlobe

Flocculus

Vermis

Rostral view

Caudal view

B

A

Figure 4-10 External views of the cerebellum. ( A ) The cerebellum viewed from above (i.e., a rostral direction). ( B) The cerebellumviewed from below (i.e., a caudal direction). Major landmarks are labeled. (Reprinted with permission from Bhatnagar, S.C. (2008). Neuro-science for the study of communicative disorders (3rd ed.). Baltimore, MD: Lippincott Williams & Wilkins.)




transmitting neural information from the cerebel-lum.

BRAINSTEM (“M-ENCEPHALON”)

The mesencephalon, part of the metencephalon,and the myelencephalon together make up what isknown as the brainstem. Figure 4-12 shows a dorsaland ventral view of the external features of the brain-stem. The mesencephalon is the midbrain and is themost rostral of the brainstem components being in

very close proximity to the thalamus. The midbrainhas a number of surface features—the superior col-liculi and inferior colliculi , collectively referred toas the corpora quadrigemina , on the dorsal surfaceand the cerebral peduncles on the ventral surface.The colliculi are bumps or swellings that overlienuclei involved with hearing and vision, whereasthe peduncles are home to critical motor pathways.The cerebral aqueduct , part of the ventricular sys-tem, courses through the midbrain. The pons (partof the metencephalon) is found in the middle of thebrainstem and acts as a bridge to the cerebellum (the

other part of the metencephalon). Ventrally, the ponshas a midline pontine sulcus which cradles the basi-lar artery ; dorsally, the pons gives rise to the largestof the cerebellar peduncles, the middle cerebellarpeduncle. The rostral aspect of the fourth ventricle isassociated with the dorsal aspect of the pons. Finally,the myelencephalon or medulla oblongata makesup the most caudal aspect of the brainstem and iscontinuous with the spinal cord. The ventral aspect ofthe medulla hosts connection points for a number ofcranial nerves critical for speech, hearing, and swal-

lowing. Also on the ventral surface are areas called thepyramids and pyramidal decussation; these regionsoverlie tracts that carry motor information to cranialand spinal nerves for muscle movement—key forspeech production to be discussed later. The dorsalaspect of the medulla houses the caudal portion ofthe fourth ventricle.

Spinal Cord

The spinal cord is the most caudal part of the CNSextending 42 to 45 cm in length from the foramenmagnum down the vertebral canal terminatingaround the rst lumbar vertebra (see Figure 4-13). Asmentioned previously, the spinal cord is continuous with the medulla at its most rostral connection buttapers off at its most inferior end as the conus medul-laris . Caudal to this region, a mass of spinal nerves arefound which are collectively called the cauda equina (horse’s tail).

SEGMENTAL (i.e., HORIZONTAL) AXIS

The spinal cord is organized into ve segments paired with the corresponding vertebrae, listed here fromsuperior to inferior: cervical, thoracic, lumbar, sacral ,and coccygeal segments . Each segment, in turn, haspairs of spinal nerves numbered and named for thesegment they are associated with for a total of 31 pairsof spinal nerves. Specically, the cervical segment has8 pairs of spinal nerves (i.e., C1 to C8), the thoracicsegment has 12 pairs of spinal nerves (i.e., T1 to T12),the lumbar segment has 5 pairs of spinal nerves (i.e.,

Dentate nucleus

Interposed nucleus: Emboliform nucleus Globose nucleus

Fastigial nucleus

Figure 4-11 Transparent view of the cerebel-lum to illustrate the deep cerebellar nuclei.(Reprinted with permission from Campbell,W.W. (2005). DeJong’s the neurologic examination (6th ed.). Philadelphia, PA: Lippincott Williams &Wilkins.)




L1 to L5), the sacral segment also has 5 pairs of spinalnerves (i.e., S1 to S5), and nally the coccygeal seg-ment has just 1 pair of spinal nerves (i.e., CO1). Allspinal nerves are “mixed” nerves, that is, they carryboth sensory and motor information. The sensory

component enters the dorsal root of the spinal nerve with its neuronal cell bodies housed in the dorsalroot ganglion outside the spinal cord. Alternatively,the motor component of the spinal nerve emergesfrom the ventral root with its neuronal cell bodies in

Medulla

Pons

Midbrain

Pons

Superior colliculi

Inferior colliculi

Fourth ventricle

Vagal trigone

Hypoglossal trigone

Midbrain

Medulla

Facial colliculus

Superior cerebellar peduncle

Middle cerebellar peduncle

Inferior cerebellar peduncle

Pyramidal decussation

Pyramids

Basilar sulcus

Cerebral peduncle

Mamillary bodies

Infundibulum

A

B

Figure 4-12 External views of the brain-stem. ( A ) Dorsal view of the brainstem withmajor structures labeled. ( B) Ventral view ofthe brainstem with major structures labeled.Note the number of cranial nerve rootletson the ventral aspect of the brainstem.(Reprinted with permission from Bhatnagar,S.C. (2008). Neuroscience for the study of com-municative disorders (3rd ed.). Baltimore, MD:Lippincott Williams & Wilkins.)




the ventral horn of the gray matter of the spinal cord

as pictured in Figure 4-14 and discussed next. A transverse section of the spinal cord illustrates

the division of gray and white matter (see Figure 4-14).The posterior aspects of the gray matter are the dorsalhorns, whereas the anterior aspects of the gray matterare the ventral horns. Consistent with neurodevelop-ment of the spinal cord, the dorsal region is involved with sensory functions and the ventral region isinvolved with motor functions. The amount of graymatter in the ventral horns is related to the amount ofskeletal muscle innervated at that level. For instance,

at the cervical and lumbar segments, there is moregray matter to serve the innervation requirements forthe muscles of the arms and legs, respectively. Graymatter surrounding the central canal is involved with ANS functions. This holds true for the white matteras well. Referring to Figure 4-14, there are three whitematter areas that are named for their anatomical loca-

tion in the spinal cord and for the fact that tracts runup (i.e., ascending tracts) and down (i.e., descendingtracts) these “columns.” These columns make up thelongitudinal axis of the spinal cord and have specicnames. They are referred to as the dorsal fasciculus (i.e., bundle), lateral fasciculus , and ventral fascicu-lus . There is more white matter as you move up thespinal cord because more neural information is trav-eling there.

LONGITUDINAL AXIS

Numerous tracts run up and down the spinal cord,bringing sensory (i.e., afferent) information in andsending motor (i.e., efferent) information out. Sen-sory information is brought to the spinal cord orbrainstem for reex reactions, to the cerebellum forintegration and adjustments to our movement pat-terns, or, primarily, to higher cortical centers forconscious perception. Motor tracts transmit neuralcommands to skeletal muscle for movement. For themost part, these tracts are specic to body sensations(e.g., touch, pain, and temperature) and body move-

ments (e.g., gross and ne motor movement) not spe-cic to speech, language, and hearing. An exception isthe tracts and nerves involved with respiratory func-tion to be discussed in the physiology section of thischapter.

Supporting Systems

The CNS could not function without the support ofother systems to provide oxygen, nutrients, wasteremoval, and protection. Protective coverings are

provided by the meninges . Oxygen and glucose arebrought to the nervous tissue by the blood system.The ventricular system produces cerebrospinaluid (CSF) for cushioning and nutrient support both within and enveloping the CNS.

MENINGES

The meninges, shown in Figure 4-15, are connec-tive tissue coverings that surround the CNS; theseare the dura mater (“tough mother”), the arachnoid

Brainstem

Brain

Cervical segment,nerves C1-8

Thoracic segment,nerves T1–12

Lumbar segment,nerves L1–5

Sacral segment,nerves S1–5

Spinal cord

Conus medullaris

Cauda equina

Coccygeal segment,nerve CO1

Figure 4-13 Lateral view of the spinal cord showing the vesegments and their corresponding spinal nerves. (Reprinted withpermission from Cohen, B.J. (2010). Medical terminology (6th ed.).Philadelphia, PA: Lippincott Williams & Wilkins.)




mater (“web”) and the pia mater (“tender mother”).The two-layered dura mater, a dense, brous con-nective tissue (tough and inelastic), is the mostsupercial of these with its outer periosteal layeradhering to the inside of the cranium and its inner

meningeal layer immediately below. Between thesetwo layers of dura are sinuses or spaces for venousblood drainage and CSF reabsorption into the blood

stream. In addition, the inner meningeal layer ofthe dura mater has three dural extensions: (1) thefalx cerebri which extends into the longitudinal s-sure, (2) the falx cerebelli which partially separatesthe cerebellar hemispheres, and (3) the tentorium

cerebelli , a horizontally oriented extension separat-ing the occipital lobe of the cerebrum from the cer-ebellum (see Figure 4-16). The dura limits excessivemovement of the brain within the skull. The durasurrounding the spinal cord is single layered withonly the meningeal layer present (i.e., the periosteallayer remains within the cranium as the meningeallayer passes through the foramen magnum anddown the spinal cord).

The arachnoid layer is in direct contact with thedura but is much thinner and more elastic than thedura. The arachnoid is an avascular, continuous,

brous, and elastic connective tissue membrane run-ning over the sulci of the cerebrum. It can be likenedto taking a piece of Saran Wrap ® and stretching itover the cerebral cortex and spinal cord making sureit adheres to the gyri but not pressing down into thesulci or spaces. Cisterns exist where the arachnoidbridges over larger spaces. The arachnoid piercesthrough the dura at the dural sinuses; these are calledarachnoid granulations (or singularly arachnoid villi;see Figure 4-17). This is where CSF diffuses into thevenous blood. An important space lies immediately

Dorsal fasciculus

Posterior root

Dorsal root ganglion

Spinal nerve

Anterior root

Ventral fasciculus

Dorsal (posterior)

Ventral (anterior)

Centralcanal

Lateral fasciculus

Dorsal horn

Ventral horn

Ventral median fissure

Figure 4-14 Three-dimensional transverse section of the spinal cord showing gray and white matter and components of atypical spinal nerve. (Reprinted with permission from Premkumar, K. (2004). The massage connection anatomy and physiology. Balti-more, MD: Lippincott Williams & Wilkins.)

Dura mater

Arachnoid

Subarachnoidspace

Pia mater

Artery

BrainFigure 4-15 A cross section illustrating the three meningeal lay-ers surrounding the central nervous system—the dura mater, thearachnoid, and the pia mater. (Reprinted with permission from Bear,M.F., Connors, B.W., Paradiso, M.A. (2006). Neuroscience exploring thebrain (3rd ed.). Baltimore, MD: Lippincott Williams & Wilkins.)




below the arachnoid called the subarachnoid space .In this space, CSF ows and cerebral arteries travel(refer back to Figure 4-15).

The pia mater is the third meningeal layer, adher-

ing closely to the cortical tissue running down intosulci and ssures following the contour of the brain

and spinal cord. The pia is a very delicate and thin col-lagenous connective tissue membrane. The pia servesas a protective barrier and is involved in the produc-tion of CSF. A sleeve of pia encapsulates blood vessels

as they travel from the subarachnoid space to piercethe cerebral cortex.

Falx cerebri

Basilar artery

Vertebral ar teries

Tentorium cerebelli

Falx cerebelli

Straight sinus

Cerebral veins

Arachnoid granulations

Superior sagittal sinus

Internalcarotid artery

Figure 4-16 Dural extensions with associated dural sinuses in a medial view of the left half of the head. Arteriessupplying blood to the brain are also labeled. (Reprinted with permission from Moore, K.L., Agur, A.M., Dalley, A.F.(2009). Clinically oriented anatomy (6th ed.). Baltimore, MD: Lippincott Williams & Wilkins.)

Cranium

Arachnoid

Subarachnoidspace (filled with CSF)

Pia mater

Cerebral cortex

Superior sagittal sinus(filled with venous blood)

Arachnoidgranulations

Dura mater

Figure 4-17 Close-up view of the superior sagittal sinus (CSF, cerebrospinal uid). (Reprinted withpermission from Anatomical Chart Company.)




VENTRICULAR SYSTEM

The ventricles and associated canals and passage- ways are developmentally derived from the cav-ity or lumen of the neural tube. The ventricles arespaces that are lined with ependymal cells (a type ofepithelial tissue) and lled with CSF. There are four

ventricles: two lateral ventricles (one in each cere-bral hemisphere), one third ventricle, and one fourthventricle. As seen in Figure 4-18, the ventricles com-municate with each other through passages. The lat-eral ventricles are connected to the third ventricle bythe interventricular foramen and the third ventricleis connected to the fourth ventricle by the cerebralaqueduct.

Each ventricle has a unique conguration. The twolateral ventricles are symmetrical and are found deepin the telencephalon. Each of these ventricles hashorns that extend into the lobes—anterior horn in the

frontal lobe, posterior horn in the occipital lobe, andinferior horn in the temporal lobe. The parietal lobehouses the body of the lateral ventricles with the cor-pus callosum forming the roof of the body. A mem-branous partition, the septum pellucidum , formsthe medial wall of the lateral ventricles. The singlethird ventricle looks like a slit-like cleft between thetwo halves of the thalamus and may be interruptedby the interthalamic adhesion. The fourth ventricleis found between the cerebellum and the pons andmedulla and resembles a diamond shape. The caudal

end of the fourth ventricle is continuous with the cen-tral canal that runs the length of the spinal cord. Thefourth ventricle also has the openings from the ven-tricles to the subarachnoid space via three apertures.One median aperture (also referred to as the foramenof Magendie) and two lateral apertures (also referredto as the foramen of Luschka) allow for CSF to ow

into the subarachnoid space to surround and cushionthe brain and spinal cord.CSF is produced by choroid plexus found in the

walls of the ventricles. Production is continuous, with approximately 130 ml being produced each 3 to4 hours. The choroid plexus consists of an intertwinedmass of pia, capillaries, and ependymal cells and, ondissection, looks like soft and delicate strands of red-colored tissue. As schematized in Figure 4-19, the CSFthen ows through the ventricles, out the median andlateral apertures into the cisterna magna and pon-tine cisterns (part of the subarachnoid space) andows superiorly toward the superior sagittal sinus via arterial pulsations with an ebb and ow. Some CSFows inferiorly to the lumbar cistern around the spi-nal cord. A small amount of CSF ows into the centralcanal of the spinal cord from the fourth ventricle. Theabsorption of the majority of the CSF occurs throughthe arachnoid granulations into the venous bloodfound in the dural sinuses. A blockage in this systemof production to absorption can result in a condi-tion called hydrocephalus, which will be discussed inChapter 5.

Lateral ventricle(body)

Lateral ventricle

(posterior horn)

Third ventricle

Lateral ventricle(anterior horn)

Interventricular foramen

Lateral ventricle(inferior horn) Cerebral aqueduct

Lateral aperture

Fourth ventricle

Median aperture

Figure 4-18 Transparent lateral view of the left cerebral hemisphere showing the ventricular system. (Reprinted with permissionfrom Anatomical Chart Company.)




BLOOD SUPPLY

Nervous tissue is incapable of storing essential nutri-ents yet has the highest metabolic rate of any tissue in

the human body. Metabolism is aerobic which meansnervous tissue requires a constant supply of oxygenvia the blood stream. The brain itself comprises about2% of an individual’s body weight yet requires around20% of available oxygen. Without this constant supplyof oxygen by way of the blood stream, the brain ceasesto function and dies. In fact, if blood circulation is dis-rupted for only 10 seconds, a loss of consciousnessoccurs; extend that time to 3 to 4 minutes and braindamage occurs.

Recall that arteries bring oxygenated blood from theheart and veins return deoxygenated blood to the heart.This is a continuous system with oxygen exchanged inthe capillary beds. This occurs for the entire nervoussystem, but the focus of this section of the chapter ison the arterial blood supply to the brain as this is mostpertinent to speech, language, and hearing.

Origin of Blood to the Brain

The blood to the brain comes from two systems: (1)the internal carotid arteries and (2) the vertebral

basilar arteries. Both of these systems originate withblood from the aorta (see Figure 4-20). The subclavianarteries arise from the aorta and, in turn, give rise tothe vertebral arteries . The vertebral arteries ascendthrough the transverse foramen of the upper six cer-vical vertebrae and enter the base of the skull at theforamen magnum. Here, they join together to formthe basilar artery, which lies on the ventral aspect ofthe pons. The common carotid arteries also extendoff the aorta and bifurcate (i.e., split in two) into theexternal carotid artery and internal carotid artery .

Medialaperture

Lateralventricle

Lateralventricle

3rd

ventricle4 th

ventricleCentralcanal

Subarachnoidspace

Duralsinuses

Lateralaperture

Lateralaperture

Arachnoid villi

Cerebral aqueduct

Interventricularforamen

Figure 4-19 Flowchart of theow of cerebrospinal uid begin-ning at the lateral ventricles andending in the dural sinuses.

Why You Need to Know Nervous tissue is incapable of storing oxygen; forthat reason, the brain is fully reliant on the bloodsupply to bring a continuous supply of oxygen.When that oxygen supply is disrupted, an ischemicevent occurs. If the disruption of oxygen is of shortduration and any behavioral symptoms resolvequickly, this is termed a transient ischemic attack. A stroke, or cerebro-vascular accident (CVA) occurswhen a disruption of oxygen extends over a longerperiod of time due to a clot or plug (e.g., plaquebuild-up) in the arteries of the brain. This results innervous tissue dying and the resultant behavioralsymptoms associated with that tissue death such asbody weakness and slurred speech.

Right cerebralhemisphere

Basilarartery

Internalcarotidartery

Externalcarotidartery

Commoncarotid artery

Subclavianartery

Aortic arch

Vertebralartery

Cerebellum

Spinalcord

Figure 4-20 Origin of the blood supply to the brain.(Reprinted with permission from Anatomical Chart Company.)




The internal carotid arteries ascend the anterior lateralneck to the base of the skull where they enter the cra-nium through the carotid canal in the petrous portionof the temporal bone. These systems join at the largeanastomoses called the circle of Willis (i.e., arterialcircle) found on the ventral aspect of the brain super-cial to the midbrain. This is an uninterrupted circle ofblood vessels that the two internal carotid arteries andthe one basilar artery feed into. Three small communi-

cating arteries (one anterior communicating and twoposterior communicating) and proximal parts of twocerebral arteries complete the circle (see Figure 4-21).This arterial circle provides a safety mechanism for theblood supply to the brain as blockage below the circle(e.g., internal carotid arteriosclerosis ) can be compen-sated for by the other arteries that feed into the circle.

Cerebral Arteries

Three pairs of cerebral arteries arise from the circle of Willis to supply blood to the telencephalon. These arethe anterior cerebral arteries (ACAs), middle cerebral

arteries (MCAs), and posterior cerebral arteries (PCAs). Although all of these arteries are critical to brain func-tion, the MCAs are especially important as they supplyblood to cortical areas critical for speech, language,and hearing. The MCAs are the largest of these pairedcerebral arteries and originate at the termination ofthe internal carotid arteries as they come into the cir-

cle of Willis. The MCAs then turn laterally to coursethrough the lateral sulci. As they course through, theMCAs give off small arterial branches referred to asthe lenticulostriate arteries to supply blood to partsof the basal ganglia and parts of the internal capsule.The MCAs emerge from the lateral sulcus to fan outand supply the majority of the lateral surface of thecerebral hemispheres via a multitude of branches asseen in Figure 4-22. Most of these branches are logi-cally named according to the part of the cortex theysupply blood to such as the orbito-frontal branch orthe posterior temporal branch as seen in the gure. All the branches off the MCA supply critical areas forlanguage and cognition. The ACAs and PCAs also giverise to multiple branches. The cortical region that is atthe distal reaches of the arterial branches is referredto as the watershed area (see Figure 4-22). The over-lap of blood supply that occurs in the watershed areais called collateral circulation.

Cerebellum, Brainstem, and Spinal Cord Arteries

Arterial branches arise from the vertebral basilar sys-

tem to supply blood to the cerebellum, brainstem,and spinal cord (refer back to Figure 4-21). Directfrom the vertebral arteries arises a singular ante-rior spinal artery that runs along the ventral midlineof the spinal cord and two posterior spinal arteriesfound on the other side of the spinal cord. In addi-tion, the vertebral arteries give rise to the paired pos-terior inferior cerebellar arteries. Branches off thebasilar artery also supply blood to the cerebellum inaddition to the brainstem. The paired anterior infe-rior cerebellar arteries emerge from the most cau-dal aspect of the basilar artery, whereas the paired

superior cerebellar arteries emerge from the basilarartery just before it joins the circle of Willis. At the junction of the basilar artery with the circle of Willis,the PCAs, mentioned earlier, also arise; these supplyblood to the midbrain. The basilar artery also givesrise to a number of small pontine arteries to supplythis part of the brainstem. Although not associated with brainstem blood supply, the basilar artery givesrise to the labyrinthine arteries that pass laterallythrough the internal auditory canal to supply bloodto structures of the inner ear for hearing and balancefunction.

Anteriorcommunicating

Lenticulostriate

Anterior cerebral

Anterior cerebral

Ophthalmic

Internal carotid

Middlecerebral

Posteriorcerebral

Superiorcerebellar

Pontinearteries

Labyrinthine Basilar

Anterior inferiorcerebellar

Vertebral

Posterior inferiorcerebellar

Anterior spinal

Posteriorcommunicating

Figure 4-21 A ventral view of the circle of Willis ( arterial circle)and arteries arising from it, and the vertebral basilar system thatsupplies blood to the brain and spinal cord. (Reprinted with per-

mission from Agur, A.M., Dalley, A.F. (2008). Grant’s atlas of anatomy (12th ed.). Baltimore, MD: Lippincott Williams & Wilkins.)




Venous System

The deoxygenated blood needs a way out of the brainto return to the heart. This occurs through the drain-age of this venous blood toward the midline of thebrain through two sets of veins: (1) deep veins and (2)

supercial veins. The deep veins drain into the infe-rior sagittal sinus and then into the straight sinus.The supercial veins drain into the superior sagit-tal sinus. Blood from all of these sinuses convergeto travel inferiorly to the internal jugular veins (seeFigure 4-23).

Angular branches

Anterior and posteriorparietal branches

Central sulcus

Rolandic branches

Prerolandic branches

Orbitofrontal branches

Orbital branchesof anterior cerebral artery

MCA emerging fromlateral sulcus

Anterior temporalbranches

Middle temporalbranches

Posterior temporal

branches

Watershed region

Figure 4-22 Lateral view of the left cerebral hemisphere showing the branches of the middle cerebral artery (MCA)and the watershed area (the border zone between arterial distributions). (Reprinted with permission from Haines, D.E.(2004). Neuroanatomy: An atlas of structures, sections, and systems (6th ed.). Baltimore, MD: Lippincott Williams & Wilkins.)

Inferior sagittal sinus

Straight sinus

Occipitalsinus

Transversesinus

Greatcerebral vein

Basal vein

Septal veins

Superior sagittal sinus

Figure 4-23 Medial view of the right cerebral hemisphere with brainstem and cerebellum removed showing cerebralsinuses for the drainage of venous blood with select veins labeled. (Reprinted with permission from Haines, D.E. (2004).Neuroanatomy: An atlas of structures, sections, and systems (6th ed.). Baltimore, MD: Lippincott Williams & Wilkins.)




Microscopic Neuroanatomy

The singular cells that comprise the nervous systemcannot be seen with the naked eye; these are the neu-rons (i.e., nerve cell) and glial cells (i.e., neuroglia)introduced in Chapter 3. There are multiple types ofneurons and multiple types of glial cells. The anatom-ical structure of these different types of cells relate totheir function.

Neurons are composed of four parts: dendrites ,cell body (i.e., soma), axon , and terminal (see Fig-ure 4-24). The diameter of the cell body varies from4 microns to 100 microns (1 micron 1/1000 mm)and is lled with cytoplasm and organelles. Theorganelles found in the cell body were covered inChapter 3; these include the mitochondria, golgi com-

plex, lysosomes, Nissl substance, microtubules, andmicrolaments. Also in the cell body is the nucleusand, within that, the nucleolus—the genetic centerof the cell. Some of these organelles extend into theneuron’s axon and terminal. Extending out from thecell body are dendrites, often viewed as branches ofa tree with buds on these branches representing den-dritic spines. The dendrites offer expanded surfacearea for communication between neurons to occur.The singular axon ranges from microns to several feetin length. The connection point of the axon with thecell body is called the axon hillock . The distal end ofthe axon has multiple terminal branches and is oftenreferred to as the presynaptic ending. The branches ofthe terminal that resemble the arms of an octopus arecollectively called telodendria . In turn, the end pointsof each teledendrite are termed terminal boutons ; theterminal boutons house neurotransmitters that arethe chemical messengers of the nervous system. Theentire neuron is encased in a double-layered plasmamembrane with channels that allow certain ionsto pass; this is called selective permeability . Thesechannels, however, are only available for exchange of

ions at certain points called the nodes of Ranvier —intervening spaces between myelin segments on anaxon where the axon communicates with the extra-cellular space.

Glial cells are found in both the CNS and PNSand outnumber the neurons by a ratio of 5:1. Thosefound in the CNS are oligodendroglia, microglia , and

Why You Need to Know Imaging the blood ow of the cerebral hemispheresis an important tool for scientists and clinicians toprovide insight into normal and abnormal brain function. Techniques that either directly or indirectlymeasure blood ow include regional cerebral blood

ow (rCBF), positron emission tomography (PET),single photon emission computed tomography(SPECT), and functional magnetic resonance imag-ing (fMRI). The underlying assumption of these tech-niques is that active brain areas require more blood ow due to the increased metabolism of the nervoustissue at that site. These imaging techniques allow usto view which brain areas are responsible for particu-lar activities such as speech. Both PET and SPECT areconsidered techniques involving nuclear medicine asradioactive isotopes (through injection or inhalation)are used to trace brain function. PET measures blood

ow through the mapping of glucose and oxygenmetabolism at the level of the neuron. This metabo-lism denotes physiological functioning and has beenused to study language and cognitive functions inaddition to speech. SPECT is similar to PET but hasless specicity. For a detailed reading of brain imag-ing techniques, you are referred to Bhatnager (2008).

•••••

Myelin

Synapticcleft

Telodendria

Dendrite

Nucleus

Axon

Terminalbouton

Postsynapticneuron

Synapticvesicles

Nucleolus

Axon hillock

Cell body(soma)

Nodes ofRanvier

Figure 4-24 A neuron (nervecell) with its functional compo-nents labeled. (Reprinted withpermission from Bhatnagar, S.C.(2008). Neuroscience for the studyof communicative disorders (3rd ed.). Baltimore, MD: Lippin-cott Williams & Wilkins.)




astrocytes (see Figure 4-25). Oligodendroglia arefound in white matter as they form and maintainmyelin in the CNS. In fact, each individual oligoden-droglia cell is responsible for providing myelin fordozens of axons! Microglia are scattered throughoutthe CNS often near and around blood vessels and, asthe name implies, have a multitude of ne, small pro-

cesses. Microglia are most active following trauma tothe CNS where they will come in and “clean up” neu-ronal debris, a process referred to as phagocytosis ,and leaving what is referred to as a glial scar. The star-shaped astrocytes are also involved with phagocytosisafter trauma but have many other functions as well.Notably, astrocytes are intricately involved with theblood–brain barrier with their processes extendingto surround capillaries.

The only glial cell found in the PNS is the Schwanncell . Schwann cells form myelin that surrounds theaxons that make up our spinal nerves and our cranial

nerves. Each Schwann cell wraps around a segment ofan axon in a jelly roll fashion. Myelin serves as an insula-tor for faster conduction and separates the axon fromthe extracellular tissue uid except at the nodes ofRanvier. The nodes of Ranvier, then, are the gaps thatexist between adjacent Schwann cells in the PNS oroligodendroglia cells in the CNS in a myelinated axon.This turns out to be critical for neuronal impulse con-duction, which will be discussed later in the chapter.Finally, ependymal cells are also found in the CNS lin-ing the ventricles and central canal and contributing

to the choroid plexus. Clearly, glial cells support andassist the neurons in both the CNS and PNS in accom-plishing their functions.

Astrocyte cell

Bloodvessel

Neuron

Oligodendrogliacell

Microglia cell Ependymalcell

Figure 4-25 The different types of glial cells. (Reprinted withpermission from Bhatnagar, S.C. (2008). Neuroscience for the study

of communicative disorders (3rd ed.). Baltimore, MD: LippincottWilliams & Wilkins.)

Why You Need to Know Brain tumors (i.e., neoplasms) are often due to theabnormal growth of glial cells. The general name for these brain tumors is gliomas but, more speci-cally, include astrocytomas, ependymomas, andoligodendrogliomas. Of particular interest to currentand future audiologists is the inaccurately namedacoustic neuroma (another term for neoplasm),which results from the pathological overproductionof Schwann cells surrounding the vestibulocochlear(VIII) nerve. The more accurate name for this tumoris a vestibular schwannoma as the tumor most oftensurrounds the vestibular portion of cranial nerve VIII.

Neurons are classied according to their numberof processes (i.e., axons and dendrites), function, andspeed of information transfer. Neurons with multipledendrites and a single axon are called multipolar neu-rons ; these are the most commonly seen in illustrationsof neurons as illustrated in Figure 4-24. The major-ity of the neurons in the brain are multipolar, oftenpart of a motor system. Those with a single dendriteand a single axon are bipolar neurons and are foundin systems involved with special senses such as thevisual and auditory systems. Those neurons with only

a single axon emerging from the cell body are unipo-lar neurons . Unipolar neurons are found in the dorsalroot ganglia next to the spinal cord and are involvedin the transmission of sensory information from thebody. Figure 4-26 illustrates these three types of neu-rons. Speed of information transfer is dependent onthe myelin covering of the axon and the diameter ofthe axon. Axons are also referred to as nerve bers.

Nerve bers are classied as Type A, Type B, orType C based on their diameter. Type A bers trans-fer information most rapidly as they are large diam-eter, myelinated axons. Type B bers have a medium

diameter and are more nely myelinated resulting ina slower speed of information transfer as compared with Type A; they are involved in smooth muscleinnervation. Type C bers are relatively slow as theyare small in diameter and are nonmyelinated; theyare involved in the transmission of pain impulses.

An example of Type A nerve bers are the motorneurons that inform skeletal muscles whether to con-tract and how much to contract; this occurs at the neu-romuscular junction . The neuromuscular junctionis the point of communication and information




transfer between the terminal branches of an axonand the muscle bers it innervates. This junction isalso referred to as the myoneural junction as “myo”refers to muscle and “neural” refers to the nerve ber.

This point of information transfer between the nerveber and the muscle bers is a synapse. Synapses alsotake place between neurons, but here, the synapse isspecic to the neuron and the muscle. The terminalbranches from a single neuron synapse with manymuscle bers. A motor unit is one motor neuron andall the muscle bers it innervates (see Figure 4-27).

Nerves of the PNS have an organization imposedby their connective tissue coverings as illustrated inChapter 3 (see Figure 3-11). A delicate connectivetissue called endoneurium surrounds the individualnerve bers (i.e., axons). These nerve bers run inbundles called fascicles; each fascicle is encased inperineurium. Fascicles, in turn, are bundled in group-

ings that form a nerve encased in epineurium. Theseconnective tissue coverings allow a peripheral nerve,such as the hypoglossal cranial nerve, to function asa unit with a specic responsibility. For instance, thehypoglossal cranial nerve provides impulses to mus-cles of the tongue for movement.

Physiology of the Nervous System

The chapter, up to this point, has been primarily con-cerned with the anatomy, or structure, of the differentparts of the nervous system with much new terminol-ogy and labels. Now your attention is turned morefully to neurophysiology. First, the means in whichneurons communicate with one another will be pre-sented. Then, the general functions of the brain areas will be covered. The bulk of this section of the chap-ter involves a discussion of cranial nerves which willbe guided by a systems approach focusing, again, onthose systems most closely tied to speech, language,and hearing functions. These are the visual system,the auditory/vestibular system, and the speech sys-

tem. Finally, neurophysiology as it relates to swallow-ing function will be addressed.

ELECTROCHEMICAL COMMUNICATION

Neurons “speak” to one another through two means:electrical changes (measured in millivolts) andchemical changes. These changes relate to movingan “at-rest” neuron to one that is actively engaged with the transmission of a message, more properlycalled impulse conduction. To understand how this works, the “at-rest” neuron should be explained. As

mentioned previously, each neuron is encased in adouble-walled plasma membrane that has channelsto allow certain ions to come in and certain ions togo out—selective permeability. An at-rest neuron hasa particular charge with the interior of the cell beingmore negative relative to the outside of the cell (seeFigure 4-28). This at-rest charge is approximately −70 mvand is referred to as the resting membrane potential(RMP) . Thus, an “at-rest” neuron is a polarized cell;this polarization is maintained by concentration gra-dients (of chemicals), electrical gradients (opposite

Multipolar Bipolar

Unipolar

Dendrite

Cell body

Axon

Cellbody

AxonCentral

process

process

Peripheral

process

Cell body

Axon

Dendrites

Figure 4-26 Classication of neurons based on their numberof processes. (Reprinted with permission from Bhatnagar, S.C.(2008). Neuroscience for the study of communicative disorders (3rded.). Baltimore, MD: Lippincott Williams & Wilkins.)

Motorunit

Musclefibers

Alphamotorneuron

Figure 4-27 A motor unit—a single alpha motor neuron andall the muscle bers (muscle cells) it innervates. (Reprinted withpermission from Bear, M.F., Connors, B.W., Paradiso, M.A. (2007).Neuroscience: Exploring the brain (3rd ed.). Baltimore, MD: Lippin-cott Williams & Wilkins.)




charges attract), and the sodium–potassium pump(SPP) . This pump exchanges internal sodium (Na )for external potassium (K ) to assist in maintainingthe concentration gradient of these two ions, which isnecessary for the at-rest charge. Specically, the at-restneuron has much more sodium (Na ) outside the cellthan inside (Na has a positive charge) and the plasmamembrane channels are closed to Na . Inside the at-rest neuron are other ions such as potassium (K ) andchloride (Cl ). Even though there are positive ionsinside the at-rest neuron, it is the uneven distributionof the ions and their electrical charges that maintainthe RMP. All neuronal signals involve changing thismembrane potential.

The membrane potential (electrical charge) can

become either more positive or more negative. Thepositive change is referred to as depolarization andmakes it easier for the neuron to initiate an impulse(called “ring”), whereas a change in the negative direc-tion is referred to as hyperpolarization and makes itharder for the neuron to re. Thus, an impulse is char-acterized by a sudden depolarization in a section of aneuron. Depolarization can occur at any location ona neuron—a dendrite, a cell body, an axon—however,the initiation of an impulse (“ring” of a neuron)occurs at the axon because its membrane houses Na channels specialized to open when voltage changes

occur. These are called voltage-gated channels.

Action Potential

An action potential, the mechanism used by the ner-vous system to communicate over distances, resultsfrom transient changes in membrane permeability. When a segment of an axon is depolarized enough,that is, reaches threshold , Na channels open and Na rushes into the cell due to the electrical and chemicalconcentration gradients (see Figure 4-29). This results in

depolarization of the next segment of the axon continu-

ing down the length of the axon until this wave of depo-larization reaches the axon terminal—this is the actionpotential. If threshold is attained, an action potentialoccurs; if threshold is not reached, an action poten-tial does not occur; this is referred to as the all or noneprinciple. The movement of the action potential downthe axon is called propagation . Propagation occurs inone direction only, traveling down myelinated axons atfast speeds up to 120 m/second, due to saltatory con-duction . Saltatory means “to jump”; thus, the impulsetransmitted down the axon “jumps” over sections ofmyelin. In reality, what is actually occurring is that the

changes in membrane potential (in the case of actionpotentials—depolarization) can only occur at the nodesof Ranvier where the ion channels in the plasma mem-brane can communicate with the extracellular space;the rest of the axon is insulated by myelin. Nonetheless,the action potential moves down the axon without dec-rement, that is, the amplitude of voltage change downthe length of the axon does not decrease. Immediatelyfollowing an action potential, for a brief period of time,the cell will not respond to a stimulus to re or respondsonly if the stimulus is especially strong; this is termed

+ –

+ + + + + + + – – – – – – –

+

– + + + + + + + – – – – – – –

+ + + – – –

+ + + – – –

Polarized plasma membrane

Cell body

Dendrites

Restingmembranepotential(RMP)of −70 mV

Axon

Figure 4-28 An at-rest neuron in its polarized state with theintracellular uid more negative than the extracellular uid. (Re-printed with permission from Bhatnagar, S.C. (2008). Neurosciencefor the study of communicative disorders (3rd ed.). Baltimore, MD:Lippincott Williams & Wilkins.)

K+Na +

Depolarization RepolarizationResting potential

Action potential propagation

Na +

Na +

Na +

Na +

Na +

Na +

K+

K+

K+

K+

K+

K+

K+

K+K+

K+ K+

K+

Na +

Na +

Na +

Na +

Figure 4-29 A schematic illustration of the propagation of animpulse (action potential) in a segment of an axon from restingpotential, to depolarization, to repolarization (Na sodium;K potassium).




the absolute refractory period and the relative refrac-tory period , respectively (see Figure 4-30). The voltagechange (in millivolts) and the time involved (in milli-seconds) in a single action potential at a segment of anaxon is illustrated in Figure 4-30. Following are the keycharacteristics of an action potential:

• Initiated by membrane depolarization• Threshold usually 10 to 15 mV depolarized rela-

tive to RMP

• All or none principle• Conducted without decrement• Refractory periodThe initial stimulus for depolarization of a cell is

either an external stimulus to our sensory systems orinternal stimulus from chemicals called neurotrans-mitters. External stimuli such as pressure to the tonguetip, light to the retina, or movement of cochlear haircells act as triggers to initiate enough depolarizationto result in an action potential. In the case of neuronto neuron or neuron to muscle communication, theinitial stimulus is the chemical transmitted by theneuron terminal. This is the chemical part of the elec-trochemical communication system.

Synapse

A synapse is an anatomically specialized junction

between two neurons or between a neuron and themuscle bers it innervates. There are multiple neuronallocations where synapses occur, with the most frequentbeing between an axon and a dendrite, termed axo-dendritic. At a synapse, the activity of the rst neuroninuences the excitability of the next neuron. Neuronsconducting neural information toward the synapseare called presynaptic cells and neurons conductingneural information away from the synapse are calledpostsynaptic cells (see Figure 4-31). A presynaptic cell

Threshold

Absolute refractory period

Actionpotential

30

0

–60

–70

–80

M i l l i v o l t s

RMP

Relative refractory period

RMP

Milliseconds

.5 1 1.5 2 2.5 3

Figure 4-30 A graph depicting the membrane potentialchanges in millivolts across time during the generation of anaction potential (RMP, resting membrane potential).

Terminal bouton

Synapticcleft

Receptorsites

Neurostransmittersubstance

Synapticvesicles

Postsynaptic neuron

PresynapticneuronFigure 4-31 An illustrationof a synapse between neurons.(Reprinted with permissionfrom Bear, M.F., Connors, B.W.,Paradiso, M.A. (2006). Neurosci-ence exploring the brain (3rd ed.).Baltimore, MD: LippincottWilliams & Wilkins.)




produces either an inhibitory or excitatory response inthe postsynaptic cell based on the chemical messengersent across the synaptic cleft. These chemical messen-gers are called neurotransmitters.

There are a number of chemicals that act as neu-rotransmitters; the focus here will be on those thatare stored in and released from the synaptic vesiclesin the terminal boutons of the axon. These are smallmolecules (see Table 4-3). Small molecule neurotrans-mitters have fast responses and short-lasting effects;these include glutamate, gamma-aminobutyric acid,acetylcholine (ACh), dopamine, norepinephrine,and serotonin. ACh is responsible for the fast syn-aptic transmission that happens at the neuromus-cular junction. Large molecules (i.e., neuropeptides)have also been found to act as neurotransmitters.The reader is referred to Bear, Connors, and Paradiso

(2007) for a detailed discussion of current thinking inregard to neurotransmitters. A presynaptic neuronmay have more than one neurotransmitter type anda postsynaptic neuron will have more than one recep-tor type to receive the neurotransmitter.

The steps involved in neurotransmitter release arelisted below:

• Depolarization (action potential) in presynapticcell results in calcium (Ca 2 ) channels opening atthe axon terminal

• Ca 2 inux into the presynaptic cell occurs

• Ca2 mobilizes synaptic vesicles• Synaptic vesicles fuse to presynaptic terminal

bouton membrane• Exocytosis occurs• Neurotransmitter substance diffuses across the

synaptic cleft• Neurotransmitter attaches to receptor sites on

postsynaptic membrane• Neurotransmitter affects the chemical gates of

the postsynaptic membrane, changing mem-brane permeability

Calcium (Ca 2 ) plays a key role, infusing into thepresynaptic terminal bouton to mobilize the syn-aptic vesicles. The vesicles then fuse to the plasmamembrane and open to release their contents (i.e., aneurotransmitter such as dopamine) into the extra-

cellular space, a process referred to as exocytosis .The neurotransmitter traverses the synaptic cleft toattach to a receptor site, if one is available for it, onthe postsynaptic membrane. Here, the neurotrans-mitter affects the ion channels changing the perme-ability of the membrane at the localized area. Thesechannels are referred to as chemically gated channelsas they respond to the neurotransmitter chemical.Changes in membrane potential at receptor sites arecalled graded potentials and can be added up (i.e.,summed) in two ways: temporally and spatially.

TABLE 4-3

SMALL MOLECULE NEUROTRANSMITTERS, WITH GENERAL LOCATION AND PRIMARY FUNCTION

Neurotransmitter Central Nervous System Peripheral Nervous System

Acetylcholine (ACh) Widespread—regulates telencephalic Neuromuscular junction— activity, critical for the sleep–wake excitatory for muscle cycle, inuences stereotyped contraction movements

Norepinephrine Thalamus, hypothalamus, cerebralcortex—adjusts levels of attentionand arousal

Dopamine Midbrain, basal ganglia, amygdala,cortex—involved in movement,motivation, and cognition

Serotonin Brainstem, diencephalon, hippocampus,amygdala, cerebral cortex—adjustslevels of attention and arousal;involved with pain control

Gamma-aminobutyric Widespread, especially basal gangliaacid (GABA) and cerebellum—critical inhibitory

function

Glutamate Widespread—excitatory; may be involved with learning and memory functions




These localized or graded potentials can have anexcitatory or an inhibitory effect on the postsynapticneuron. Excitatory postsynaptic potentials (EPSPs) have a localized depolarizing effect, increasing thelikelihood that the postsynaptic neuron will initiate anaction potential. For example, the neurotransmitterglutamate would result in an EPSP. Inhibitory post-

synaptic potentials (IPSPs) have the opposite effect. An IPSP results in a localized hyperpolarizing of themembrane, decreasing the likelihood for the initiationof an action potential. The neuron can be thought ofas a mini processor of information as it integrates thetype of message the neurotransmitters are communi-cating via the receptor sites (i.e., IPSPs and/or EPSPs).Furthermore, the integration of EPSPs necessary toresult in a ring of an action potential is referred to assummation, either over time (i.e., temporal) or area(i.e., spatial). Temporal summation is the combiningof rapid, sequential excitatory potentials generated atthe same synapse, whereas spatial summation refersto the combining of excitatory potentials generated atdifferent synapses on the same cell.

This electrical–chemical communication systemof graded potentials at the sensory receptors or syn-apse site and the subsequent generation of actionpotentials results in the transmission of coded neu-ral messages throughout the entire nervous system.Different parts of the nervous system are specializedto communicate specic types of neural information.The various functions of the different areas of the CNS

and the PNS (in regard to cranial nerves especially)are covered next.

Functional Neuroanatomy

The study of brain anatomy and its correlates to behav-ior has been going on for some time. Franz Joseph Gall,an Austrian medical student, proposed one of the earlyexamples of this in the early 19th century. He believedbumps on the skull reected underlying mounds ofbrain tissue that correlated with different aspects of

personality and other behavioral traits. This was calledphrenology . The notion of correlating brain regions with particular language behaviors (localizationtheory) was scientically corroborated by the obser-vations of Paul Broca (1824–1880) and later, Carl Wer-nicke (1848–1904). Broca identied a frontal lobe areain the left hemisphere of the brain that, when lesioned,resulted in signicant decits of expressive language. Wernicke observed specic difculties with the com-prehension of language when the superior aspect ofthe left hemisphere temporal lobe was damaged.

There are distinct types of cerebral cortex in thehuman brain related to its evolution. The neocortex is the “newest” of the cortical areas (making up morethan 90% of the cortical area) and has six layers. Thisvertical organization relates specically to the typeof neuron found in that cellular layer. The six layersare: (I) molecular, (II) external granular, (III) exter-

nal pyramidal, (IV) internal granular, (V) internalpyramidal, and (VI) multiform layer. Flow of neuralinformation occurs in both the horizontal and thevertical direction across these layers connecting cellsto other cortical areas or to subcortical structures. Theremainder of the telencephalic cortex, older in regardto evolution, is the two-layered olfactory cortex andthe single-layered hippocampal cortex. It is the neo-cortex that sets humans apart from other mammalianspecies; in fact, when clinicians and scientists refer tothe “cortex,” they are most often referring to the neo-cortex. The cellular makeup (i.e., cytoarchitecture )across regions of the cerebral cortex has been wellstudied.

CEREBRAL FUNCTION

Brodmann investigated the cytoarchitecture of thecerebral hemispheres at the turn of the 20th centuryand discovered multiple areas with different cellu-lar anatomy that could be related to various humanbehaviors. He numbered approximately 50 differ-ent areas; this cytoarchitectural map and number-

ing system is often referred to in neurological elds.Table 4-2 lists select Brodmann areas for the corticalregions most involved with speech, language, andhearing. Figure 4-32 illustrates this map on both a lefthemisphere lateral view and the medial surface of theleft hemisphere with select numbers emphasized fortheir clinical importance to the speech and hearingeld. Another way to view the functional neuroanat-omy of the brain is in regard to cortical regions associ-ated with particular functions.

The cerebral cortex can be subdivided into pri-mary areas, association areas (which are further

subdivided into unimodal and multimodal associa-tion areas), and limbic areas (see Figure 4-32). Pri-mary areas have a one-to-one correlation to motorand sensory functions and receive projections fromthe thalamic nuclei associated with motor and sen-sory functions. If a primary area is stimulated (as inthe case of cortical mapping studies) or is damaged,then predictable motor and/or sensory behaviorsor decits, respectively, will be seen. Primary areasinclude the precentral gyrus of the frontal lobe , Brod-mann area 4, commonly referred to as the motor




strip or primary motor cortex . The motor cortexgives rise to projection tracts to the brainstem andspinal cord for volitional movement of muscles ofthe head, neck, and body. Caudal to the motor strip isthe postcentral gyrus of the parietal lobe , Brodmannareas 3, 1, 2, commonly called the sensory strip orprimary somatosensory cortex . This area receives

sensory information (i.e., touch, vibration, pain, andtemperature) via tracts that travel from the brain-stem and spinal cord transmitting conscious sensa-tions from sensory receptors in the head, neck, andbody. The special senses of hearing and vision havetheir own primary cortical regions. Heschls’ gyrus,located on the most superior aspect of the superior

Medial view

Unimodal associationcortex (Wernicke’s area)

Primaryvisualcortex

Unimodalassociationcortex (vision)

Primary auditorycortex

Multimodal associationcortex (P-T-O)

Primary somatosensory cortex

Primary motor cortexUnimodal associationcortex (premotor)

Multimodalassociation cortex

(prefrontal)

Unimodal association

cortex (Broca’s area)

Lateral view

Figure 4-32 Brodmann’s cytoarchitectural map. Brodmann numbers associated with cortical areas most pertinent to speech, language,and hearing are circled. Primary, unimodal association, and multimodal association cortical areas are labeled on the lateral view of the

left cerebral hemisphere (P-T-O, parietal–temporal–occipital). (Reprinted with permission from Kiernan, J.A. (1998). Barr: The humannervous system: An anatomical viewpoint (7th ed.). Philadelphia, PA: Lippincott Williams & Wilkins.)




temporal gyrus in the temporal lobe , was numberedby Brodmann as area 41 and 42, and functions asthe primary auditory cortex (Heschl’s gyrus) wheresound is consciously perceived. The primary visualcortex , Brodmann area 17, is found surrounding thecalcarine ssure primarily on the medial aspect ofthe occipital lobe . Note that each of the four lobes

of the cerebral hemispheres has one primary corti-cal region.Single-function, or unimodal, association areas

are adjacent to each of the primary cortical areas andare involved with the same functions and receive orgive projections to the corresponding primary area. When stimulated or damaged, these areas reectbehaviors that are related to their sensory or motorfunction but in a less specic and localized way ascompared with their primary counterparts. Five uni-modal association areas are shown in Figure 4-32.The premotor cortex, Brodmann area 6, is foundrostral to the motor strip and provides projectionsto the motor strip. The inferior frontal gyrus, Brod-mann areas 44 and 45, is found at the inferior endand just anterior to area 6. This area is commonlyreferred to as Broca’s area and provides projectionsto area 4 regarding movement for speech. The soma-tosensory association area, Brodmann numbers 5and 7, is immediately caudal to the sensory stripand receives projections from the same. The audi-tory association cortex is especially important forlanguage and hearing function. This is Brodmann

area 22, commonly referred to as Wernicke’s area .The auditory association cortex is critical for apply-ing meaning to what we hear and receives projec-tions directly from the primary auditory cortex. Thevisual association cortex takes up the remainder ofthe occipital lobe; these are Brodmann areas 18 and19. The visual association cortex receives projec-tions from the primary visual cortex and works toperceive, interpret, and attach meaning to the visualstimuli in our environment. Primary and unimodalassociation areas take up much of the surface areaof the cerebral cortex; what remains are the multi-

modal association cortices.The two multimodal association areas receive mul-

tiple inputs from the single-function association areasdescribed earlier. The parietal–temporal–occipital(P-T-O) region is located at the conuence of thoselobes and includes Brodmann areas 39 and 40. TheP-T-O is surrounded by sensory areas and provides forthe integration and association of multiple sensoryinputs. The other complex, multimodal associationcortex can be found at the most anterior aspect of thebrain and is referred to as the prefrontal cortex . The

prefrontal cortex is expansive, corresponding to Brod-mann areas 8, 9, 10, 11, 12, and 46. The prefrontal cortexreceives converging inputs from multiple areas of thebrain and thalamus. This area of the brain is respon-sible for higher cognitive processes such as reasoningand executive function (i.e., planning, organization,monitoring, and controlling of behavior). The prefron-

tal cortex is also home to our personality.Limbic areas of the brain include cortical areas(cingulate gyrus, parahippocampal gyrus, and uncus)in addition to the subcortical nuclei of the hippocam-pus and amygdala. The paired mammillary bodiesare also considered part of the limbic system and canbe found on the exposed ventral surface of the dien-cephalon. These structures, along with the tracts thatconnect them, make up the limbic system. The limbicsystem is responsible for regulating emotional andmotivational aspects of behavior. It is also criticallyinvolved in memory, especially as it relates to newlearning.

Why You Need to Know The importance of the hippocampus in memory function was made evident by a famous case—H.M.H.M. underwent surgery for epilepsy in 1953 toremove nervous tissue from both medial temporallobes (where the hippocampi and their connectionsare housed). Subsequent to the surgery, H.M. couldnot form any new memories. For example, H.M.

could not recall a conversation he had just had orcould not recall a magazine he had just looked at.His memories from before the surgery were intactand he was able to learn new motor activities(although he was not able to consciously recollectdoing so).

As presented earlier in this chapter, all of theseareas of the cortex, whether primary, association,or limbic, require tracts to communicate with oneanother and with subcortical structures such as the

thalamus. Neural impulses travel along the tracts tocommunicate across hemispheres (commissural), within hemispheres (association), and at lower braincenters (projection). For example, the left prefrontalcortex communicates with the right prefrontal cortexby way of the corpus callosum, a commissural tract.The left hemisphere primary auditory cortex com-municates with Wernicke’s area by way of short asso-ciation bers, and the somatosensory cortex receivesthalamic input via tracts traveling through the inter-nal capsule, a projection ber system.




NEURAL SYSTEMS

Neural systems refer to the different neural circuitrypatterns of the peripheral and central nervous systems working together to achieve a specic function. Thissection of the chapter focuses on those neural systemskey to speech, language, and hearing function. Theseconsist of the visual system, the auditory/vestibularsystem, and the motor speech system. Also included isthe neural circuitry involved in swallow function.

Cranial Nerves

A key part of the neural circuitry for the systems mostinvolved in speech and hearing are the cranial nerves(CNs). Cranial nerves do for the head and neck whatthe spinal nerves do for the rest of the body: (1) they

provide motor and sensory innervation to musclesand structures of the head and neck, (2) they areinvolved with the innervation of our special senses—most notably vision and audition, and (3) they playan important role in the ANS such as pupil dilationand saliva production. There are 12 pairs of cranialnerves with all but two pairs (CN I and CN II) enter-

ing or exiting the brainstem. The cranial nerves arenumbered using Roman numerals I to XII. They arenamed for their function (e.g., olfactory ), or the partof the head/neck they innervate (e.g., optic ), or by vir-tue of the nerve’s anatomy (e.g., trigeminal —havingthree parts). Table 4-4 lists each cranial nerve nameand number, associated system, general function,and general location of neural cell bodies. The cranialnerves will be discussed in more detail as they relateto each system presented.

TABLE 4-4

NUMBERS AND NAMES OF CRANIAL NERVES WITH GENERAL FUNCTION AND CELL BODY LOCATION

Cranial Nerve System Function Location of Brainstem Nuclei a

I Olfactory Olfactory Sensory Nasal cavity a

II Optic Visual Sensory Retina a of the eyeIII Oculomotor Visual Motor Midbrain Autonomic nervous Midbrain systemIV Trochlear Visual Motor Midbrain V Trigeminal Motor speech and Motor Pons

swallowing Sensory Pons (extending rostral tomidbrain and caudal tomedulla)

VI Abducens Visual Motor Pons VII Facial Motor speech and Motor Pons swallowing Sensory Medulla Autonomic nervous Pons system VIII Vestibulocochlear Audition and balance Sensory Pons/medulla (also known as the

auditory or acoustic)IX Glossopharyngeal Motor speech and Motor Medulla swallowing Sensory Medulla

Autonomic nervous Medulla system X Vagus Motor speech and Motor Medulla swallowing Sensory Medulla Autonomic nervous Medulla system XI Spinal accessory Motor speech and Motor Medulla swallowing Cervical spinal cord XII Hypoglossal Motor speech and Motor Medulla swallowing

a Cell bodies for cranial nerves I and II are not located in the brainstem.




Visual System

The visual system is obviously important to languagefunction in regard to reading comprehension and oralreading as well as perceiving and interpreting the non-verbal visual signals relied upon to supplement a com-municator’s message. Vision begins peripherally with

light acting as the stimulus entering the eye and endscentrally with the processing of visual informationin the single-modality association cortex and evenbeyond, to multimodal association areas of the brain.

A brief review of the structure of the eyeball willserve to assist in understanding the input from thevisual elds to our retinas. The different parts ofthe eyeball are labeled in Figure 4-33. The cornea isthe transparent covering of the eye that bends andfocuses the incoming light rays. The sclera is the lateralcontinuation of the cornea and is often referred toas “the white of our eye.” The lens of the eye invertsthe visual image projection onto the retina. The iris isthe colored ring that surrounds and controls the sizeof the pupil, the opening through which light enters.The choroid layer is deep to the sclera and providesvascularization to the eye. The most inner layer of theeye is the retina, which we will return to shortly.

The eye maintains its spherical shape via a liq-uid lling; the anterior cavity of the eye is lled withaqueous humor (a watery substance) and the poste-rior cavity is lled with vitreous humor (a jelly-likesubstance). Furthermore, the anterior cavity has two

chambers: an anterior chamber between the corneaand iris and the posterior chamber between the iris

and the lens. The canal of Schlemm connects thesetwo chambers for regular drainage of the aqueoushumor into the venous system; this is a critical sys-tem that regulates intraocular pressure. Glaucomais a condition of increased intraocular pressure thatresults from problems with either overproduction ofthe aqueous humor or dysfunction of this canal.

Returning to the retina, it is here that the nervoussystem’s involvement in vision begins. The retinadevelops from diencephalic tissue; therefore, it actsin a way like a “mini-brain.” The retina is multilayered with three nuclear layers and two synaptic layers (seeBhatnagar, 2008, or Nolte, 1999, for a detailed discus-sion of the retinal layers). The focus here is on the outernuclear layer of the retina that houses the sensoryreceptors for vision—the rods and cones . Returning toFigure 4-33, it can be seen that the retina is interruptedby the optic disc—a “hole” in the back of our eye. Theoptic disc is the exit point for the axons making up cra-nial nerve II (the optic nerve) as well as the entry pointfor blood vessels supplying the eye. Due to the lack ofsensory receptors at the disc, any image falling there will not be perceived and, hence, we have a blind spot.Interestingly, this blind spot goes unnoticed, as ourbrain makes up for the missing information throughperceptual processes in the visual cortex at the occipi-tal lobe. Another key feature of the retina is the fovea . At the fovea, intervening neural layers are shifted tothe side so that light focuses directly on the sensoryreceptors there for increased resolution.

The rods and cones are referred to as photorecep-tors . Rods are sensitive to light and are found in most

Anteriorchamber

Anterior cavity

Retina

Choroid

Sclera

Optic nerve

Optic disk

Posteriorchamber

Fovea

Posterior cavity

Vitreoushumor V

i s u a

l i m a g e

Cornea

PupilIris

Lens

Aqueoushumor

Figure 4-33 Anatomical structures of the eye-ball. (Reprinted with permission from Bhatnagar,S.C. (2008). Neuroscience for the study of communi-cative disorders (3rd ed.). Baltimore, MD: LippincottWilliams & Wilkins.)




abundance lateral to the fovea. There are around100 million rods in each retina. Rods assist us greatlyin “night vision,” helping us to see shades of grayand perceive movement and shapes. The retina alsocontains cones, found in greatest abundance at thefovea; nonetheless, cones are much less in numberas compared with rods. There are around 6 millioncones, the photoreceptors responsible for perceivingform and color. Thus, cones are responsible for visual

acuity. Light is transferred to neural information bythe photoreceptors and passed on to axons makingup the optic nerve via the nuclear and synaptic lay-ers of the retina. The optic nerve transmits this neuralinformation toward the CNS.

The primary visual pathway is our system for sightand begins with the optic nerve as illustrated in Figure4-34. The optic nerve from each eye transmits visualinformation from left and right visual elds (what yousee with your eyes straight forward) toward the opticchiasm . At the chiasm, the outer bers of the opticnerves stay ipsilateral while the inner bers cross, or

decussate, to the contralateral hemisphere. It is at theoptic chiasm that bers get “sorted out” so that thebers carrying information from the right visual eldare destined for the left hemisphere and the berscarrying information from the left visual eld are des-tined for the right hemisphere. The signicance of thiscrossing over will be elucidated in Chapter 5 duringthe discussion of lesion effects on the visual systemfollowing a neurological trauma such as stroke. Fromthe chiasm, the bers continue back as the optic tract to synapse at the LGN of the thalamus. Fibers fan

out from the thalamus as they project back towardthe occipital lobe as the optic radiations . Finally,synapses occur at the primary visual cortex, Brod-mann area 17, at the occipital cortex surrounding thecalcarine ssure. The surrounding single-functionassociation areas, 18 and 19, further process visualinformation.

Small secondary visual pathways exist that sendaxons to the hypothalamus and midbrain. Those

going to the hypothalamus play a role in the sleep– wake cycle by relaying information regarding theamount of light in our environment. Other axonsdiverge from the optic tract to synapse with the nucleiof the superior colliculi found in the midbrain. Visualreexes important to maintain the position of our eyesand control the xation of the eyes to keep objectsfocused on the fovea for the best resolution are partof this system.

Our eyes move in synergy to draw attention tovisual elds and focus light on our fovea. The cranialnerves responsible for these eye movements are the

oculomotor (III), trochlear (IV), and abducens (VI)and are shown in Figure 4-35. Each of these cranialnerves innervates muscles associated with a particu-lar eyeball movement. The oculomotor is responsiblefor moving our eyes upward, downward, inward, andmedially. Importantly, CN III also innervates the mus-cle responsible for elevating the eyelid (i.e., levatorpalpebrae superioris). Damage to this cranial nerve,then, results in a droopy eyelid, called ptosis . Theoculomotor nucleus for CN III is located centrally inthe midbrain and its nerve bers exit from the ventral

Right optic tract

Right lateralgeniculate nucleus (LGN)

Opticradiations

Primary visual cortex

Left optic nerve

Optic chiasm

Leftvisual field

Rightvisual field

Figure 4-34 Primary visual pathway showing theinformation from the visual elds coming to the retinasand the projection from the retinas to the primary visualcortex in the occipital lobes. (Reprinted with permissionfrom Bear, M.F., Connors, B.W., Paradiso, M.A. (2007).Neuroscience: Exploring the brain (3rd ed.). Baltimore, MD:Lippincott Williams & Wilkins.)




I Olfactory bulb

Olfactory tract

II Optic nerve

III Oculomotor n.

IV Trochlear n.

V Trigeminal n.

VI Abducens n.

VII Facial n.

VIII Vestibulocochlear n.

IX Glossopharyngeal n.

X Vagus n.

XI Spinal accessory n.

XII Hypoglossal n.

Figure 4-35 Ventral aspect of the brainshowing cranial nerve locations. (Reprintedwith permission from Cohen, B.J., Taylor, J.J.(2009). Memmler’s the human body in healthand disease (11th ed.). Baltimore, MD: WoltersKluwer Health.)

surface of the brainstem (see Figure 4-36 for a view ofall the brainstem nuclei associated with the cranialnerves). The trochlear cranial nerve enables our eyesto move downward and outward. The trochlear nerveis engaged when we walk downstairs. The motornucleus for the trochlear is found just caudal to the

oculomotor nucleus at the junction of the midbrainand pons. CN IV’s bers emerge from the dorsal sur-face of the brainstem where they immediately decus-sate to curve around the brainstem and join the othercranial nerves on the ventral side. The abducenscranial nerve innervates muscles associated withmoving the eye laterally (i.e., abduction—away frommidline). This is easily tested by visually tracking anobject from one side of the visual eld to the other.The abducens motor nucleus is found in the caudalpons with its bers emerging from the ventral surfaceof the brainstem.

Cranial nerve III, the oculomotor, also has an ANScomponent. It is part of the parasympathetic systeminnervating smooth muscle to adjust the lens of theeye for accommodation—to focus and adjust formoving targets and distances. It is also involved inpupil constriction; this is tested by the pupillary lightreex. Any ANS component of a cranial nerve has itsown nuclei in the brainstem and CN III is no excep-tion. The Edinger–Westphal nucleus, found next tothe motor nucleus of CN III, gives rise to parasympa-thetic bers that exit as part of the oculomotor nerve.

These cranial nerves will be returned to in the nextsection of the chapter, as they are related to the ves-tibular system as well.

Why You Need to Know Lesions involving the visual system have varyingeffects. Damage to the primary visual tract, includ-ing the optic nerve, may result in various visual elddecits depending on the extent and site of damage.Damage to the cranial nerves involved in eyeballmovement may result in diplopia (i.e., doublevision) or strabismus (i.e., tilting of the eye), whathas commonly been referred to as “lazy eye.”

Auditory and Vestibular Systems

A case does not need to be made in regard to the audi-

tory system’s involvement in speech, language, and,of course, hearing. The sense of hearing supports ourfunctioning and enjoyment of life. In regard to speechand language, the ability to perceive and understandthe acoustic signal generated by the vocal tract pro-vides crucial feedback for learning. Separate chap-ters (see Chapters 12 and 13) in this text explain theauditory and vestibular system in detail as well asthe pathologies associated with damage to those sys-tems. Here, the focus is on cranial nerve VIII, the ves-tibulocochlear nerve, and the tracts associated with




the auditory and vestibular systems. Cranial nerve VIII divides into two branches in the periphery as itsname implies: the vestibular branch and the cochlearbranch. We will look rst at the auditory componentof this system, which includes the cochlear branch of

the eighth cranial nerve.

Auditory (Cochlear) Component

The auditory pathway begins at the peripheralsensory receptors for hearing, the hair cells of thecochlea. These are analogous in some ways to therods and cones of the retina. The stereocilia (thread-like processes) residing on top of the hair cellsbend and deect secondary to basilar membranemovement (and other components of the organ ofCorti), thereby generating action potentials. Details

regarding the transduction of mechanical vibrations(i.e., the movements) of the hair cells into neuralinformation are covered in Chapter 12. Processes ofthese hair cells go to the cell body found in the spi-ral ganglion of the cochlea. Axons from here project

through the modiolus in the center of the cochleaand proceed through the internal auditory canal(found in the petrous portion of the temporal bone)to the brainstem. Figure 4-37 diagrams the auditorypathway from the brainstem up to primary auditorycortex. Cranial nerve VIII enters the brainstem adja-cent to the inferior cerebellar peduncle at the pons-medullary junction where bers from the cochlearcomponent will synapse at the ipsilateral cochlearnuclear complex—here starts the auditory brainstem.The cochlear complex is composed of a total of four

Edinger Westphal nucleusOculomotor nucleus

Trochlear nucleus

Vestibular nuclei

Trigeminal nucleus

Abducens nucleus

Facial nucleus

Superior salivary nucleusInferior salivary nucleus

Nucleus ambiguous

Foramen magnum

Anterior horn ofcervical spinal cord

Mesencelphalic nucleus

Main sensory nucleus

Spinal trigeminal nucleus

Cochlear nuclei

Nucleus solitarious

Hypoglossal nucleus

Dorsal vagal nucleus

Superior colliculus

Afferent Efferent

Figure 4-36 Dorsal view of the brainstem with the nuclei associated with cranial nerves pictured. Nucleireceiving afferent projections are illustrated on the left half of the diagram and nuclei giving rise to effer-ent projections are illustrated on the right half of the diagram. It should be noted that all of these nuclei arepaired (i.e., one in each half of the brainstem). For ease of illustration, only one of each nucleus (except thetrochlear) is pictured. (Reprinted with permission from Bhatnagar, S.C. (2008). Neuroscience for the study ofcommunicative disorders (3rd ed.). Baltimore, MD: Lippincott Williams & Wilkins.)




nuclei, one dorsal and one ventral on each side ofthe brainstem (refer back to Figure 4-36). From here,the auditory pathway becomes more complex due tomultiple nuclei for synapses and multiple opportu-nities for axons to decussate prior to continuing their

ascent. Nonetheless, there are four main relay nucleibetween the cochlea and the cortex. These are thecochlear nuclei already mentioned followed by thesuperior olivary nucleus , the inferior colliculi, andthe MGN of the thalamus.

Figure 4-37 illustrates the auditory pathway andpossible crossover points for axons. Fibers of thecochlear branch of CN VIII bifurcate and synapse atthe cochlear nuclei. The bers then travel to synapseat either the ipsilateral superior olive or the contral-ateral superior olive via the trapezoid body; hence,some bers decussate at this point. From there, bers

ascend in a tract called the lateral lemniscus ; the cellbodies along this tract form the nuclei of the laterallemniscus. Here, some bers cross over to the otherside as well. The bers then ascend to synapse inthe midbrain at the inferior colliculi (recall that thesuperior colliculi are related to vision). From here,the bers travel via the brachium of the inferior col-liculus to synapse at the MGN of the thalamus (recallthat the lateral geniculate nuclei are associated withthe visual system). Finally, the bers travel via theauditory radiations (similar to the optic radiations)

to synapse at the primary auditory cortex, Brodmannarea 41.

The auditory system is considered redundant withits multiple synapses and decussations. Thus, auditoryinformation from one ear is ultimately shared with

each cerebral cortex. Despite this intermixing of audi-tory signals, there remains what is called a contralat-eral effect. That is, a majority of auditory informationreaching the primary auditory cortex originates in thecontralateral ear.

There is now evidence to support the presence ofdescending, efferent auditory pathways which appearto act as a feedback mechanism. Chapter 12 presentsmore information specic to the efferent olivoco-chlear pathway . These descending tracts serve toinhibit the reception of sound providing for auditorysharpening of the acoustic signal.

Vestibular Component

The sensory receptors for the vestibular component ofthe eighth cranial nerve are the hair cells found in thesemicircular canals, the utricle and the saccule. Thesemicircular canals, more specically the crista amp-ullaris within the canals, are involved in the percep-tion of angular movements of the head in space (i.e.,dynamic equilibrium), whereas the macula withinthe utricle and saccule of the vestibule are involved inperceiving the position of the head relative to gravity

Nucleiof laterallemniscus

Auditoryradiations

CN VIIICochlear nuclei

Superior olivarynucleus

Laterallamniscus

Auditorycortex

Medialgeniculate

nucleus (MGN)

Inferiorcolliculus

Trapezoidbody

Figure 4-37 Auditory pathway from the co-chlea to the primary auditory cortex. (Reprintedwith permission from Bear, M.F., Connors, B.W.,Paradiso, M.A. (2007). Neuroscience: Exploring thebrain (3rd ed.). Baltimore, MD: LippincottWilliams & Wilkins.)




(i.e., static equilibrium). A more thorough discussionof the vestibular apparatus’ anatomy and physiologycan be found in Chapter 12. The cell bodies for thesehair cells are located in the vestibular ganglion foundbetween the vestibular apparatus and the internalauditory canal. The axons making up the centralprojections for the cell bodies continues as CN VIII’s

vestibular component to enter the brainstem at thepons-medullary junction.The bers from the vestibular component of the

eighth cranial nerve synapse at the vestibular nuclei;in turn, projections from these nuclei travel either inan ascending or descending direction as tracts (seeFigure 4-38). Indicative to the importance of equilib-rium and balance, there are a total of eight vestibu-lar nuclei in the rostral medulla, four on each sideof the brainstem. Axons from these nuclei give riseto a tract called the medial longitudinal fasciculus (MLF). The ascending bers of the MLF synapse atthe cranial nerve nuclei for those nerves innervatingeye movement. Recall from the previous section thatthese are the oculomotor (CN III), trochlear (CN IV),and abducens (CN VI) nuclei. Thus, the ascendingMLF is critical for eye movement reexes secondaryto changes in head position.

The descending bers of the MLF make up the

medial and lateral vestibulospinal tracts . The lateralvestibulospinal tract is critical for vestibular reex reac-tions (e.g., extensor or antigravity muscles) to maintainbody balance and make the appropriate posture adjust-ments. For example, if you spin until you feel dizzyand then stop, the staggering that follows is a result ofexaggerated lateral vestibulospinal tract activity (Nolte,1999). The medial vestibulospinal tract is responsible forstabilizing head position as we move and to coordinatehead position with eye movements as described earlier.

In addition to the ascending and descending tractsdescribed earlier, a number of bers from the ves-tibular nuclei travel directly to the cerebellum. Theseprojections travel via the inferior cerebellar peduncleto synapse in the older parts of the cerebellum (i.e.,occulonodular lobe, vermis, and fastigial nucleus)to provide information regarding head position. Thecerebellum, in turn, sends projections back out to thevestibular nuclei to inuence muscle adjustmentsrequired for the maintenance of balance.

Motor Speech SystemCN VIII,

vestibularcomponent

Vestibularnuclei

Ascending MLF

Thalamus

Vestibulospinaltract

Vestibulocerebellarfibers

Oculomotornucleus

Trochlearnucleus

Abducensnucleus

Figure 4-38 Dorsal view of the brainstem showing tractsassociated with the vestibular system, including the ascendingand descending medial longitudinal fasciculus (MLF) (CN, cranialnerve). (Reprinted with permission from Bhatnagar, S.C. (2008).Neuroscience for the study of communicative disorders (3rd ed.).Baltimore, MD: Lippincott Williams & Wilkins.)

Why You Need to Know The vestibuloocular reex allows eye direction tostay stable in space to aid visual focus. In fact, thesemicircular canals of our inner ears developed inparallel with the muscles that control the move-ments of our eyes; these two systems work together

for this reex. You can demonstrate this reex to yourself by shaking your head while reading thistext; although your head is moving your eyes willadjust via reexive movements. Alternatively, if youshake the text back and forth while reading, it willbe much more difcult, if not impossible, to read.This is because your semicircular canals cannotreceive any afferent information from the textbookto make the necessary eye movement adjustments!

Why You Need to Know The motor speech system involves peripheral and cen-tral nervous system mechanisms to literally “producespeech.” Although the label “motor speech” emphasizesthe motor aspect of speech production, the sensorymechanisms are critical to providing the feedbacknecessary to coordinate and modulate our muscu-loskeletal system to produce intelligible and naturalsounding speech. The term “motor speech” is aptbecause it is routinely used to describe communicationdisorders secondary to disruption in these systems.




Half of our cranial nerves are involved with speechproduction. These are the trigeminal (CN V), facial(CN VII), glossopharyngeal (CN IX), vagus (CN X),spinal accessory (CN XI), and hypoglossal (CN XII). Asseen in Table 4-4, the majority of these cranial nerveshave sensory and motor components. Three of them,the facial, glossopharyngeal, and vagus, also serve the

ANS. The last two, spinal accessory and hypoglossal,are motor only. An idea or “thought” that initiates speech produc-

tion comes from our cognitive systems that are housedin the multimodal association cortices of our brain.Language is intricately tied to cognition. For exam-ple, associating and accessing memories (prefrontalcortex) to word retrieval (P-T-O cortex) requires mul-tiple regions of the brain to work together in a coordi-nated, parallel fashion. Of course, this whole processof formulating an idea and converting it into languageoften begins with sensation of the world around us.For example, a particular smell may evoke an image of your grandmother and inspire you to say somethingabout her. This “idea” is then conveyed, via tracts, tolanguage centers of the brain—Wernicke’s area (Brod-mann area 22) and Broca’s area (Brodmann area 44,45). Recall that these areas are single-function, or uni-modal, association cortices. Broca’s area, along withother premotor cortices, basal nuclei, cerebellum,and sensory strip send projections to the motor cortex(Brodmann area 4) to direct volitional motor activity. We now turn to the tracts that will bring the messages

to the cranial nerves and spinal nerves involved inspeech production.

Corticospinal and Corticobulbar Tracts

Motor bers that direct movements of our body, head,and neck originate in the motor cortex (i.e., precen-tral gyrus). The bers that run from the cortex to thespinal cord to innervate efferent bers of the motorcomponent of the spinal nerves make up the corti-cospinal tract . The emphasis here is on the bersthat run from the motor cortex to the motor nucleihoused in the brainstem that give rise to the cranial

nerves referred to as the corticobulbar tract . Thesetwo tracts together (corticospinal and corticobul-bar) are often referred to as the pyramidal tracts. Thename pyramidal comes from the fact that these tractsarise from the pyramidal cells (the largest of these areBetz cells), named for their shape, in cortical layer Vof the cerebral cortex. In addition, the majority of thecorticospinal tract decussates at the denoted area ofthe pyramids in the caudal medulla. This accountsfor contralateral control of body movement, that is,the left hemisphere motor cortex controls right bodymovement and vice versa. Nonetheless, by using the

more anatomical names for these tracts, the tracts’origination and destination becomes transparent.Specically, the corticospinal tract begins at the cor-tex (“cortico-”) and ends at the spinal cord (“-spinal”), whereas the corticobulbar tract begins at the cortexand ends at the “bulb” (“-bulbar”) which refers to themedulla due to its shape.

Why You Need to Know Clinicians use the terms upper motor neuron(UMN) and lower motor neuron (LMN) whenspeaking of the effects of a disruption of the motorsystem. Basically, UMNs refer to neurons of thecorticospinal and corticobulbar tracts and LMNsrefer to the neurons of the cranial and spinal nervesincluding their origination in the brainstem andspinal cord, respectively.

Neural information for respiratory control involvesa complex array of neural signals beginning at themotor cortex (i.e., precentral gyrus) and travelingvia the corticospinal tract. Neural information owsfrom the cortex down through the internal capsule,the ventral midbrain (i.e., cerebral peduncle) andthrough the medulla (i.e., pyramids) to innervate neu-ronal cell bodies in the anterior horns of the cervical,thoracic, and lumbar regions of the spinal cord forvolitional respiratory control. It should be noted thatthe majority (around 85%) of the corticospinal bers

decussate (crossover) at the pyramidal decussation inthe caudal medulla. Again, this means that the major-ity of neural information directing volitional move-ment in one half of our body is mediated by the motorsignals arising in the contralateral hemisphere. Spe-cically, corticospinal projections arising from the lefthemisphere innervate movement on the right side ofthe body, whereas projections arising from the righthemisphere innervate movement for the left half ofthe body.

The corticospinal tract is signicant for speech pro-duction in regard to respiratory function. Volitional

respiratory control occurs during breathing activitiessuch as meditative breathing or voluntarily taking adeep breath; whenever you have conscious controlover your breathing, this is volitional. Involuntary, orautomatic, respiration is the norm of course. Auto-matic respiratory control requires constant inputfrom nuclei in the pons and medulla that send projec-tions to the same ventral horn cells in the cervical andthoracic regions of the spinal cord. From these ventralhorns, neural projections are sent out via the ventralspinal roots to innervate muscles of respiration. Mostnotable is spinal nerve C4, part of the phrenic nerve,




which innervates the diaphragm muscle, our primaryand critical muscle for inspiration.

The corticobulbar tract sends neural commandsto the cranial nerve motor nuclei in the brainstemresponsible for innervating muscles of the head andneck. Here, we are concerned with motor speechfunction, but these same neural mechanisms andmuscles are involved with swallow function. The

corticobulbar tract begins at the lateral aspect of themotor cortex. The motor cortex has a topographicalorganization referred to as the motor homunculus (see Figure 4-39) that very specically indicates thecortical region, giving rise to neurons controllingparticular parts of our face and neck including thevocal tract (i.e., oral cavity, nasal cavity, pharynx, andlarynx). Fibers from the motor cortex converge andtravel via the anterior limb of the internal capsule,continue to descend through the cerebral peduncle(ventral midbrain) giving off bers to both sides of

the brainstem to innervate the motor nuclei of cranialnerves V (pons), VII (pons), IX (medulla), X (medulla), XI (medulla), and XII (medulla). Note that four of thesix cranial nerves involved with speech house theircell bodies in the medulla with the facial motor nucleiclose by at the junction of the pons and medulla (referback to Figure 4-36). It should be emphasized that thecorticobulbar tract from one hemisphere provides

neural information to cranial nerve nuclei in both theleft and right halves of the brainstem. This “doublecoverage” serves as an important safety mechanismshould one cerebral hemisphere be compromised byneurological insult (e.g., tumor or stroke). An excep-tion to this double coverage rule is discussed later withregard to the facial and hypoglossal motor nuclei.

Trigeminal Nerve

Cranial nerve V, the trigeminal, is the largest of the cra-nial nerves. It emerges from the lateral ventral aspect

L e

g

H i p

T r u n k

N e c k

H e a d

A r m

E l b o w

F o r e a r m H a n d

F i n g e r s T h u m b E y e

F a c e

Li p s

J a w

T o n g u e

P h a r y n x

Toes

Foot

Figure 4-39 A coronal section of the motor ho-munculus showing the topographical representationof the right half of the body in the primary motorcortex of the left cerebral hemisphere. The samerepresentation exists in the right cerebral hemispherefor the left half of the body. A sensory homunculus,not pictured here, represents the body for conscioussensation at the primary sensory cortex. (Reprintedwith permission from Bear, M.F., Connors, B.W.,Paradiso, M.A. (2006). Neuroscience exploring the brain (3rd ed.). Baltimore, MD: Lippincott Williams &Wilkins.)




of the pons (refer back to Figure 4-35) and has bothsensory and motor functions. The trigeminal is respon-sible for transmitting sensory information regardingtouch, pressure, pain, and temperature from the head,face, and teeth including senses from the mucousmembranes of the oral and nasal cavities. Next time you get a toothache, you can thank the trigeminal

nerve. This cranial nerve also transmits propriocep-tive information from facial and lingual muscula-ture. Proprioception refers to an internal awarenessof muscle movement, position, and posture. Motorfunction of the trigeminal is primarily responsible for jaw movement: innervating the muscles that openand close the jaw and lateralize movement for chew-ing or mastication . Refer to Chapter 10 for a thoroughdiscussion of the musculoskeletal anatomy associ-ated with jaw movement. In addition, the trigeminalinnervates one velar (i.e., soft palate) muscle—thetensor veli palatini —and one middle ear muscle—the tensor tympani .

The trigeminal has three branches (“tri-” means“three”). The ophthalmic branch is sensory only andtransmits information from the forehead, upper eye-lid, eyeball, and mucous membranes of the nasalcavity. The maxillary branch is also sensory only,transmitting information from the upper lip, lateralnose, upper cheek, mucous membranes of the nasalcavity, the roof of the mouth (i.e., hard palate), andthe upper teeth and jaw. The mandibular branch issensory and motor, transmitting sensory informa-

tion from the lower lip, chin, posterior cheek andtemple, external ear, lower jaw and teeth, inside of thecheeks, oor of the mouth and tactile, pain, and tem-perature information from the anterior two-thirds ofthe tongue. However, the mandibular branch doesnot transmit any taste sensation: that is left to othercranial nerves. As mentioned earlier, motor impulsestravel by way of the mandibular branch to muscles ofmastication (e.g., masseter, temporalis, mylohyoid),the middle ear (tensor tympani), and velum (tensorveli palatini).

The trigeminal has three brainstem nuclei for sen-

sation associated with it (refer back to Figure 4-36).Fibers from the sensory component of CN V syn-apse here upon entry into the brainstem; the nuclei where the synapse occurs depends on the sensoryinformation a given ber is carrying. The mesen-cephalic nucleus , as the name implies, extends intothe midbrain and receives proprioceptive informa-tion. The main sensory nucleus , found in the pons,receives tactile sense information. The spinal trigem-inal nucleus , located in the pons and medulla andextending into the cervical spinal cord (as the name

indicates), primarily receives information regardingpain and temperature. In this way, sensory informa-tion from the head is already being organized but hasnot reached conscious sensation yet, as that happensin the cortex.

The sensory bers that arise from the sensory nucleiof the trigeminal ascend to the cortex by way of the

thalamus. Fibers from the main sensory nuclei ascendipsilaterally as part of the medial lemniscus pathwayor contralaterally as the dorsal trigeminal tract to syn-apse in the ventral posterior medial (VPM) nucleus of the thalamus. Following another synapse, the bersthat arise from the VPM ascend via the internal cap-sule to the postcentral gyrus (Brodmann areas 3, 1, 2), where conscious sensation occurs for tactile sensa-tion from the head. Fibers from the spinal trigeminalnucleus ascend contralaterally either as the spinaltrigeminal tract (and merge with Lissauer’s tract ) oralong with the spinothalamic tract (coming from thespinal cord) to synapse again in the thalamus at the VPM. From here, bers follow the same route throughthe internal capsule to the cortex for conscious sen-sation of pain and temperature. Similar to the motorrepresentation at the primary motor cortex, a sensoryhomunculus exists for the somatosensory cortex.Sensations from the head and face are received at theinferior lateral aspect of the sensory strip.

Keeping with one trigeminal motor branch, thereis one trigeminal motor nucleus (refer back to Figure4-36). The motor nucleus of CN V is centrally located

in the pons. This motor nucleus receives both ipsilat-eral and contralateral input (recall “double coverage”)from the motor cortex via the corticobulbar tract. A synapse occurs at the motor nucleus and bersemerge from the lateral aspect of the ventral pons asthe motor component of CN V’s mandibular branch.

Facial Nerve

Cranial nerve VII, the facial, innervates the muscles offacial expression, among other functions. It emergesfrom the ventral junction of the pons and medulla just lateral to the abducens nerve (refer back to Fig-

ure 4-35) and has components serving all three func-tions: sensory, motor, and autonomic. Its sensorycomponent is smaller than its motor component butis critical for our enjoyment of life, as it picks up tastesensation from the anterior two-thirds of the tongue.Motorically, CN VII supplies innervation to the manymuscles involved with lip movement for speech (seeChapter 10 for detailed information regarding thesemuscles) such as the orbicularis oris. In addition,this cranial nerve innervates eyelid depressors, so wecan sleep and blink to protect the eye and maintain




moisture (recall that CN III, the oculomotor, inner-vates muscles elevating the eyelid). In addition, thefacial nerve innervates the tiny stapedius muscle(within the middle ear), which responds to loud noiseby dampening excessive movement of the ossicles(see Chapter 12 for more information regarding thestapedial reex). The autonomic component is part

of the parasympathetic nervous system and providesstimulation to glands that produce saliva.The facial cranial nerve has three brainstem nuclei

associated with it, one for sensation, one for motorfunction, and one for autonomic function (refer backto Figure 4-36). Fibers carrying sensation for taste enterthe brainstem to synapse in the nucleus solitarius. Thenucleus solitarius, located in the medulla, is a sharednucleus that receives input from afferent bers of cra-nial nerves IX and X as well. Fibers from this nucleusascend to synapse at the VPM nucleus of the thala-mus in the same manner as sensations carried by thetrigeminal. From here, projections travel via the inter-nal capsule to the gustatory cortex located at the ante-rior insular cortex and the frontal operculum overlyingit. Association bers from here project to the orbitalcortex to integrate taste information with olfaction.

The motor nucleus of cranial nerve VII is housedin the rostral medulla (see Figure 4-36). Unique tothe facial motor nucleus is that the lower half of thenucleus receives input from only the contralateralcorticobulbar tract. This lower half has the cell bod-ies that give rise to the axons innervating muscles of

facial expression for the lower half of the face. This is anexception to the “double coverage” safety mechanism, which means that if a lesion occurs (e.g., stroke, tumor)affecting the corticobulbar bers in one hemisphere,the effects will be seen in the contralateral lower face.This is most clearly manifested as a droopy half of thelower face with marked impairments in raising that lipcorner. The motor nucleus that sends projections outto innervate muscles of the upper face receives corti-cobulbar input from both hemispheres as expected.

Cranial nerves that have ANS components havededicated nuclei for the particular ANS function.

Specically for the facial cranial nerve, the superiorsalivary nucleus contains the cell bodies that giverise to its parasympathetic component. This nucleusis found in the rostral medulla adjacent to the motornucleus of CN VII. Its bers travel with cranial nerve VII to innervate sublingual and submandibular glandsfor the production of saliva.

Glossopharyngeal Nerve

Cranial nerve IX, the glossopharyngeal, is involved with the tongue and pharynx as its name implies. It

emerges from the lateral ventral aspect of the medullabelow cranial nerve VIII (refer back to Figure 4-35)and has all three functions: sensory, motor, and auto-nomic. It provides sensory information from the upperthroat (i.e., pharynx) and completes the special senseof taste by transmitting information from the poste-rior one-third of the tongue (recall that the facial cra-

nial nerve does the job for the anterior two-thirds). Youare able to gag or to be consciously aware of a nastysore throat, thanks to CN IX! The glossopharyngeal’smotor component innervates some pharyngeal (e.g.,stylopharyngeus) and lingual (e.g., palatoglossus)muscles (see Chapter 10). Similar to the facial cranialnerve, the glossopharyngeal’s autonomic componentis part of the parasympathetic nervous system andprovides stimulation to the parotid glands that pro-duce saliva.

A brainstem nucleus is associated with each of theglossopharyngeal functions. Fibers carrying sensoryinformation synapse, along with facial nerve sensorybers, at the nucleus solitarius already described (referback to Figure 4-36). Fibers from this nucleus ascendto the thalamus to synapse at the VPM nucleus fortaste, tactile, pain, and temperature sensations. Thebers then continue on via the internal capsule to ter-minate at the tongue and pharyngeal regions of thesensory homunculus of the postcentral gyrus for mostof these conscious sensations. Projections associated with taste go to the gustatory cortex as describedearlier. Efferent projections that comprise the motor

component of the glossopharyngeal nerve arise fromthe rostral end of a shared brainstem nucleus foundin the medulla called the nucleus ambiguous (seeFigure 4-36). The ANS bers of the glossopharyngealnerve that innervate the parotid gland arise from theinferior salivary nucleus.

Vagus Nerve

Cranial nerve X, the vagus, is best known to speechclinicians and speech scientists for its prominent rolein voice production, yet, as elucidated later, the vagusis involved with numerous functions in addition to

voice. The vagus is a large, prominent cranial nerveemerging from the lateral aspect of the medulla justcaudal to the glossopharyngeal nerve (refer back toFigure 4-35). Like the glossopharyngeal nerve, it hasall three functions: sensory, motor, and autonomic.The sensory functions are many; those most relevantto speech and swallowing are listed here. The vagustransmits sensation from the mucosal surfaces of thelower pharynx, larynx, trachea and bronchi, esopha-gus, and stomach. In addition, it conveys informa-tion from a small number of taste buds around the




epiglottis . This is thought to have a protective effectfrom ingesting toxic substances, as these taste budspick up bitterness.

As alluded to above, cranial nerve X innervates allof the intrinsic muscles of the larynx (e.g., lateral andposterior cricoarytenoids, interarytenoids); these arethe muscles that have both their origin and insertion

within the larynx itself. Chapter 8 provides detailedcoverage of these muscles. The vagus also inner-vates all the pharyngeal muscles with the exceptionof one, and all the velar muscles with the exceptionof one. The stylopharyngeus (a pharyngeal muscle)is innervated by the glossopharyngeal cranial nerveand, as mentioned previously, the tensor veli pala-tini (velar muscle) is innervated by the trigeminalcranial nerve. The vagus is a critical part of the para-sympathetic division of the ANS, innervating glands,cardiac muscle, and the smooth muscle of bloodvessels, trachea, bronchi, esophagus, stomach, andintestines. Thus, the vagus is involved with breath-ing, cardiac function, and digestive function—criti-cal indeed!

The vagus (which means “wanderer”) wandersthroughout the body by way of multiple branches;three of these branches are particularly relevant tospeech production as they innervate the muscles of thevelum, pharynx, and larynx. The pharyngeal branch provides motor innervation to the velar muscles (withthe exception of the tensor veli palatini) and the pha-ryngeal constrictor muscles. The superior laryngeal

nerve is a branch of the vagus that further divides intoexternal and internal laryngeal branches. The externalbranch of the superior laryngeal nerve provides motorinnervation to muscles of the inferior pharynx (i.e.,inferior constrictor muscle and cricopharyngeus) andto one intrinsic laryngeal muscle—the cricothyroid. As you will learn later (see Chapter 8), the cricothy-roid muscle is our primary muscle for changing thepitch of our voice. The internal branch of the superiorlaryngeal nerve carries sensory information from thelarynx above the vocal folds and from the tongue baseand epiglottis. The recurrent laryngeal nerve (RLN) is

the primary cranial nerve branch involved with voice.The name “recurrent” is apt secondary to the fact thatthe nerve on the left side extends down toward theheart prior to looping under the aortic arch and thenascending back up to innervate muscles on the leftside of the larynx. The RLN on the right side extendsdown and loops under the subclavian artery. Under-standably, the RLN is at risk for being damaged dur-ing thoracic surgery or secondary to thoracic trauma.The RLN transmits sensation from the larynx belowthe vocal folds as well as from the superior esophagus.

Importantly, it is this branch of CN X—the RLN—thatinnervates all the intrinsic laryngeal muscles with theexception of the cricothyroid.

The three different brainstem nuclei associated with the vagus are found in the medulla. Afferentbers bringing in the variety of sensations the vagusis responsible for go to different nuclei depending on

the sensation. The bers carrying taste information join the afferent bers from cranial nerves VII and IXto synapse in the nucleus solitarius. As mentionedearlier, these bers then ascend to synapse in the VPMnucleus of the thalamus. Projections for taste sensa-tion from the thalamus travel to the gustatory centerat the insular cortex and frontal operculum for theconscious sensation of taste. The many bers carryingsensation from the viscera (e.g., organs of the thoraxand abdomen) also go to the nucleus solitarius. Thebers transmitting pain, temperature, and touch fromthe inferior pharynx, larynx, esophagus, and regionsof the outer ear join afferent bers from cranial nerve V to synapse in the spinal trigeminal nucleus. Fibersthen ascend to the VPM nucleus of the thalamus andon to the postcentral gyrus as previously described.

Two brainstem nuclei give rise to CN X’s efferentprojections. The nucleus ambiguous (refer back toFigure 4-36) is a shared nucleus as mentioned ear-lier, giving rise also to efferent bers of cranial nervesIX (glossopharyngeal) and XI (spinal accessory). Thebers from this nucleus innervate those skeletal mus-cles of the velum, pharynx, and larynx served by the

branches of the vagus described earlier. The dorsalvagal nucleus (see Figure 4-36) is the major parasym-pathetic nucleus of the brain. Fibers from this nucleusprovide parasympathetic innervation to the thoracicand abdominal viscera.

Spinal Accessory Nerve

Cranial nerve XI is named spinal accessory becauseit has a spinal component that innervates musclesof the neck and shoulders and a cranial componentthat provides assistance to the vagus nerve. The spinalaccessory cranial nerve has only a motor function. The

cranial root is the most caudally located of the cranialnerves, emerging from the lateral aspect of the ventralmedulla very near the spinal cord (refer back to Figure4-35). It serves to assist the pharyngeal and recurrentbranches of the vagus in innervating muscles of thevelum, pharynx, and larynx with the exception of thepalatoglossus muscle. The spinal root arises fromthe anterior horns of the cervical spinal cord (C1 toC5) to innervate the muscles that turn our head (e.g.,sternocleidomastoid) and shrug our shoulders (e.g.,trapezius).




Hypoglossal Nerve

Cranial nerve XII, the hypoglossal, is responsiblefor tongue movement; therefore, it is critical in bothspeech and swallow function. The hypoglossal alsohas only a motor component. It emerges from theventral medulla medial to the other medullary cranialnerves (see Figure 4-35). It provides motor innervationto all the intrinsic and extrinsic muscles of the tongueexcept for the palatoglossus (CN IX’s responsibility).In addition, the hypoglossal nerve also innervatessome of the extrinsic laryngeal muscles (also referredto as the strap muscles of the neck), especially thoseinvolved with lowering the larynx (i.e., the infrahyoidmuscles).

Given its singular function, all efferent bers thatcomprise cranial nerve XII arise from a single nucleus.The hypoglossal nucleus is found in the medulla adja-cent to midline (refer back to Figure 4-36). This motornucleus receives the majority of its input from thecontralateral cerebral hemisphere via the corticobul-bar tract. This, again, is an exception to the “doublecoverage” rule. This means that a lesion to one cere-bral hemisphere can result in signicant weakness inthe contralateral side of the tongue. For example, aright cerebral hemisphere lesion involving the lateralprecentral gyrus (see Figure 4-39) would affect the leftside of the tongue.

Swallow Function

The neural circuitry responsible for swallowing hasmuch overlap with the circuitry for motor speechfunction, although the reexive nature of swallowingdictates control by the swallow center located in themedulla. Nonetheless, the cranial nerves discussedearlier along with their afferent and efferent innerva-tions are all critical. Thus, the cranial nerves involved with swallow function include the trigeminal (V ),facial (VII), glossopharyngeal (IX), vagus (X), spinalaccessory (XI), and hypoglossal (XII). A brief presen-tation of swallow physiology will assist the reader inunderstanding the importance of these cranial nerves

and the structures they innervate. Swallowing, ordeglutition , occurs in four stages: (1) oral prepara-tory stage , (2) oral stage , (3) pharyngeal stage , and(4) esophageal stage (see Chapter 10).

The oral preparatory stage involves preparingthe food and/or drink for swallow. This includesthe introduction of food to the oral cavity requiringactive involvement of the lips and the manipulationof that food once in the oral cavity requiring addi-tional involvement of the jaw and tongue. Chewing,

or mastication, manipulates the food into a bolus —a cohesive mass of food in preparation of the swal-low. Cranial nerves involved with this stage of theswallow are indicated in Table 4-5 and include thetrigeminal (jaw movement), facial (lip seal and cheektension), and hypoglossal (tongue movement). Inaddition, the velum is depressed while all this foodpreparation is going on so nasal breathing can occur.This requires the involvement of the glossopharyn-geal, vagus (pharyngeal branch), and spinal acces-sory cranial nerves. As you can imagine, the time for

this stage varies widely and is dependent on howmuch the food is enjoyed and how quickly the foodis ingested.

The oral stage of the swallow starts the momentthe bolus begins to move from the anterior to theposterior oral cavity. This stage is quite quick in thenormal swallow, averaging about one second; thisis referred to as oral transit time . Cranial nervesinvolved with tongue movement are primary duringthis stage (see Table 4-5). Of course, that means thehypoglossal cranial nerve is heavily involved withassistance from the trigeminal to maintain elevation

of the jaw.The pharyngeal stage of the swallow is largely

reexive and considered involuntary. That is, what we think of as the swallow is automatically initi-ated once the bolus reaches the posterior oral cavity(near the region of the posterior faucial pillars ; seeChapter 10). Certainly, a swallow can be voluntarilyinitiated as well; although you may be surprisedthat swallowing suddenly becomes more difcult when thinking about it, especially when swallowing

TABLE 4-5

CRANIAL NERVES ASSOCIATED WITH SPEECHPROCESSES AND SWALLOW STAGES

Cranial Nerve Speech Process Swallow Stage

V. Trigeminal Articulation Oral preparatory Resonance VII. Facial Articulation Oral preparatory

OralIX. Glosso- Articulation Oral pharyngeal Resonance Pharyngeal X. Vagus Phonation Pharyngeal Resonance Esophageal XI. Spinal Phonation Pharyngeal accessory Resonance XII. Hypoglossal Articulation Oral preparatory Oral




your saliva in multiple successions (give this a try).This stage of the swallow involves moving the bolusfrom the posterior oral cavity into the esophagus.Multiple synchronous events must happen for thisswallow reex to occur. The velum must elevate toclose off the nasal cavity requiring innervation ofvelar muscles from the trigeminal, vagus, and spinal

accessory cranial nerves (see Table 4-5). The tonguemust continue to be active in propelling the bolustoward the esophagus requiring hypoglossal involve-ment. Pharyngeal muscles must be active as well,narrowing and constricting the pharynx to assistbolus movement; this requires innervation from theglossopharyngeal, vagus, and spinal accessory cra-nial nerves. At the same time, the larynx must moveup and forward and the vocal folds must close, all toprotect the airway from bolus entry (i.e., aspiration ),requiring major activity from the RLN (recall this isan important branch of cranial nerve X) to close thevocal folds and to draw the epiglottis down and backto cover the opening to the larynx. The hypoglossalcranial nerve is also involved here, as it innervatesneck muscles that elevate the larynx.

The cricopharyngeus, along with bers from theinferior constrictor muscle, make up the sphinctermuscle found at the opening to the esophagus, col-lectively called the upper esophageal sphincter orUES. The UES relaxes or opens during the pharyn-geal phase to accommodate the incoming bolus.The specic innervation of the UES continues to be

studied. The glossopharyngeal nerve, pharyngeal andrecurrent branch of the vagus nerve, and the spinalaccessory nerve are all involved. Once initiated, theswallow occurs quickly. This timing is referred to aspharyngeal transit time (PTT) .

The pharyngeal stage of the swallow is mediated bythe swallow reex center in the brainstem. Sensationsare transmitted from the posterior oral cavity to thereticular swallowing center in the pons and medulla.This swallow center then sends input to the motornuclei of cranial nerves V, VII, IX, X, XI, and XII as wellas to the respiratory centers of the medulla to coordi-

nate the reexive muscle activity for the swallow witha brief cessation of breathing. Once the bolus passesinto the esophagus, the pharyngeal stage is completedand breathing resumes.

The esophageal stage of the swallow is involuntaryand involves the transport of the bolus from the supe-rior esophagus to the stomach. The movement of thebolus occurs through peristaltic , or wavelike, actionof the esophagus requiring 10 to 20 seconds depend-ing on the consistency of the food being swallowed.

The parasympathetic component of the vagus isinvolved with esophageal innervation below the levelof the cricopharyngeus muscle (i.e., superior openingof the esophagus).

The special senses of taste and smell inuence theswallow through the subjective, conscious experi-ence of taste and the stimulation of saliva production.

Taste, or gustation, has been discussed in the previ-ous section by covering the specic functions of eachcranial nerve. By way of review, cranial nerves VII, IX,and, to a much lesser degree, X have afferent bersfrom taste buds to the nucleus solitarius in the brain-stem. From here, bers travel to the VPM nucleus ofthe thalamus and on to the gustatory center of theinsular cortex. The insular cortex also receives projections from the olfactory system. The olfactory sys-tem includes the last cranial nerve to be discussed,cranial nerve I—the olfactory nerve.

The olfactory nerve is responsible for the senseof smell. It has only this sensory function and is one oftwo cranial nerves that does not enter or emergefrom the brainstem (can you recall the other?). Theolfactory nerve’s cell bodies are located in the olfac-tory bulbs (refer back to Figure 4-35) on the ventralsurface of the frontal lobe. The sensory receptors forsmell are found in the epithelium of the nasal cavi-ties. The actual nerve is made up of the unmyelinatedshort axons projecting through the cribriform plate of the ethmoid bone (see Chapter 10) to the olfac-tory bulb. Projections from here travel caudally to

multiple areas including the anterior medial tempo-ral poles (primary olfactory cortex) with secondaryprojections to the limbic system, orbital gyri, insularcortex, and hypothalamus. The limbic system con-nects smell to emotion and aggressive responses; theorbital gyri of the frontal lobe connects smell to odordiscrimination; the insula connects smell to taste(recall that the gustatory center is there); and thehypothalamus connects smell to hunger and thirstsignals.

Summary A foundation was laid in this chapter for you to appre-ciate the importance of the nervous system in theproduction of speech, in the sensory ability to hear,and in the reception and expression of language. Thechapter began by stressing, again, the necessity tounderstand and use terminology, in this case neuro-logical terms. The organization of the nervous systeminto its mature form begins in neurodevelopment




with the ultimate differentiation into the corticaland subcortical components of the telencephalon,the different thalamic regions of the diencephalon,the three areas of the brainstem (mesencephalon,metencephalon, and myelencephalon), and the con-nections to the cerebellum and the spinal cord. Thesomatic and autonomic divisions of the PNS are also

involved with functions important to the speech and

hearing professional, most notably the cranial nervesand the cervical spinal nerves. These nerves, withtheir sensory, motor, and autonomic components,are responsible for the special senses of audition,balance, vision, smell, and taste. They also serve topick up sensations and provide motor commands forstructures and muscles involved in respiration, pho-

nation, resonation, articulation, and swallowing.



PART 3

Knowledge Outcomes for ASHA Certication for Chapter 5• Demonstrate knowledge of the etiologies of uency disorders (III-C)

• Demonstrate knowledge of the characteristics of uency disorders (III-C)• Demonstrate knowledge of the etiologies of voice and resonance disorders (III-C)• Demonstrate knowledge of the characteristics of voice and resonance disorders (III-C)

• Demonstrate knowledge of the etiologies of receptive and expressive language disorders (III-C)• Demonstrate knowledge of the characteristics of receptive and expressive language disorders

(III-C)• Demonstrate knowledge of the etiologies of swallowing disorders (III-C)• Demonstrate knowledge of the characteristics of swallowing disorders (III-C)• Demonstrate knowledge of the etiologies of cognitive aspects of communication (III-C)• Demonstrate knowledge of the characteristics of the cognitive aspects of communication (III-C)

• Demonstrate knowledge of the prevention related to cognitive aspects of communication (III-C)

Learning Objectives• You will be able to relate lesion site(s) with probable communication disorder(s).• You will be able to describe the medical etiologies associated with neurogenic communication

disorders.• You will be able to dene aphasia and differentiate the types of aphasia.• You will be able to compare and contrast cognitive-communicative impairments associated

with traumatic brain injury and dementia.• You will be able to dene the motor speech disorders (dysarthrias and apraxia of speech) and

differentiate the types of dysarthria.

CHAPTER 5

Pathologies Associated with the Nervous System


a- without, absent, negative a phasia

arterio- artery arterio sclerosis

brady- slow brady kinesia

dys- bad or difcult dys arthria

hemi one-half hemi paresis

hyper too much hyper tonic

hypo too little hypo tonic

kinetic/kinesia movement hyper kinetic

83





neo- new neo cortex

-oma tumor, growth astrocyt oma

-osis state of disease arterioscler osis

-rrhea ow, discharge logo rrhea

scler- scar, plaque multiple scler osis-sia abnormal or pathological state dyskine sia

Introduction

This chapter now applies your knowledge from Chap-ter 4. To understand neurological disorders, it is neces-sary to understand the neurological systems and howa lesion to those systems results in various symptoms .The term lesion is rather generic, as it applies to any dis-ruption to the nervous system as a result of any etiol-ogy . As a student of the nervous system, you will soonrealize that the behaviors seen with a given disorder arequite closely associated with the site of lesion in the ner-vous system (Duffy, 2005). The notion of lesion site andits correlation to symptomatology will be returned to inthe discussion of the various communication disordersassociated with neuropathology. Each of the commu-nication disorders discussed in this chapter has a listof symptoms associated with it. A symptom is a devia-tion from normal function; a collection of symptoms

is called a syndrome . These communication disordersinclude: aphasia , cognitive-communicative disorders ,apraxia of speech (AOS) , and dysarthria . Prior to dis-cussing the disorders of most pertinence to the eld ofspeech–language pathology, an overview of the manymedical etiologies that give rise to these communica-tion disorders is presented. Brookshire (2003) remindsus that clinicians who wish to treat individuals with neu-rogenic communication disorders must have at least abasic knowledge of the anatomy and physiology of thenervous system and what can go wrong with it.

Neuropathologies

A number of traumas, disorders, and diseases of thenervous system may result in a communication dis-order. Various signs (i.e., objective data reported by aphysician) and symptoms are associated with disrup-tion to the nervous system (Brookshire, 2003). Thesigns and symptoms reect the location of the lesionrather than the cause. Nonetheless, the etiology ofnervous system breakdown is important as it directs

medical management and future outcomes. As youcan imagine, there are many neurologic problemsthat can result in symptoms specic to a communica-tion disorder. This chapter will highlight those that aremost often seen by speech–language pathologists.

NERVE CELLS AND GLIAL CELLSRecall that the neuron, or nerve cell, is the basicfunctional unit of the nervous system. Therefore, alldisruptions involving the nervous system impact theneuron. Nonetheless, certain pathologies specicallytarget certain types of neurons (e.g., motor neurons) orparts of the neuron (e.g., myelin sheath composed ofoligodendroglia in the central nervous system [CNS]).Three presented here are the degenerative disordersof amyotrophic lateral sclerosis (ALS),multiple scle-rosis (MS), and Parkinson’s disease (PD). In addition,

various neoplasms or tumors can occur that affectnervous system function. Amyotrophic lateral sclerosis is commonly referred

to as “Lou Gehrig’s disease,” named after the famousbaseball player who suffered from it. ALS is a disease ofthe motor neurons (see Figure 5-1). More specically,the motor cell bodies in the anterior horns of the spi-nal cord, the cranial nerve nuclei, and the precentralgyrus are affected, as are the motor neurons compris-ing the corticospinal and corticobulbar tracts. Thisresults in both upper motor neuron (UMN) and lowermotor neuron (LMN) symptoms. Thus, symptoms

are motor and progressive in nature. Early symptomsmay manifest in limb weakness or in weakness ofthe muscles of the head and neck resulting in speechand swallowing problems. Onset of the disease is inadulthood and life span ranges, on average, from 1 to5 years with death usually due to respiratory failure(Duffy, 2005).

Multiple sclerosis is primarily a disease of the whitematter. In MS, the myelin sheath degenerates but theaxon remains intact as illustrated in Figure 5-2. Recallthat myelin in the CNS is made up of a particular type



CHAPTER 5 PATHOLOGIES ASSOCIATED WITH THE NERVOUS SYSTEM 85

of glial cell, the oligodendroglia. Although neuronaltransmission can still occur, it does so in a disruptedmanner. The process of demyelination and glialcell proliferation happens concurrently (Bhatnagar,2008). This results in the forming of plaques in the white matter of the CNS with a predilection for thebrainstem, periventricular white matter, spinal cord,and optic nerves (Duffy, 2005). Symptoms reect the

area of lesion, thus both sensory and motor systemsmay be affected. MS strikes young adults usuallybetween 20 and 40 years of age. The exact cause isunknown, but MS is thought to be among the auto-immune disorders. There are multiple types of MSbased on disease progression: (1) benign with sud-den onset but complete or near complete remission;

(2) relapsing–remitting with periods of exacerbationfollowed by incomplete or nearly full remission; (3)chronic progressive with slow onset and continu-ous symptoms worsening; and (4) malignant withsevere, rapid progression (Cobble, Dietz, Grigsby, &Kennedy, 1993; Kraft, Freal, Coryell, Hanan, & Chit-nis, 1981; both as cited in Yorkston, Miller, & Strand,1995).

Parkinson’s disease is named for James Parkinson, aBritish physician who rst described it back in 1817.This disease involves the basal ganglia. More speci-cally, PD is a result of the degeneration of dopamineproducing neurons in the substantia nigra. Dop-amine is a neurotransmitter that plays a large rolein the transmission of neural information regardingmovement. Figure 5-3 illustrates that the substantianigra, located in the midbrain, is functionally a partof the basal ganglia circuit with tracts connecting itto the striatum. In the case of basal ganglia function,dopamine is an inhibitor and works synergistically with acetylcholine (Ach) in the striatum to regulate

Degeneratingaxon

Atrophiedmusclefibers

Dendrites

Cellbody

Musclefibers

Axon

Dendrites

Cellbody

Normal motor unit Motor unit affected by ALS

Figure 5-1 A normal motor unit and a motor unit affected byamyotrophic lateral sclerosis (ALS). (Reprinted with permissionfrom Anatomical Chart Company.)

Normalaxon

(intact myelin)

Damagedaxon

(damagedmyelin)

Rapidimpulse

conduction

Slowimpulse

conduction

Figure 5-2 Demyelination of an axon due to multiple sclerosis.(Reprinted with permission from Smeltzer, S.C., Bare, B.G. (2000).Textbook of medical-surgical nursing (9th ed.). Philadelphia, PA:Lippincott Williams & Wilkins.)

Striatum

Dopamine system

Substantianigra

Figure 5-3 An illustration of the dopaminergic connections ofthe substantia nigra in the midbrain to the rest of the basal gan-glia. (Reprinted with permission from Bear, M.F., Connors, B.W.,Paradiso, M.A. (2007). Neuroscience: Exploring the brain (3rd ed.).Baltimore, MD: Lippincott Williams & Wilkins.)




movement. Cardinal symptoms of PD include bra-dykinesia (i.e., slowness of movement), rigidity, andresting tremor. Diagnosis of PD is usually made laterin life, 60 years and older although younger peoplecan get the disease (see Why You Need to Know box).

tissue from the dura mater can give rise to menin-giomas .

DISRUPTION OF SUPPORTING SYSTEMS

Recall that the blood supply, meningeal coverings,and ventricular system all act to support the work ofthe CNS. These systems do not communicate neuralinformation but are critical to the neuron’s ability todo so. Disease and injury can disrupt these supportsystems and result in damage to the nervous tissue.

Inammation of the meninges is called meningitis

which specically affects the pia mater and the arach-noid mater, collectively referred to as the leptome-ninges . This includes the subarachnoid space and thecerebrospinal uid (CSF) traveling in it. Meningitisis caused by the entry of microorganisms by way ofthe blood stream into the CSF. These microorganismsare typically bacterial or viral. Bacterial meningitis istreated with intravenously administered antibiotics, whereas the treatment for viral meningitis is directedmore at the symptoms than the cause because virusesdo not respond to antibiotic treatment. The onset ofmeningitis is rapid, over the course of a few days,

with symptoms including headache, fever, vomiting,lethargy, stiff neck, and confusion. Otitis media , leftuntreated, is one of many potential causes of menin-gitis (see Chapter 13 for a detailed discussion of otitismedia). Several different bacteria (e.g., pneumococ-cal, haemophilus inuenzae type B) are responsiblefor meningitis with meningococcal bacteria being theleading cause of bacterial meningitis in children 2 to18 years of age (Centers for Disease Control and Pre-vention, 2007).

Why You Need to Know Parkinson’s disease is medically treated and man-aged through medication such as leva-dopa( L -dopa) used to synthetically replace the dimin-ishing dopamine in the substantia nigra. Whenthe medication is working as it should, the patientis “on;” when it is not, the patient is “off.” Follow-ing is an excerpt from actor Michael J. Fox’s (2002)memoir called Lucky Man describing this “on/off”phenomenon:

When I’m “off,” the disease has complete authorityover my physical being. I’m utterly in its possession.Sometimes there are ashes of function, and I can beeffective at performing basic physical tasks, certainly feeding and dressing myself (though I’ll lean towardloafers and pullover sweaters), as well as any chorecalling for more brute forces than manual dexter-ity. In my very worst “off” times I experience the fullpanoply of classic Parkinsonian symptoms: rigidity,shufing, tremors, lack of balance, diminished smallmotor control, and the insidious cluster of symptomsthat makes communication—written as well asspoken—difcult and sometimes impossible. (p. 214)

Neoplasms refer to tumors (an abnormal prolifer-ation of cells) of the CNS. Tumors that originate within the CNS are almost always of glial cell origin(called gliomas ), a common type being astrocy-tomas . These types of tumors are usually benign,meaning they rarely travel away, or metastasize,beyond their place of origin. Alternatively, tumorsoriginating in other areas of the body may wellmetastasize to the CNS. As can be seen in Figure 5-4,tumor growth in the CNS displaces surrounding ner-

vous tissue resulting in elevated intracranial pres-sure. Symptoms will reect the location of the tumorand may include double vision, cognitive impair-ment, nausea, seizures, and headache (Bhatnagar,2008). Gliomas are named for the cell that gives riseto them; in addition to astrocytomas, there are oligo-dendrogliomas and ependymomas. Acoustic neuro-mas are tumors that arise from the Schwann cellsthat comprise the myelin surrounding the eighthcranial nerve. Lastly, although not glial in origin,

Normal coronalview of brain

Intracerebraltumor

Figure 5-4 Intracerebral tumor resulting in displacement ofnervous tissue. Note the mass effect on the ventricle and theherniation of tissue at the brainstem. (Reprinted with permis-sion from Smeltzer, S.C., Bare, B.G. (2000). Textbook of medical-surgical nursing (9th ed.). Philadelphia, PA: Lippincott Williams &Wilkins.)




The meninges can also be impacted by physi-cal trauma to the head via penetration through themeninges to the brain. This is referred to as open head

injury and will be discussed later.The ventricular system includes the choroid plexus,the ventricles, the associated foramen, the subarach-noid space, and the CSF that ows through it all. Anydisruption of this system results in a buildup of CSFand associated increase in intracranial pressure. Dis-ruptions can take two forms: a blockage somewherein the ow of CSF or an inadequate drainage of theCSF into the venous sinuses. Both of these problemsresult in hydrocephalus .

There are two types of hydrocephalus. Commu-nicating hydrocephalus refers to a breakdown of the

drainage mechanism of the CSF into the sinuses, whereas noncommunicating hydrocephalus resultsfrom an obstruction to CSF ow from the ventricles tothe subarachnoid space (Bhatnagar, 2008). The mostcommon site of occlusion is at the cerebral aqueductand is typically caused by surrounding brain tissueedema or the presence of tumors (Brookshire, 2003).Regardless of the cause, hydrocephalus results inincreased CSF pressure, thereby enlarging the ven-tricles and shifting the surrounding brain tissue out

of the way. Communicating hydrocephalus is alsoreferred to as “normal pressure hydrocephalus” (Brad-ley, 2002) because it is not accompanied by increasedintracranial pressure. Infantile hydrocephalus resultsin enlarged head size. In infants, the cranial sutures(see Chapter 10) are not yet fused, so the increasedintracranial pressure results in an expansion of the

cranium. Hydrocephalus is often surgically treatedquite successfully. The typical treatment for noncom-municating hydrocephalus is the placement of anintraventricular shunt that drains excess CSF from theventricular system to the patient’s neck or abdomenas seen in Figure 5-5.

Blood supply to the brain is an absolutely criticalsupporting system. The most common vascular dis-ease interrupting this blood supply and resulting incommunication disorders is stroke or cerebrovas-cular accident . Stroke occurs when there is a suddendisruption of blood supply to the brain, thus cuttingoff oxygen and glucose to the nervous tissue. Thisdecrease in oxygen is called ischemia . If the bloodsupply is returned fairly rapidly (i.e., within hours)and there are no residual symptoms, this is referred toas a transient ischemic attack (or event) (TIA). If theloss of blood supply lasts too long, the resulting effectis an area of infarct . In regard to the CNS, an infarct isa localized area of dead nervous tissue.

Figure 5-6 illustrates various examples of cardio-vascular disease that can lead to stroke. There aredifferent types of strokes related to their etiologies—

ischemic stroke and hemorrhagic stroke . Ischemicstroke is further subdivided as thrombotic or embolic in nature. Thrombosis refers to the gradual buildup ofmaterial, typically plaque on arterial walls that ulti-mately occludes the artery. This is often a result of ath-erosclerosis , which refers to the process whereby fattydeposits, cholesterol, calcium, and other substancesbuild up within the walls of an artery (American Heart Association, 2007). This buildup rst creates a severenarrowing of the artery lumen (called stenosis ) prior tototal occlusion (see Figure 5-6B). Figure 5-6C picturesa thrombus as a result of such plaque buildup on an

arterial wall. Illustrated in Figure 5-6D is an embolus, which refers to material traveling in the blood streamuntil it gets to an artery or capillary too narrow to passthrough. Varied embolic material exists such as bloodclots due to heart disease or a breaking off of plaquebuildup in the carotid or vertebral arteries. Infarctsdue to ischemia account for roughly 80% of strokes,the remaining 20% are due to hemorrhage.

Most simply, hemorrhage refers to a burst bloodvessel (see Figure 5-6E). Here, we are concerned with

Why You Need to Know Through the practice of immunization, bacterialmeningitis has been signicantly reduced. Just 20 years ago, Haemophilus inuenzae type B (Hib) bac-teria was the most common form of life- threateningbacterial meningitis in children younger than 5

years. In 1991, the Hib vaccine was approved forinfants 2 months of age. A physician training inpediatrics today will likely never see a case of Hibmeningitis. The current incidence of Hib diseaseis 1.3/100,000 children; 3% to 6% of those casesare fatal and up to 20% of surviving patients havepermanent hearing loss or other long-term sequelae.Menactra is a new vaccine that offers protectionsagainst the meningococcal bacteria. This vaccine isrecommended for children at their routine preado-lescent visit (11 to 12 years old) and college fresh-man living in dorms. “Meningococcal infections can

be treated with drugs such as penicillin. Still, aboutone of every ten people who get the disease dies fromit and many others are affected for life. This is whypreventing the disease through the use of vaccineis important for people at highest risk” (Center forDisease Control and Prevention, 2007).




a burst blood vessel in the CNS. The impact of this

bleeding is twofold: (1) the nervous tissue beyond thepoint of hemorrhage does not receive its oxygen andglucose and (2) the pooling of blood puts pressureon surrounding nervous tissue and shifts it out of the way; this is referred to as a mass effect . Hemorrhagesare labeled according to where they occur; three loca-tions of hemorrhage are shown in Figure 5-7. Hemor-rhages can occur within the meningeal layers, that is,epidural, subdural, and subarachnoid. Those associ-ated with the dura are typically caused by blows tothe head as in traumatic brain injury (TBI). Hemor-rhages can also occur subcortically; these are called

intracerebral (or parenchymal ) hemorrhages. Fre-quent sites of intracerebral hemorrhage include thethalamus, basal ganglia, cerebellum, or brainstem(Duffy, 2005). A common precursor to this type ofhemorrhage is chronic high blood pressure (hyper-tension). Another antecedent to hemorrhage is thepresence of an aneurysm (see Figure 5-8). An aneu-rysm is a weakening of the arterial walls so that theybegin ballooning out over time. A ruptured aneu-rysm is often the cause of subarachnoid hemorrhage(Duffy, 2005). Lastly, abnormally formed capillary

beds (arteries and veins) called arteriovenous mal-

formations can result in weakened vessel walls andbecome enlarged to the point of rupture.

Tube inserted intolateral ventricle viacraniotomy

Drainage tube in peritonealcavity, with extra length toallow for growth of child

Enlargedlateralventricle

Enlargedfourthventricle

Hydrocephalus

Normal

Normallateralventricle

Normalfourthventricle

A BFigure 5-5 A . Shunt placement for infantile hydrocephalus. B . Shown are normal ventricles and enlarged ventricles as a result ofhydrocephalus. ( A . Reprinted with permission from Bear, M.F., Connors, B.W., Paradiso, M.A. (2007). Neuroscience: Exploring the brain (3rd ed.). Baltimore, MD: Lippincott Williams & Wilkins. B . Reprinted with permission from Anatomical Chart Company.)

Why You Need to Know Risk factors for stroke fall into treatable anduntreatable categories. Untreatable risk factorsinclude the greatest risk factor, age. Males and females have similar rates of stroke once womenare postmenopause. Family history and race play arole especially in blood clotting disorders. Race alsoinuences dietary habits. Medical conditions suchas a previous stroke or heart attack also increaserisk. Treatable risk factors are those variables thatcan be changed or controlled; changing certainbehaviors can help to prevent stroke from occurring.These include treating medical conditions such ashigh blood pressure, cardiac arrhythmia, and theoccurrence of TIAs. Lifestyle factors that increasestroke risk include smoking, type II diabetes,hyperlipidemia (too much fatty tissue in the bloodstream), and obesity (Reinmuth, 1994).




Blood

Endothelium

Stenosis

Plaquebuildup

Thrombus

Embolus

Burstartery

A B C

D E

Healthy artery

Figure 5-6 A normal, healthy artery and cutaways of arteries illustrating cardiovascular disease. A . Normal, healthy artery. B . Buildupof plaque within an artery. C . Thrombosis. D . Embolus. E. Hemorrhage.

Epiduralhemorrhage

Subduralhemorrhage

Intracerebralhemorrhage

Figure 5-7 Three sites of hemorrhage affecting the brain. (Reprinted with permission from LifeART image copyright © 2010. LippincottWilliams & Wilkins. All rights reserved.)




CEREBRAL HEMISPHERES

A number of neuropathologies cross neural sys-tems and affect multiple nervous system functions.

Three of these will be discussed here: encephalitis,TBI , and dementia . In all cases, cognitive and lim-bic system functions are especially vulnerable todisorder.

Generalized brain tissue inammation most oftendue to viral causes is termed encephalitis . This viralinfection of the brain tissue causes swelling, especiallyin the temporal lobes. A common viral cause is theHerpes simplex virus, but there are a number of otherviruses that may result in encephalitis. Symptoms aresimilar to meningitis including severe headache, con-fusion, and fever sometimes accompanied by drowsi-

ness, irritability (in children), and seizures. Medicaltreatment for encephalitis involves the administra-tion of antiviral agents if the cause is Herpes simplex;otherwise, the treatment is primarily symptomatic.Survivors of encephalitis may have neurological de-cits in the areas of cognition, motor abilities, vision,and epilepsy as well as associated behavioral andemotional changes.

Brain damage refers to any type of injury to the brainfrom any cause and at any age, whereas TBI refers tobrain damage as a result of physical trauma. There are

two categories of TBI: open (penetrating) head injury and closed (nonpenetrating) head injury (see Table 5-1).Open head injury results from a penetrating wound tothe head that pierces through the protective menin-geal layers and impacts brain tissue. Examples of thistype of injury include gunshot wounds or depressedskull fractures. The effects of penetrating head injuriesare largely focal, but the physical force of the traumato the brain also sets up impact-induced shock wavesthat propagate through nervous tissue (Kirkpatrick &DiMaio, 1978).

Middle cerebralartery

Aneurysm

Figure 5-8 An aneurysm of the middle cerebral artery. (Reprinted with permission from Anatomical ChartCompany.)

TABLE 5-1

MECHANISMS OF TRAUMATIC BRAIN INJURY

1. Penetrating (open) head injury 2. Nonpenetrating (closed) head injury i. Discrete lesions (a) Concussion (b) Contusion 1. Coup 2. Contrecoup (c) Hematoma (d) Ischemic brain damage ii. Diffuse lesions (a) Diffuse axonal injury (b) Hypoxia




Closed head injuries (CHIs) are the result of blunttrauma to the head along with linear and rotationalacceleration of the brain within the skull. This move-ment results in the stretching of axons and bloodvessels (Strich, 1961) as well as the back and forthmovement of the brain within the cranial cavity. Asa result, lesions due to CHI can be focal or diffuse.

Focal damage is most likely to occur when the brainis in motion due to the mechanical forces associated with the brain shifting forward into the anterior andmiddle cranial fossa (see Chapter 10; Adams, Graham,Murray, & Scott, 1982).

Concussion, contusion, hematoma, and ischemicbrain damage are among the discrete effects of CHI. A concussion is the most minor of brain injuries. Itresults in an alteration of consciousness for a shortperiod of time and may be accompanied by a distur-bance of vision or equilibrium. A contusion is a moreserious consequence of head injury caused by theimpact of the brain and skull during trauma. Contu-sions result from minor hemorrhages or tearing ofblood vessels at the site of impact and are generallyassociated with blows or falls. The most vulnerableareas for contusion are the orbitofrontal, anterotem-poral, and lateral temporal cortices (Sohlberg &Mateer, 2001). The TBI term coup refers to the contu-sion at the site of impact, and the term contrecoup refers to the contusion opposite the site of impactas illustrated in Figure 5-9. For example, if the site ofimpact is the left hemisphere orbitofrontal cortex, the

expected contrecoup contusion would be the righthemisphere posterior occipital lobe. Another discreetlesion as a result of TBI is a hematoma, an accumula-

tion of blood. Hematomas are named for their loca-tion such as “epidural” or “subdural.” Lastly, areas ofbrain tissue can be affected by ischemia with the mostsusceptible areas being boundary zones between theanterior cerebral artery (ACA) distribution and themiddle cerebral artery (MCA) distribution.

Although there are a number of discreet or focal

lesions that may occur as a result of TBI, the diffuselesions may have the most lasting impact on function.Diffuse lesions refer to damage to the brain that is notlocalized to one particular region. These lesions are theresult of damage to the nerve bers (i.e., axons) or thegeneralized effect of hypoxia. The damage and shear-ing of CNS white matter is referred to as diffuse axonalinjury (DAI). Hypoxia refers to decreased oxygenationof neural tissue resulting from systemic hypotension(low blood pressure), increased intracranial pressure,or secondary to seizure activity or cardiopulmonarycompromise (e.g., heart attack). Patients typicallypresent with a mixed type of damage, that is, both focaland diffuse, although one type usually predominates.

Forwardmovement

Backwardmovement

Coupinjury

Contrecoupinjury

Figure 5-9 Coup and contrecoup focal areas of contusion inhead injury. (Reprinted with permission from LifeART image copy-right © 2010. Lippincott Williams & Wilkins. All rights reserved.)

Why You Need to Know Computerized tomography (CT) and magnetic reso-nance imaging (MRI) are the primary neuroimagingtools used for diagnostic purposes in clinical set-tings. In addition, newer technologies are built uponthese imaging techniques. CT scans make use of aseries of x-ray images or slices allowing for differentcross sections of the live brain, or body, to be viewed. Although CT scans do not produce pretty pictures,they are incredibly useful in detecting abnormalitiessuch as an infarct following a stroke or the occur-rence of a hemorrhage. Alternatively, MRIs producean image that has much better resolution, or pic-ture, using an imaging technique that draws uponmagnetic properties of hydrogen atoms in our bodyto, again, view sections of the live brain or body. Inthe case of TBI, the x-rays used with CT are preferableto detect skull fractures while MRI is preferable todetect DAI.

Dementia is a disorder characterized by a progres-sive decline in cognitive abilities that typically strikesin later years. Difculty with memory is typically oneof the earliest and most devastatingly affected of thecognitive processes. In addition to memory, an indi-vidual must evidence other decits including at leastone of the following: apraxia, agnosia , aphasia, orexecutive function impairment. In turn, these multi-ple decits impact the individual’s ability to carry outsocial and occupational roles (American Psychiatric




Association, 1994). Dementias can be grouped ascortical dementias or subcortical dementias accordingto the primary locale of brain damage. Dementia ofthe Alzheimer’s type is classied as a cortical dementiaand accounts for approximately 50% of the cases seen(Katzman & Bick, 2000). It is progressive and irrevers-ible. Life expectancy after diagnosis ranges from 3 to23 years with an average of 8 years (Lubinski, 2005).

Alzheimer’s dementia results in progressive atro-phy of the cerebral cortex due to the breakdown ofneurons at the cellular level. Predominate pathologiesat the cellular level include the presence of neuriticplaques and neurobrillary tangles which are shown

in Figure 5-10. Neuritic, or amyloid, plaques are aresult of clumps of beta-amyloid protein fragmentsthat congregate in the extracellular space through-out the CNS. These plaques are thought to stimulatefree radical production and, in turn, cause neuronalcell death (Cummings, Vinters, Cole, & Khachatu-rian, 1998). The tangles refer to intracellular twistedstrands of tau protein. Tau protein functions in nor-mal cells to promote axonal growth and development(Cummings et al., 1998). Even though AD is classiedas a cortical dementia affecting neurons in the medialtemporal lobe and widespread association cortices,

these histologic changes also occur subcortically, par-ticularly in the hippocampus. Neuronal cell death incertain nuclei leads to a disruption of neurotransmit-ter production particularly affecting the cholinergicsystem. ACh is the neurotransmitter of the cholinergicmechanism. ACh in the CNS is involved with learningand memory. This has become a promising area ofneuropharmacological research and therapy (Massey,2005). This combination of neuronal cell death and ACh depletion leads to the dementia syndrome of the Alzheimer’s type.

More recent research has explored the role of genesin causation of Alzheimer’s disease (AD) . Genetics is apredominant factor in early-onset AD, also referred toas familial AD, which typically affects individuals from30 to 60 years of age. The genetic difference is due toa mutation of specic genes resulting in an individualhaving a 50/50 chance of getting the disease if theirparent had it. The genetic mutation causes abnormalproteins to be formed in a cell; in the case of AD, morebeta-amyloid protein is formed and, as indicated ear-lier, this protein is part of the plaques leading to cellbreakdown. More common, however, is late-onset AD,occurring after the age of 60. Genetics still play a role

but not nearly as strong. In this case, genetic variants increase the risk of developing the disease. This riskis related to a gene called the apolipoprotein E gene(APOE); there are three forms of this gene with APOE € 4 most directly related to increasing the risk of devel-oping AD. Better understanding of the role of genesin AD is a priority of research. For more on the role ofgenes and other causative factors associated with thisdevastating disease, access the information providedby the National Institutes of Health ( www.nih.org ).

Beta amyloidproteinfragments

Neurites

White matter Cerebral cortex(gray matter)

AxonNeuronal cellbody

Alzheimer’s Normal

NeurofibrillarytanglesA B

Figure 5-10 Microscopic brain tissue changes in Alzheimer’s disease. A . Amyloid plaques. B . Neurobrillary tangles. (Reprinted withpermission from Anatomical Chart Company.)

Why You Need to Know The exact cause, and therefore prevention, of AD is unknown at this time. However, researchhas discovered associated risk factors. Like heartdisease and stroke, there are untreatable risk factors such as age and genetics. Treatable risk factors include overall cardiovascular health (e.g.,cholesterol levels, blood pressure) and diabetescontrol. Nonmedical variables under our controlinclude educational level, social engagement,cognitive stimulation (e.g., doing puzzles, reading

http://www.nih.org/

http://www.nih.org/




Pick’s disease is another type of cortical dementiaand is grouped under a broader heading of demen-tias called frontotemporal dementias . Pick’s dis-ease is named for the neurologist, Arnold Pick, whorst identied the pathology back in 1892. Thus, theabnormal cells involved with this disease are referredto as Pick cells; these cells include abnormal depositsof the tau protein which are referred to as Pick bod-ies. Interestingly, in this dementia, the affected areasof the cortex remain localized to the frontal and ante-rior temporal lobes, which is different from the dif-fuse cortical atrophy associated with dementia of the Alzheimer’s type. Because of this localized damage,early symptoms are associated with emotion andlanguage functions.

A type of dementia that can be cortical, subcorti-cal, or a combination is that resulting from vasculardisease. In fact, this type of dementia is referred toas vascular dementia or multi-infarct dementia. Thistype of progressive cognitive loss is a result of mul-tiple “mini-strokes” throughout the brain having a

cumulative effect on function.Dementias of the subcortical classication are asso-ciated with degenerative diseases of the basal ganglia.Huntington’s disease affects the telencephalic basalganglia and results in devastating movement disor-ders and, ultimately, dementia. As already discussed,Parkinson’s disease (PD) is primarily a movementdisorder but, in some cases, the disease can also beaccompanied by an associated dementia.

All of the neuropathologies just reviewed mayresult in a communication disorder. These commu-nication disorders may be due to a breakdown or

damage to cortical language regions (e.g., aphasia),to various motor nuclei and tracts (e.g., apraxia ordysarthria), or to widespread cortical and subcorticalmechanisms supporting cognitive and limbic func-tions (e.g., cognitive-communicative impairments).It should be noted here that an individual may pres-ent with multiple communication disorders at a giventime. The next section of the chapter presents each ofthese disorders by making reference to typical neuro-pathologies resulting in the disorder, dening the dis-order, and explaining its subtypes.

Neurologic CommunicationDisordersAPHASIA

Aphasia refers to language impairment as a result ofbrain damage to the language dominant hemisphere,

almost always the left hemisphere. The languageproblems are primarily in form (phonology, morphol-ogy, and syntax) and in content (semantics) for bothexpression and reception. The pragmatic function oflanguage is largely intact for individuals with aphasia,as many skills that govern and regulate language useare housed in the right hemisphere of the brain. Thebrain damage is typically due to an ischemic stroke tothe language-dominant hemisphere. However, apha-sia can also be the result of any lesion affecting theperisylvian region, referred to as the language zone(see Figure 5-11). Stroke due to hemorrhage, tumorssuch as gliomas, or focal lesions due to TBI can alsoresult in aphasia.

A stroke can occur anywhere within the CNS, butthe middle cerebral artery (MCA) is particularly at riskfor embolic ischemic strokes. This is due to the MCAbeing almost a direct continuation of the internalcarotid system and, therefore, any plaque or clots mov-ing in the blood stream up toward the brain tend totravel this path prior to becoming lodged and occlud-ing an artery. Recall that the arterial distribution of theMCA includes the majority of the lateral cortex of the

frontal, parietal, and temporal lobes for both right andleft hemispheres. In the language-dominant hemi-sphere, such a stroke results in language impairment.The type of impairment depends on where along thearterial distribution the stroke occurs.

the newspaper, going to museums), and aerobicexercise to increase oxygen to the brain. Althoughit is not known whether any of these activities willactually prevent the onset and progression of AD,it certainly will not hurt and will denitely helpdecrease risk of other health conditions such asheart disease or depression.

Lateral(Sylvian)fissure

Perisylvianlanguage

zoneFigure 5-11 The perisylvian language zone. (Reprinted withpermission from Anatomical Chart Company.)




Aphasia can be further dened as an acquiredlanguage impairment affecting both expressive andreceptive abilities. Expressive modalities of languageinclude verbal (i.e., spoken) and graphic (i.e., written)expression. Receptive modalities of language includeauditory and reading comprehension. In addition,the interpretation and use of gestures for communi-

cation are affected. All of these language modalitiesare affected to some degree in aphasia, although theseverity across modalities is inuenced by the sizeand site of the lesion (i.e., brain damage). In fact,aphasias are classied into subtypes based on effectsto the various modalities. For example, an individual with an ischemic stroke involving the left hemisphereinferior frontal gyrus would likely evidence signi-cant decits in expression and less severe decits incomprehension. Conversely, a stroke affecting theleft hemisphere superior temporal gyrus would likelyresult in signicant decits in comprehension butbetter verbal expression skills. Nonetheless, both sce-narios would show problems across all modalities.

The most basic way to classify the aphasias is intononuent and uent types. These types are correlatedto a general site of lesion and broadly differentiated bysymptomatology (see Table 5-2). Persons presenting with nonuent aphasias have lesions to the inferiorfrontal lobe involving Broca’s area, the anterior insu-lar cortex, and surrounding tissues. These individualshave concomitant motor symptoms of contralateralhemiparesis of the limbs; typically right-side hemipa-

resis, as the left hemisphere is language dominant inthe vast majority of people. In addition, due to uni-lateral upper motor neuron (UUMN) involvement, acontralateral lower facial droop and tongue weaknessis expected. Persons with uent aphasias have lesionsinvolving the superior temporal lobe often extending

into the inferior parietal lobe. These individuals donot show motor impairment but may have visual elddecits consistent with a lesion involving the opticradiations of the primary visual pathway.

Nonuent versus uent distinctions are madebased on characteristics of verbal output. A nonu-ent speaker uses language the way a text message via

a cell phone may be written—with the fewest words,grammatical markings, and punctuation to get themessage across. Hence, a nonuent speaker hasmore content (e.g., nouns and verbs) than functor words (e.g., conjunctions, prepositions, and articles)present in their speech. This symptom of aphasia isreferred to as agrammatism , which literally means“without grammar.” As the nonuent label implies,their speech is effortful with many hesitations, revi-sions, and interrupted melody. These speakers areusually quite aware of their errors, which may in turnincrease frustration or decrease their willingness toattempt to speak. Alternatively, uent speakers soundgood. Their speech is produced without effort and hasappropriate melodic contours. Grammatical mark-ings are present although their use may be in error;this symptom is called paragrammatism . Inferredfrom verbal output and lesion site, the symptom thatmost impacts the communication of uent speak-ers is their decreased comprehension. They maymanifest this by behaviors such as failing to respondappropriately to verbal input, being unable to followcommands, giving quizzical facial expressions, and/

or making requests for repetition. Also evident is theirdecreased ability to monitor their own speech andmake self-corrections. Table 5-2 provides a summarylist of the expected language characteristics associ-ated with the nonuent and uent classications.

Multiple types of aphasia fall under these broadcategories of nonuent and uent. Traditionalistsin aphasia use a classication scheme developed byGeschwind and others out of the Boston School ofMedicine (Goodglass, 1993). This scheme furtherclassies aphasia into syndromes (a collection ofsymptoms) based on (1) lesion site, (2) uency, (3)

speech, (4) word retrieval, (5) repetition, and (6) com-prehension (Brookshire, 2003). Symptom patternsacross these categories result in the classication. Thedifferent aphasia syndromes broken down accordingto their uent or nonuent verbal output are Non- uent: Broca’s aphasia, transcortical motor apha-sia, and global aphasia; Fluent: Wernicke’s aphasia,conduction aphasia, transcortical sensory aphasia,and anomic aphasia. Each type is briey discussednext, but you are referred to texts devoted to aphasiafor further discussion of this classication scheme

TABLE 5-2

SPEECH AND LANGUAGE CHARACTERISTICSASSOCIATED WITH NONFLUENT ANDFLUENT APHASIA

Nonuent Aphasia Fluent AphasiaDecreased melodic line Adequate melodic lineDecreased utterance Normal or extended length utterance lengthText message speech Adequate grammar (may

have errors in use)Effortful articulation Effortless articulation Word retrieval Word retrieval difculties difcultiesBetter comprehension Better expression than than expression comprehension




and the use of these labels to describe aphasia (e.g.,Brookshire, 2003; Goodglass, 1993)

Nonuent Aphasias

Broca’s aphasia is named for the physician, PaulBroca, who rst documented speech and language

decits due to brain damage involving the languagedominant hemisphere. This syndrome results froma lesion to Brodmann areas 44 and 45. Verbal outputis nonuent and agrammatic with effortful and halt-ing speech, most likely due to a motor programmingdisorder called apraxia of speech (AOS) that often co-occurs with Broca’s aphasia (AOS will be discussedlater in this chapter). Word retrieval is considered fairfor content words but often masked by speech dif-culty. Speech repetition (i.e., immediately repeatinga word or phrase) is marked by misarticulated andhalting speech. Writing abilities may be the strongeroutput modality, as graphic language abilities willnot be compromised by AOS but the dominant writ-ing hand may be motorically involved. Auditory andreading comprehension is fair to good as compared with expressive abilities.

Transcortical motor aphasia is the result of whitematter tracts being disconnected from cortical lan-guage centers in the frontal lobe; hence, this is oftenreferred to as anterior isolation syndrome (Brook-shire, 2003). Lesions are to the anterior superior fron-tal lobe, Brodmann areas 8 and 9. Individuals with

this type of aphasia are nonuent speakers who lackinitiation exemplied by severely impaired sponta-neous speech (LaPointe, 1994). Speech abilities and word retrieval are variable while repetition abilitiesare remarkably strong. Comprehension is good rela-tive to expression.

Global aphasia, as the name implies, is a result ofa large, widespread lesion to the perisylvian languagezone as a result of blockage at the proximal MCA.Individuals with this type of aphasia are nonuentand may have severely limited verbal output calledverbal stereotypes (e.g., “where where,” “da wanni,”

“nuts”), overlearned or automatic phrases (“one,two, three . . .”) or expletives. Written output is alsoextremely limited. Word retrieval is poor as is theirability to repeat. In keeping with the global nature ofthe decit, comprehension is also poor.

Fluent Aphasias

Wernicke’s aphasia, a type of uent aphasia, wasnamed for Karl Wernicke, an early localization-ist, who, like Paul Broca, found particular language

symptoms associated with damage to the brain. Incontrast to Broca’s area, Wernicke’s area is located inthe posterior superior temporal gyrus of the languagedominant hemisphere, Brodmann area 22. Damageto this region results in uent, yet empty, verbal pro-ductions with unintended word substitutions. Thesesubstitutions are called verbal (or semantic ) para-

phasias , and may or may not be related to the target word (e.g., television/computer vs. fork/computer). Word retrieval is poor as is repetition with the pres-ence of these paraphasias. In fact, individuals with Wernicke’s aphasia may produce words not found intheir language called neologisms . A string of neolo-gisms along with inappropriate use of real words isreferred to as jargon . As expected, comprehension ispoor; therefore, awareness of these errors is often notpresent. This decreased awareness may result in effu-sive output of speech, referred to as press of speech or logorrhea .

Similar to the transcortical motor aphasia describedearlier, transcortical sensory aphasia results fromdamage to white matter tracts cut off from posteriorlanguage zones and has been referred to as a poste-rior isolation syndrome. Site of lesion is associated with the posterior superior parietal lobe, Brodmannarea 7 or around the complex association areas ofthe parietal–temporal–occipital (P-T-O) lobes. Verbaloutput is uent but empty with variable speech; theymay evidence verbal paraphasias. Word retrieval ispoor but repetition skills are remarkably intact. Com-

prehension is poor.Conduction aphasia is most likely a result of a lesionimpacting the arcuate fasciculus, the tract connecting Wernicke’s to Broca’s area. Verbal output is uent andgood but may include literal (or phonemic) para-phasias . In literal paraphasia, an individual uninten-tionally substitutes phonemes in the target word ortransposes phonemes in the target word (e.g., domtu-tor for computer or comtuper for computer ). The pro-duction of literal paraphasias impacts a fair ability toretrieve words. Interestingly, repetition is signicantlyimpacted because of the disconnection between the

comprehension and formulation/production centersfor language. That is, problems with repetition aredue to the disconnection rather than comprehensionas these individuals have relatively intact comprehen-sion abilities.

Anomic aphasia is the mildest of the aphasia syn-dromes and is associated with “. . . lesion sites that areremote from each other” (Goodglass, 1993, p. 214).Goodglass indicates possible lesion sites resulting inanomic aphasia to include the frontal lobe, the angu-lar gyrus, or the inferior temporal gyrus, with each of




these sites resulting in slightly different versions ofanomia. Verbal output is uent, but word retrievalis only fair with verbal paraphasias evident. Thisimpaired word retrieval is also apparent in writing.Repetition and comprehension is fair to good relativeto verbal expression.

Table 5-3 highlights a language characteristic ofeach syndrome that assists in making an accurateclassication. That said, it should be noted that evenexperienced diagnosticians often cannot classify anindividual’s aphasia into a syndrome type. In fact, theaccuracy of identied syndrome is quite dependenton the rigor of the classication criteria used and

ranges from 30% to 80% accuracy (Goodglass, Kaplan,& Barresi, 2001).

COGNITIVE-COMMUNICATIVE DISORDERS

“Cognitive-communicative disorders encompassdifculty with any aspect of communication thatis affected by disruption of cognition” (AmericanSpeech-Language-Hearing Association, 2005, p.1).Disrupted cognitive processes that can impact com-munication abilities include attention, memory,reasoning, and executive function. The neurologic

underpinnings for these functions rely on complexassociation areas, that is, the prefrontal cortex andP-T-O cortex and their connections to one another andthe limbic system. Thus, any pathology that impactsthese systems can result in a cognitive-communica-tive disorder. These pathologies include stroke, TBI,dementia, anoxia, meningitis, encephalitis, tumors,and hydrocephalus. Although many types of traumaor disease may result in disrupted cognition, theexpected pattern of disruption differs. Following isa discussion of the cognitive decits associated with

communicative breakdown due to right hemispherebrain damage, TBI, and dementia.

Right Hemisphere Syndrome

Similar to aphasia, right hemisphere syndrome (RHS)results from a collection of symptoms displayed fol-

lowing damage to a cerebral hemisphere. In this case,the damage is to the nondominant hemisphere forlanguage, most often the right hemisphere. In most ofthe patients seen, the damage is due to stroke. How-ever, right hemisphere damage can be incurred dueto other causes such as focal brain injury, tumor, orother disease processes.

Much has been written about hemispheric dif-ferences. For example, analytical and logic-orientedpeople have been referred to as “left hemispherethinkers,” whereas more creative and intuitive peo-ple have been called “right hemisphere thinkers.”This tendency to categorize people according tohemispheric dominance is associated with their styleof thinking. Although oversimplied, there is sometruth to this notion. The left hemisphere is associ-ated with more linear processing, perceiving detail,and being heavily involved in linguistic encodingand decoding and the motor planning for speech. Alternatively, the right hemisphere processes infor-mation more holistically with parallel processing,enabling us to see the gestalt or “big picture.” Thus,the right hemisphere excels in the simultaneous

integration of information and is heavily involvedin visual perception and spatial relationships. As thefamed author Carl Sagan (1977) reminds us, we needboth hemispheres to function optimally as humanbeings:

There is no way to tell whether the patterns extractedby the right hemisphere are real or imagined withoutsubjecting them to left hemisphere scrutiny. On theother hand, mere critical thinking, without creativeinsights, without the search for new patterns, is sterileand doomed. To solve complex patterns in changingcircumstances requires the activity of both hemi-spheres: the path to the future lies through the corpuscallosum. (p. 191)

Individuals with RHS have been described as hav-ing language without communication (Burns, 1985).These individuals have most of their linguistic abili-ties intact, masking what can be more subtle cogni-tive decits. The problems associated with damageto the nondominant hemisphere for language,most typically the right hemisphere, fall under thebroad categories of visuospatial decits, affect and

TABLE 5-3

DISTINGUISHING LANGUAGECHARACTERISTICS OF APHASIA SYNDROMES

Aphasia Syndrome Distinguishing Features

Broca’s AgrammatismTranscortical motor Preserved repetition ability Global Profound impairment across

all language modalities Wernicke’s Empty speechTranscortical sensory Preserved repetition ability Conduction Marked impairment of

repetition Anomic Primary difculty in word

retrieval




prosody, and higher cognitive functions. The cogni-tive functions impacted are most likely grounded indifculties with attention and integration (Myers,1999). Myers has characterized a “typical” individual with RHS as displaying the following: (1) adequatesupercial conversation; (2) at voice or affect; and(3) communication partner perceptions of inatten-

tion, insensitivity, and poor pragmatics or use of lan-guage (e.g., eye contact, turn taking).

Visuospatial Decits

One of the most interesting decits seen followingright hemisphere damage is that of neglect . Neglectis dened as the failure to report, respond, or orientto novel or meaningful stimuli contralateral to theside of lesion; hence, left hemispatial neglect maybe present with right cerebral hemisphere damage. What makes this complex disorder fascinating isthe interplay of multiple perceptual and cognitivesystems including attentional mechanisms, inten-tion, awareness, and internal mental representa-tions (Brookshire, 2003). The most severe neglecthas been associated with lesions to the right parietallobe especially posterior inferior lesions (Mesulam,1981), but the frontal lobes are also implicated. Indi-viduals present with many behavioral symptoms ofneglect including (1) failure to respond to stimuli inthe left hemispace (i.e., to the left of body midline);(2) attending only to the right side during activities ofdaily living such as dressing the right half of their body

or only eating food from the right side of their plate;and (3) motor behaviors such as bumping into door- ways and walls to their left (Myers, 1999). Neglect canalso directly affect the communicative acts of writingand reading with writing oriented on the right side ofthe page or reading only the words presented to rightof midline.

A number of other perception-based impairmentscan be part of RHS. Constructional impairments reect difculty in drawing, copying, or utilizingobjects in constructing gures and products. Con-structions evidence distortion and disorganization

and may reect impairments in attention, perception,and neglect. Prosopagnosia refers to an inability torecognize familiar faces and is associated with righttemporal occipital lesions with long-term difcul-ties associated with bilateral lesions (Benson, 1989).Denial of illness, termed anosognosia , is a commonsequela of right hemisphere damage and is correlated with parietal lobe damage. The extent of denial var-ies among patients, ranging from indifference towardtheir decits to complete denial of ownership of theirvery own limbs (Brookshire, 2003).

Affect and Prosody

Individuals with RHS may exhibit symptoms of ataffect exhibited in decreased facial expression as wellas lack of prosodic contours in their speech. Interest-ingly, these problems are not only expressive but alsoreceptive. That is, individuals with RHS also exhibitdifculties “reading” facial cues, body language, andthe prosodic features of others’ speech. Hence, manyadults with RHS have difculty using and appreciat-ing emotion in daily life situations (Brookshire, 2003).Emotional competence involves both mood andaffect. Mood is the inner emotional state, whereasaffect is the external manifestation of mood. The lim-bic system is clearly involved with emotion and mood,but the ability to appropriately express emotion (viaaffect) and to interpret others’ emotions seems to bemediated by the nondominant hemisphere for lan-guage, that is, the right hemisphere for most adults(Tucker & Frederick, 1989).

The prosodic disturbances often seen are referredto as aprosodia —decits in the ability to both under-stand and produce prosodic features. Prosody is partof speech production. It includes the perceptualfeatures of pitch, loudness, and duration in speech. Acoustically, the speech signal is altered in frequency,intensity, and timing, respectively. These alterationscome together to provide the contour or intonation ofspeech that, in turn, signals meaning. The combina-tion of aprosodia and disturbed emotional expressionand interpretation is a part of the matrix of RHS.

Higher Cognitive Functions

Individuals with RHS exhibit impairment in attentionand integration. In fact, Myers (1999) postulates thatdifculties in attention and integration may be at theroot of many of the symptoms individuals with RHSmanifest.

The right hemisphere is dominant for arousalmechanisms that direct us to attend to importantstimuli in our environment. For example, the fron-tal eye elds (represented in Brodmann area 8 in thesuperior frontal lobe) are involved in orienting themovement of the eyes and head to the contralateralspace (Bhatnagar, 2008). Following right hemispheredamage, many individuals evidence problems withfocusing, sustaining, and shifting (i.e., alternating anddividing) attention. Because attention is a fundamen-tal cognitive process that supports other cognitiveand language tasks, the impact of decits here can beseen in issues of neglect, emotion, reading, writing,and pragmatics.

The diminished ability to pull together relevantdetails while ignoring irrelevant details to integrate




information and draw inferences is a distinguishingfeature of RHS. The impact of this lack of integra-tion on discourse abilities was noted in 1979 whenMyers described the discourse of individuals withright hemisphere damage as “. . . wend ing [italicsadded] their way through a maze of disassociateddetail, seemingly incapable of ltering out unnec-

essary information” (cited in Myers, 2005, p. 1147).She further described the communication decits ofindividuals with RHS, when they exist, as being irrel-evant and often peppered with excessive informationand literal responses to questions and events. Fur-ther research has determined that these individualsare able to make simple inferences, but difculty isseen with generating inference in less predictable andnovel situations.

Pragmatics refers to the social use of language andfollows conventional rules in a given society. Theserules include use of personal space, appropriate turntaking and eye contact, and maintaining topic andappropriate topic switching. Pragmatic problemsare not always present following right hemispheredamage (Lehman-Blake, Duffy, Myers, & Tompkins,2002). When they are, these individuals exhibit prob-lem behaviors such as decreased eye contact, givingup their conversational turn, inappropriately ter-minating conversations, and engaging in excessiveand ego-oriented speech (Kennedy, Strand, Burton,& Peterson, 1994; Prutting & Kirchner, 1987). None-theless, as Lehman-Blake et al. (2002), Kennedy et al.

(1994), and Brookshire (2003) remind us, pragmaticimpairments may or may not be present. Therefore,it is important to (1) understand the individual’s prag-matic style prior to injury and (2) undertake a carefulanalysis of pragmatic skills.

Traumatic Brain Injury

The decits seen following TBI are as widespread andvaried as the injury itself. Recall from a previous sec-tion that TBI is a result of a combination of focal anddiffuse damage to the brain due to some outside force.

The damage can be further complicated by the body’sreaction to the trauma (e.g., intracranial pressure) andother secondary factors (e.g., anoxia). Although focaleffects of TBI can result in the communication disor-ders of aphasia, dysarthria, and those associated withRHS, the focus here will be on the cognitive sequelaemost often noted with TBI. Alternatively, other pathol-ogies can result in similar cognitive symptomatologyas in TBI. These include meningitis, encephalitis, andanoxic events (e.g., near drowning or excessive bleed-ing). Attention, memory, and executive functions are

nearly always affected with associated problems inspeed of processing, reasoning, and problem solving. Although not focused on here, personality changesand behavioral symptoms (e.g., impulsivity) are alsocommon following TBI. Attention, memory, and exec-utive functions share neural systems and are espe-cially vulnerable to injury in TBI (Sohlberg & Mateer,

1989). These are the anterior frontal and temporalbrain regions mentioned earlier. Recall, however, thatthese areas connect to other brain regions via tracts.For example, connections between limbic systemstructures such as the cingulate gyrus and subcorticalsystems such as the thalamus have been implicatedin higher level attentional mechanisms (Mateer &Ojemann, 1983).

Medical recovery following TBI occurs in more of astepwise fashion as compared with vascular diseasesuch as stroke (Brookshire, 2003). Recovery follow-ing TBI has a predictable course, but time to movethrough stages of recovery varies and is dependent ona number of variables such as severity of injury andsecondary effects. A common scale utilized to makegross judgments of recovery level is the Rancho Los Amigos Levels of Cognitive Functioning Scale , tradi-tionally an eight-point descriptive scale (revised toinclude two advanced levels of recovery) to determinefunctional severity based on behavioral symptomsand to denote amount of assistance required to func-tion (Bushnik, 2000; see Table 5-4).

Why You Need to Know The best way to “treat” TBI is to prevent it from hap-pening or at least decrease the impact of injury. Oneway to do this is to put laws in place that requirethe use of protective equipment such as child safetyseats, seat belts, and compulsory helmet use formotorcycle and bicycle riders. Improving highwaysafety and imposing speed limits also prevents orlessens the impact of TBI. Special playground surfaces help as well. When a brain injury does occur,improved emergency technology and paramedic

skill along with swift medical response such ashelicopter transport work to lessen the effects of theinjury.

Attention , or the ability to concentrate, refers toone’s ability to scan, select out, and respond to rel-evant stimuli in the environment and maintain thisbehavior over time. Ability to focus, screen out dis-tractions, and sustain attention is foundational toother cognitive processes. For example, if you donot attend to new information in the classroom you




shift, planting a ower, or carrying out computer com-mand sequences without thinking. Priming refers tothe notion that previous exposure to information read-ies the brain to recall associated information.

Some types of memory are interdependent onexecutive functions, to be discussed in the next sec-tion. One is prospective memory or “remembering to

remember,” that is, remembering to carry out a task inthe future. The second type is called metamemory andcan be thought of as “memory about memory” or hav-ing knowledge and making judgments about one’s ownmemory abilities. This type of memory is called upon when learning new information as personal judg-ments are made regarding acquisition of knowledge.For example, this type of memory is used when study-ing for an exam. Another type of memory that requiresexecutive functions is working memory . Workingmemory takes information from the senses (e.g., audi-tory, visual) and relates that to stored semantic mem-ories that are retrieved for comparison purposes. Inaddition, working memory is involved in making judg-ments about the worthiness of encoding incomingsensory information to store long term. The locationof memory in the brain is widespread and dependenton specic type of memory. Table 5-6 lists areas of thebrain associated with various types of memory.

Executive functions allow us to put our thoughtsand desires into action. Consider the job of a goodcompany executive; that executive generates plansand actions to reach certain company goals. To do

that the executive delegates tasks and oversees, ormonitors and controls, progress toward goals, makingadjustments when necessary. Executive functioningcan be viewed as having an umbrella function over theother cognitive processes of attention, memory, andreasoning. Components of executive function includeanticipation and goal selection, organization andplanning, initiation, awareness and self- monitoring,and use of feedback to make adjustments to plans.

Dementia

Individuals suffering from dementia, of many types, willdemonstrate communication difculties grounded intheir cognitive decline. The various disease processesnoted earlier (e.g., Alzheimer’s, Pick’s disease, multi-infarct) result in dementia and the associated cogni-tive-communicative impairment. A popular scale forgrossly rating cognitive decline following dementia

diagnosis is the Global Deterioration Scale (Reisberg,Ferris, de Leon, & Crook, 1982); Table 5-7 presents thelevels for this scale.

The earliest symptoms of AD are changes in per-sonality (e.g., becoming defensive) and memory. Earlyimpairments are reected in a breakdown of episodicmemories and executive functioning especially at thelevel of working memory. Working memory requiressustained attention and is a component of executivefunctioning (Sohlberg & Mateer, 2001). Individuals withdementia have difculty holding on to what was justheard or seen to make these judgments and/or encode

information into long-term memories (Bayles, 2006).Santo Pietro and Ostuni (2003) present the char-

acteristics of communication loss across the stagesof Alzheimer’s type dementia in regard to memory,understanding, speech and language skills, and socialskills. The following is summarized from their work.

The communication decits during the earlystage of dementia are relatively mild and reect thememory problems already mentioned. Individualslose their orientation to time, their ability to retrieverecent memories, or their ability to use short-term

TABLE 5-6

NEUROANATOMICAL REGIONS ASSOCIATEDWITH MEMORY PROCESSES

Memory Process Neuroanatomy

Working memory Prefrontal cortex Declarative memory Neocortex and medial–

temporal/diencephalicbrain regions

Semantic memory All sensory associationcortices

Procedural memory Basal gangliaPriming Neocortex

TABLE 5-7

STAGES OF THE GLOBAL DETERIORATIONSCALE USED IN DESCRIBING COGNITIVEDECLINE IN INDIVIDUALS WITH DEMENTIA

Stage Label and Clinical Phase

1 No cognitive impairment; normal2 Very mild cognitive decline; forgetfulness

3 Mild cognitive decline; early confusional4 Moderate cognitive decline; late

confusional5 Moderately severe cognitive decline; early

dementia6 Severe cognitive decline; middle dementia7 Very severe cognitive decline; late

dementia

From Reisberg, B., Ferris, S., de Leon, M.J., & Crook, T. (1982). The global deterioration scale for assessment of primarydegenerative dementia. American Journal of Psychiatry, 139 ,1136–1139.




memory to hold on to a short list or a phone number.Conversation may seem abrupt or they may becomeargumentative. This may be due to decreased abilitiesto comprehend more complex or rapidly presentedinformation. They may lose their train of thought andhave difculties keeping up with conversation. Wordretrieval is affected, but at this stage, they are often

aware of errors and make attempts at self-correction.Communication during the middle stage is quiteaffected and difculties are immediately obvious.Orientation is impacted for both time and place;however, they still know who they are. Memory prob-lems become more apparent in conversation withmore egocentrism and less perspective taking, lessquestioning, less initiation, and rare self-correction. Auditory and reading comprehension is impactedalthough they retain the ability to read extra-linguisticcues (e.g., facial expressions). Individuals at this stagealso retain the mechanics of reading such as in oralreading and demonstrate the ability to comprehendat the single word or the short phrase level in a mean-ingful context (Bourgeios & Hopper, 2005).

Communication is devastated in the late stage of Alzheimer’s type dementia. All orientation is lost: per-son, place, and time. They cannot form new memo-ries nor even recognize family members. Awarenessof the rules of social engagement is lost as is a desireto communicate. In fact, at this stage, the patient maylose speech production and comprehension alto-gether and appear to be mute.

Primary progressive aphasia (PPA) is a subtype offrontotemporal dementia, labeled as such because ofthe areas of the brain that are degenerating. PPA dif-fers from the clinical picture seen with Alzheimer’sdementia, as it manifests itself in progressive declineof language abilities followed by a decline in cogni-tion. The term aphasia applies because the initiatingsymptoms are in language. It differs from aphasiaassociated with stroke or other focal lesions due to its(1) insidious onset; (2) focal affect on the language-dominant hemisphere; (3) progressive worsening ofsymptoms; and (4) ultimate cognitive involvement. In

addition to the progressive aphasia, progressive AOShas also been noted with certain individuals (Duffy,2005). AOS is a motor speech disorder that will be dis-cussed in the next section.

MOTOR SPEECH DISORDERS

A myriad of speech disorders are associated withlesions involving the motor centers and pathways ofthe central and peripheral nervous systems. Recallfrom Chapter 4 the many structures, tracts, and nerves

responsible for planning and executing motor actions.Centrally, these include the premotor cortex, theanterior insular cortex, the precentral gyrus, the cor-ticospinal and corticobulbar tracts, the basal ganglia,the cerebellum and associated tracts, the brainstem(i.e., cranial nerve motor nuclei), and the spinal cord(i.e., anterior horns). Peripherally, recall the motor

component of the cervical spinal nerves and the cra-nial nerves involved with motor execution. Theseare the trigeminal (V), facial (VII), glossopharyngeal(IX), vagus (X), spinal accessory (XI), and hypoglossal(XII). Any neuropathology that affects these systemshas the potential to result in a motor speech disorder;thus, stroke, tumor, degenerative disease, or TBI mayresult in a motor speech disorder.

Motor speech disorders are dened as “. . . speechdisorders resulting from neurologic impairmentsaffecting the motor planning, programming, neu-romuscular control, or execution of speech” (Duffy,2005, p. 6). There are two motor speech disorders: AOS and dysarthria. Duffy denes AOS as a “. . . motorspeech disorder characterized by a disturbance inmotor planning or programming of sequential move-ment for volitional speech production” (p. 5) anddysarthria as a “. . . speech disorder characterized bydisturbances in speech muscle control due to paralysis, paresis, weakness, slowness, incoordination,and/or altered muscle tone” (p. 5). These same motorproblems resulting in speech difculties are oftenalso manifested in other parts of the body. For exam-

ple, an individual with uncoordinated speech mayalso show uncoordinated body movements. Thus,individuals with these disorders look like they havemotor problems.

Apraxia of Speech

AOS is rarely found in isolation; rather, it is typicallyconcomitant with aphasia. This makes sense whenone thinks of the lesion sites associated with AOS.Lesions resulting in this motor speech disorder arealways in the language-dominant hemisphere but not

necessarily localized to one particular region. None-theless, AOS is most often seen following lesions tothe third frontal convolution, or Broca’s area, with theanterior insular cortex often implicated as well (Miller,2002). This is consistent with the speech descriptionof those with nonuent aphasia described earlier inthis chapter. Second, the supplementary motor areais important for planning and programming of voli-tional movements (Duffy, 2005). Other areas of lesionhave also been implicated in AOS such as subcorticallesions involving the basal ganglia or regions of the




parietal lobe including the somatosensory cortex andthe supramarginal gyrus (Square-Storer & Apeldoorn,1991). These areas are responsible for the integra-tion of sensory information, a prerequisite for skilledmotor activity (Duffy, 2005).

The process of motor planning and programmingcan be looked at as a sort of bridge between language

formulation and motor execution (Halpern, 2000). Aproblem in language formulation is aphasia; a problemin motor execution is dysarthria; a problem with thebridge is AOS. This bridge seems to require a “. . . trans-formation of the abstract phonemes to a neural codethat is compatible with the operations of the motorsystem” (Duffy, 2005, p. 309). This transformation isresponsible for “. . . connecting the inner language pro-cesses into the endless number of speech utterances”(Halpern, 2000, p. 218). A breakdown in this motor pro-cess results in interesting speech symptoms.

Individuals with AOS have speech output thatreects a concentrated effort to sequentially and voli-tionally produce phonemes for intelligible speech. Wertz, LaPointe, and Rosenbek (1984) describe thisspeech as consisting of “islands” of uent, intelligiblespeech interrupted by periods of effortful, off-targetgroping for the speech sounds. These islands of u-ent speech are usually automatic phrases that areproduced without thinking. For example, a client maybe struggling to say a target word when all of a sud-den he says “gosh, this is just so hard!” perfectly clear.However, when asked to repeat that utterance, he is

unable to do so without hesitation and effort.Speech output secondary to AOS can be describedin regard to articulatory disturbance and prosodic dis-turbance. Symptoms evident in articulation includeinconsistent trial and error responding, increased dif-culty with increased utterance length and complexity,and frequent speech sound substitutions. Symptomsresulting in the disrupted prosodic contours of speechinclude slow speech rate, hesitations, and difculty ini-tiating speech (known as articulatory groping ).

Dysarthria

Dysarthria is actually a syndrome or a collection ofmotor speech symptoms reective of the disturbedmotor system. Darley, Aronson, and Brown (1975)completed a seminal study and subsequently pub-lished a now classic text categorizing and describ-ing six types of dysarthria that are very specicallyrelated to site of lesion (a seventh type was described years later). It is important to note that it is the siteof lesion rather than the etiology of the lesion thatdetermines the type of dysarthria. For example, a

brainstem stroke, ALS, or an acoustic neuroma can allresult in symptoms associated with accid dysarthria.The original six types of dysarthria are accid, spas-tic, ataxic, hypokinetic, hyperkinetic, and mixed. Theseventh type, a relatively mild dysarthria, is namedfor its lesion site—unilateral upper motor neuron(UUMN) dysarthria. Unlike AOS, dysarthria reects

impairment in the ability to execute motor move-ment for speech production. Also unlike AOS, dysar-thria often affects all speech processes—respiration,phonation, resonation, articulation, and prosody— whereas AOS primarily impacts articulation andprosody. Speech characteristics associated with thedisrupted processes for dysarthria are highlighted inTable 5-8. Each of the subtypes of dysarthria, along with its correlated lesion site, is described next.

UUMN dysarthria results from lesions to the UMNsand is the mildest of the dysarthrias. More specically,the lesion involves disruption to the tracts carrying

TABLE 5-8

SPEECH SYMPTOMS COMMONLY ASSOCIATEDWITH THE DYSARTHRIA TYPES

Dysarthria Type Speech Symptoms

Unilateral upper Imprecise articulation motor neuronSpastic Strained-strangled phonation Hypernasal resonance Slow, imprecise articulationFlaccid Short breath groups Breathy phonation Reduced loudness Inhalatory stridor Hypernasal resonance Nasal air emission Imprecise articulation Ataxic Loudness and pitch variations Normal resonance Irregular articulatory

breakdownsHypokinetic Breathy phonation Reduced loudness Monotone vocal quality

Normal resonance Imprecise articulation Rapid speech rateHyperkinetic Intermittent strained phonation (dystonia) Phonatory arrests Normal resonation Intermittent, slow, articulatory

distortionsHyperkinetic Abrupt phonatory arrests (chorea) Normal resonation Intermittent, quick, articulatory

distortions




is responsible for coordinating movement through thecontrol of range, force, direction, and timing of move-ments. When this is disrupted, movements becomeuncoordinated and lack synergy. In fact, the resultingdysarthria is often described as “drunken speech.”This lack of coordination crosses all speech systems,especially impacting the prosodic features of speech.

Hypokinetic dysarthria is caused by damage to thebasal ganglia system, specically involving the sub-stantia nigra. This is the dysarthria associated withthe degenerative disorder of Parkinson’s disease (PD).The name refers to the decreased (hypo) movement(kinetic), or bradykinesia, seen in PD. Additional motorsymptoms include muscle rigidity, resting tremor,and difculty initiating movement. It is common tosee individuals with PD presenting with stooped pos-ture, decreased facial expression (i.e., masked facies),and a shufe in their walk (i.e., festinating gait). Mostspeech processes are affected with notable symptomsin phonation and articulation.

Hyperkinetic dysarthria is classied into two types ofdysarthria that are both a result of involuntary move-ments but named for the speed of these movements.Dysarthria associated with slow, writhing movementis called slow hyperkinetic dysarthria such as withdystonia. These uncontrolled movements slowly buildto a peak and are sustained before subsiding. Quickhyperkinetic dysarthria is associated with chorea.In contrast to dystonic movement patterns, choreicmovements are fast, only briey sustained if at all, and

unpredictable. Pathologies affecting the basal gangliaand associated circuitry in the cerebral hemispheresare responsible for hyperkinetic dysarthrias. Thesepathologies include congenital cerebral palsy of theathetoid type resulting in dystonia and degenerativeHuntington’s disease resulting in chorea. However,often times the pathology underlying these disruptivemovement disorders is unknown (Duffy, 2005).

Mixed dysarthrias, as the name implies, result froma combination of two or more of the above types. Thismost often occurs with degenerative disorders suchas amyotrophic lateral sclerosis (ALS) or multiple

sclerosis (MS) or when trauma affects multiple localesof the nervous system such as with traumatic braininjury (TBI) or multiple strokes. The speech systemsaffected will vary dependent on the combination ofdysarthria types.

Swallowing Disorders

Swallowing impairments are referred to as dys-phagia . Dysphagia has multiple etiologies; here, the

neural information to the brainstem and spinal cord.Symptoms of UUMN are seen contralateral to the siteof lesion and are manifested in lower facial weaknessand tongue weakness. For this reason, articulationis most often impacted. However, lesions to UMNsmay also result in damage to tracts that are importantfor posture, muscle tone, and reexes (Duffy, 2005).

Because of the site of lesion, these individuals oftenpresent with aphasia and/or AOS. In fact, interven-tions for those communication disorders are a prior-ity over a mild dysarthria.

Spastic dysarthria results when bilateral lesions tothe UMNs occur. Bilateral lesions result in signicantdysarthria and are also called pseudobulbar palsy .This is because the lesion occurs above the level ofthe brainstem (i.e., the bulbar region). These bilaterallesions result in lack of inhibitory neural informationreaching the cell bodies that give rise to the LMNs inthe brainstem and spinal cord. This, in turn, results inmuscle weakness, too much muscle tone (i.e., hyper-tonia ) with limited range of movement, and exagger-ated reexes. The pathology involved is often bilateralstrokes or TBI, but other etiologies (e.g., degenerativedisease) account for some cases.

Lesions affecting the LMNs result in accid dys-arthria . Recall that LMNs include motor neuron cellbodies (located in the brainstem or the spinal cord),the peripheral nerves (cranial nerves or spinal nerves),the neuromuscular junction, and, end with the musclebers innervated. Lesions occurring anywhere along

the LMN can result in accid dysarthria; thus, eti-ologies vary. These include, but are not limited to,brainstem stroke, TBI or other induced trauma (e.g.,surgeries), ALS, myasthenia gravis (a disorder of theneuromuscular junction), and muscular dystrophies.In contrast to spastic dysarthria, there is decreasedmuscle tone (i.e., hypotonia ), muscle weakness, andatrophy of the affected muscles. The extent and sever-ity of speech systems affected are contingent on siteof lesion. If a lesion occurs peripherally, closer to theinnervation of the targeted muscle, then the symp-toms will reect that interruption. For example, if

the recurrent laryngeal branch of the vagus nerve isdamaged during thoracic surgery, symptoms will bespecic to the phonatory system. Alternatively, symp-toms are more pervasive and severe when a lesionoccurs higher up (i.e., at or near the brainstem), thusimpacting multiple cranial nerves. In this case, allspeech systems will likely be affected.

Ataxic dysarthria results from damage to the cer-ebellum and/or the tracts associated with it. Degen-erative disease, stroke, TBI, and tumor are the mostcommon causes of lesion. Recall that the cerebellum




focus is on swallowing difculties due to acquiredneurologic disorders. It is appropriate that a discus-sion of dysphagia follows motor speech disorders,especially dysarthria, because these disorders oftenco-occur. This is due to the impact of the associatedpathology on the motor system and the resultantaffects on the muscles across the different stages

of the swallow. The pathologies resulting in neu-rogenic dysphagia are similar to those mentionedearlier and include stroke, TBI, tumors, and degen-erative diseases (Corbin-Lewis, Liss, & Sciortino,2005). Unlike the dysarthrias, a clear correlationbetween lesion site and expected symptoms doesnot exist for neurogenic dysphagia. Instead, theswallowing impairment is described based on thedisrupted stage(s) of the swallow (these stages weredescribed in Chapter 4).

Lesions resulting in decreased or disorderedmovement of the facial, labial, and lingual muscula-ture results in oral preparatory and oral stage impair-ments. Lesions involving the LMNs of the facial,trigeminal, and hypoglossal cranial nerves will obvi-ously result in problems at these stages of swallow.However, lesions to higher cortical centers, such asthe UMNs, the cerebellum and its tracts, or the basalganglia and their tracts, can also result in problemsin these stages. Pathologies associated with theselesions are consistent with that already mentioned.Notable symptoms include drooling, reduced mas-tication and bolus formation, pocketing of food, and

difculty propelling the bolus posteriorly to initiatethe swallow. Oral transit delay can result in food anddrink passing inadvertently into the hypopharynx,entering the laryngeal vestibule, and possibly pen-etrating the vocal folds (see Chapter 8) with resultantaspiration. Aspiration is dened as food, drink, orsaliva that enters the airway (i.e., trachea) below thelevel of the true vocal folds.

The pharyngeal stage is highly automatized andrequires rapid integration of multiple movementsfor a safe swallow to occur. The velum elevates toclose the nasopharyngeal port at the same time as

the larynx moves up and forward and the epiglot-tis moves down and back. A lesion impacting themovements required for this stage of the swallowis of priority concern as the result can be aspira-tion. Pathologies affecting this stage are those thatresult in large, multiple, or diffuse nervous systemlesions such as multiple strokes, TBI, and degen-erative diseases (Corbin-Lewis et al., 2005). Symp-toms associated with problems in this stage includea delayed trigger of the swallow reflex and food anddrink getting hung up (called residue ) in the val-

leculae and pyriform sinuses. The individual withproblems in this stage will often cough or chokeor, more seriously, not feel anything penetrate theairway. When the later happens, it is referred to assilent aspiration .

The esophageal stage of the swallow requires intactfunction of the upper esophageal sphincter to allow

the bolus to enter and proper motility of the skeletaland smooth muscle of the esophagus to propel foodto the stomach. Problems with this stage are primar-ily under the purview of the gastroenterologist. Textsdevoted to swallowing disorders review the variousdisorders that inuence esophageal function (e.g.,Corbin-Lewis et al., 2005; Crary & Groher, 2003; Loge-mann, 1998).

Dysphagia can also be the result of limited cogni-tion due to neuropathology. Swallowing concerns areespecially prevalent in the later stages of dementia. Although these individuals may have adequate func-tion across stages of the swallow, their cognitive de-cits impact remembering to chew and rememberingto swallow! This can even be a problem earlier in thecourse of the disease, as they may not even remem-ber to eat. All of this can result in malnutrition anddehydration for the individual which, in turn, impactscognitive functioning as evidenced by increased con-fusion and lethargy.

A stagnate bolus of food in the oral cavity impactsa safe swallow. If chewing is not adequate, a bolus toolarge for safe passage into the esophagus may enter

the airway and result in aspiration and/or penetra-tion—an episode of choking. Likewise, holding a mas-ticated bolus in the oral cavity for a prolonged periodof time increases the risk of aspiration or penetra-tion as well. Imagine someone laying down for theirafternoon nap following lunch or a snack. As you canimagine, mealtime assistance with reminders to chewand swallow as well as follow-up oral hygiene is abso-lutely critical for these individuals.

Individuals with end-stage dementia pose uniquechallenges in regard to dysphagia management. At this stage, individuals may refuse food by turn-

ing away, gagging, or spitting food out. The choiceto provide nutrition and hydration support throughtube feeding or going with a palliative care approachneeds to be decided upon. At this time, the speech–language pathologist serves an important role ineducating staff and family regarding options and out-comes. Although it may sound unkind to withholdnutritional support, persons with advanced demen-tia on tube feedings have been found to not fare anybetter than those without tube feedings in regard toaspiration risk (Finucane, Christmas, & Travis, 1999).




Alternatively, palliative care refers to providing foodand/or drink that are accepted by the individual suchas using ice chips on the lips for comfort.

Summary

This chapter presented the many communication dis-orders that result from neurologic disturbance. Theneuropathologies that can result in communicationbreakdowns are also many and varied including car-diovascular incidents, trauma, and disease. The resul-tant communication disorders can be in language(e.g., aphasia), cognition (e.g., disorders secondary toright hemisphere damage, TBI, or dementia), speech(e.g., AOS, dysarthria), or any combination. Key to thisdiscussion of the various neurogenic communicationdisorders is understanding the neurological substrates

associated with the various disorders. Referring back toChapter 4 of this part will greatly assist you in connect-ing neuropathology to neuroanatomy and physiology.Conversely, understanding various neurological disor-ders assists in meaningful application of the detailedinformation presented in Chapter 4.

Clinical Teaser—Follow-Up

At the beginning of this part, you were asked to note any terms or concepts in the case study that were unfamiliar to you. As you read Chapter 4, you were to pay particularattention to the anatomy and physiology pertinent to thiscase. Now we return to the case for fur ther discussion.

Following the format of Chapter 5, we can interpret this case regarding etiology, neuropathology, and result-ing communication disorder(s). Sisi suffered an ischemicstroke affecting the frontal branch of the middle cerebralartery. Based on site of lesion and symptoms, brain areasdamaged included the left precentral gyrus (Brodmannarea 4), the third frontal convolution (Brodmann areas44, 45), and the anterior insular cortex. The lesion mayhave extended into subcortical white matter as well. In-formation from the speech–language evaluation leads to

the conclusion that Sisi evidences unilateral upper motorneuron dysarthria and nonuent aphasia. More informa-

tion is required to determine if apraxia of speech (AOS) is

present. What information from Chapters 4 and 5 assistedyou in drawing these conclusions? What information doyou need to (1) further classify this aphasia as a particu-lar syndrome and (2) determine if AOS is present? Lastly,would you expect swallowing ability to be affected and ifso, which stage(s)?



PART 2 SUMMARYPart 2 (Chapters 4 and 5) presented information critical to understand the basic func-tions of the nervous system and what can go wrong with it to result in a communica-tion disorder. The understanding of the nervous system and its pathologies preparesthe reader for the subsequent chapters of this book. The brain is the overseer of body

function via the conversion of thought to action and sensation to integration in gen-eral and for speech production specically. Thus, muscles of the speech and swal-lowing mechanism—respiratory, phonatory, resonatory, and articulatory—all receiveinnervation via spinal and cranial nerves which, in turn, receive neural commandsfrom higher cortical centers and pathways. Also, sensory receptors send neural infor-mation, via spinal and cranial nerves, to the central nervous system. This sensory feed-back includes auditory information and both conscious and unconscious informationregarding muscle position. Thus, it can be appreciated that the nervous system allowsfor a continuous feed forward and feedback mechanism for speech and swallowingthrough messages sent to muscle for movement and messages received at the brainfor thought and response. Damage can occur to the nervous system in a number of ways: by disease or by injury such as stroke or traumatic brain injury. This damagemay, in turn, result in disorders of communication. The communication disorder isa result of where damage occurs in the nervous system and can take the form of anacquired language disorder (e.g., aphasia), a motor speech disorder (e.g., dysarthria orapraxia of speech), or a cognitive-communicative disorder. There are different typesof aphasia (e.g., Broca’s aphasia) and different types of dysarthria (e.g., accid dysar-thria) depending on lesion site. There are also different manifestations of cognitive-communication disorders which are variably described based on lesion site (e.g., righthemisphere damage), type of injury (e.g., traumatic brain injury) or disease (e.g.,dementia). This part concludes with a brief description of the impact of neurologicaldamage on swallowing function across the stages of the swallow as well as the impactdementia has on eating and swallowing.

PART 2 REVIEW QUESTIONS 1. Describe the components of the fully developed central nervous system using

neurodevelopmental (i.e., “-encephalon”) terminology. 2. Name two gyri and sulci associated with each of the four lobes of the cerebrum:

frontal, parietal, temporal, and occipital. 3. Describe the ow of cerebrospinal uid beginning with the lateral ventricles and

ending with the dural sinuses. 4. How do glial cells differ from neurons? Name four types of glial cells and de-

scribe each one’s function. 5. List the steps for an action potential beginning with a stimulus to the presynap-

tic neuron, resulting in depolarization. 6. Dene IPSP and EPSP. What is the difference between the two? 7. What communication disorder is most likely to result from a lesion to the follow-

ing areas of the central nervous system: brainstem, Brodmann area 22, hip-pocampus, orbital gyri, and cerebellum?

8. What communication disorder is most likely to result from the following medicaletiologies: right hemisphere stroke; left hemisphere stroke; amyotrophic lateralsclerosis, Alzheimer’s dementia; Parkinson’s disease; and encephalitis?

106



Anatomy,Physiology, andPathology ofthe Respiratory System

PART 3



PART 3CHAPTER 6

Anatomy and Physiologyof the Respiratory System


brachial pertaining to the arm and shoulder brachial nerve

cardiac pertaining to the heart cardiac impression

chondro- pertaining to cartilage chondro -osseous juncture

-clavius pertaining to the clavicle sub clavius

-cleido- pertaining to the clavicle sterno cleido mastoid

costal pertaining to the ribs costal pleura

costarum pertaining to the ribs levator costarum brevis

crico- pertaining to the cricoid cartilage crico tracheal ligament

dorsi pertaining to the back latissimus dorsi

glottic pertaining to the glottis, the variable-sized sub glottic pressure opening between the vocal folds

ilio- pertaining to the ilium lateral ilio costalis

inter- between inter vertebral disc

intra- within or inside of intra tracheal membrane

lumbo- pertaining to the lumbar region of the vertebral column quadratus lumbo rum

111



processes (III-B)

Learning Objectives• You will be able to describe the framework that supports the respiratory system.• You will be able to describe the lungs and their linkage to the thoracic cavity.• You will be able to discuss the muscles that mediate inspiration and expiration.• You will be able to dene the basic concepts involved in respiration, including but not limited

to airow, Boyle’s law, elastic recoil, gravity, pressure, torque, and volume.• You will be able to explain the mechanics of quiet, vegetative breathing.• You will be able to discuss the differences in respiratory mechanics between quiet, vegetative

breathing and breathing to support vocal activity.



112 PART 3 ANATOMY, PHYSIOLOGY, AND PATHOLOGY OF THE RESPIRATORY SYSTEM


odontoid shaped like a tooth odontoid process

osseo- pertaining to bone chondro- osseo us juncture

parietal pertaining to the wall of a cavity parietal pleura

pectoral pertaining to the chest pectoral is major

pelvic pertaining to the pelvis pelvic girdleperi- around or surrounding peri cardium

phrenic pertaining to the diaphragm phrenic nerve

pulmo- pertaining to the lungs alveoli pulmo ni

sacral pertaining to the sacrum sacral foramina

serratus having a sawtooth or jagged appearance serratus anterior

spiro- pertaining to the process of breathing spiro meter

sterno- pertaining to the sternum sterno cleidomastoid

sub- below or inferior to sub clavius

tracheal pertaining to the trachea intra tracheal membrane vertebro- pertaining to the vertebral or spinal column vertebro sternal

Clinical Teaser

Richard is a 35-year-old teacher who comes to your speechand language clinic complaining of an inability to producea strong, clear voice. It seems that every time he attempts

to speak, he just does not seem to have enough breath tospeak in a clear voice for any more than a few seconds at a

time. He suspects he has asthma, but denies that there is afamily history of the disorder. Richard claims to be healthyotherwise. When you ask him, he admits that he has beensmoking for approximately 10 years—perhaps, a pack toa pack and a half each day. He also relates to you that hiscondition seems to be worse after his three-times-weeklyexercises. Finally, through further inquiry, you learn thatRichard has had chronic gastroesophageal reux disease forwell over 15 years. You note that he presents a pronouncedstridor upon inhalation. Being well versed in the anatomy and physiology of therespiratory system, you suspect that a number of thingscould be causing the problem. Immediately coming to mind

are asthma, emphysema, neuropathology, and paradoxicalvocal fold movement (PVFM) disorder. You suggest to yourclient that he get a complete medical work up from hispersonal physician. Your client does indeed follow up with your suggestion.His primary care physician conducts a general health check-up. All medical signs do not appear to support a diagnosisof asthma. Because of Richard’s history of cigarette smoking,

the doctor suspects that perhaps he is in the initial stages ofemphysema. The doctor refers the patient to a pulmonaryspecialist for further evaluation. The pulmonary specialist conducts a thorough assess-ment of Richard, including respiratory measures (e.g.,vital capacity [VC], ow-volume loop testing) and endos-copy. An endoscopic examination reveals no subglottic

inammation typically seen in asthma patients. In fact, all testing seems to reveal normal structure and function of the respiratory system. Not able to provide a denitivediagnosis, the pulmonary specialist refers Richard to anotolaryngologist. Taking into consideration the information that has beenobtained to this point, the otolaryngologist has Richard en-gage in vigorous exercise for 20 minutes before conductingan endoscopic examination. The doctor notices right away

that Richard’s stridor is more pronounced. The doctor be-gins the endoscopic exam, which immediately reveals an ab-normal adduction of the vocal folds during inhalation with asmall posterior, triangular glottal chink. Further testing sup-ports a diagnosis of PVFM disorder. Note any terms or concepts in the foregoing case study

that are unfamiliar to you. As you read the rst chapter of this part, pay particular attention to the anatomy and physi-ology pertinent to this case, then try to relate that informa-

tion to the discussion of respiratory pathologies presentedin Chapter 7.



CHAPTER 6 ANATOMY AND PHYSIOLOGY OF THE RESPIRATORY SYSTEM 113

sounds such as consonants and vowels. The net resultof these activities is speech production.

The remainder of this chapter will be devoted toa thorough discussion of the anatomy and physiol-ogy of the respiratory system. It is expected that uponreading this chapter, you will be well versed in thestructure and mechanics of respiration.

Anatomy of theRespiratory System

In describing the anatomy of the respiratory system, itmay be helpful to use the analogy of building a house.First, a foundation is laid and the house’s frameworkis erected. Once the framework is in place, electriciansand plumbers will install the electrical and plumbingsystems. Then, carpenters will ll the wall, oor, andceiling spaces with insulation. Finally, the inner andouter walls of the house will be constructed. In manyinstances, the builder may install appliances prior tocompletion of the house.

Take the framework rst. In anatomy, the framework is the skeletal system. The skeletal system iscomposed of bones, cartilages, and connective tissuesuch as membranes, ligaments, and tendons. Nervesand blood vessels can be viewed as the electrical andplumbing systems. The house’s insulation correspondsto muscles; that is, muscles are an integral part of theskeletal system in much the same way that insulation

is an integral part of the house’s framework. Finally, themucous membranes that cover the muscles, nerves,and blood vessels are analogous to the walls of thehouse. Any organs that may be part of a particular sys-tem (e.g., the lungs as part of the respiratory system)can be thought of as the house’s appliances.

Keeping this analogy in mind, the anatomy of therespiratory system will be presented in a logical order.First, the framework will be discussed (i.e., bones, car-tilages, membranes, ligaments, and tendons). Then,muscles that are an important component of the sys-tem will be presented. Following the muscles, mucousmembranes and organs will be described in detail.Finally, a brief discussion will be provided about theneural underpinnings of the respiratory system (struc-tures of the circulatory system will not be discussed).

THE FRAMEWORK FOR THERESPIRATORY SYSTEM

The framework of the respiratory system includesve structures: the vertebral (or spinal) column, therib cage, the pectoral girdle, the pelvic girdle, and

Introduction

Now that you have a basic understanding of the ner-vous system—the battery that drives the entire speechand hearing mechanisms—it is time to take a closerlook at the three systems that comprise the humanvocal mechanism. These three are the respiratory,phonatory, and articulatory/resonance systems. Theanatomy and physiology of the phonatory system willbe discussed in Chapter 8, and the articulatory/reso-nance system will be presented in Chapter 10. Yourattention is turned toward the respiratory system inthis chapter.

As discussed in Chapter 4, the nervous system canbe envisioned as the apparatus that overrides the entirevocal mechanism. In other words, each of the threesystems that comprises the vocal mechanism is able tofunction and contribute to the process of speech pro-duction because of the inuence of the nervous system(see Figure 6-1). The greatest contribution the nervoussystem makes to the vocal mechanism is through theinnervation of voluntary muscles that comprise eachof the systems of speech production. However, the ner-vous system may also inuence the vocal mechanismthrough the autonomic nervous system.

The respiratory system can be thought of as thepower source for speech production. It is throughour expired air that energy is created to cause pho-nation of the vocal folds, thereby producing a com-plex tone that is further modied as it passes through

the vocal tract. In other words, the respiratory sys-tem provides input to the phonatory system by wayof expired air from the lungs. In turn, the phonatorysystem is responsible for producing the vocal tone(this will be discussed at length in Chapter 8), which isthen modied through the processes of articulation and resonance (see Chapter 10) to produce speech

Figure 6-1 A schematic overview of the speech productionmechanism.

Nervous System

Respiratorysystem

Articulatory/ resonance

system

Phonatorysystem

Speechproduction




the trachea and bronchial tree. These ve structures will be examined more closely in the paragraphs thatfollow.

The Vertebral (Spinal) Column

The vertebral—or spinal—column makes up the axisof the human body (see Figure 6-2). It is composedof 32 or 33 individual bones stacked upon each other

vertically. An individual bone is referred to as a ver-tebra. In the upper regions of the vertebral column(i.e., the cervical, thoracic, and lumbar regions), thevertebrae for the most part do not actually make con-tact as they are stacked upon each other; instead, car-tilaginous discs (called intervertebral discs ) residebetween adjacent vertebrae throughout most of thelength of the vertebral column. These discs are non-existent in the fused vertebral structures known as thesacrum and coccyx, which are the lowermost regionsof the vertebral column.

Figure 6-3 shows the landmarks of a typical ver-tebra. Anteriorly, a vertebra has a corpus or body.Proceeding posteriorly from the corpus are two legsor pedicles. The two pedicles are joined together bylaminae that form the neural arch . The pedicles andneural arch create an inner chamber immediatelyposterior to the corpus. This chamber is called the

vertebral foramen. When the majority of vertebraeare stacked vertically, this foramen becomes a pas-sageway from the base of the skull to the lower back.The spinal cord resides within this passageway. At the juncture where each pedicle meets a lamina, a somewhat laterally directed process emerges, one on theright-hand side and one on the left. These are calledtransverse processes . Finally, proceeding posteriorlyfrom the point where the two lamina meet is anotherprocess called the spinous process . When one runsa nger down the center of their back, they will feelbumps along its length. These are the spinous pro-

cesses. The vertebrae are bound together by a seriesof anterior and posterior longitudinal ligaments, as well as several accessory ligaments, thereby formingthe vertebral column.

In a typical adult, the vertebral column is approxi-mately 72 to 75 cm in length. It is divided into regionsand the individual vertebrae are coded accordingto their sequence in any given region. Proceedingat the base of the skull and moving toward the tail-bone, these regions are the cervical, thoracic, lumbar,sacral, and coccygeal regions.

2

3

4

5

2

3

4

5

6

7

8

9

10

122

23

4567

1

2

3

4

5

1

2

3

4

5

67

8

9

10

11

12

1234567 C7

C5C4

C1C2C3

C6

T1T2

T3T4

T5T6

T7T8T9

T10

T11

T12

L1

L2

L3

L4

L5

Cervicalregion

Thoracicregion

Lumbarregion

Sacralregion

(five fusedvertebrae)

Coccygealregion (threeor four fused

vertebrae)A BFigure 6-2 The human vertebral column with individual verte-brae numbered. A . Anterior view. B . Lateral view. (Reprintedwith permission from Cohen, B.J., Taylor, J.J. (2009). Memmler’s

the human body in health and disease (11th ed.). Baltimore,MD: Wolters Kluwer Health.)

Lamina

Pedicle

Vertebralforamen

Spinous process

Transverseprocess

Corpus (body)

Figure 6-3 Landmarks on a typical human vertebra (superiorview). (Reprinted with permission from Cohen, B.J., Taylor, J.J.(2009). Memmler’s the human body in health and disease (11th ed.).Baltimore, MD: Wolters Kluwer Health.)




The cervical region is found in the neck. It consists ofseven vertebrae coded C1 through C7. C1 and C2 alsohave names. C1 is known as the atlas because it artic-ulates with the skull. Similar to the mythological char-acter of the same name, the atlas can be envisioned asholding the weight of the world (i.e., the skull) on itsshoulders. C2 is also referred to as the axis because ofits articulation with C1. The axis has a special processknown as the dens or odontoid process , upon whichthe atlas rests and rotates (see Figure 6-4). This actionallows us to turn our head from side to side. In addi-tion to the landmarks mentioned earlier for a typical

vertebra, the cervical vertebrae have a distinguishingcharacteristic. On the proximal end of the transverseprocesses are small holes called transverse foram-ina (C7 may or may not have these). The purpose ofthese foramina is to provide a passageway for somenerves and blood vessels as they pass through theneck region. Incidentally, an interesting fact aboutcervical vertebrae is that most mammals have thesame number. This means that a giraffe and a humanhave the same number of cervical vertebrae, althoughobviously the giraffe’s are much larger (as much as 8½inches in length!).

The thoracic region of the vertebral column con-sists of 12 vertebrae coded T1 through T12. As oneproceeds from T1 to T12, the individual vertebraebecome larger. In addition to the typical landmarks,the thoracic vertebrae are unique in that they housethe articular facets for the ribs. These facets can befound along the posterolateral aspects of the corpusand the transverse processes.

The lumbar region consists of ve vertebrae that arevery large in size by comparison to the other vertebrae.The large size is necessary to support the individual’s

weight. The lumbar vertebrae are coded L1 throughL5. Other than their large size, the lumbar vertebraehave no uniquely distinguishing landmarks.

The sacral and coccygeal regions consist of a num-ber of fused vertebrae. The sacrum is composed ofve vertebrae whose discs have ossied. The overallshape of the sacrum is somewhat like a wedge. The

sacrum contains four pairs of sacral foramina . Theseallow nerves and blood vessels to pass from the pel-vic region into the lower extremities. The coccyx is theterminal region of the vertebral column and consistsof three or four fused vertebrae. Collectively, the coc-cygeal vertebrae resemble a rattlesnake’s rattle.

The Rib Cage and Sternum

The primary organs of respiration are the lungs. Thetwo lungs are housed within the rib cage, also referred toas the thoracic cavity. The rib cage is composed of 12pairs of ribs arranged vertically (see Figure 6-5). Theuppermost ribs and the lowermost ribs are somewhatsmaller than the ribs in the middle of the rib cage.This gives the rib cage a barrel-like appearance. Anat-omists refer to the individual ribs by number along with a letter “R” to indicate “rib.” For example, therst pair of ribs is labeled R1 and the last pair of ribsis labeled R12.

Figure 6-6 is an illustration of a typical rib. The keylandmarks of a typical rib are the shaft (the length ofthe rib), neck and head (the posterior terminal end of

the rib that articulates with thoracic vertebrae), andcostal groove (a depression running along the lengthof the shaft on the undersurface of the rib, whereblood vessels and nerves are housed). Finally, the cos-tal angle (also known as the “angle of the rib”) is theabrupt change in curvature of the rib as it is bent intwo directions, causing it to appear twisted upon itsaxis.

Posteriorly, all 12 pairs of ribs articulate with thevertebral column. One would think that because thereare 12 pairs of ribs and likewise 12 thoracic vertebrae,each rib would articulate with its corresponding ver-

tebra. However, the articulations are not that simple.Table 6-1 summarizes the articulations of the ribs withthe thoracic vertebrae. The posterior articulations arebetween the head of the ribs and the corpora (the plu-ral of corpus) of the thoracic vertebrae, and betweenthe neck of the ribs and the transverse processes ofthe thoracic vertebrae (with the exception of R11 andR12, which do not articulate with the transverse pro-cesses). The head of each rib is held in place by thearticular capsule, radiate ligament, and interarticularligament. The neck of each rib is held in place by the

Foramen for densFacet for dens

Dens or odontoidprocess

Atlas (C1)

Axis (C2)

Posterosuperior view

Figure 6-4 Articulation of the atlas (C1) with the axis (C2).(Reprinted with permission from Anatomical Chart Company.)




articular capsule, anterior costotransverse ligament,posterior costotransverse ligament, ligament of theneck of the rib, and ligament of the tubercle of the rib.The joints formed by these articulations are arthrodialor slightly gliding joints. Because of this arrangement,the lateral rib cage can rotate upward and outward or

downward and inward, somewhat analogous to rais-ing and lowering the handle on a water bucket. Thisincreases and decreases the transverse volume of thethorax.

Unlike their posterior attachments, not all of the ribshave an anterior articulation. R1 through R10 articu-late anteriorly with the sternum , more commonlyknown as the breastbone (see Figure 6-7). The ster-num is an elongated bone that has three parts. From

A B

R1

R2

R3

R4

R5

R6

R7

R8

R9

R10

R11

R12 Thoracicvertebrae Thoracic

vertebrae

Chondro-osseus juncture

Sternum

R12

R11 R10

R9

R8

R7

R6

R5

R4

R3

R2

R1

Figure 6-5 The human rib cage. A . Anterior view. B . Posterior view. (Reprinted with permission from LifeART imagecopyright © 2010. Lippincott Williams & Wilkins. All rights reserved.)

HeadNeck

Articularfacets

Site ofarticulationwith costalcartilage Costal

groove

Costalangle

Shaft

Figure 6-6 Landmarks on a typical human rib. (Reprinted withpermission from Tank, P.W., Gest, T.R. (2008). Lippincott Williams& Wilkins atlas of anatomy. Baltimore, MD: Lippincott Williams &Wilkins.)

TABLE 6-1

ARTICULATIONS OF THE RIBS WITH THETHORACIC VERTEBRAE

Articulates with And the TransverseRib Number the Corpus of Process of

1 T1 T1 2 T1 and T2 T2 3 T2 and T3 T3 4 T3 and T4 T4 5 T4 and T5 T5 6 T5 and T6 T6 7 T6 and T7 T7 8 T7 and T8 T8 9 T8 and T9 T9 10 T10 T10 11 T11 (None) 12 T12 (None)




superior to inferior, these parts are the manubrium,corpus, and xiphoid (or ensiform) process. Landmarkson the manubrium include the suprasternal (or jugu-lar) notch and the clavicular notches. The supraster-nal notch is on the superior surface of the manubriumand can be felt by pressing down on the bone at themidline base of the neck. The clavicular notches areon the superior-lateral surfaces of the manubrium andare the point of articulation of the sternum with theclavicles (or collarbones). The corpus of the sternumis the anterior point of articulation for most of the ribs,as described more fully later. The xiphoid process does

not have a direct articulation with any of the ribs. It is adelicate structure that should never be depressed dur-ing articial resuscitation.

The ribs themselves do not actually come in contact with the sternum; rather, the articulations between ribsand sternum are accomplished by a series of cartilagesthat extend from the anterior terminals of the ribs.R1 through R7 have direct articulations with the sternum,that is, each rib has its own cartilage that makes contact with the sternum. Because of this, R1 through R7 are

referred to as vertebrosternal (or “true”) ribs becausethey have direct articulations with the vertebral columnand the sternum. R8 through R10 also have articulations with the sternum, but these attachments are more indi-rect. The cartilages for these ribs merge and join withthe cartilage of R7 before making a single articulation with the sternum. Because of this, R8 through R10 arereferred to as vertebrochondral or “false” ribs. Finally,R11 and R12 do not have an anterior attachment at all.Because their only articulation is with the vertebral col-umn, they are referred to as vertebral or “oating” ribs.In terms of the specic location of the articulations forR1 through R10, R1 articulates with the lateral surfaceof the manubrium immediately inferior to the clavicularnotch. R2’s articulation is at the juncture between themanubrium and corpus of the sternum. Finally, theremaining ribs articulate with the sternum along the lat-eral edge of its corpus. All costal articulations with thesternum are held in place by a series of radiate sterno-costal ligaments.

Two types of joints are formed by the articula-tions of the ribs with the sternum. The joint formedby the articulation of R1 with the manubrium is a

synchondrosis, which means that the joint ossies with age. The joints formed between R2 through R10and the sternum are synovial, which allow a varietyof movements. Considering the synovial action of theribs’ anterior articulations, the anterior rib cage canmove upward and outward or downward and inward,similarly to raising and lowering the handle on an old water well pump. This action creates slight increasesand decreases in the anteroposterior dimension ofthe thorax. It should be noted that this anterior actionoccurs simultaneously with the action of the lateralrib cage by virtue of the ribs’ posterior articulations

with the vertebral column.

The Pectoral Girdle

The pectoral girdle refers to the bony structure in thechest region that provides support for the upper extrem-ities (see Figure 6-8). Two bones comprise the pectoralgirdle: the clavicle and the scapula . The clavicle wasmentioned briey earlier. It is also known as the col-larbone. There are two clavicles: each one articulatesmedially with the manubrium of the sternum at the

Suprasternal notch

Clavicular notch

Sternal angle

Corpus (body)

Xiphoid process

Figure 6-7 Landmarks on a human sternum. (Reprinted withpermission from Agur, A.M., Dalley, A.F. (2008). Grant’s atlas ofanatomy (12th ed.). Baltimore, MD: Lippincott Williams & Wilkins.)

Why You Need to Know If pressure is placed directly upon the bony xiphoidprocess, it can break off of the body of the sternum.Being somewhat spearheaded in shape, the xiphoidprocess could be driven into the liver, resulting in arupture of this vital organ that may prove fatal.




clavicular notch. The lateral articulation of the clavicleis with the scapula (or shoulder blade), more speci-cally at the acromion which is its most lateral point.Therefore, each clavicle runs horizontally along theshoulder from the sternum to the scapula. The twoscapulae are somewhat triangular in shape and liedorsal to the upper seven or eight ribs. The scapulaeare literally suspended in place by their articulations with the clavicles. Besides the acromion, each scapula

has another important landmark—the glenoid fossa .The glenoid fossa is a crater-like depression in whichthe head of the humerus (the upper bone of the arm)rests. Being inquisitive, you no doubt wonder what thepectoral girdle has to do with respiration. The answeris that several muscles that play a part in respirationhave their origin somewhere on the pectoral girdle.The same is true of the pelvic girdle.

The Pelvic Girdle

The pelvic girdle (see Figure 6-9) is to the lower extrem-

ities as the pectoral girdle is to the upper extremities.It consists of a pair of coxal bones. Each coxal bonehas three parts: the ilium , the ischium , and the pubis .The pubis from each coxal bone merges anteriorly atthe pubic symphysis . This joint is generally immov-able but will “soften” in females during late pregnancyto allow the baby’s head to pass through. The sacrumof the vertebral column articulates with the iliumposteriorly, forming the sacroiliac joint. The sacrumand coccyx together with the coxal bones is referredto as the bony pelvis. The acetabulum , a crater-like

depression along the lateral aspect of the ischium, isthe point of articulation with the femur—the large,upper leg bone. Finally, running obliquely from theanterior superior iliac spine to the pubic symphysison either side are the inguinal ligaments . These liga-ments separate the contents of the lower abdomenfrom the lower extremities.

The Trachea and Bronchial Tree

The trachea (or windpipe) is a singular tube composedof a series of vertically arranged rings of cartilage thatextends from the level of C6 to T5 (see Figure 6-10).

Scapula

Clavicle

Anterior view Posterior view

Articulation withthe manubrium ofthe sternum

AcromionprocessGlenoid

fossa

Figure 6-8 The pectoral girdle showing the articulation of the clavicle with the scapula. (Reprinted withpermission from Tank, P.W., Gest, T.R. (2008). Lippincott Williams & Wilkins atlas of anatomy. Baltimore, MD:Lippincott Williams & Wilkins.)

Sacrum

Iliac crest

Ilium

Pubis

Ischium

Pubic symphysis

AcetabulumCoxalbones

Coccyx

Figure 6-9 The pelvic girdle showing the spatial relationshipsof the coxal bones, sacrum, and coccyx. (Reprinted withpermission from Tank, P.W., Gest, T.R. (2008). Lippincott Williams& Wilkins atlas of anatomy. Baltimore, MD: Lippincott Williams& Wilkins.)




Its superior articulation is with the cricoid cartilage, which is the base of the larynx. This articulation isheld together by the cricotracheal ligament . To artic-ulate with the cricoid cartilage, the rst tracheal ringmust be large by comparison with the other tracheal

rings. At its inferior terminal, the trachea bifurcatesat the carina , forming two main stem bronchi—onebronchus proceeds to the left lung while the otherproceeds to the right.

In all, the trachea is composed of approximately 16to 20 horseshoe-shaped rings of hyaline cartilage. Therings are incomplete posteriorly; this posterior regionis lled by brous tissue and smooth muscle bers.The esophagus runs immediately behind and paral-lel to the trachea. The cartilaginous rings do not actu-ally touch each other, as they are stacked vertically. Asmall space exists between adjacent rings. The spaces

are lled with a broelastic membrane called theintratracheal membrane . This membrane is actuallydouble layered. At each ring, the two layers separate.One layer covers the interior of the trachea, while theother covers the outside. Between the rings, the twolayers come together to form a single unit. Supercialto the inner layer of the intratracheal membrane (i.e.,inside the trachea) is a mucous membrane consistingof pseudostratied ciliated, columnar epithelial cells.Goblet cells are also located here; their purpose is tosecrete mucous. The cilia within the mucous mem-

brane continuously push the mucous (and any for-eign material it may trap) upward toward the larynx.Finally, phagocytic cells assist by ingesting bacteriaand other undesirable organisms to prevent infec-tion. With the cartilaginous rings and intratrachealmembrane taken together, the net result is a tube thatis approximately 11 to 12 cm in length and 2 to 2½ cm

in diameter.

Trachea

Larynx

Hyoid bone

Trachealcartilages

Figure 6-10 Anterior view of the human trachea. (Reprintedwith permission from Premkumar, K. (2004). The massage connec-tion anatomy and physiology. Baltimore, MD: Lippincott Williams &Wilkins.)

Why You Need to Know The word “phagocytic” comes from the Greek term“phagein” which literally means to eat. Phagocyticcells ingest and destroy foreign matter such asmicroorganisms. As such, they could be consideredthe immune system’s rst line of defense againstdisease within the respiratory system.

As mentioned earlier, the trachea terminates infe-riorly by bifurcating into two main stem bronchi.The bronchi will divide two more times into lobar (orsecondary) bronchi and then again into segmental(or tertiary) bronchi. The three generations of bron-chi form what is known as the bronchial tree (seeFigure 6-11). Only a part of the main stem bronchi layoutside the lungs. The main stem bronchi pierce the

Trachea

Main stem(primary) bronchus

Carina

Lobar(secondary)bronchus

Segmental(tertiary)bronchus

Right Left

Figure 6-11 Anterior view of the human bronchial tree.(Reprinted with permission from Anatomical Chart Company.)




lung tissue at the hilum so that all further parts of thebronchial tree are housed entirely within the lungs.

The two main stem bronchi are approximately halfthe diameter of the trachea. The right bronchus issomewhat larger than the left bronchus in diameter,but it is also shorter in length. The two main stembronchi are similar in structure to the trachea, except

that they are not quite as cartilaginous and insteadconsist of more smooth muscle tissue. The right bron-chus divides into three lobar bronchi, whereas the leftbronchus divides into two.

cles of respiration are categorized as either muscles ofinspiration or muscles of expiration. That said, it mustbe emphasized that sometimes there is not a cleardichotomy between muscles that are inspiratory andmuscles that are expiratory. As you will see, a smallnumber of muscles are involved in both inspiration andexpiration. For example, a small number of muscles

within the rib cage can be either inspiratory or expira-tory in their function. Similarly, the muscles we typi-cally classify as abdominal wall muscles (and thereforeexpiratory) are often active during inspiration.

In describing muscles—whether they are musclesof respiration, phonation, or articulation/resonance—the origin and insertion are usually highlighted as wellas the action of the muscle. To act upon a body part, amuscle must have two attachments (usually to bone orcartilage). The point of attachment that remains rela-tively constant during muscle contraction is the originand is usually the proximal structure. The insertion isusually the distal attachment and is associated withthe body part that moves during contraction. In somecases, the action of a single muscle may be notewor-thy because of its importance, but in most instances,it is the action of several muscles as a group thatcauses a particular body part to move. As the musclesare being discussed in the sections that follow, thesecharacteristics will be described more fully. It shouldbe noted that in the vast majority of cases muscles arepaired, even though the discussion may refer to themin the singular case. If the discussion does not men-

tion that a particular muscle is unpaired, you shouldassume that the muscle is paired.

The Muscles of Inspiration

The majority of muscles involved in respiration assistin regulating inspiration. These muscles are foundthroughout the thoracic region as well as the neck. Toassist you in remembering the muscles, the musclesof inspiration have been organized into two groups:(1) primary muscles and (2) secondary muscles.The secondary muscles are subclassied according

to their general location: (1) ventral thorax; (2) dor-sal thorax; and (3) neck. The origins, insertions, andactions of the muscles of inspiration are summarizedin Table 6-2.

Primary Muscles of Inspiration

Three muscles perform the greatest work during inspi-ration. They are the diaphragm , external intercostals ,and internal intercostals . Of these, the diaphragm isunpaired, while the external and internal intercostalsare paired.

Why You Need to Know For people with the afiction, asthma is an immunesystem response to certain stimuli (e.g., cold air,physical exertion, allergens) that affects the bronchi.Spasms within the bronchi lead to inammation oftheir internal membranes. The inammation cre-

ates an obstruction that results in greater resistanceto inspired air. This pathological condition will bediscussed in greater detail in Chapter 7.

Each lobar bronchus supplies a specic lobe of thelungs. Being the astute student you are, you quicklydeduce that the right lung has three lobes while theleft lung has two. Within each lung, the lobes are fur-ther divided into smaller regions called segments.The lobar bronchi divide into the same number ofsegmental bronchi as there are segments in that lung

(i.e., the three lobar bronchi of the right lung will fur-ther divide into 10 segmental bronchi, whereas thelobar bronchi of the left lung will divide into eightsegmental bronchi).

The segmental bronchi will continue to divideapproximately 20 times until the last generations aremicroscopic in size. As the bronchi continue to divide,there will be less and less cartilage and more and moresmooth muscle. The last generation of bronchi gives way to the bronchioles, which in turn give way to theterminal bronchioles. Finally, the terminal bronchi-oles give way to the alveolar ducts, which open intothe air sacs where the exchange of oxygen and carbondioxide takes place at the alveoli pulmoni .

THE MUSCLES OF RESPIRATION

We turn our attention now to the muscles of respira-tion. A cycle of respiration has two phases: inspira-tion (i.e., breathing in) and expiration (i.e., breathingout). For each of these phases of respiration, there is aseries of muscles whose action facilitates that particu-lar phase. Therefore, for discussion purposes, the mus-




TABLE 6-2

MUSCLES OF INSPIRATION WITH THEIR ORIGINS, INSERTIONS, AND ACTIONS

Muscle Origin Insertion Action

Diaphragm

External intercostals

Internal intercostals

Lateral iliocostalis cervicisLateral iliocostalis thoracis

Latissimus dorsi

Levator costarum brevis

Levator costarum longus

Pectoralis major

Pectoralis minor

Scalenus anterior

Scalenus medius

Scalenus posterior

Serratus anterior

Serratus posterior superior

Sternocleidomastoid

Subclavius

Sternal: xiphoid processCostal: inner aspect of

R7–R12 Vertebral: lumbar

vertebraeLower border of R1–R11

Lower border of R1–R11

Outer surfaces of R3–R6Upper edges of R7–R12

Spines of lower thoracic

vertebrae, lumbarvertebrae, sacrum,and R10–R12

Transverse processes ofC7 and T1–11

Fasciculi of lower fourbrevis muscles

Medial clavicle andentire length ofsternum

Anterior aspect of R2–R5

Transverse processes of C3–C6Transverse processes of

C2–C7Posterior tubercles of

C6–C7, and in somecases C5

R1–R8 and in somecases R9

Spinous process of C7and T1–T2 or in some

cases T3Sternum: anterior

manubriumClavicle: proximal

(sternal) endJunction of R1 and

its cartilage

Central tendon

Upper surface of the ribimmediately below

Upper surface of the ribimmediately below

C4–C6Lower edges of R1–R6

Upper humerus

Tubercle and angle ofthe rib immediatelybelow

Second rib below theirorigin

Greater tubercle of thehumerus

Coracoid process of thescapula

Inner border of uppersurface of R1

Upper surface of R1

Outer surface of R2

Outer surface of the ribsand inner surface ofthe scapula

Lateral to the angle ofR2–R5

Two heads unite andattach to the mastoidprocess

Inferior surface ofthe clavicle, near theacromion of thescapula

The primary muscle of inhalation; increases the longitudinal

volume of the thoracic cavityand compresses the abdominal

viscera As each successive upper rib isanchored, the rib immediatelybelow is elevated

The portions of these musclesalong the anterior rib cage(i.e., sternum) act similarly tothe external intercostals

Elevates R3–R6 Works in concert with the lateral

iliocostalis cervicis to stabilizethe back of the rib cage wall

With the humerus xed, the bers

of this muscle that insert intoR10–R12 will elevate them

Elevates the posterior rib cage

Elevates the lower posterior ribs

With the humerus xed, elevatesthe sternum and anterior ribs

With the scapula xed, elevatesR2–R5

Elevates R1

Elevates R1

Elevates R2

With the scapula xed, elevatesR1–R8 and in some cases R9

Elevates R2–R5

With the head xed, elevates thesternum and clavicle

With the clavicle xed, elevatesR1




The Diaphragm

The diaphragm is the primary muscle of respiration,essentially being the workhorse of inspiration (seeFigure 6-12). It is a single muscle that separates thethorax from the abdomen and is bi-domed, similarlyto the humps on a camel. The dome on the right-handside is situated a bit higher than the dome on theleft because the liver occupies the upper right-handquadrant of the abdomen. The diaphragm is amongthe largest muscles in the body. As it lies in place, itlooks rather large and resembles an open umbrella.However, if you were to remove the diaphragm andspread it out at on a table, you would note that it is

relatively thin and broad.The muscle bers insert into a core of connective

tissue called the central tendon , which is actually anaponeurosis that resembles a trifoliate leaf (somewhat like the maple leaf on a Canadian ag). Becausethe diaphragm separates the thorax from the abdo-men, it is perforated with several openings to allowstructures to pass from the thorax to the abdomen.Noteworthy are the (1) aortic hiatus, which allows theaorta to pass through to the abdomen; (2) foramenvena cava, which allows the vena cava to pass through

to the abdomen; and (3) the esophageal hiatus, which

allows the esophagus to pass through on its way to thestomach.The diaphragm has three points of origin: a ster-

nal portion that attaches to the posterior surface ofthe xiphoid process; a costal portion that anchorsonto the lowermost six ribs; and a lumbar por-tion that attaches to L1 through L3 by way of twolegs called crura. Of these three attachments, thelumbar attachment is inexible. Since the lumbarattachment is inferior to the body of the diaphragm,contraction will result in the diaphragm descend-ing toward its lumbar attachments. In other words,

during contraction, the diaphragm lowers towardthe contents of the abdomen, thereby increasingthe longitudinal (or vertical) volume of the thorax.Because of its costal and sternal attachments, con-traction of the diaphragm will also pull down on thesternum and lower six ribs. In addition to these threepoints of origin, the diaphragm also has connectionsto the lungs (by way of the visceral pleura ; a morethorough discussion of the pleurae can be found inthe section that describes the lungs) and the brouslayer of the pericardium .

Figure 6-12 A superior view of the human diaphragm with pertinent landmarks. (Reprinted with permission from Agur, A.M., Dalley, A.F.(2008). Grant’s atlas of anatomy (12th ed.). Baltimore, MD: Lippincott Williams & Wilkins.)

Muscle fibers

Foramenvena cava

Central tendon

Muscle fibers

Esophagealhiatus

Central tendon

Aortic hiatus

Pericardial sac

Pleural cavity

Thoracicvertebra

Rib




The Intercostal Muscles

The external and internal intercostals also play a sig-nicant role in inspiration. As their name implies, theintercostal muscles can be found between the ribs (seeFigure 6-13). The terms external and internal refer totheir relative position to each other—the externals are

supercial and the internals are deep. The 12 pairs ofribs have 11 spaces between them. Not surprisingly,there are 11 pairs of internal and external intercostalmuscles. The bers of the intercostal muscles are ori-ented obliquely (i.e., diagonally) although in oppositedirections (essentially crisscrossing each other). Thiscrisscrossing of the two muscles occurs throughoutmost of the distance between each adjacent pair ofribs. However, at the sternal and vertebral terminals,only one of the two muscles can be found. At the ver-tebral terminal, the external intercostals continueall the way to the vertebral column but the internalintercostals stop short of it. At the sternal terminal,the opposite is true. The internal intercostals proceedall the way to the sternum, but the external intercos-tals terminate approximately at the chondro-osseous juncture (the point where the rib ends and the carti-lage that continues to the sternum begins). Any spacethat is not occupied by either the internal or externalintercostal muscle is occupied by connective tissue.

The external intercostal muscles are stronger thanthe internal intercostals. The net action of the exter-nal intercostal muscles is to expand the rib cage

by elevating the ribs. The origin for each externalintercostal muscle is the rib immediately above, andthe insertion is the rib immediately below. As eachexternal intercostal muscle contracts, the lower rib to which it is attached elevates. The sum of the contrac-tion of all 11 pairs of external intercostals then is anincrease in the transverse volume of the thorax.

The internal intercostal muscles may actually havea dual purpose. Not only do they apparently assistin inspiration, but they are also thought to assist inforced expiration. The ventral bers of the internalintercostals (i.e., from the sternum to approximatelythe chondro-osseous juncture) act in much the same way as the external intercostals. However, the greaterlength of the internal intercostals (i.e., from thechondro-osseous juncture to a few centimeters awayfrom the vertebral column) has the opposite effect onthe ribs. Along the lateral and posterior wall of the ribcage, the internal intercostal muscles lower the ribs.

The intercostal muscles are thought to have anadditional function besides elevating and loweringthe rib cage. Evidence seems to suggest that thesemuscles also keep the intercostal spaces rigid dur-ing respiration so that they do not bulge out duringexpiration or get drawn in during inspiration (Agur& Dalley, 2005). One might expect that by expandingthe rib cage, the outward force that is placed on theribs will generate an inward force on the intercostalspaces. Similarly, the inward force that is generatedby contraction of the rib cage will generate an out-

ward force on the intercostal spaces. The intercostalmuscles serve to make the intercostal spaces rigid toprevent these forces from acting upon them.

Secondary Muscles of Inspiration

In all, 14 additional muscles can be considered mus-cles of inspiration, and any number of them may becalled upon to assist when there is a greater demandfor air intake. All of them are paired muscles. Thesesecondary muscles include the lateral iliocostaliscervicis , lateral iliocostalis thoracis , latissimus dorsi ,levator costarum brevis , levator costarum longus ,

pectoralis major , pectoralis minor , scalenus anterior ,scalenus medius , scalenus posterior , serratus anterior ,serratus posterior superior , sternocleidomastoid , andsubclavius . In the following sections, these muscleshave been subclassied according to their location:ventral thorax, dorsal thorax, and neck.

The Ventral Thorax

There are four pairs of muscles situated withinthe ventral thorax. These are the pectoralis major ,pectoralis minor , subclavius , and serratus anterior

Internalintercostal(externalintercostalhas beenexcised)

Externalintercostals

Externalintercostal

Internalintercostals

(externalintercostalshave been

excised)

Lateral viewof rib cage

Figure 6-13 The internal and external intercostal muscles.(Reprinted with permission from Agur, A.M., Dalley, A.F. (2008).Grant’s atlas of anatomy (12th ed.). Baltimore, MD: LippincottWilliams & Wilkins.)




(Figure 6-14 illustrates all four of these muscles). Theprimary purpose of these muscles is to assist in mov-ing the arm and shoulder. However, they may play aminor role in respiration by assisting in deep inspira-tion, such as what would occur during vigorous exer-cise or yawning. The pectoralis major is a fan-shapedmuscle that has three attachments: the clavicle, thesternum, and the humerus. The clavicular and ster-nal attachments are this muscle’s origin while thehumerus is the insertion. When the pectoralis majorcontracts and the humerus is in a xed position, it will

elevate the sternum and with it the anterior aspect ofthe ribs attached thereon.

The pectoralis minor is deep to the pectoralis majorand runs from the anterior aspect of R2 through R5to the scapula. When this muscle contracts and thescapula is in a xed position, the net effect will beelevation of ribs 2 through 5.

The subclavius gets its name from the fact that itcourses immediately below and parallel to the clavi-cle. Its origin is the chondro-osseous juncture of therst rib and its insertion is the inferior surface of the

Pectoralismajor

Serratus anterior(anterior view)

Subclavius

Pectoralis minor(pectoralis majorhas beenexcised)

Serratus anterior(anterior view)

Serratus anterior(lateral view)

Figure 6-14 Muscles of the upper thorax, including the pectoralis major and minor, subclavius, and serratus anterior. (Reprinted withpermission from Agur, A.M., Dalley, A.F. (2005). Grant’s atlas of anatomy (11th ed.). Baltimore, MD: Lippincott Williams & Wilkins.)




rst pair of longus muscles originates on the trans-verse processes of T7 and inserts onto R9, whereasthe last pair of longus muscles originates on the trans-

verse processes of T10 and inserts onto R12. As theirnames imply, the levator costarum muscles elevatethe posterior rib cage when they contract.

Finally, the serratus posterior superior is illustratedin Figure 6-18. The term “serratus” refers to the factthat this muscle has a jagged appearance as it insertsinto the ribs. The serratus posterior superior origi-nates on the spinous processes of C7 through T3 andthen inserts lateral to the angle of R2 through R5. When it contracts, it elevates ribs 2 through 5.

The Neck Muscles

Four pairs of muscles in the neck region may contributeto inspiration. These are the scalenus anterior , scalenusmedius , scalenus posterior , and sternocleidomastoid . All of these muscles are illustrated in Figure 6-19. Asa whole, these four neck muscles serve to elevate therst two ribs, sternum, and clavicle. The net effect ofthis action is a slight increase in the anteroposteriordimension of the rib cage, such as would be needed fordeep inhalation during strenuous exercise or yawning.

The three scalenes are among the deepest musclesin the neck. They originate on the transverse processes

and posterior tubercles of most of the cervical ver-tebrae and then insert either onto R1 (the scalenusanterior and medius) or R2 (the scalenus posterior).

Contraction of the scalenus anterior and scalenusmedius will result in elevation of the rst rib, whereascontraction of the scalenus posterior will result inelevation of the second rib.

The sternocleidomastoid is an interesting musclenot only in its architecture but also in its action. It hasthree attachments, as its name implies: the sternum,the clavicle, and the mastoid process (the roundedpart of the base of the skull immediately posteriorto the ear). The primary purpose of this muscle is toallow us to turn our head from side to side. It accom-plishes this action because of how it is situated. The

mastoid process is behind the axis of the body (i.e.,the vertebral column), but the sternum and clavicleare anterior to the axis. With the sternum and clavi-cle anchored, the sternocleidomastoid will pull uponthe mastoid process, thereby turning the head to oneside. However, the head turns to the side that is oppo-site to the muscle that is contracting. That is, whenthe sternocleidomastoid on the right side of the neckcontracts, it turns the head to the left, and vice versa.If the mastoid process is anchored, the sternocleido-mastoid will slightly elevate the sternum and clavicle.

Levator costarumbrevis

Levator costarumlongus

Posterior view of theposterior rib cage

Figure 6-17 The levator costarum muscles (brevis and longus).(Modied with permission from Moore, K.L., Agur, A.M.,Dalley, A.F. (2009). Clinically oriented anatomy(6th ed.).Baltimore, MD: Lippincott Williams & Wilkins.)

Serratusposteriorsuperior

Serratusposteriorinferior

Posterior viewof the rib cage

Figure 6-18 The posterior serratus muscles (superior and in-ferior). (Modied with permission from Moore, K.L., Agur, A.M.,Dalley, A.F. (2009). Clinically oriented anatomy (6th ed.). Baltimore,MD: Lippincott Williams & Wilkins.)




As a unied, coordinated whole, the muscles ofinspiration serve to increase the longitudinal, trans-verse, and anteroposterior volumes of the thoraciccavity. Having the lungs contained within, expan-sion of lung tissue will also occur in any of these threedimensions that are at work. A more thorough discus-sion of these mechanics is reserved for the section on

Physiology of the Respiratory System.

The Muscles of Expiration

The muscles of expiration are generally located in theabdomen and are categorized into two groups: pri-mary muscles and secondary muscles. The primarymuscles are found within the wall of the abdomen andhence they are referred to as abdominal wall muscles. All of the secondary muscles of expiration (with theexception of the quadratus lumborum) can be found

within the thorax. The quadratus lumborum is a deepabdominal muscle. Table 6-3 summarizes the origins,insertions, and actions of the muscles of expiration.

Primary Muscles of Expiration

Four pairs of muscles within the abdominal wall playa part in expiration. These are the external oblique ,

internal oblique , rectus abdominus , and transver-sus abdominus . Removal of the epidermis of theabdomen will reveal the external oblique and rectusabdominus along with a network of connective tis-sue that binds the muscles together. The connectivetissue includes the lumbodorsal fascia posteriorly,the inguinal ligament inferiorly, and the abdominalaponeurosis anteriorly. Of particular note is the latter.The abdominal aponeurosis forms the linea alba (lit-erally, “white line”) at the midline of the belly, cours-ing from the xiphoid process to the pubic symphysis.

Sternocleidomastoid

Scalenus anteriorScalenus posterior

Scalenus medius

Lateral view of the neck

Figure 6-19 Muscles of the neck, including the sternocleidomastoid and scalenus muscles (anterior, medius, and posterior). (Reprintedwith permission from Agur, A.M., Dalley, A.F. (2008). Grant’s atlas of anatomy (12th ed.). Baltimore, MD: Lippincott Williams & Wilkins.)




With the linea alba positioned vertically in the middleof the abdomen, the muscles of the abdominal wallare all paired with one on each side of midline.

Upon dissection of the epidermis and connectivetissue, the external oblique and rectus abdominus arethe rst muscles in view. The external oblique is thelargest and strongest of all the abdominal wall mus-cles (see Figure 6-20). It is broad and thin, originat-ing on the posterior surfaces of the lower eight ribs

and terminating at the anterior aspect of the iliaccrest as well as the abdominal aponeurosis. As itsname implies, the bers of the external oblique runin a diagonal direction. When this muscle contracts,it pulls the lower ribs downward and also compressesthe anterior and lateral walls of the abdomen.

To be able to view the internal oblique, the externaloblique and rectus abdominus must be removed. Thebers of the internal oblique also course in a diagonal

TABLE 6-3

MUSCLES OF EXPIRATION WITH THEIR ORIGINS, INSERTIONS, AND ACTIONS


External oblique


Internal oblique

Lateral iliocostalislumborum

Lateral iliocostalis thoracis

Latissimus dorsi

Quadratus lumborum

Rectus abdominus

Serratus posterior inferior

Subcostals

Transversus abdominus

Transversus thoracis

Posterior surfaces andlower borders ofR5–R12

Lower border of R1–R11

Lateral half of inguinalligament and anterioriliac crest

Lumbodorsal fascia,lumbar vertebrae, andposterior surface ofthe coxal bone

Upper edges of R7–R12

Spines of lower thoracicvertebrae, lumbarvertebrae, sacrum,

and R10–R12Iliac crest and

iliolumbar ligament

Crest of the pubis

Spinous process of

T11–T12 and L1–L3Same course as theinternal intercostals

Inner surfaces ofR6–R12, diaphragm,and transversusthoracis

Posterior surface ofsternum, xiphoidprocess, and R5–R7

Anterior half of iliaccrest and abdominalaponeurosis

Upper surface of the rib immediately below

Linea alba and thecartilages of R10–R12and in some cases R9

Lower edges of R7–R12

Lower edges of R1–R6

Upper humerus

Transverse processes ofL1–L4; lower borderof R12

Cartilages of R5–R7 andxiphoid process

Inferior border of

R8–R12Same as the internalintercostals but maytraverse more thanone rib

Deepest layer of theabdominal aponeu-

rosis and the pubis

Lower borders and inner surfaces of R2–R6

Pulls the lower ribs downwardand compresses the anteriorand lateral walls of theabdomen

The portions of these musclesalong the sides and back of therib cage pull down on the ribs

Pulls the lower ribs downwardand compresses the anteriorand lateral walls of theabdomen

Depresses the lower six ribs

Works in concert with the lateraliliocostalis lumborum to

stabilize the back of the ribcage wallContraction of this muscle as

a whole compresses the lowerportion of the rib cage wall

Pulls down on R12

Pulls down on the sternum andlower ribs and compresses theanterior abdominal wall

Depresses R8–R12

Pull down on the ribs to whichthey are inserted

Compresses the anterior andlateral walls of the abdomen

Pull downward on R2–R6




kept rigid, contraction of these muscles will depressthe ribs, thereby decreasing thoracic volume while atthe same time generating increased intra-abdominalpressure by compressing the anterior and lateralabdominal walls.

Secondary Muscles of Expiration

There are eight pairs of secondary muscles of expi-ration. They include the internal intercostals, lateraliliocostalis lumborum, lateral iliocostalis thoracis,latissimus dorsi, quadratus lumborum, serratus pos-terior inferior, subcostals, and transversus thoracis. Allof these muscles are found in the thorax except thequadratus lumborum, which is found deep within theabdomen.

You may recall that the internal intercostals, lateraliliocostalis, and latissimus dorsi were all describedearlier in the section that described the muscles ofinspiration (refer back to Figures 6-13, 6-15, and 6-16,respectively). These muscles play a dual role in res-piration. You learned earlier that the portions of theinternal intercostals that abut the sternum functionsimilarly to the external intercostals, that is, they per-form an inspiratory function. However, when the lat-eral and posterior portions of the internal intercostalscontract, they depress the rib cage, which is an expi-ratory function. Similarly, the latissimus dorsi playsan inspiratory role when only the costal portion ofthis muscle contracts, but it plays an expiratory role when the entire body of the muscle contracts. When

the whole muscle contracts, the latissimus dorsi com-presses the lower portion of the rib cage. Finally, thelateral iliocostalis is a muscle that has three parts:cervicis, thoracis, and lumborum. The cervicis andthoracis bundles are involved in inspiration, whereasthe lumborum and thoracis bundles are involved inexpiration. The lateral iliocostalis lumborum origi-nates at the lumbodorsal fascia, lumbar vertebrae,and posterior surface of the coxal bone and insertsinto the lower edges of ribs 7 through 12. When it con-tracts, it depresses the lower six ribs. The lateral ilio-costalis thoracis works with the lumborum bundle by

simply stabilizing the back of the rib cage (which italso does with the lateral iliocostalis cervicis duringinspiration).

The remaining three pairs of expiratory muscles within the thorax—the serratus posterior inferior, sub-costals, and transversus thoracis—all serve to depressa number of the ribs. The serratus posterior inferiorbegins on the spinous processes of T11 through L3and inserts into the inferior border of R8 through R12(see Figure 6-18). When this muscle contracts, it pullsdown on ribs 8 through 12. The subcostal muscles(see Figure 6-22) can be seen running in an oblique

direction on the internal surface of the lower ribs neartheir angles, in relative proximity to the vertebral col-umn. The specic ribs into which they insert differfrom person to person. Contraction of these muscles

will pull down on the ribs to which they are attached.Finally, the transversus thoracis muscles resemble thelegs of a spider as they extend from the posterior sur-face of the sternum, xiphoid process, and R5-R7 to theposterior surfaces of R2 through R6 (see Figure 6-23). When this muscle contracts, it pulls downward onribs 2 through 6.

The nal secondary muscle of expiration is thequadratus lumborum (see Figure 6-24). To see thismuscle from the ventral side of the body, the abdomi-nal contents (e.g., intestines, stomach, liver) must beremoved. The point of origin for this muscle is the

iliac crest and iliolumbar ligament. Its insertion is thetransverse processes of L1–L4 and the lower border ofthe 12th rib. Its action is thought to be to anchor R12during forced expiration.

NEURAL INNERVATION OF THE MUSCLESOF RESPIRATION

In Chapter 4, you were introduced to the human ner-vous system. A thorough discussion of the nervoussystem was provided there, and therefore will notbe provided here. However, it is important that you

Internalintercostals

Subcostalmuscles

Interior view of theposterior rib cage

Sternum

Thoracicvertebrae

Figure 6-22 The subcostal muscles. (Reprinted with permis-sion from Agur, A.M., Dalley, A.F. (2008). Grant’s atlas of anatomy(12th ed.). Baltimore, MD: Lippincott Williams & Wilkins.)




understand the neural innervation of the many of theimportant muscles of respiration because in manycases, pathology of the respiratory system may be aresult of nerve damage (see Chapter 7 for a more thor-ough discussion of the impact of neurological impair-ment on breathing).

Table 6-4 provides a summary of most of the mus-cles of inspiration and expiration and their neuralconnections. In all, 23 spinal nerves (8 cervical, 12thoracic, and 3 lumbar) are involved in the motorinnervation of the muscles of respiration. In addition,the sternocleidomastoid is innervated in part by acranial nerve.

As was mentioned earlier in this chapter, thediaphragm is the primary muscle of respiration,accounting for the longitudinal dimension of tho-racic cavity expansion. The diaphragm is innervatedby the phrenic nerve , which arises from the thirdthrough fth cervical spinal nerves. Two branchesof the phrenic nerve pass through the neck in proxim-ity to the scalenus anterior muscle and carotid arteryon their way to the thoracic cavity. The left phrenicnerve proceeds directly to the diaphragm to inner-vate it, but the right phrenic nerve passes through the

Transversethoracis muscles

Posterior viewof sternum

Interior of theanterior rib cage

Figure 6-23 The transversus thoracis muscles. (Modied with permission from Agur, A.M., Dalley, A.F. (2008).Grant’s atlas of anatomy (12th ed.). Baltimore, MD: Lippincott Williams & Wilkins.)

Quadratuslumborum

Figure 6-24 The quadratus lumborum muscle. (Modied withpermission from Moore, K.L., Agur, A.M., Dalley, A.F. (2009).Clinically oriented anatomy (6th ed.). Baltimore, MD: LippincottWilliams & Wilkins.)




foramen vena cava at the level of T10 and then risesto meet the diaphragm. In addition to innervating thediaphragm, the phrenic nerves also provide sensoryinnervation to the mediastinum, pleurae , liver, andgall bladder.

Both sets of intercostals muscles (i.e., external andinternal) are innervated by the intercostal nerves, which are formed by the anterior (i.e., ventral) rami ofspinal nerves T1 through T11. Each intercostal musclereceives its own intercostal nerve. However, the tho-racic spinal nerves innervate more than just the inter-costal muscles.

The remaining muscles of inspiration are inner-vated by various combinations of cervical and/or tho-racic spinal nerves. The pectoralis major and minorare innervated by C5 through C8. The subclaviusreceives its innervation from cervical spinal nerves 5and 6. The three pairs of scalenus muscles are inner-vated by C2 through C8. The levator costarum mus-cles (brevis and longus) receive innervation from C8as well as thoracic spinal nerves 1 through 11. Theserratus anterior receives innervation from cervical(C5–C7) and thoracic (T2 and T3) spinal nerves. Theserratus posterior superior is innervated by T2 andT3. Finally, the sternocleidomastoid is the only mus-cle that receives innervation from a cranial nerve (thespinal accessory nerve—cranial nerve XI). However, italso receives motor commands from cervical spinalnerves 1 through 5.

The muscles of expiration within the abdominal wall are all innervated by spinal nerves T7 throughT12; the internal oblique and transversus abdominusare innervated by the rst lumbar spinal nerve (L1)as well. The quadratus lumborum is innervated byT12 in addition to L1–L3. The subcostals are inner-

vated by the intercostal nerves (T1 through T11). Thelatissimus dorsi (which is also classied as a muscleof inspiration) is innervated by cervical spinal nerves6 through 8. The serratus posterior inferior is inner-vated by T9 through T12. Finally, the transversus tho-racis receives its innervation from thoracic spinalnerves 2 through 6.

THE LUNGS AND PLEURAE

The two lungs consist of spongy, porous tissue and arehoused within the rib cage, one on the right-hand side

and the other on the left (see Figure 6-25A). Betweenthe two lungs, posterior to the sternum, and anterior tothe vertebral column is the mediastinum, which con-tains all of the thoracic viscera except the lungs (seeFigure 6-25B). These viscera include the heart and peri-cardium, aorta, vena cava, phrenic nerves, esophagus,trachea, main stem bronchi, lymph nodes of the centralthorax, and lesser blood vessels and nerves. The medi-astinum is encapsulated by loose connective tissue.

A comparison between the two lungs reveals thatthe right lung is larger than the left, but it is also

TABLE 6-4

NEURAL INNERVATION OF SELECTEDMUSCLES OF RESPIRATION

Muscle Innervation

Diaphragm C3–C5 (phrenic nerve)External intercostals T1–T11 (intercostal

nerves)

External oblique T7–T12Internal intercostals T1–T11 (intercostal

nerves)Internal oblique T7–L1Latissimus dorsi C6–C8Levator costarum muscles C8–T11Pectoralis major C5–C8Pectoralis minor C5–C8Quadratus lumborum T12–L3Rectus abdominus T7–T12Scalenus muscles C2–C8Serratus anterior C5–C7; T2 and T3Serratus posterior inferior T9–T12Serratus posterior superior T2 and T3Sternocleidomastoid Spinal accessory (cranial

nerve XI); C1–C5Subclavius C5 and C6Subcostal T1–T11 (intercostal

nerves)Transversus abdominus T7–L1Transversus thoracis T2–T6

Why You Need to Know Damage to the phrenic nerves will result in paraly-sis of the diaphragm. Because the diaphragm isresponsible for mediating longitudinal expansionof the thorax—and hence accounts in part for tidalvolume—an individual with paralysis of the dia-

phragm will require a ventilator to assist in respi-ration. The good news is that since the diaphragmreceives bilateral innervation, it would be difcult(although not impossible) to completely paralyze it.That would require a pathological condition thatis more central rather than peripheral. Paralysisand its effect on the breathing mechanism will bediscussed in more detail in Chapter 7.

Secondary to the diaphragm, the intercostal mus-cles play a signicant role in the inspiratory process.




shorter in part because of the liver below it. The leftlung is smaller because the heart occupies some of thespace of the left lung, in a concavity called the cardiacimpression . Both lungs are divided into lobes: theright lung has three lobes separated by the oblique

and horizontal ssures, whereas the left lung has twolobes separated by the oblique ssure. You may recallfrom the discussion of the bronchial tree that eachlobe receives its own lobar or secondary bronchus. Although the bronchial tree has considerable smoothmuscle tissue within it (especially as the tree dividesfurther and further), lung tissue has very few smoothmuscle bers. This means that the action of the lungsis passive; that is, the lungs must rely on outside forcesto act upon them to make them expand and contractduring respiration. The interior volume of an averageadult male’s lungs is approximately 5 liters (5000 cc);

in an average adult female, the volume is approxi-mately 4 liters (4000 cc). That is, for an adult female,the capacity of air for each lung would be equivalentto a 2-liter bottle of your favorite soft drink.

In adults, there are approximately 300 million alveolipulmoni—small pits or depressions within the air sacsof the lungs. At birth, there are approximately 25 mil-lion alveoli. That number increases to the adult num-ber of 300 million by age 8 years, and remains at thatnumber throughout life. The alveoli pulmoni consistof Type I and II cells as well as phagocytic cells. Type I

cells are epithelial cells arranged in a single layer. TypeII cells are responsible for producing pulmonary sur-factant, a somewhat soapy substance that breaks upsurface tension within the alveoli during respiration.Phagocytic cells in the lungs assist in eliminating any

bacteria or other organisms that have found their wayto the alveoli. The alveoli pulmoni are engorged withan elaborate system of capillaries where carbon diox-ide is released from the bloodstream so that it can beexhaled, and oxygen is taken up by the bloodstreamso it can be distributed throughout the body.

Mediastinum

Sternum

Heart

Esophagus

Aorta

Vertebra

Obliquefissure

Horizontalfissure

Obliquefissure

RIGHT LEFT

A B

Lung

Figure 6-25 The human lungs and mediastinum. A . Anterior view of the lungs. B . Transverse section through the lungs and medi-astinum. (Reprinted with permission from Agur, A.M., Dalley, A.F. (2008). Grant’s atlas of anatomy (12th ed.). Baltimore, MD: LippincottWilliams & Wilkins.)

Why You Need to Know A baby born prematurely tends to have underde-veloped lungs. For example, Type II cells may notbe fully developed, leading to a reduction in the

production of pulmonary surfactant resulting in anincrease in surface tension within the alveoli. Thebaby may show signs of respiratory distress and maybe placed on a ventilator until the lungs developmore fully to allow her to breathe independently.Similarly, underdevelopment of phagocytic cellsmay leave the baby susceptible to infectious pro-cesses such bacterial or viral pneumonia.

Each lung is somewhat triangular in shape, withthe apex extending into the root of the neck and the




base making contact with the diaphragm. Each lungis enclosed within a double-layered membrane calledthe pleurae. The pleurae that surround each lungare independent of each other. This is a protectivemechanism; if the pleura of one lung is compromised,the other lung will not be affected. The pleurae notonly line the lungs but also line the inner surface of

the rib cage, superior surface of the diaphragm, andmediastinum. The outer layer of each pleura linesthe inner surface of the ribs and hence is referred toas the costal (or parietal ) pleura . The inner layer cov-ers the diaphragm and is known as the visceral pleura.The thoracic visceral pleura continues beyond thediaphragm and is continuous with the visceral lin-ing of the abdomen. A potential space exists betweenthe two pleurae; this space is referred to as the pleu-ral cavity or intrapleural space and contains a serousuid that allows the two layers to glide upon eachother without friction during respiration.

The two layers of the pleurae adhere to each otherand are airtight. This vacuum is known as pleurallinkage and essentially binds the lungs to the inte-rior of the rib cage and to the superior surface of thediaphragm. Approximately 75% of the surface of thelungs is in contact with the interior wall of the rib cage.The remaining 25% is in direct contact with the supe-rior surface of the diaphragm as well as indirectly withthe abdominal wall muscles. This means that the dia-phragm must exhibit greater movement than the ribcage to effect comparable changes in lung volume.

Because of pleural linkage, whenever the rib cageand/or diaphragm are displaced, the lungs will alsodisplace proportionately. Analogous to Mary andher little lamb (i.e., the rib cage and the diaphragmare Mary and the lungs are her little lamb), whereverMary goes, the lamb is sure to follow. This is a veryimportant part of the physiology of breathing.

Physiology of theRespiratory System

In the rst half of this chapter, the physiology of respi-ration was alluded to during the discussion of variousanatomical structures. In this section of the chapter, amore thorough and integrated discussion of respira-tory physiology will be presented. With a rm under-standing of the anatomical structures of respiration, you should have little difculty comprehending howthe process of respiration takes place. The clinician intraining must be able to describe respiratory physiol-ogy as it relates to normal, quiet breathing (referred toas vegetative breathing), and then be able to describe

the changes that take place when respiration is usedfor the purpose of vocal activity. Before discussing theactual mechanics though, you need to understandsome basic concepts that are related to breathing.

BASIC CONCEPTS

Volume, Pressure, and Airow

To understand the mechanics of inspiration, you mustunderstand some very basic concepts. Two of theseare volume and pressure. These two concepts are inte-grally related to each other. According to Boyle’s law ,assuming temperature is kept at a constant, volumeand pressure will be inversely related to each other. Inother words, as the value of one increases, the value ofthe other decreases proportionately. This very simplelaw of physics applies to gases, and of course, the air we breathe is a gas. Figure 6-26 illustrates the rela-tionship. Assume we have two containers, one beinglarger than the other. Assume also that each containeris lled with the very same number of air molecules.Because one container is larger than the other, itsinterior volume is also larger. The air molecules in thelarger container “spread out” to ll the interior volumeof that container. For the smaller container, the airmolecules are more compacted because they do nothave as much interior space to occupy as the largercontainer. Because the air molecules in the smallercontainer are compacted, they exert a greater amountof pressure within the container as compared with thelarger container where the molecules are not quite ascompacted. If there was a way to further reduce theinterior volume of the container, the air pressure within would continue to increase as its volume gets

A B

Less pressure

Greaterpressure

Figure 6-26 A schematic representation of Boyle’s law. Asvolume decreases (as depicted when going from container A tocontainer B), air molecules are more compacted, resulting ingreater pressure within the container.




smaller and smaller. The inverse is also true: if youmake the container larger and larger, its interior vol-ume will also get larger and larger and along with it,the pressure within will continue to decrease.

Now let us move from the containers to the humanlungs. The lungs are also containers of air, and theirinterior volume can be manipulated. Recall from

the discussion of anatomy that the lungs consist ofrelatively few smooth muscle bers, so they must bemanipulated by external forces. As the lungs expand,their interior volume increases. As the lungs contract,their interior volume decreases. Taking Boyle’s lawinto consideration, as the lungs expand, the air pres-sure within the alveoli decreases because the air mol-ecules “spread out” to occupy the increased volume.Conversely, as the lungs contract, the air pressure within the alveoli increases because the air moleculesbecome more compacted.

To understand the process of inspiration, one mustalso understand uid mechanics. The term “uid” isused to denote any gas or liquid. One of the principlesof uid mechanics states that a uid will always owfrom areas of greater pressure to areas of lesser pres-sure. Of course, this implies that there are two areas(referred to as gradients) of pressure. Recall fromthe discussion immediately above that one gradientof pressure is within the lungs. This is referred to aspulmonary pressure . The other gradient of pressureis the air outside the body—what we commonly referto as atmospheric pressure . If pulmonary pressure

is equal to atmospheric pressure, there will be noow of air from one gradient of pressure to the other.However, if either of these pressures changes relativeto the other, air will ow from the gradient of greaterpressure to the gradient of lesser pressure.

Understanding these basic concepts, you are wellequipped to comprehend how inspiration takes place.Before a breath is taken, when the lungs are at resting volume , pulmonary pressure and atmospheric pres-sure are essentially equivalent. Expansion of the lungscauses their interior volume to increase, therebyresulting in a decrease in pulmonary pressure rela-

tive to atmospheric pressure. Because uids alwaysow from gradients of greater pressure to gradients oflesser pressure, the air outside the body will enter therespiratory passageway and ll the lungs until pul-monary pressure once again is equal to atmosphericpressure, at which time airow will cease. The indi-vidual has just “taken a breath,” that is, inspired air.

Notice that humans inspire air by creating negativepressure within the lungs. Because of this, humans arereferred to as negative pressure breathers. Some ani-mals are positive pressure breathers. For example, a

frog generates positive pressure by pufng its cheeksin and out like a piston. A frog has no diaphragm, so itcannot generate negative pressure in its lungs.

Passive Forces

When the thorax expands during inspiration, sev-

eral physical phenomena are set into motion. Theseare referred to as passive forces and include elasticrecoil , torque , intra-abdominal pressure , and gravity .Newton’s Third Law of Motion comes into play here.It states that for every action, there is an oppositeand equal reaction. Elastic recoil, torque, and intra-abdominal pressure are all forces that conform to thisbasic law. First, because the lungs are composed ofelastic tissue, they have the ability to be “stretched”during inspiration. Expansion of lung tissue creates acertain force, and there is an opposite and equal forcethat acts upon the lungs to collapse them. This is elas-tic recoil. Second, rib cage expansion is accomplishedby rotation of the ribs upon their longitudinal axes.The force that is generated by this rotation is knownas torque. Once again, when the ribs rotate upon theiraxes, an opposite and equal force exists in oppositionto the torque that is created. Third, when the dia-phragm contracts, it descends toward the abdomen.Think of the diaphragm as acting somewhat like apiston. As it descends, it applies downward pressureon the abdominal contents, creating what is referredto as intra-abdominal pressure. Intra-abdominal

pressure exerts itself proportionately on the inferiorsurface of the diaphragm, attempting to force the dia-phragm back to its resting position.

In part, these three phenomena account for theexpiratory phase of respiration along with gravity.Gravity assists the expiratory phase by acting uponthe ribs. As the ribs are elevated during inspiration,gravity pulls on them to lower them back to their rest-ing position. The net effect of these four passive forcesis contraction of the rib cage, which subsequentlyresults in expiration. In some cases, these passiveforces are all that is needed to mediate expiration. In

other cases, expiration is more active (i.e., it requirescontraction of certain muscles).

Lung Volumes and Capacities

Obviously, the lungs are not always completely lled with air, neither are they ever completely empty. Infact, at rest when an individual is between breaths,the lungs are about 40% full of air. An individual cannotforce out all the air in his lungs, neither does hetypically breathe in as deeply as he possibly can




during quiet vegetative breathing. As such, the lungshave certain volumes. A lung volume is a discreet unitthat is independent of all other volumes. In other words, volumes do not overlap. Tidal volume (TV) is the air that is normally exchanged during a com-plete respiratory cycle (i.e., an inspiration followed byan expiration). In a typical adult male, TV is approxi-

mately 600 cubic centimeters (cc) or milliliters (ml)and in adult females TV is approximately 450 cc.The lungs have volumes that extend beyond a nor-

mal tidal inspiration and a normal tidal expiration.These are referred to as inspiratory reserve volume(IRV) and expiratory reserve volume (ERV) , respec-tively. A typical adult has an IRV of approximately2500 cc and an ERV of approximately 1000 cc. You canreach your IRV by taking a normal tidal inspiration,stopping, and then gulping in as much additional airas you can. IRV will be the amount of additional air you gulped in. By the same token, you can access yourERV by taking a normal tidal expiration, stopping, andthen forcing out all the air you can. The additionalair you forced out (before you started wheezing andcoughing!) is ERV.

Even upon forcing out as much air as possible, someair will remain in the lungs. This is known as residual volume (RV) and remains in the lungs to keep themfrom collapsing. RV is approximately 1100 cc in a typi-cal adult. Finally, air lls structures within the respi-ratory passageway outside the lungs—the oral andnasal cavities, larynx, trachea, and bronchi. These

are referred to as dead air spaces, and they containapproximately 150 cc of air. Incidentally, upon inspira-tion, the rst 150 cc of air to enter the lungs will comefrom the dead air spaces. Conversely, the nal 150 ccof air released from the lungs upon expiration will llthese dead air spaces.

Although lung volumes are discreet, independentunits, lung capacities are not. Lung capacities areformed by the combination of lung volumes. Humansonly use a portion of their total lung volume duringvegetative breathing and vocal activity. When thereis a greater demand for air (e.g., when exercising or

when engaging in vocal activity), we have the ability tocall upon our IRV and/or ERV. In other words, healthylungs have the capacity to meet our every demandfor air. Lung capacities include inspiratory capacity(IC), functional residual capacity (FRC), vital capac-ity (VC), and total lung capacity (TLC) . IC can beexpressed as TV IRV. In other words, an individual’sIC is the amount of air he or she can maximally inhalefrom a resting expiratory level. FRC is equal to ERV RV;that is, FRC is the amount of air in the lungs at a restingexpiratory level. The formula for VC is IRV TV ERV.

It is the amount of air a person can maximally andforcibly exhale upon taking a deep inspiration. Finally,TLC is the combination of all lung volumes (IRV TV ERV RV).

Why You Need to Know All lung capacities are important from a clinicalstandpoint, but VC is very likely of greatest clinicalinterest to a speech–language pathologist because itincludes TV, IRV, and ERV—all of the volumes thatmay come into play during vocal activity. One candetermine by using a mathematical formula theexpected VC for a given individual. For adult males,expected VC can be determined by multiplyingthe person’s age by 0.112, subtracting that number from 27.63, and then multiplying the result by thatindividual’s height (in centimeters, or cm). Foradult females, one would multiply the individual’s

age by 0.101, subtract that number from 21.78, andthen multiply the result by the individual’s height(in cm). VC is typically used as a general indica-tor of an individual’s ability to provide breathsupport for vocal activity. In some cases, personswith voice disorders or neuromotor problems willexhibit a diminished ability to provide adequatebreath support for speech. In these cases, VC maybe considerably less than what the clinician mayexpect. An instrument called a spirometer is used tomeasureVC, and norms exist to give the clinician anidea as to how much VC a person should be able togenerate. Although beyond the scope of this textbookto discuss, there are other instruments that we use tostudy respiration. These include, but are not limitedto, the pneumotachometer and plethysmograph . Amore thorough discussion of instrumentation andits use in studying respiratory physiology can be found in Hixon, Weismer, and Hoit (2008).

Lung volumes and capacities can vary considerablyfrom person to person. An individual’s size, gender,and age often inuence his or her lung volumes and

capacities. For example, VC tends to change with age.It rst increases gradually up until a person reachesthe age of 20 years, levels off until age 25 years, andthen decreases at the rate of approximately 100 cceach year thereafter. Similarly, a person’s position(e.g., lying down vs. standing up) and posture will alsoaffect measurements of lung volume and capacity. Inthe supine position, for example, resting lung volumedrops from 40% to about 20% because of the effectof gravity. The strength of the muscles that assist inmediating respiration will also have an effect on these




measures. Finally, disease processes may also affectlung volumes and capacities (a more thorough dis-cussion of some of these disease processes can befound in Chapter 7).

Breathing and the Exchange of Air

A typical human takes approximately 12 breaths perminute when engaging in quiet, vegetative breathing.Of course, for more strenuous activity, the number ofbreaths taken per minute will increase—in some cases,quite dramatically. In the section immediately above, it was mentioned that TV is approximately 600 cc (or ml) foran adult male and 450 cc for an adult female. In other words, with each breath, a typical male exchangesapproximately 600 cc and an adult female exchangesapproximately 450 cc of air. Considering an averageof 12 breaths per minute, a typical male exchangesapproximately 7.2 liters of air per minute (12 breathsper minute times 600 cc equals 7200 cc or 7.2 liters).This is known as the individual’s minute volume . Aperson’s maximum minute volume is the amount ofair that person can maximally exchange each minute(assuming he or she does not hyperventilate duringthe process!). Maximum minute volumes range fromapproximately 150 to 170 liters, which indicates thathumans only use a fraction of their VC during quietbreathing.

consumed by that individual in a minute is 320 cc(minute volume 8000 cc of air; 8000 cc of air 20%oxygen 1600 cc of oxygen; 1600 cc of oxygen 20%actually consumed 320 cc). If you do your math right, you will realize that approximately 4% of inspired air isactually consumable oxygen (20% of 20% is 4%).

The human body must have oxygen to functionproperly. The air we breathe actually contains rela-tively little oxygen—only about 20% of atmosphericair is oxygen; the remaining 80% is nitrogen, carbondioxide (0.04%), and other elements and compounds. Although only one-fth of air is oxygen, it is still morethan enough to sustain life. In fact, only 20% of the

oxygen humans inspire is actually consumed by thebody! Expired air is composed of approximately 16%oxygen, 4% carbon dioxide, and 75% nitrogen. Notethat the carbon dioxide we breathe out is 100 timesgreater than the carbon dioxide we breathe in. Withmore than 6 billion people on earth breathing, wegenerate a lot of carbon dioxide. Of course, plants usecarbon dioxide like humans use oxygen.

Let us do some more math. If a person has a respi-ratory rate of 16 breaths per minute with TV mea-sured at 500 cc per breath, the total amount of oxygen

Figure This Out What would a typical adult female’s minute volumebe if she took 12 breaths per minute with an averageTV of 450 cc?

Why You Need to Know Emphysema, a disease that adversely affects thealveoli and elasticity of the lungs, can dramati-cally alter blood oxygen levels. Consumable oxygenmay be well below 4% of inspired air in individualswho present with this disease. Emphysema will bediscussed in greater detail in Chapter 7.

THE PROCESS OF VEGETATIVE BREATHING

Inspiration

Now that you understand the basic concepts involvedin respiration, a question that may come to mind is“How do the lungs expand so that pulmonary pres-sure will decrease resulting in the sequence of eventsthat creates inspiration?” Your knowledge of respi-

ratory muscles now comes into play. Recall fromthe discussion of anatomy that certain muscles areresponsible for inspiration. These muscles are sum-marized in Table 6-2. The action of all these muscles will result in expansion of the thoracic cavity in threedimensions—longitudinal, transverse, and antero-posterior—although all three dimensions may not beacted upon at any given time.

Vegetative breathing is primarily an automatic func-tion (i.e., you do not have to consciously think abouttaking a breath) that is regulated by the lower brain cen-ter for breathing housed within the medulla oblongata.

This center does two things: (1) regulates the levels ofoxygen and carbon dioxide in the arterial blood and (2)controls the rhythmic pattern of breathing. Wheneverthe medulla senses that there is too much carbon diox-ide and not enough oxygen in the blood, it sends neu-ral signals to the nerves that control respiratory muscleactivity. The appropriate muscles that enable us to yawn contract. A yawn is simply a reexive behaviormediated by the lower brain center for breathing.

The diaphragm is responsible primarily for longitu-dinal expansion of the thoracic cavity. As this muscle

Figure This Out How much oxygen would a person consume perminute if he has a TV of 550 cc and a respiratoryrate of 14 breaths per minute?




contracts, it descends toward the abdomen. Becauseof its attachments, the diaphragm not only expandsthe thoracic cavity in the vertical dimension (i.e., lon-gitudinally), but it also pulls down on the lower ribcage and distends the abdominal wall outward. Thisgenerates negative pressure within the thorax. Whena person is standing or sitting in an upright position,

muscles in the chest wall and abdominal wall contractto prevent the rib cage from being “sucked” inward bythe negative force being generated by the diaphragm.The counteraction of the abdominal wall musclesalso exerts an upward force on the diaphragm, whichassists the diaphragm in lifting the rib cage. Althoughthe diaphragm remains in a contracted (i.e., lowered)position, its body is spread out superiorly and laterallyby the intra-abdominal pressure exerted upon it bycontraction of the abdominal wall muscles. Becausethe diaphragm has attachments to the lower ribs, thenet effect will be an expansion of the lower rib cage.In this way, not only does the diaphragm mediate lon-gitudinal expansion of the thorax but also assists intransverse expansion. When an individual is lying inthe supine (i.e., “belly up”) position, gravity will exertan inward force on the diaphragm so that the abdom-inal muscles do not need to contract.

The external intercostal muscles are second only tothe diaphragm in terms of their importance to vegeta-tive breathing. During shallow breathing, the externalintercostals may not even be called upon; their con-tribution to inspiration becomes more pronounced

when you take a deeper than normal breath (e.g., yawning or sighing). Recall that the external inter-costals course from each rib to the rib immediatelybelow. As these muscles contract, they pull up on therib below. The articulations the ribs have with the tho-racic vertebrae and sternum allow the ribs to rotateon their longitudinal axes. The ribs evert, resulting ingreater lateral thoracic volume.

During quiet, vegetative breathing, there may bemeasurable upward and forward movement of the ster-num, as the anterior ribs are acted upon by the internalintercostal muscles. This movement will create a slight

increase in the anteroposterior dimension of the thoraciccavity. Contraction of the neck muscles will also gener-ate a slight increase in the anteroposterior dimension ofthe thorax, but these muscles are usually not involved inthe process unless vegetative breathing becomes strenu-ous. For example, as an individual engages in heavy aer-obic exercise, the demand for more oxygen may causethe individual to contract the neck muscles as he or shestrains to get more air into the lungs.

The majority of muscles involved in inspirationare relegated to a secondary role. The remaining

inspiratory muscles of the thorax (as well as the neckmuscles just mentioned) typically do not play a role ininspiration unless there is a greater demand for oxy-gen by the body or if an individual wants to generateconsiderable vocal volume (i.e., yell or scream). Underthese scenarios, the secondary muscles contract tofurther expand the transverse and anteroposterior

volumes of the thoracic cavity.It should be noted that intrapleural pressure (thepressure within the potential space between the cos-tal and visceral pleurae) is always negative throughoutrespiration. At rest (i.e., between breaths), intrapleuralpressure is approximately −6 cm H 2O. During inspira-tion, the contraction of the diaphragm pulls on thevisceral pleura. This generates even more negativeintrapleural pressure (from −6 cm H 2O to approximately−10 cm H 2O). Boyle’s law plays a role here. Expansionof the rib cage and descent of the diaphragm increasesthe volume within the intrapleural space, which causesthe drop in pressure. Upon expiration, contraction ofthe rib cage and elevation of the diaphragm gener-ates greater (i.e., more positive) intrapleural pressure,although overall the pressure is still negative.

What does this mean in terms of inspiring air? As was mentioned briey in the section on anatomy, notonly are the lungs made of elastic tissue, they also actas a unit with the diaphragm and rib cage because ofpleural linkage (remember Mary and her little lamb).The visceral and costal pleurae act like two compressedplates of glass with liquid between them, meaning that

they glide upon each other but do not separate. Longi-tudinal and transverse expansion of the lungs createsgreater volume within the alveoli pulmoni. The greatervolume in the alveoli results in lower pulmonary pres-sure by comparison to atmospheric pressure (pulmo-nary pressure is approximately −2 cm H 2O relative toatmospheric pressure). Air will ow from outside thebody to within the lungs to equalize the drop in pres-sure. Once the pressure is equalized, airow ceasesand you are at the end of the inspiratory phase of therespiratory cycle (i.e., pulmonary pressure is 0 cm H 2Orelative to atmospheric pressure).

Why You Need to Know Under certain pathological conditions such asasthma or chronic bronchitis, the individual maycontract the neck muscles in an attempt to creategreater lung volume to compensate for reduced tidalinspiration due to the obstruction within the bron-chi. These pathological conditions will be discussedin Chapter 7.




Expiration

Once air gets into the lungs, how do we get it out? Doesit require additional muscle activity? From the discus-sion about respiratory anatomy, you know that thereare certain muscles that are classied as muscles ofexpiration. However, for quiet, vegetative breathing,the action of these muscles is typically negligible. Infact, the expiratory muscles (especially the abdominal wall muscles) actually assist in the process of inspira-tion . What then serves as the impetus for expiration?

For the most part, passive forces act upon the thoraxto contract it. As was mentioned earlier, these passiveforces include elastic recoil, torque, intra-abdominalpressure, and gravity. As the muscles of inspiration relax,these forces act upon the thorax to compress it. As thethorax compresses back to its resting position, the alve-oli within the lungs are compressed as well. Compres-sion of the alveoli results in an increase in pulmonary

pressure relative to atmospheric pressure (i.e., pulmo-nary pressure is now 2 cm H 2O relative to atmosphericpressure). With pulmonary pressure being greater thanatmospheric pressure, air will ow from the lungs tooutside the body. The lungs deate until they reach theirresting volume, which is also the point at which pulmo-nary pressure once again equals atmospheric pressure(i.e., the pressure differential is 0 cm H 2O).

With these passive forces at work, what prevents thethorax from compressing before we have a chance touse the oxygen from the air? The answer is the inspira-tory muscles (especially the external intercostals) andthe abdominal wall muscles. Upon inspiration, the dia-phragm almost immediately relaxes. However, the exter-nal intercostals and the abdominal wall muscles remainactive throughout inspiration. This prevents the rib cagefrom contracting prematurely. Interestingly enough, when the external intercostal muscles start to relax,the internal intercostal muscles may contract, exertinga downward and inward force on the ribs to assist indeating the thorax. Once the thorax has returned to itsresting state, another cycle of respiration begins.

The Respiratory CycleDuring quiet, vegetative breathing, the inspiratoryphase is active. In other words, muscles are alwaysinvolved in the process. Muscles of inspiration areneeded to initiate the inspiratory phase. Other thanthe possible contraction of the internal intercostals,the expiratory phase is usually passive. Newton’sThird Law of Motion acts upon the thorax to initiateexpiration by generating the passive forces of elasticrecoil, torque, and intra-abdominal pressure. Gravityalso plays a role in the expiratory process.

If one were to time a typical cycle of respiration dur-ing quiet, vegetative breathing, it would be evident thatthe timing of the inspiratory and expiratory phases isalmost equivalent. The inspiratory phase accounts forapproximately 40% of the respiratory cycle, whereasthe expiratory phase accounts for 60% of the cycle. Asan example, if a complete cycle of respiration takes

2 seconds to complete, inspiration will account for800 msec (0.8 seconds) of the cycle, while expiration willaccount for the remaining 1200 msec (1.2 seconds).

When the thorax is at rest (i.e., when a person isbetween breaths), the air in the lungs occupies approx-imately 40% of VC. This is referred to as resting lungvolume. The TV that is created during quiet, vegetativebreathing accounts for an additional 10% of VC. Thismeans that on average, only 50% of VC is used duringquiet, vegetative breathing. When we yawn, we go intoIRV. For example, inspiration during a vigorous yawncan occupy as much as 90% or more of VC. You canimagine that an activity like physical exercise will alsocause us to utilize more of our IRV and thus VC.

THE PROCESS OF BREATHINGFOR VOCAL ACTIVITY

When an individual uses the breath stream for vocalactivity, the respiratory system undergoes distinctphysiological changes. These changes affect boththe mechanics and timing of the respiratory cycle.The primary difference between vegetative breathing

and using the breath stream for vocal activity is theintroduction of the phonatory system into the equa-tion. The vocal folds remain abducted (i.e., separated)during vegetative breathing, but they adduct (i.e.,come together) during vocal activity. The phonatorysystem will be described more fully in Chapter 8. Inthis section, we will describe respiratory physiologyas it relates to vocal activity. More specically, we willdiscuss what happens when we engage in two vocalactivities—continuous, steady phonation and con-versational speech.

Continuous Phonation

Continuous, steady phonation is dened as the sus-taining of phonation with little variation in pitch orintensity. An example of this would be sustaining avowel sound or a single musical note. The speakerinspires air and then continuously phonates until heor she runs out of breath.

During vocal activity, expired air is used to gener-ate vocal fold vibration. Because inspired air is notinvolved in phonation, the mechanics of inspiration




do not change considerably from what one wouldobserve during quiet, vegetative breathing. The samephenomena that explain vegetative inspiration stillapply. To inspire air, the individual simply contracts thediaphragm, external intercostal muscles, and possiblysome secondary muscles of inspiration. The internalintercostals and abdominal wall muscles contract to

stiffen the rib cage so that the intercostal spaces arenot sucked in by the negative pressure. The net result ofthis muscle activity is expansion of the thorax. Becauseof pleural linkage, the lungs expand as well. Pulmonarypressure decreases relative to atmospheric pressurebecause of the increased volume within the alveoli. Airenters the lungs to equalize the drop in pressure.

Although the basic inspiratory mechanics are thesame for continuous vocal activity as they are for veg-etative breathing, an observable difference is that IRV will likely be called into play during continuous vocalactivity. In other words, the speaker will take a deeperbreath than he or she normally would during vegetativebreathing. If the speaker is asked to sustain continuousphonation until he or she runs out of breath, then ERV will also be accessed. This will necessitate a change inexpiratory mechanics as well.

Take note of Figure 6-27. The upper part of the g-ure shows the changes in lung volume that occur dur-ing continuous vocal activity. Point “A” represents the

peak of the volume trace. Here, the speaker has takena deep breath, essentially going into IRV. Then, thereis a gradual decrease in lung volume throughout thevocal activity until it “bottoms out” (point “B”). Thespeaker is below resting lung volume; in other words,the speaker has accessed ERV. Now note the tracebelow the volume trace. This second trace represents

pulmonary pressure. You can see that although lungvolume diminishes over time throughout continu-ous vocal activity, pulmonary pressure remains rela-tively constant. Pulmonary pressure is what we use toset the vocal folds into vibration (except at the vocalfolds, it is referred to as subglottic pressure ). At a nor-mal loudness level, it only takes approximately 5 to8 cm H 2O of subglottic pressure to maintain vocal foldvibration.

In terms of inspiration, accessing IRV means thatmore air is introduced into the alveoli. The speaker isin a condition of high lung volume (point “A” in Figure6-27). High lung volume means greater pulmonarypressure. Greater pulmonary pressure means greaterrelaxation pressure (remember that for every action,there is an opposite and equal reaction). To counterthe increased relaxation pressure, we must put a brakeon the expiratory forces (referred to as the checkingmechanism ) that act to make the rib cage collapse(Hixon, Mead, & Goldman, 1976). This is accomplishedby the chest wall inspiratory muscles (i.e., the externalintercostals primarily, but other muscles may also beactive). Refer back to Figure 6-27. Note the muscles that

are involved in inspiration (from the beginning of thegraph to point “A”). The diaphragm and external inter-costals contract simultaneously, but the diaphragmrelaxes almost immediately. The external intercostalsremain active beyond relaxation of the diaphragm. Thisis done to counter the increased relaxation pressure athigh lung volume as the speaker begins to phonate onexpired air. Note also that the abdominal wall muscles(e.g., the external obliques and rectus abdominus) arealso active during inspiration. These muscles contractto counter the negative force on the intercostal spaces.

Diaphragm

External intercostals


External obliques

Rectus abdominus

Latissimus dorsi

Volumein litersrelativeto mid

respiration

Pressure(cm H 2O)

Time (seconds)

1

0

−1

−24

0

5 10 15 20 25 30 35 40

B

A

Figure 6-27 Muscle activity during steady, continuousphonation.

Why You Need to Know Any neuromuscular disease or disorder that affectsthe braking mechanism of the external intercostalmuscles will have a concomitant effect on phona-tion time, that is, an individual’s ability to main-tain vocal fold vibration beyond a few seconds.The individual may not be able to speak but a fewwords before running out of breath. Neuromuscularpathologies will be discussed in greater detail inChapter 7.




At the point of the vertical dotted line in Figure6-27, when the external intercostal muscles relax,the speaker is approaching resting lung volume (i.e.,is in mid lung volume), but phonation continuesuninterrupted. As the speaker continues to phonate,expiratory rib cage muscles (i.e., internal intercos-tals) contract to maintain the steady (5 to 8 cm H 2O)

subglottic pressure to sustain vocal activity. Thespeaker continues to phonate and begins to tap intoERV. At this point, the speaker is below resting lungvolume, and pulmonary pressure is negative in rela-tion to atmospheric pressure (i.e., the speaker is atlow lung volume). However, subglottic pressure forphonation remains a steady 5 to 8 cm H 2O. To be ableto do this, the speaker has to apply even greater mus-cular pressure on the breathing mechanism. At thispoint, the abdominal wall muscles (especially theexternal obliques and rectus abdominus) becomeactive. By contracting these muscles, greater intra-abdominal pressure is exerted upon the diaphragm, which in turn exerts greater pressure on the lungs. As the speaker continues more and more into ERV,expiratory thoracic muscles (e.g., latissimus dorsi)and additional abdominal muscles become activeuntil the speaker runs out of breath (point “B” inFigure 6-27).

It should be noted that muscle activity duringvocal activity is not an all-or-none event. In other words, it is not a matter of the inspiratory musclescontracting rst, then relaxing, and then nally the

expiratory muscles contracting. Breathing for vocalactivity requires a coordinated and overlappingeffort between all of the muscles of inspiration andexpiration. This way, rib cage wall and abdominal wall volume will decrease at a constant rate through-out phonation. Lung volume will also decrease at arelatively constant rate throughout phonation, pro-viding the steady and constant pulmonary pressurethat is necessary to initiate and maintain vocal foldvibration.

Conversational Speech

The physiological changes that occur during con-versational speech are even more remarkable thanfor continuous, steady phonation. In the latter case,vocal pitch and intensity remain somewhat constantthroughout phonation. In the case of conversationalspeech, we vary our vocal pitch, intensity, and qual-ity quite a bit. Changes in vocal pitch and intensityare what allow us to vary our lexical stress and into-nation. For example, in some contexts, lexical stressallows us to differentiate the meaning of words (say

the word “record” with stress on the rst syllable andthen with stress on the second syllable). Similarly,intonation also plays a part in conveying the meaningof our utterances (e.g., say the sentence “We are goingto the store tonight” rst with a rising intonation at theend of the sentence and then with a falling intona-tion). Nine of the 24 consonant sounds in English are

produced without vocal fold vibration. Therefore, inconversational speech, there are intermittent periods where vocal fold vibration is either “on” or “off.”

Another difference between continuous, steadyphonation and conversational speech is that we donot typically utilize a large portion of IRV or ERV forconversational speech. We tend to take quick, rapidinspirations (going slightly into IRV) and then speakuntil we go a little into ERV. We could use all of IRV andERV to speak, but it would cause a disruption in ourability to produce conversational speech in a smooth,uninterrupted manner.

Because of these changes, respiratory physiologyis once again altered somewhat. Volume and pressurechange considerably throughout our conversationalspeech. For conversational speech, lung volume is pri-marily a mid-range event. Remember that VC at rest-ing lung volume is approximately 40%. Normal tidalinspiration adds another 10% to VC, meaning that weonly use about 50% of our VC for vegetative breath-ing. During conversational speech at a normal inten-sity level, inspiration accounts for approximately 60%of VC; in other words, we utilize only a small portion

of our IRV. We then speak on expired air and continueuntil we are relatively close to resting lung volume. Insome cases, we might even go into ERV a bit (to about30% to 35% VC). In these cases, the checking mecha-nism during high lung volume and the active contrac-tion of muscles of expiration during low lung volume will not likely come into play to the degree they wouldduring steady, continuous phonation. We do not typi-cally go well into IRV unless we want to increase ourvocal intensity (such as in yelling or screaming), and we do not go too far into ERV unless we continue tospeak until we run out of breath (such as might occur

when we are excited or when we are trying to hold theoor during conversation).

For such activities like singing, reading loudly, or yelling, we do go more into our IRV and may use moreof our ERV. According to Hixon (1973), our inspirationaccounts for approximately 80% of VC when we readloudly and as much as 85% to 90% when we yell orsing classically. At the end of expiration, we are usu-ally around 35% VC. In other words, for vocal activ-ity produced at greater intensity, we typically usebetween 45% and 55% of our VC. Naturally, if we go




more and more into our ERV, we will utilize more andmore of our VC.

What are the physiological mechanisms duringconversational speech? In essence, we tend to “charge”the respiratory system during conversational speechby taking quick inspirations intermittently through-out our speech. Slight upward and downward varia-

tions in pulmonary (and hence, subglottic) pressureoverride our expiratory breath stream and allow us toalter our vocal pitch, intensity, and quality. We gener-ate slight increases in pulmonary pressure to medi-ate lexical stress and slight decreases in pulmonarypressure at the end of breath groups where pitch andintensity tend to level off.

Once again, the same basic mechanics apply forinspiration during conversational speech as they dofor vegetative breathing and steady, continuous pho-nation. The difference, of course, is whether we requireas much braking activity by the external intercostalsat high lung volume or more active participation ofthe expiratory abdominal and chest wall muscles atlow lung volume. The greatest change in physiologyinvolves the expiratory phase.

The expiratory phase is mediated by the expiratoryabdominal and chest wall muscles. These muscles aretypically not involved in inspiration during conversa-tional speech. This allows these muscles to be at theready to drive expiration as soon as the inspiratoryphase has ended. When the abdominal wall musclescontract, they generate greater intra-abdominal pres-

sure that exerts itself upon the diaphragm. This resultsin three actions. First, it increases the diaphragm’sradius of curvature and elongates its principal musclebers. This allows the diaphragm to produce quick,powerful inspirations so that there are minimal dis-ruptions to running speech. Second, upward force onthe diaphragm generates an upward force on the ribcage, which elevates it. This in turn stretches the bersof the expiratory rib cage muscles to allow them toproduce quick expiratory pulses for varying lexicalstress and vocal intensity. Finally, inward incursionof the abdominal wall muscles prevents an outward

excursion of the abdomen when the diaphragm actsupon the rib cage to elevate it. If this did not takeplace, there would be a reduction in the expiratorychest wall muscles’ ability to generate the expira-tory pulses necessary to effect changes in intensity,stress, and intonation. That is, if the expiratory chest wall muscles contracted without opposition from theabdominal wall muscles, the inward pressure gener-ated by the expiratory chest wall muscles would sim-ply dissipate by outward excursion of the abdomen.

The abdominal muscles then mechanically “tune” thebreathing mechanism for inspiration and expirationduring conversational speech.

The Respiratory Cycle

It should be clear to you that dramatic changes

occur to the respiratory cycle during vocal activity.First and probably most obvious are the mechani-cal changes that take place, especially during theexpiratory phase. Perhaps not quite as obvious arethe changes that occur to the timing of respira-tion. As you learned earlier in this chapter, duringquiet, vegetative breathing, inspiration accounts forapproximately 40% of the respiratory cycle, whileexpiration accounts for the remaining 60%. Dur-ing vocal activity, the ratio between inspiration andexpiration changes dramatically to approximately10% and 90%, respectively. This makes sense whenone considers what is going on physiologically dur-ing vocal activity. Because the vocal folds adduct forphonation, they create an obstacle to the expiredair so that it takes longer for the expiratory phaseto be completed. To a lesser degree, the checkingmechanism of the external intercostal muscles dur-ing expiration also causes the expiratory phase to beprolonged. In addition, we tend to utilize more ofour VC during vocal activity than what we do duringquiet, vegetative breathing. We use varying amountsof our inspiratory and expiratory reserve volumes

during vocal activity. These volumes are not utilizedas much during tidal breathing.

Summary

This chapter provided a thorough description and dis-cussion of the anatomy and physiology of the respira-tory system. The respiratory system is the power sourcefor vocal activity. Without adequate breath support,humans would not be able to generate a vocal tone,that is, they would not have a voice. Indeed, there are

many pathological conditions that may result in poorbreath support for speech, and as expected, individu-als exhibiting any of these pathologies will also havevoice problems. Some of these pathologies will bediscussed in Chapter 7. Then, in Chapter 8, a thoroughdiscussion of the phonatory system will be presented.Through a discussion of the phonatory system, youshould gain a greater appreciation for the impor-tant role respiration plays in the process of speechproduction.



PART 3

Knowledge Outcomes for ASHA Certication for Chapter 7• Demonstrate knowledge of the biological basis of the basic human communication

processes (III-B)• Demonstrate knowledge of the neurological basis of the basic human communication

processes (III-B)• Demonstrate knowledge of the etiologies of voice and resonance disorders (III-C)• Demonstrate knowledge of the etiologies of swallowing disorders (III-C)

• Demonstrate knowledge of the characteristics of swallowing disorders (III-C)

Learning Objectives• You will be able to list and briey describe the medical etiologies associated with respiratory

pathologies.• You will be able to explain the impact of respiratory pathologies on speech breathing and

voice production.• You will be able to explain the impact of respiratory pathologies on swallowing.

CHAPTER 7

Pathologies Associated with the Respiratory System


chemo- responding to chemicals chemo receptor

de- decrease de saturation

hyper- increased or excessive hyper ination

hypo- decreased or reduced hypo xemia

-itis infection bronch itis

mechano- responding to movement mechano receptor

-ologist specialist pulmon ologist

oro- pertaining to the oral cavity oro pharynx

-osis state of disease tubercul osis

pneumo- pertaining to the lungs pneumo nia

sclera-/sclero- scar, plaque multiple sclero sis

-sia abnormal or pathological state dyskine sia

143



CHAPTER 7 PATHOLOGIES ASSOCIATED WITH THE RESPIRATORY SYSTEM 145

return the blood to the heart’s left side (Kersten,1989). An example of the impact of less efcientoxygen exchange is chronic emphysema. Individu-als have enlarged hearts due to the extra effortrequired by the heart to pump oxygenated blood tomuscles and organs. Alternatively, many of the dis-orders listed in Table 7-1 impact systems beyond the

cardiopulmonary. Such is the case with congenitaldisorders such as muscular dystrophy (MD) , aninherited disease of progressive muscle deteriora-tion and weakness, and neurological disorders suchas multiple sclerosis (MS) , a disease of the centralnervous system affecting the myelin covering of theaxons. Also, some disorders may be only temporaryor transient in nature with proper medical treat-ment, such as those associated with allergies suchas asthma and hay fever or infections of the lungssuch as pneumonia or tuberculosis. Other disor-ders progressively worsen with respiratory func-tion decreasing over time such as with amyotrophiclateral sclerosis (ALS) (also known as Lou Gehrig’sdisease).

Speech–language pathologists (SLPs) becomeinvolved when respiratory function impacts speechbreathing beyond the acute phase. Thus, individuals with chronic breathing problems may benefit fromevaluation and intervention for speech breathing. You will recall from Chapter 6 that our respiratorysystem is extremely flexible, generating positiveand negative pressures for inspiration and expira-

tion, respectively, that go well beyond that neededfor conversational speech. Because of this excess“reserve,” individuals with significantly reducedrespiratory capacity can often speak intelligibly atadequate intensities, although those same indi-viduals may not have long utterances or be able tospeak loudly or shout with as much success. Whenlung volume and capacities become too small forfunctional speech, then the patient becomes ven-tilator dependent and collaborative work with therespiratory therapist begins and/or efforts switchto the use of augmentative and alternative commu-

nication systems.This chapter now turns to a brief description of

some of the respiratory pathologies an SLP mayencounter in his or her practice. As mentioned earlier,a number of disorders resulting in respiratory difcul-ties can be medically managed without a referral forspeech therapy services. However, it should be under-stood that whenever the breath stream is compro-mised, speech production is also likely compromised.The extent to which SLPs intervene is presented ingreat detail in Hixon and Hoit’s (2005) comprehensive

text on evaluation and management of individuals who have speech breathing disorders.

AIRWAY OBSTRUCTION

A number of respiratory difculties are secondaryto obstructions in the upper and lower airways that

hinder the ow of air and gas exchange at the alve-oli. Selected respiratory disturbances will be dis-cussed as they relate to the power supply for speechproduction.

Asthma and Paradoxical Vocal Fold Movement

Asthma and paradoxical vocal fold movement(PVFM) can be mistaken for one another, as theyboth are a function of airway obstruction and bothresult in sudden difculty breathing. However, thereare a number of differences that distinguish the two. A hallmark symptom of PVFM is difculty breathingin air (Hixon & Hoit, 2005), whereas asthma is betterdescribed as difculty breathing out . Further, PVFMis an upper airway obstruction that occurs second-ary to sudden adductor spasms of the vocal folds thatinterfere with normal breathing (Mathers-Schmidt,2001). In contrast, asthma is a lower airway obstruc-tion due to constriction of both large and smallpulmonary passages (e.g., bronchi, bronchioles).In asthma, there is abnormal sensitivity of smoothmuscle surrounding the bronchioles causing them

to close and trapping air inside the lungs (Goodman,2003). In addition, an “asthma attack” brings aboutinammation of the bronchial lining and the produc-tion of mucus as depicted in Figure 7-1A. Abnormal“noise” when breathing is heard with both disorders,but again, there are differences. Asthma is associated with wheezing and a concomitant patient complaintof tightness in the chest; this wheezing emanates fromthe pulmonary passages. The sound associated withPVFM is inhalatory stridor . Stridor is caused by thecreation of air turbulence during inspiration throughthe adducted vocal folds; thus, the sound emanates

from the larynx. Further, when the vocal folds fullyadduct during breathing, dyspnea or complete cessa-tion of breathing can occur.

There are varying views espoused in the literatureconcerning the etiologies of PVFM. It has been con-sidered an organic disorder similar to asthma in thatit may be brought on by a response to environmen-tal allergens and/or strenuous exercise. Alternatively,it may be a functional disorder with a psychologicalcomponent (see Chapter 9, for a discussion of organicversus functional voice disorders). Mathers-Schmidt




(2001) blends the two views and considers PVFMa complex, heterogeneous laryngeal disorder. The American Speech-Language-Hearing Association (n.d.)concurs by including the following as possible trig-gers for PVFM:

• Shouting/coughing.• Physical exercise.• Acid reux.• Cold air breathing.• Smoke and air pollution.

• Psychosocial issues.• Neurological issues.It should be noted that an individual can pres-

ent with both PVFM and asthma. When obstructionoccurs to the lower airway, accessory muscles of res-piration come into play to assist the primary musclesin moving air in and out of the lungs.

Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD)

is a general and nonspecific term that refers tochronic bronchitis and emphysema as illustratedin Figure 7-1B. Chronic bronchitis is the continu-ous over production of mucus due to the structuralchanges of the bronchi because of environmentalpollutants and allergens such as smoking (see Why You Need to Know Box). Emphysema results in thebreaking down of the walls of the air sacs resultingin clumps of alveoli and decreased surface area forgas exchange (see Figure 7-2). Furthermore, thealveoli become thick walled and lose their elastic-

ity. COPD then impacts both ventilation and respi-ration. Through medical treatment, ventilation ismaintained by medication administered throughinhalers and nebulizer treatments. Respirationis managed but cannot be improved by the use ofoxygen support. You may have seen individuals car-rying or pulling oxygen tanks attached to tubinginserted into their nose by way of nasal cannulae ;most likely, these individuals have COPD (althoughlung cancer may also be the culprit). In addition,individuals with advanced emphysema are termed

“pink puffers” by medical personnel, as they havea ruddy complexion and are short of breath (the“puffing”), often breathing through pursed lips.

Individuals with COPD are able to speak conver-sationally but may use shorter breath groups or getfatigued more easily with speech. A breath group issimply the quantity of speech, as measured by num-ber of syllables or words, produced in a single breath. As you can imagine, as lung volume decreases, breathgroup length also decreases. Along with the reducedphrase length, expect the reduced lung volumes andcapacities to also result in lower subglottic pres-

sure and reduced vocal intensity all while requiringincreased respiratory effort on the part of the speaker(Seikel, King, & Drumright, 2005). The fatiguing effectof speaking is related to decreased oxygen in the bloodstream. Hixon and Hoit (2005) provide a clinical exam-ple of managing speech breathing to decrease fatiguein an individual with moderate emphysema. In clientsat risk for desaturation during speaking activities,monitoring of oxygen saturation (SpO 2) levels and/orend-tidal breathing partial pressure of carbon dioxide(PCO 2) is done under the direction of a pulmonolo-

ASTHMA

Musclespasm Edema

Mucus

Emphysema ChronicbronchitisCOPD

A BFigure 7-1 Airway obstruction. A . The triad of symptoms secondary to an asthma attack. B . The combination of emphysema andchronic bronchitis results in chronic obstructive pulmonary disease (COPD). (From Kersten, L. (1989). Comprehensive respiratorynursing: A decision making approach. Philadelphia, PA: W.B. Saunders.)




gist and with the assistance of a respiratory therapist(Hixon & Hoit, 2005). Hixon and Hoit suggest using apulse oximeter to monitor oxygen saturation (SpO 2)to assist in determining the type of speaking behav-ior that causes desaturation and teach strategies to

reduce this (e.g., incorporating nonspeech breathsbetween speech breaths).

tion of blood with uid buildup in the lungs as well asother tissues. Congestion refers to this buildup of uidand concomitant swelling (i.e., edema). Causes aremany and include years of uncontrolled high bloodpressure and coronary artery disease. Individuals with

CHF have chronic shortness of breath and persistentcoughing up of phlegm. Most typically, the left ven-tricle or chamber of the heart fails and blood backsup into tissues (e.g., the swelling seen in the lowerextremities) and organs. Lung congestion, or pulmo-nary edema , occurs with this left-sided heart fail-ure. This uid then lls the alveoli and prevents gasexchange or respiration from occurring. Speech isimpacted due to decreased lung volume and decreasedability to generate and sustain the subglottic pressuresnecessary for continuous speech with adequate loud-ness. In addition, patients with CHF present with a wetor gurgly sounding voice and persistent coughing; thismakes it hard to determine at bedside if they are at riskfor aspiration of food and drink because these symp-toms mimic those that indicate swallowing problems.

MUSCULOSKELETAL CONDITIONS

Conditions affecting voluntary skeletal muscleinclude the various forms of muscular dystrophy(MD). Muscular dystrophies are inherited geneticdiseases resulting in degeneration of skeletal muscle

Respiratorybronchiole

Alveolarsac

Increasedmucoussecretions

Damagedcilia

Epithelialcell

Smoothmuscle

Alveolarsac

Bronchiole

Bronchiolesand alveoli

Chronicbronchitis

Emphysema

Bronchiole lumen

NORMAL:

COPD:

Figure 7-2 An illustration of airwayobstruction in chronic bronchitis andthe breakdown of alveolar walls inemphysema (chronic obstructive pulmo-nary disease [COPD]) comparedwith normal respiratory function.(Modied with permission fromNettina, S.M. (2009). Lippincott manual ofnursing practice (9th ed.). Philadelphia:Lippincott Williams & Wilkins.)

Why You Need to Know Smoking is clearly linked to lung disease attribut-ing to 438,000 deaths in the United States each year.The majority of these deaths are a result of COPD(chronic bronchitis and emphysema) and lungcancer (Centers for Disease Control, 2005). Althoughprevalence rates have declined in young adults 18to 24 years of age in the United States, smoking is

still the most prevalent in this age group (AmericanLung Association, 2007). Furthermore, adult malesand females who smoke lose an average of 13.2 and14.5 years of life, respectively, as compared withnonsmokers.

Congestive Heart Failure

The weakening of the heart’s ability to efciently andadequately pump blood leads to congestive heartfailure (CHF) . This, in turn, causes decreased circula-




and associated progressive muscle weakness. Thetypes of MD vary in terms of age of onset, distribu-tion of affected muscle groups, rate of progression,and extent of muscle weakness (National Institute ofNeurological Disorders and Stroke, n.d.). Althoughinvolvement of the muscles of respiration are not arequired characteristic of the disease, it is often the

case that MD results in such severely weakened respi-ratory muscles that the patient’s breathing becomes ventilator dependent.

Individuals with MD may present with a varietyof respiratory issues affecting speech breathing. Theprogressive muscle weakness leads to reduced lungcapacities and decreased ability to generate adequatesubglottic pressures for phonation (Seikel et al., 2005).Furthermore, Seikel and colleagues indicate that thereduced range of motion seen in individuals with MD,as well as other dysarthrias of the accid type, canresult in reduced breath groups, impaired prosody,

and reduced vocal intensity.Spinal column deformities, when severe, also

hinder breathing abilities. Scoliosis (also termedkyphoscoliosis ) refers to a lateral (i.e., sideways)spinal curvature that is a deviation from the normalvertical line of the spine or vertebral column. Fig-ure 7-3A illustrates a right thoracic scoliosis, as thespinal deviation is to the r ight at the thoracic regionof the vertebral column. According to the NationalScoliosis Foundation (n.d.a), scoliosis is found in2%–3% of the US population, affecting infants to

adults with an average age of onset between 10 and15 years. If the lateral curvature is severe, the ribcagemay press against the lungs and heart and compro-mise cardiopulmonary function.

The vertebral column is aligned in the center of ourback and has two areas of normal anterior curvatureat the cervical and lumbar regions. These curves are

important to maintain an erect posture and providefor maximal mechanical efciency for breathing. Thus,structural deformities of the vertebral column willlimit the natural and efcient expansion and recoil ofthe ribcage. Lordosis refers to abnormally large ante-rior curvatures of the vertebral column. All of us have alittle bit of what may be referred to as “swayback.” Typi-cally, an underlying disease is at the root of a seriouslordosis such as with MD (National Scoliosis Founda-tion, n.d.c). Kyphosis (or “round back”) is the oppositeof lordosis. It is an abnormal increase in the posteriorcurvature of the vertebral column (National Scoliosis

Foundation, n.d.b). This is most often seen in the tho-racic vertebral region where we have a certain degreeof natural rounding. Figure 7-3B shows these spinalcurvatures via a lateral view. You might be familiar withDowagers hump , often associated with aging women.This hump is a type of kyphosis due to a collapse of thevertebrae in the upper thoracic region because of lowbone density or osteoporosis . The key to minimizingor avoiding this is prevention through consuming ade-quate levels of calcium and vitamin D and performing weight-bearing exercises.

Kyphosis LordosisA B

Figure 7-3 Deviations of the spinal column. A . Scoliosis. B . Kyphosis and lordosis. (Modied with per-

mission from Stedman’s medical terminology (2010). Baltimore: Lippincott Williams & Wilkins.)




NEUROLOGICAL PATHOLOGIES

Neurological traumas and diseases are numerous as you read about in Chapter 5. Those disorders of thenervous system that result in dysarthria likely have arespiratory component. Neurological damage impact-ing ventilation and respiration can be widespreadfrom the central nervous system to the peripheral ner-vous system. In the central nervous system, the uppermotor neurons (UMNs), the control circuitry of thecerebellum and basal ganglia, the medullary respira-tory center, the brainstem cranial nerve nuclei, andthe anterior horns of the spinal cord are all involved inbreathing. In the peripheral nervous system, the lowermotor neurons (LMNs), the neuromuscular junction,and the muscles of inspiration and expiration are allinvolved. You are referred back to Chapter 5 on neu-rological pathologies for a discussion of the variousdysarthrias associated with the neuropathologies

mentioned in this chapter. Here, the focus will be on

select pathologies that have a signicant respiratorycomponent involved with management and treat-ment. These include spinal cord injuries and progres-sive neurological diseases.

Prior to a discussion of certain neurological pathol-ogies, a review of the central nervous system controlof respiration is in order. As presented in Chapter 4,central control of respiration is both conscious andunconscious in nature. Voluntary control over breath-ing is evidenced in simple activities such as taking abig breath, holding the breath, and breathing fasteror slower, and in more complex activities such asbreathing for speech production. Voluntary neuralmechanisms for breathing include frontal lobe motorcortices (e.g., premotor cortex, motor strip), parietallobe somatosensory areas, the basal ganglia, thala-mus, and cerebellum. In addition, breathing changesassociated with emotions are mediated by the limbic

lobe (see Figure 7-4). Next time you become emotional,

Lung changes sensedby mechanoreceptors

Cerebralcortex

Respiratorycenter

C3C4C5

Limbicsystem

Bloodstream changessensed by chemoreceptors

DiaphragmOther respiratory

muscles

Phrenicnerve

Figure 7-4 The brainstemrespiratory center with input fromhigher brain regions, the vascularsystem, and the lungs and outputto the muscles of respiration.(Modied with permission fromPremkumar, K. (2004). The massageconnection anatomy and physiology .Baltimore: Lippincott Williams &Wilkins.)




take special note of the effect on your breathing. Infact, you may not even be able to generate and controlthe breath to speak in emotionally charged situations. Although volitional and emotional breathing occurs,our breath is primarily involuntarily controlled as dic-tated by blood chemistry.

Importantly, minute changes in blood chemistry

sensed by peripheral chemoreceptors in the bloodstream and carbon dioxide levels in cerebrospinaluid by central chemoreceptors at the level of themedulla indirectly control breathing. The medullaryrhythmicity center with separate inspiratory andexpiratory centers controls automatic breathing. Inthe pons, the apneustic area promotes inspiration andthe pneumotaxic area inhibits inspiration; togetherthese areas provide input to the medulla to regu-late respiratory coordination. These critical brain-stem respiratory centers may be suppressed throughtrauma, or “narcotized” by drugs or alcohol (see Why You Need to Know box).

mucosa involved with the upper airway structures ofthe velopharyngeal port, the pharynx, the larynx, andthe accessory neck muscles for breathing. Twenty-threespinal nerve pairs (i.e., 8 cervical, 12 thoracic, and theupper 3 lumbar pairs) are involved with innervatingboth the primary and accessory muscles of respiration. You are encouraged to refer back to Chapter 6 to review

the neural innervation for the muscles presentedthere. The motor commands that are sent out from thebrainstem and spinal cord are mediated by the affer-ent input not only from the chemoreceptors but alsofrom the mechanoreceptors located in the pulmonaryapparatus itself (e.g., alveoli) and those located in thechest wall responding to muscle stretch (Hixon & Hoit,2005). Damage to any of these nerves can have a detri-mental effect on respiration.

Spinal Cord Injury

Trauma involving the spinal cord at almost any levelcan impact breathing with trauma at the cervical levelbeing the most severe (see Figure 7-5). For example,Christopher Reeve, the well-known actor and advo-cate for spinal cord research, suffered a high cervicalspinal cord injury (SCI) (C1-C2) during an equestrianrace resulting in quadriplegia and the need for venti-lator supported breathing for the remainder of his life. According to the National Spinal Cord Injury Statis-tical Center (n.d.), spinal cord injuries have a varietyof causes with sports-related injuries accounting for

approximately 9% of cases. The leading cause of spi-nal cord injuries is motor vehicle accidents (approxi-mately 48%) followed by falls (approximately 23%).Similar to traumatic brain injury (TBI), spinal cordinjuries are most prevalent in young adult men.

Why You Need to Know Excessive drinking by college students can result inpulmonary aspiration and/or respiratory failureand death. This excessive drinking is often referredto as “binge drinking” roughly dened as ve ormore drinks in two hours for men or four or moredrinks in two hours for women. As the body is unableto metabolically keep up with the alcohol, the effectsare ultimately revealed in decreased heart rate,breath rate, and gag reex. In turn, the decreasedgag reex may result in pulmonary aspiration ofvomit, potentially fatal due to its asphyxiation ofthe lungs. In addition, both cardio and pulmonaryeffects are seen when blood alcohol levels (from 0.35to 0.40) suppress the medullary respiratory center.Hence, never let a drunk friend “sleep it off;” insteadstay with your friend and call for help if breathingrate is reduced (i.e., eight breaths or less per minute;recall that a normal quiet breathing rate is around12 breaths per minute), if they are unconscious or

semiconscious and do not rouse to a shout or pinch,if their skin is cold or clammy and has a bluishcomplexion, or if they are vomiting without waking! ANY of these signs warrant getting help. Of course, you want to avoid this situation by urging friends, family, and yourself to drink in moderation if at all.

Select cranial nerves and a number of spinal nervepairs are also involved in ventilation. Cranial nervesIX (glossopharyngeal), X (vagus), XI (spinal acces-sory), and XII (hypoglossal) innervate muscles and

Spinal cord

Esophagus

Compression,hemorrhage, and

edema at site of injury

1st rib

Figure 7-5 An illustration of cervical spinal cord injury. (Modi-ed with permission from Anatomical Chart Company.)




Trauma to the spinal cord is often secondary tofractured vertebrae due to displaced bone and/ordiscs that compress the cord itself (Young, 2003),although one can suffer vertebral fracture withoutSCI. When the spinal cord is involved both tissue grayand white matter of the CNS can be impacted as wellas spinal nerves of the PNS carrying afferent and effer-

ent neural information to and from the spinal cord,respectively. Thus, SCI disrupts sensory, motor, andautonomic nervous system functions. The body loca-tion and extent of the disruption is dependent on thelevel and severity of the injury.

One way to classify SCI is “complete” or “incom-plete” in regard to the amount of remaining functionbelow the level of injury. The level of injury refers tothe spinal cord segments and vertebrae and their cor-responding numbers: cervical (1–8), thoracic (1–12),lumbar (1–5), and sacral (1–5). Complete SCI refersto no function below the level of the injury, that is, nosensation or voluntary movement on either side ofthe body below the level of injury. An incomplete SCIis dened as some function present below the levelof injury. In addition, symptoms can also be sec-ondary to autonomic nervous system disruption.These symptoms can include disruption of boweland bladder control, blood pressure regulation, andbody temperature regulation. More specically to theinterest of the SLP is weakness or paralysis of respi-ratory muscles for speech breathing and for swallowsafety. For example, if the injury results in weakened

or paralyzed intercostal and abdominal muscles, thepatient will not be able to produce a productive coughand will be at increased risk for aspiration and pneu-monia. An SCI above C4 may require a ventilator forbreathing.

Hixon and Hoit (2005) present two case examplesof clients with SCI. Here, a brief summary of each caseis presented to give you a glimpse at the type of inter-ventions that can be done to assist individuals with SCIto gain improved speech function. A young woman with a C6 injury as a result of a fall was quadriplegic with limited residual function in her arms and hands.

Although she could speak, her breath support forspeech was severely limited due to weakened musclesof respiration. Her voice lacked intensity, she spoke inshort breath groups, and became fatigued with speak-ing. Due to the level of her injury, innervation to thediaphragm was spared (recall that the diaphragm isinnervated by the phrenic nerve that arises at C3–C5,above her level of injury). Following the SLP’s evalu-ation and consultation with the pulmonologist , anelastic wrap-around binder was used to position theabdominal wall inward and support the body trunk.

This treatment resulted in longer breath group pro-ductions and improved vocal intensity. A second cli-ent was described as a young adult male who suffereda C2 level SCI following a motor vehicle accident. Dueto the level of SCI, he was left with paralysis of thediaphragm, muscles of the rib cage, and muscles ofthe abdomen. As expected, he required a ventilator to

breath. After extensive medical consultation and test-ing, he was determined to be a candidate for a phrenicnerve pacer (see Figure 7-6). A phrenic nerve paceracts as a respiratory neural prosthesis that electricallystimulates the phrenic nerves for diaphragm contrac-tion and resultant inspiration (Hoit & Shea, 1996). Thepacer, along with abdominal binding and behavioraltreatment, resulted in such good speech productionthat he often sounded like a normal speaker (Hixon& Hoit, 2005).

Why You Need to Know A phrenic nerve pacer, also called a diaphragmaticpacer, is an electrode that is placed in the cervicalregion behind the phrenic nerve with a radiof-requency receiver that communicates with anexternal radiofrequency transmitter. The patient isintroduced to the pacer gradually and stimulationis adjusted according to ventilation needs. Potentialcandidates for this type of pacer include individu-als with SCI, ALS, and MS, whereas individualswith COPD would not be candidates (Hoit & Shea,1996).

Progressive Neurological Diseases

The diseases that result in degeneration of certainaspects of the nervous system vary widely in rate ofsymptom progression. Some diseases progress slowlysuch as Parkinson’s disease (PD), some diseases prog-ress rapidly such as amyotrophic lateral sclerosis(ALS) and some are widely variable in progressionrate such as multiple sclerosis (MS). Entire texts aredevoted to the speech and swallowing disorders and

management associated with these diseases (e.g., Yorkston, Miller, & Strand, 2003). Here, a brief over-view of selected diseases is presented along with adescription of each disease’s potential impact onbreathing.

Freidreich’s Ataxia

Freidreich’s ataxia (FA) is a hereditary spinocerebellardegenerative disorder named for the German physi-cian who rst described its symptoms in 1863. It is anautosomal recessive genetic disease meaning that the




affected individual must inherit two affected genes,one from each parent. For this reason, there may beno apparent family history as each parent would be

“silent carriers.” Signs and symptoms associated withthis type of ataxia include a progressive loss of bal-ance and coordination beginning with a poor gait andprogressing to include the trunk and upper extremi-ties. Initial symptoms typically occur between 5 and15 years of age; however, rate of progression varies widely across individuals (Muscular Dystrophy Asso-ciation, n.d.). In addition, muscles atrophy over timeand individuals may develop scoliosis. FA also affectsthe heart and can result in congestion as describedpreviously; these symptoms are managed medically. As the disease progresses, speech and swallowing are

also affected by decreased muscle coordination andtiming of movements. Respiratory effects with ataxicdysarthria in general include reduced coordinationbetween speech processes and within the processof respiration itself. For example, decreased abilityto coordinate inspiration and expiration with result-ing inappropriate timing and explosive expiratorybursts may occur (Seikel et al., 2005). Thus, respira-tory control is an apt target for intervention along with targeting improved timing of tongue, jaw, and lipmovement.

Multiple Sclerosis

Multiple sclerosis (MS) is a progressive disease thatresults in multiple lesions of the oligodendrogliacomprising the myelin in the central nervous sys-tem. Thus, disrupted myelin can occur in the brain,spinal cord, or optic nerves. Sclerosis refers to thescar tissue that is left to replace patches of destroyedmyelin, producing lesions known as MS plaques. Asmentioned earlier, the progression is highly variableacross individuals with the most common patterninvolving remission and relapse. Relapsing-remittingMS is typied by nearly full remissions following anexacerbation of symptoms with a period of stabilityor incomplete remissions with a chronic progres-sion of symptoms. MS is usually diagnosed in youngadults between the ages of 18 and 40 years and ismore common among woman than men. Life expec-tancy is not affected for 85% of those diagnosed withMS (Yorkston, Miller, & Strand, 1995). Table 7-2 liststhe various types of MS based on progression of thedisease.

Given the varied lesion sites associated with MS,symptoms may also be varied. Motor, sensory, andvisual systems may be impacted with symptoms ofunilateral vision loss, sensory loss, and/or motor weakness and spasticity (Johnson & Jacobson, 2007). When dysarthria is present, it is the mixed type, mostoften a spastic–ataxic type with respiratory and pho-natory symptoms prominent (Darley, Aronson, &Brown, 1975; Duffy, 2005). More specic to respira-

tion, Chiara, Martin, and Sapienza (2007) state thatthe dysfunctional neural control of expiratory mus-cles in particular results in reduced subglottic pres-sure for adequate speech production. This, in turn,leads to phonatory problems. The additional difcultyin coordinating respiratory and phonatory functionmay also result in reduced breath groups. Nonspeechrespiratory characteristics can include decreased vital

Antenna

Radiofrequencytransmitter

Electrode

Radio frequency

receiverPhrenic nerve

Lung

Diaphragm

Figure 7-6 An implanted phrenic nerve pacer. (From a Googleimage search of “phrenic nerve pacer.”)

TABLE 7-2

MULTIPLE SCLEROSIS SUBTYPES BASED ONPROGRESSION CHARACTERISTICS

Subtype Course of Disease

Benign One or few episodesRelapsing–remitting Deterioration followed by

near complete recovery Remitting–progressive Gradual accumulation of

decitsProgressing Sudden onset and continuous

progression withoutremission




capacity and, more rarely, the need for ventilatorysupport (Darley, Brown, & Goldstein, 1972).

Parkinson’s Disease

Parkinson’s disease (PD) is also a progressive disor-der of the central nervous system. In the case of PD,the basal ganglia are involved; more specically, the

dopamine producing neurons of the substantia nigradegenerate. This results in the characteristic symp-toms of bradykinesia, rigidity, and resting tremor.Individuals with PD often present with a masked-likeface, a stooped posture, and a “pill-rolling” movementof the hands. As can be seen in Figure 7-7, the trunkexion of an individual with PD is one problem thatcompromises the respiratory system. The onset of PDis typically in the sixth or seventh decade of life and itsrate of progression varies.

Individuals with PD have a decreased ability toautomatically execute learned motor plans. Thisincludes the ease at which they can utilize the respi-ratory system for efcient and effective speech pro-duction. Duffy (2005) notes that the primary speechissues for individuals with PD center on phonation,articulation, and prosody. Specic respiratory symp-toms that are reected in speech breathing difcultiesinclude decreased vital capacity, decreased chest wallexcursion, decreased respiratory muscle strength,irregular breathing patterns, and increased breathing

rate. These symptoms may be due to an “. . . alterationin the agonistic/antagonistic relationship betweenrespiratory muscles during breathing” (Duffy, 2005,p. 198). Furthermore, individuals with PD evidence abowing of the vocal folds which further hinders theability of the respiratory and laryngeal systems to col-laborate for loud, clear speech production. The inter-

action between these two systems is exemplied wellin the Lee Silverman Voice Treatment program, orLSVT (see Why You Need to Know box).

Head bent forward

Masklike facial expression

Rigidity

Stooped posture

Bradykinesia (absence or poverty of normal movement)

Tremor

Figure 7-7 A woman exhibiting symptoms of Parkinson’sdisease. (Modied with permission from LifeART image copyright© 2010 Lippincott Williams & Wilkins. All rights reserved.)

Why You Need to Know The Academy of Neurologic Communicative Dis-orders and Sciences (ANCDS) has taken the leadin providing systematic reviews of treatment andpresenting practice guidelines in the various areasof neurologic communication disorders. One suchreview was a paper on behavioral management

of respiratory/phonatory dysfunction in dysarthria(Yorkston, Spencer, & Duffy, 2003). Among stud-ies reviewed were those by Ramig and colleagues,who investigated the effects of Lee Silverman VoiceTreatment (LSVT) with individuals with Parkinson’sdisease. LSVT focuses on the voice through effortfuland repetitive exercises at the respiratory and pho-natory levels to increase loudness, and in so doing,improve speech quality. The ANCDS concluded thatevidence supporting LSVT is good for immediateposttreatment improvement and has some evidencethat supports long-term maintenance of treatmenteffects (Yorkston et al., 2003).

Amyotrophic Lateral Sclerosis

As mentioned in Chapter 5, ALS is a progressive dis-ease of the motor neurons (refer back to Figure 5-1)that results in both UMN and LMN symptoms. Earlysymptoms may be manifested in limb weakness or in weakness of the muscles of the head and neck result-ing in speech and swallowing problems (i.e., bulbarsymptoms). Onset of the disease is in adulthood and

life expectancy ranges on average from 1 to 5 yearspostdiagnosis. However, a quarter of individualsdiagnosed with ALS survive for more than 12 years(Bromberg, 1999). Death is usually due to respiratoryfailure (Duffy, 2005).

Consistent with involvement of upper and lowermotor neurons, a mixed dysarthria of the spastic-accidtype is common in individuals with ALS. Those speechcharacteristics most indicative of respiratory involve-ment include decreased loudness, reduced breathgroups, and decreased use of prosody manifested in




monoloudness and monopitch. In addition, individuals with ALS may exhibit decreased ability to generate sub-glottic pressure sufcient for coughing (Duffy, 2005).Shortness of breath and decreased vital capacity whilein the supine position, as well as weakness of the dia-phragm, inspiratory and expiratory chest wall muscles,and abdominal muscles can all be expected (Hixon &

Hoit, 2005).

Tracheotomy andMechanical Ventilation

Individuals with a variety of respiratory pathologiesresulting in airway obstruction and/or muscle weak-ness may depend on articial airways and/or venti-lators to meet their respiratory needs. Many of theetiologies associated with these patient groups havealready been discussed in this or previous chapters;these include stroke, TBI, SCI, laryngeal or chesttrauma, and pulmonary, cardiopulmonary, and neu-rodegenerative diseases. Most typically, these patientspresent in intensive care units (ICUs) either in theacute stage of trauma or, alternatively, at end stages ofprogressive disease.

Tracheotomy often follows oral/nasal endotra-cheal intubation (see Figure 7-8). A tracheotomy refersto the surgical incision (see Figure 7-9) made aroundthe second or third tracheal rings, whereas a tracheo-stomy refers to the opening made by the incision. This

opening is also referred to as the stoma . Furthermore,a tracheostomy tube is a short articial airway that isinserted into the trachea through the stoma during

the surgery (also see Figure 7-9). This tube allows fora direct airway into the lower respiratory passages,bypassing upper airway obstruction due to trauma,disease, or surgery. Notice in Figure 7-10 that the tra-cheostomy tube is inserted below the subglottic spacedirectly into the trachea, and thus it is below the truevocal folds. This has important implications for voic-ing possibilities.

A tracheostomy tube has multiple components. As

pictured in Figure 7-11, the outer most tube is referredto as the outer cannula and the innermost tube isthe inner cannula. The obturator is necessary for

Tracheal tube

Carina

Tracheal tube

Figure 7-8 Endotracheal tube placement. (Modied withpermission from LifeART image copyright © 2010 LippincottWilliams & Wilkins. All rights reserved.)

Tracheotomy

Incision in trachea

Tracheostomy tubeinserted in tracheal opening (stoma)

Figure 7-9 Tracheotomy and tracheostomy. (Modied with permission from Moore, K.L, Agur, A.M., Dalley, A.F.( 2010).Essential clinical anatomy (4th ed.). Baltimore: Lippincott Williams & Wilkins.)




tube insertion. A tracheostomy tube can be cuffed oruncuffed. For a cuffed tube, a small balloon (or cuff)surrounds the outer cannula. This cuff can be inated

or deated. When the cuff is inated, expired air can-not travel up to the larynx but instead is directed backout of the stoma. When the cuff is deated, expired airis free to travel around the cannula and up throughthe larynx as long as the stoma is occluded. In this

condition, a deated cuffed tracheostomy tube actsin the same way as an uncuffed tube.

There are different options when it comes to speak-ing with a tracheostomy tube in place. For example,one can deate a cuffed tracheostomy tube or simply wear an uncuffed tube. When either an uncuffed ordeated cuffed tube is worn and the stoma is occluded,

expired airow is directed superiorly through the larynx. This allows the air to pass between the adductedvocal folds and through the oral and nasal cavities,thereby allowing for speech to occur. The stomacan be occluded either manually with a nger or byusing a speaking valve (see Figure 7-12). This is a oneway valve that is tted on the stoma end of the tra-cheostomy tube that allows the patient to breathe inthrough the valve, but on expiration the pressure ofexpired air closes the valve so that air is redirected tothe upper airway similar to manual occlusion (see the Why You Need to Know box for a discussion of vari-ous speaking valves). The speaking valve then allowsthe patient to speak on expired air without having tomanually occlude the stoma.

When it comes to deating a cuffed tube or using anuncuffed tube, a caveat is in order. There may be con-traindications regarding cuff deation. For instance,the patient may be at risk for aspiration due to exces-sive oropharyngeal and tracheal secretions. There-fore, working closely with nursing staff and obtainingmedical clearance prior to targeting voice and speechproduction is imperative. Similarly, decisions must be

made regarding the necessity and advantage of plac-ing a tracheostomy tube over the more short-termendotracheal intubation. Many texts offer in-depthdiscussion of these matters for the SLP (e.g., Johnson& Jacobson, 2007).

Vocal folds

SubglottalspaceThyroid gland

Inflated cuff

Figure 7-10 Sagittal view of the placement of a tracheostomytube. (Modied with permission from Stedman’s medical dictionary (2005) (28th ed.). Baltimore: Lippincott Williams & Wilkins.)

Outer cannula Cuff

Balloon forcuff inflation/ deflation

Inner cannula Obturator

Figure 7-11 Components of a tracheostomy tube. (Modied with permission from Pillitteri, A. (2009). Maternal and child health nursing: Care of the childbearing and childrearing family (6th ed.). Philadelphia:Lippincott Williams & Wilkins.)




Patients may require mechanical ventilation—or a breathing machine—for breath support due tohypoxemia, hypercapnia , or both. Hypoxemia refers

Figure 7-12 An example of a speaking valve (Aqua PMV 007;Passy-Muir Inc., Irvine, CA). (From Passy-Muir Web site productcatalog (http://www.passy-muir.com/products/pmvs/pmv007.aspx).)

Why You Need to Know A number of considerations must be given prior tothe placement of a speaking valve for a tracheos-tomy and/or ventilator-dependent patient. Oftentimes, an SLP is consulted early in the process forconsideration of a speaking valve. The preplacementevaluation of the patient is conducted ideally withcollaboration among team members—the SLP, the

respiratory therapist, and the nursing staff underthe direction of the pulmonologist. Areas theSLP will be directly responsible for includean in-depth oral motor examination, evaluationof cognitive and motivational status for speaking,and adequate alertness throughout most of theday to support verbal communication (Johnson& Jacobson, 2007). In addition, the SLP should beknowledgeable regarding the various types of speak-ing valves that are available as well as manufac-turer support. Fortunately, professional meetingssuch as the annual convention of the AmericanSpeech-Language-Hearing Association provideextensive opportunities to view and learn abouttracheostomy tubes and the various speaking valvesavailable through demonstration and interactiondirectly with manufacturers’ representatives.

Intravenous (IV) bag

Pump

Heart monitor

Nasogastric tube

Electrodes

IV Catheter

Endotrachealintubation

Mechanicalventilator

Figure 7-13 A patient inan intensive care unit on me-chanical ventilation for breathing.(From http://www.medem.com/medem/images/jamaarchives/

JAMA_Practice_HealthCare_ lev20.)

http://www.passy-muir.com/products/pmvs/pmv007.aspx


http://www.medem.com/medem/images/jamaarchives/JAMA_Practice_HealthCare_lev20









to low pulmonary artery oxygen levels and hypercapniarefers to elevated blood carbon dioxide levels. Ventila-tors are set according to air pressure, air volume, andrespiratory rate. A number of factors play into thesesettings such as disease state and medical status of thepatient. Regardless, it is the physician, most typically apulmonologist, who determines the settings and works

with a team of professionals to carry out the orders andkeep the physician informed. This team includes a respi-ratory therapist, a nurse, and, often, an SLP. Althoughmechanical ventilation is common in intensive care andacute settings, sometimes it is necessary over the longterm and therefore is also seen in home health settingsand long-term care settings. Indeed, some individualsfunction remarkably well for a number of years withportable ventilators. It should also be noted that a num-ber of less invasive means are available to assist a patient with the work of breathing if full ventilator support isnot needed (e.g., a full facial mask that delivers positivepressure to the patient’s airway). Figure 7-13 illustratesa patient on a ventilator; the pictured scene is typical ofthe number of tubes and machines utilized in an ICU.

SLPs may work with patients as they are weanedfrom ventilators and tracheostomy tubes to sponta-neously breathe on their own. A speaking valve maybe a good intermediate step for this weaning processas the patient goes from full breathing through a tra-cheostomy tube to the complete occlusion of the tubethrough capping it (Johnson & Jacobson, 2007).

Summary

This chapter provided an introduction to a numberof respiratory pathologies that can affect speechbreathing and the potential role of the SLP. When

disease or trauma disrupts one’s ability to breathe,the power source for voice and indeed all of speechis curtailed. Difficulties range from total inability touse the breath for speech as in intubated patientsto primary impact on the ability to coordinate andcontrol the airstream for the most efficient use forspeech as seen in patients with ataxic dysarthria.

Because respiration serves as the very foundationof speech, understanding the various patholo-gies and their impact on the air supply equips thespeech–language professional to target respiratorymanagement in a team setting to achieve the bestoutcome possible for speech.


Your study of Chapter 7 should have informed you ofa number of factors that support the physician’s diag-nosis of PVFM disorder. In thinking about respiratory

pathologies, PVFM disorder is a result of airway obstruction, where the vocal folds themselves get in the way ofinspiration. This was noted in the case description re-garding inhalator y stridor. Recall that str idor is caused by

the creation of air turbulence during inspir ation throughadducted vocal folds. Indeed, a hallmark symptom of thisdisorder is difculty breathing in. Another clue that thismay be a case of PVFM disorder is the close associa-

tion of symptoms to physical exercise . Other trigger s forPVFM include smoking and acid reux, both exhibitedby this patient. Although the diagnosis of PVFM disorderis accurate, the physician would likely take the oppor-

tunity to educate Richard regarding what he is doing tohis lungs through his smoking behavior and the possibleoutcome of chronic bronchitis and emphysema. Qualityof life is often diminished when one is forced to live withCOPD. This could turn out to be a real issue for Richardif he does not defeat his smoking habit.



PART 3 SUMMARYPart 3 (Chapters 6 and 7) presented information regarding respiratory anatomy, physi-ology, and pathology. The understanding of the respiratory system and its patholo-gies prepares you to build on this foundational knowledge for speech production as we move to the upstream speech systems of phonation, articulation, and resonance.

Respiration serves as the power supply for speech production. Air pressures, volumes,and ows are generated in the pulmonary apparatus by active (i.e., muscles) and pas-sive (e.g., elastic recoil of the lungs) forces. The movement of air in and out of thelungs through the process of ventilation is critical for the life-sustaining process ofrespiration but also quite literally gives us air to speak on. Thus, pathologies that affectventilation for respiration also affect our power supply for speech. These pathologiesare many and varied, resulting from diverse etiologies such as airway obstruction,musculoskeletal deformities, and neurologic disease. Some of these pathologies aretransient in nature and are resolved with acute medical intervention (e.g., asthma);others are persistent and move into chronic and oftentimes progressive stages such aschronic obstructive pulmonary disease, muscular dystrophy, and amyotrophic lateralsclerosis. Chapter 7 concluded with an introduction to the breath support systemsof tracheostomy and mechanical ventilation. The speech–language pathologist needsto be aware of the impact these diseases and support systems have on breathing forspeech production to effectively intervene with these patients given a team approach(e.g., doctors, respiratory therapists).

PART 3 REVIEW QUESTIONS 1. Describe the support framework for the respiratory system in as much detail as

possible. 2. How does the exchange of oxygen and carbon dioxide take place within the

lungs? 3. What is the difference between lung volume and lung capacity? List and describe

as many of the volumes and capacities as you can. As far as breath support forspeech or other vocal activity is concerned, which lung capacity is probablymost relevant, and why?

4. How do the inspiratory and expiratory phases of respiration change from vegeta-tive to vocal function?

5. Explain how passive forces act during respiration. 6. Describe how inspiration takes place, using such terms as pulmonary pressure,

atmospheric pressure, and Boyle’s law. 7. What are the neural underpinnings of the respiratory system? How might neuro-

logical pathology affect breathing? 8. Contrast ventilation with respiration and indicate one respiratory pathology that

compromises each. 9. How do the respiratory symptoms associated with paradoxical vocal fold move-

ment disorder differ from symptoms associated with asthma? 10. Why do individuals with chronic obstructive pulmonary disease speak on

shorter breath groups? 11. Why do individuals with congestive heart failure speak with decreased loudness? 12. Name two musculoskeletal conditions that may impact breathing for speech.

158




13. Why would an individual with a spinal cord injury at C1/C2 be a better candi-date for a phrenic nerve pacer than an individual with a spinal cord injury atC6/C7?

14. Providing therapy on the timing of the respiratory cycle and coordination of thestructures involved with ventilation is appropriate for an individual with whattype of progressive neurological disease?

15. Individuals with pathologies affecting the respiratory system often have in-creased risk for aspiration. Why?

16. What impact could an uncuffed or deated cuffed tracheostomy tube have onswallow safety?



PART 4Anatomy,Physiology, andPathology of thePhonatory System



163



processes (III-B)

Learning Objectives• You will be able to discuss the framework that supports the phonatory system.• You will be able to list and describe the muscles that mediate phonator y activity.• You will be able to dene the basic concepts involved in phonation, including but not limited

to airow, Bernoulli effect, fundamental frequency, harmonics, octaves, and subglottic pressure.

• You will be able to describe the mechanics of phonation in terms of the Myoelastic Aerody-namic Theory and the Cover–Body Model.

CHAPTER 8

Anatomy and Physiologyof the Phonatory System


ary- pertaining to the arytenoid cartilages ary epiglottic folds

cerato- horns cerato cricoid ligaments

crico- pertaining to the cricoid cartilage crico tracheal membrane

genio- pertaining to the chin genio hyoid muscles

glosso- pertaining to the tongue glosso epiglottic folds

hyo- pertaining to the hyoid bone hyo thyroid membrane

infra- below infra hyoid muscles

inter- between inter arytenoid muscles

musculo- pertaining to muscles musculo cartilaginousmyo- pertaining to muscles myo elastic aerodynamic theory

para- beside; to the side of para median position

pars part of a larger anatomical structure pars oblique

stylo- pertaining to the styloid process stylo hyoid ligament

sub- below sub glottic pressure

supra- above supra hyoid muscles

thyro- pertaining to the thyroid cartilage thyro arytenoid muscles



164 PART 4 ANATOMY, PHYSIOLOGY, AND PATHOLOGY OF THE PHONATORY SYSTEM

Clinical Teaser

Destiny is a typical 15-year-old sophomore in high school.She has many friends and is a very sociable person. She is ac-

tive in extracurricular school activities, especially cheerleadingand singing in the school choir. She has a younger sister andan elder brother at home. Because of all the activities she andher siblings are into, home life is a bit chaotic. The entire fam-ily is quite vocal and there is a lot of yelling among Destinyand her siblings. Destiny loves being the center of attention;however, she constantly has to vie for her parents’ attentionalong with her brother and sister. It seems like the child whois loudest is usually the one noticed by mom and dad. Over the past several months, Destiny has noticed thather voice fatigues very rapidly over the course of a typicalday. She also notices that her vocal pitch is much lower thanit normally is. She has been struggling with the vocal aspectof her cheerleading and also notices that while she sings shehas trouble hitting the high notes. Her voice quality is veryhoarse and there is a certain degree of breathiness in her

voice as well. Although it is sometimes painful for Destiny to cheerlead and sing, she continues to do so. Destiny’s parents have also noticed the deterioration ofher voice over the last couple of months. They are concerned

that Destiny’s voice is worsening. They call their primary carephysician who examines Destiny and then recommends her

to an otorhinolaryngologist, or ENT doctor. The ENT con-ducts a more thorough examination of Destiny’s voice. Sheuses a beroptic endoscope with stroboscopy to observe theanatomy and physiology of Destiny’s vocal folds as she pho-nates. Based on the examination, the ENT diagnoses Destinywith bilateral vocal nodules, approximately 1.5 mm in size, on

the juncture of the anterior one-third of the length of the

vocal folds. The ENT refers Destiny to your clinic and recom-mends that she receive voice therapy. Note any terms or concepts in the foregoing case study

that are unfamiliar to you. As you read the rst chapter of this part, pay particular attention to the anatomy and physi-ology pertinent to this case. We will return to this case at

the conclusion of this part.

Introduction

In Chapter 4, you learned that the nervous systemis the control center for speech production in muchthe same way the CPU is the control unit for a com-puter. The respiratory, phonatory, and articulatory/resonance systems then can be thought of as thecomputer’s peripherals, although these peripheralshave quite different functions than the peripherals you’d see with a computer. You learned in Chapter 6that the respiratory system is the power source forspeech production. In this chapter, your attention

will be turned toward the phonatory system—themotor or generator for speech production. The pho-natory system is responsible for the creation of thevocal tone. In other words, it is the system by whichhumans generate voice. An acoustic signal is pro-duced by vibration of the vocal folds. This signal isthen modied and transformed as it passes through

the vocal tract on the way out the lips. The process ofmodication and transformation is accomplished bythe articulatory/resonance system, which will be thefocus of Chapter 10. For now, you will learn to appre-ciate the beauty and sophistication of the humanvocal mechanism.

Anatomy of the Phonatory System

In Chapter 6, a house building analogy was used to

describe the anatomy of the respiratory system. To alesser extent, the same analogy can be used to describethe anatomy of the phonatory system. Recall that thehouse building analogy involved the construction ofa foundation and framework (i.e., bones, cartilages,and connective tissue); installation of insulation (i.e.,muscles); erection of walls (i.e., mucous membranes);and installation of the electrical system (i.e., thenervous system).

In the sections that follow then, the anatomy of thephonatory system will be presented according to thisanalogy. The foundation and framework (i.e., bones,cartilages, and connective tissue) will be discussedrst. Then, muscles that are important to the func-tion of the phonatory system will be presented (i.e.,the insulation). Following the muscles, mucous mem-branes (i.e., the walls) will be described. Finally, theneural underpinnings (i.e., the electrical system) ofthe phonatory system will be presented.

THE FRAMEWORK FORTHE PHONATORY SYSTEM

The foundation or framework of the phonatory sys-tem includes the hyoid bone and the larynx . Thehyoid bone can be thought of as the superior bound-ary of the phonatory system. The larynx is a muscu-locartilaginous structure that resides inferiorly tothe hyoid bone and is attached to it by membranes.The trachea is immediately inferior to the larynx andis also attached to it by a membrane or ligament (thetrachea was described more fully in Chapter 6 as partof the respiratory system). Figure 8-1 provides anillustration of the phonatory system.



CHAPTER 8 ANATOMY AND PHYSIOLOGY OF THE PHONATORY SYSTEM 165

The Hyoid Bone

The hyoid bone can be seen in Figure 8-1 and is furtherillustrated in greater detail in Figure 8-2. It is locatedin the upper region of the neck approximately at thelevel of the third cervical vertebra (C3) and is imme-diately superior to the larynx. Upon inspection, the

hyoid is somewhat horseshoe or U shaped, with theopen end facing posteriorly (i.e., toward the esopha-gus). An interesting fact about the hyoid bone is thatit does not articulate with any other bone, but ratherit is suspended in place by the stylohyoid ligaments coming from the styloid processes of the temporalbones of the skull.

Technically, although the hyoid bone and larynxare connected, the hyoid is not considered an integralcomponent of the larynx. Rather, the hyoid is consid-ered part of the tongue complex, serving as the pointof attachment for several tongue muscles comingfrom above. Not only do muscles make attachmentsto the hyoid bone from above, but muscles also makeattachments to the hyoid from below. As such, thehyoid bone is literally suspended in place by a total of22 or 23 pairs of muscles. Many of these muscles willbe presented later in this chapter.

As illustrated in Figure 8-2, the hyoid bone con-sists of a corpus (i.e., body), two greater cornua (i.e.,horns), and two lesser cornua. The corpus has a con-vex anterior surface and a concave posterior surface.Projecting posteriorly and somewhat superiorly are

the two greater cornua, each one attached to a lateralborder of the corpus. The lesser cornua rise superiorlyfrom the juncture of the corpus and greater cornua.They resemble “devil’s horns.” Both the greater andlesser cornua, as well as the corpus of the hyoid, arethe point of origin or insertion of muscles.

Mandible

Hyoid bone

Thyroidcartilage

Trachea

Clavicle

Sternum

Mastoid

process

Styloidprocess

Stylohyoidligament

Figure 8-1 The phonatory system, including the larynx, hyoidbone, and other associated structures. (Modied with permissionfrom Moore, K.L., Dalley, A.F., Agur, A.M. (2009). Clinically orientedanatomy (6th ed.). Baltimore, MD: Lippicott Williams & Wilkins.)

Greater cornu

Lesser cornu

Fibrocartilage

Corpus

Greater cornu

Lesser cornu

Corpus

Right anterolateral view of hyoid bone

Anterosuperior view of hyoid bone

Figure 8-2 Anterolateral and anterosuperior views of thehyoid bone, with selected landmarks. (Modied with permissionfrom Moore, K.L., Dalley, A.F., Agur, A.M. (2009). Clinically orientedanatomy (6th ed.). Baltimore, MD: Lippicott Williams & Wilkins.)

Why You Need to Know The hyoid bone is variable from specimen to speci-men. For example, in some instances, one or bothlesser cornua may be absent. This does not create aproblem for the person who has this condition. Themuscles will simply attach to an alternate structure.

The Larynx

The human larynx is a complex musculocartilaginousstructure found in the anterior region of the neck (seeFigures 8-1, 8-3, and 8-4) approximately from the levelof the third cervical vertebra (C3) to C6. For most peo-ple (especially males), the larynx can be located quitereadily by the prominent bulge extending outward inthe neck, commonly referred to as the Adam’s apple.In reality, the Adam’s apple is a landmark on the larg-est of all the cartilages composing the larynx.




As seen in Figure 8-3, the larynx is composed of atotal of nine cartilages along with their connectingmembranes and ligaments. Although there are ninecartilages in total, only six have distinct names asthree of the cartilages are paired. The three unpairedcartilages are the thyroid, cricoid , and epiglot-tis . The three paired cartilages are the arytenoids, cuneiforms , and corniculates . The thyroid, cricoid,and arytenoids are all classied as hyaline cartilage, which has a tendency to ossify with advanced age.The remaining cartilages (i.e., epiglottis, cuneiforms,and corniculates) are classied as elastic cartilage. In

the following paragraphs, a more thorough descrip-tion will be provided for each cartilage, along with theconnecting membranes that are noteworthy.

Thyroid Cartilage

The thyroid cartilage is further illustrated in Figure8-4. It is the largest of all the laryngeal cartilages. Thethyroid is formed by two quadrilateral-shaped platesof cartilage called the thyroid laminae . The two lami-nae are fused together at midline anteriorly, form-ing the thyroid angle . In adult males, this angle is

approximately 90 degrees; in adult females, the angleis approximately 120 degrees. The fusion of the twolaminae is not complete. Instead, the two laminaeseparate superiorly forming the thyroid notch . Imme-diately below the thyroid notch is the point where thethyroid cartilage projects most anteriorly. This pointof projection is called the thyroid prominence or the Adam’s apple. The manner in which the two laminaefuse anteriorly means that the thyroid cartilage is simi-lar in shape to the hyoid bone with an open posterior.On each thyroid lamina, there may be a prominentridge running obliquely along the surface. This ridge

is referred to as the oblique line , and actually may be atendon for the sternothyroid and thyrohyoid musclesthat attach to the larynx at this point.

An examination of Figure 8-4 (A, B, and D) revealstwo pair of cornua projecting superiorly and inferi-orly (one pair of each is found at the posterior termi-nus of each thyroid lamina). By comparison, the twosuperior cornua are longer yet more slender thanthe two inferior cornua . The superior cornua projectsuperiorly, posteriorly, and somewhat medially (i.e.,they take an upward, backward, and slightly inward

Epiglottis

Triticialcartilage

Superior cornu Oblique line

Laryngealprominence

Lamina

Thyroidcartilage

Cuneiform cartilage

Arytenoidcartilage

Cricoidcartilage

Corniculate cartilage

Apex

Muscular process

Vocal processBase

Arytenoid articular facetThyroid articular facet

Anterior arch

Posterior quadrate lamina

POSTERIOR ANTERIOR

Lateral view Anterior view

Epiglottis

Triticial cartilage

Petiolus

Superior cornu

Thyroid notch

Laryngealprominence

Lamina

Inferior cornu

Corniculate cartilageApex

Vocal processMuscular process

BasePosterior quadratelamina

Anterior arch

Cuneiformcartilage

Cricoidcartilage

Fovea oblonga

Arytenoid cartilage

Triangular fovea

Thyroidcartilage

Inferior cornu

Petiolus

Arcuate ridge

Figure 8-3 The cartilages of the larynx with selected landmarks. (Modied with permission from Agur, A.M., Dalley, A.F. (2008).Grant’s atlas of anatomy (12th ed.). Baltimore, MD: Lippincott Williams & Wilkins.)




direction). The superior cornua articulate indirectly with the greater cornua of the hyoid bone by way ofthe lateral hyothyroid ligaments (in fact, the entiresuperior surface of the thyroid cartilage articulates with the inferior surface of the hyoid bone by way ofthe hyothyroid membrane ; the lateral hyothyroidligaments are simply a thickening of the hyothyroid

membrane where the superior cornua of the thyroidcartilage articulate with the greater cornua of thehyoid). The inferior cornua of the thyroid cartilagearticulate directly with the cricoid cartilage and are heldin place by the capsular ligaments , which are actuallycomposed of a series of ligaments: the anterior, poste-rior, and lateral ceratocricoid ligaments. The union of

Hyothyroidmembrane

Thyroidnotch

Inferior cornu

Capsular(ceratocricoid)ligaments

Epiglottis

Superiorcornu

Thyroidlamina

Obliqueline

Medialcricothyroidligament

Lateralcricothyroid

ligaments

Anterior archof the cricoid

Cricotrachealligament

A B

Epiglottis

Hyothyroidmembrane

Thyroidlamina

Thyroidprominence

Thyroid angle

Cricothyroidligaments

Anterior arch ofthe cricoid

Triticialcartilage

Superiorcornu

Obliqueline

Inferiorcornu

Posteriorquadratelamina of

the cricoid

C

Epiglottis

Hyothyroidmembrane

Corniculatecartilage

Arytenoidcartilage

Vocal processMuscular process

Vocal ligament


the cricoid

Hyoepiglotticligament

Thyroepiglotticligament

Thyroidprominence


D

Petiolus

Posteriorcricothyroidligament

EpiglottisHyothyroidmembrane

Superiorcornu


ArytenoidcartilageVocal

ligament

Inferior cornu

Capsular(ceratocricoid)

ligaments Posteriorquadratelamina ofthe cricoid

Figure 8-4 Various views of the larynx: ( A ) anterior view, ( B) right lateral view, ( C ) sagittal view, and ( D ) posterior view. (Modiedwith permission from Tank, P.W., Gest, T.R. (2008). Lippincott Williams & Wilkins atlas of anatomy. Baltimore, MD: Lippincott Williams& Wilkins.)




the thyroid and cricoid cartilages forms the bilateralcricothyroid joints . These joints will be described inmore detail later in this section on anatomy as well asin the section on physiology.

Epiglottis

The epiglottis is further illustrated in Figures 8-3 and8-4. It somewhat resembles a leaf, with a broad bodytapering into a short, slender stalk. The broad por-tion is referred to as the corpus, and the stalk is calledthe petiolus . The anterior, or lingual, surface of thecorpus is convex and its surface is relatively smooth.The posterior surface of the corpus is concave andappears pitted.

The epiglottis has a vertical orientation. Superiorly,the corpus lies immediately posterior to the root ofthe tongue and the corpus of the hyoid bone. As illus-trated in Figure 8-5, the anterior surface of the corpusis continuous with the root of the tongue by way of asingle medial and two lateral glossoepiglottic folds .The medial glossoepiglottic fold is separated from thetwo lateral glossoepiglottic folds by two pits called valleculae . The corpus of the epiglottis is anchored

to the interior surface of the corpus of the hyoidbone by the hyoepiglottic ligament (see Figure 8-4C). Adipose tissue forming a fat pad lies between the epi-glottis and hyoid bone. Inferiorly, the petiolus extends just behind the thyroid notch and is anchored thereby the thyroepiglottic ligament (see Figure 8-4C).

Arytenoid Cartilages

Greater detail for the arytenoid cartilages is providedin Figure 8-6. The two arytenoids lie on the posteriorsloping border of the posterior quadrate lamina of the

cricoid cartilage, forming the cricoarytenoid joints .The arytenoids resemble a three-sided pyramid withan apex and a base. The three sides include the medialsurface, posterior surface, and anterolateral surface.The medial surfaces of the arytenoids face eachother. The posterior surfaces are on the same planeas the posterior quadrate lamina of the cricoid. Themedial and posterior surfaces of each arytenoid are ata 90-degree angle. The anterolateral surface then pro-ceeds from the medial surface to the posterior surface.

The medial surface of each arytenoid is nonde-script. The posterior surface houses some important

muscles that will be discussed in detail later. Theanterolateral surface of each arytenoid is the mostdetailed of the three surfaces. The anterolateral sur-faces have several landmarks including the triangu-lar fovea, arcuate ridge , and fovea oblonga . The twofoveae are depressions on the anterolateral surface;the triangular fovea is found toward the apex of thearytenoid and the fovea oblonga lies along the base.The arcuate ridge separates the triangular fovea fromthe fovea oblonga. Each of these three landmarksserves as a point of attachment for muscles.

Why You Need to Know The thyroid cartilage is variable from specimen tospecimen. For example, in about one-third of thepopulation, there are small foramens in the regionof the superior cornua where blood vessels maypass as they enter the interior of the larynx (Zemlin,Simmon, & Hammel, 1984). For about 5% of thepopulation, one of the superior cornua may be miss-ing. Although the thyroid cartilage has a symmetricshape for most people, there may be a few caseswhere the cartilage exhibits asymmetry.

Cricoid CartilageGreater detail for the cricoid cartilage is provided inFigures 8-3 and 8-4. This cartilage serves as the low-ermost border or base of the larynx and articulates with the rst cartilaginous ring of the trachea by wayof the cricotracheal ligament . The cricoid is smallerthan the thyroid cartilage, but it is also more stout.The cricoid is composed of two parts: an anteriorarch and a posterior quadrate lamina . The two partsare continuous so that the cricoid cartilage is a cir-cular ring, similar to a signet ring. The anterior arch

lies immediately below the angle of the thyroid wherethe two thyroid laminae meet. The posterior quadratelamina is somewhat broad so that it occupies a por-tion of the open space in the posterior region of thethyroid cartilage.

There are three landmarks of note on the cricoidcartilage. The rst landmark is a pair of oval articularfacets along the lateral margin of the cricoid wherethe anterior arch ends and the posterior quadratelamina begins. These facets are the point of articula-tion of the cricoid cartilage with the inferior cornua ofthe thyroid cartilage, forming the cricothyroid joints

mentioned earlier. The second landmark is a verti-cally oriented ridge along the midline of the posteriorquadrate lamina with two shallow depressions oneither side of the ridge. The ridge is the point of inser-tion of some bers from the esophagus, whereas theshallow depressions are the point of insertion forthe posterior cricoarytenoid (PCA) muscles. Finally,the third landmark is a pair of articular facets along thesuperior surface of the posterior quadrate laminathat serve as the point of articulation of the cricoidcartilage with the two arytenoid cartilages.




Soft palate

Esophagus

Trachea

Hard palate

Tongue

Valleculae

Hyoid bone

Epiglottis

Thyroid cartilage

Pyriformsinus

Vallecula

Medialglossoepiglotticfold

A

B

Epiglottis

Vocal folds

Tongue

Figure 8-5 Mid-sagittal (A ) and superior ( B) views of the laryngeal region with selected landmarks. ( A : Modied withpermission from Anatomical Chart Company; B : Modied with permission from Snell, R. (2004). Clinical anatomy (7th ed.).Philadelphia, PA: Lippincott, Williams & Wilkins.)




In addition to the three landmarks of the antero-lateral surface, there are other noteworthy landmarkson the arytenoid cartilages. Along the base of eacharytenoid where the anterolateral surface meets theposterior surface is a prominent, laterally directedlandmark known as the muscular process . Similarly,along the base where the anterolateral and medial sur-faces meet is an anteriorly directed landmark called the vocal process . These two processes serve as a point ofattachment for some very important muscles that willbe presented later.

Cuneiform and Corniculate Cartilages

To understand the paired cuneiform and corniculate

cartilages, you must know that two folds of tissue runalong the interior of the larynx from the lateral bordersof the corpus of the epiglottis to the arytenoid carti-lages. These folds are referred to as the aryepiglotticfolds (see Figure 8-7). Both the cuneiform and cornic-ulate cartilages are embedded within the aryepiglotticfolds, thereby providing a measure of stability to thefolds. The corniculate cartilages rest atop the apexes

of the arytenoids, and the cuneiform cartilages arefound immediately anterolateral to the corniculates.Because they are embedded within the aryepiglotticfolds, you would not be able to see these cartilages butinstead would see little bumps in the posterior regionof the aryepiglottic folds. The two medial bumps arethe corniculate tubercles and the two lateral bumps

are the cuneiform tubercles (see Figure 8-7).Laryngeal Joints

Two pairs of joints are formed by articulation of thearytenoid and thyroid cartilages with the cricoid carti-lage. The joints formed by articulation of the arytenoidcartilages with the cricoid cartilage are the cricoarytenoid joints. Bilateral articulation of the thyroid cartilage withthe cricoid cartilage creates the cricothyroid joints.

The cricoarytenoid joints are formed by the articula-tion of the arytenoid articular facets located on thebase of the muscular process of each arytenoid carti-lage with the cricoid articular facets located on the lat-eral sloping border of the posterior quadrate lamina ofthe cricoid cartilage. The arytenoid articular facets areconcave, whereas the cricoid articular facets are con-vex. These articulations result in saddle joints thatallow for rocking and some limited gliding movement. A series of ligaments hold these joints in place. Foreach joint, a posterior cricoarytenoid ligament limitsthe amount of forward movement of the arytenoidcartilage upon the cricoid, whereas an anterior cri-coarytenoid ligament limits the amount of backward

movement. As you will learn in more detail later, thelateral and posterior cricoary tenoid muscles (LCAs andPCAs, respectively) and the interarytenoid (IA) muscles(i.e., oblique and transverse arytenoids) act upon this joint by moving the arytenoid cartilages backward, forward, laterally, and medially upon the posterior quad-rate lamina of the cricoid.

The cricothyroid joints are created by articulationof the inferior cornua of the thyroid cartilage with thecricoid cartilage in the region, where its anterior archends and posterior quadrate lamina begins. On eachside, the ceratocricoid ligaments (anterior, lateral,

and posterior) loosely hold the joints in place. The cri-cothyroid joints are pivot joints, allowing the cricoidand/or thyroid cartilages to pivot upon the axes cre-ated by these joints. This is accomplished by contrac-tion of the cricothyroid, thyroarytenoid, and superiorthyroarytenoid muscles that act upon this joint.

The Laryngeal Membranes

An intricate series of membranes binds the various car-tilages of the larynx into a singular unit. Some of thesemembranes have one of their attachments to a laryngeal

Triangular fovea

Arcuateridge

Foveaoblonga

Vocalprocess

Muscularprocess




the cricoid

Anterior view

Figure 8-6 Relationship of the arytenoid cartilages to the cricoidcartilage. (Modied with permission from Oatis, C.A. (2008). Kinesi-ology (2nd ed.). Baltimore, MD: Lippincott Williams & Wilkins.)

Ventricular fold

Corniculate tubercle

Cuneiformtubercle

Aryepiglotticfold

Epiglottis

Vocal fold

Figure 8-7 The aryepiglottic folds with corniculate andcuneiform tubercles. (Modied with permission from Agur, A.M.,Dalley, A.F. (2008). Grant’s atlas of anatomy (12th ed.). Baltimore,MD: Lippincott Williams & Wilkins.)




cartilage, but the other attachment is to a structure out-side the larynx. These are referred to as extrinsic mem-branes. Conversely, there are other membranes whoseattachments are found entirely within the cartilaginousconnes of the larynx. These are called intrinsic mem-branes. Incidentally, the muscles that will be discussedlater are also classied as either extrinsic or intrinsic for

the same reason as the membranes discussed here.Extrinsic Laryngeal Membranes

Three major membranes anchor the larynx in placesuperiorly and inferiorly. As was mentioned earlier,immediately superior to the larynx is the hyoid boneand immediately inferior is the trachea. The extrinsicmembranes then bind the larynx to the hyoid boneand trachea. All three of these membranes were men-tioned previously, but for the sake of enhancing yourlearning, they bear mentioning again. The three extrin-sic membranes are the hyothyroid, hyoepiglottic, andcricotracheal. The prex and root of each of these words indicates where the membrane is located.

As its name indicates, the hyothyroid membraneoccupies the space between the inferior border ofthe hyoid bone and the superior surface of the thy-roid cartilage (refer back to Figure 8-4). This mem-brane is somewhat thicker in its mid-region and alsoposteriorly where it bridges the space between thegreater cornua of the hyoid and the superior cornuaof the thyroid cartilage. In these regions, the hyothy-roid membrane is referred to as the medial and lateral

hyothyroid ligaments. In many cases, small cartilagescalled the triticial cartilages are embedded within thelateral hyothyroid ligaments. The triticial cartilages were not mentioned as components of the larynxbecause they reside outside the cartilaginous con-nes of that structure.

As you have probably already discerned, the hyoepi-glottic membrane binds the epiglottis to the hyoidbone. More specically, it is an unpaired, elastic liga-ment found midline that connects the lingual surfaceof the corpus of the epiglottis to the upper, posteriorsurface of the corpus of the hyoid bone. Recall from aprevious section that the epiglottis is bound in place

by two ligaments. The hyoepiglottic membrane is oneof them. The other—the thyroepiglottic ligament—isnot classied as an extrinsic membrane because itresides completely within the larynx (attaching thepetiolus of the epiglottis to the thyroid cartilage).

The cricotracheal membrane binds the cricoid car-tilage (i.e., the base of the larynx) to the rst trachealring. Because of the size of the cricoid cartilage, therst tracheal ring tends to be larger than all of theother tracheal rings. The membrane courses fromthe inferior border of the cricoid to the superior bor-der of the rst tracheal ring, thereby providing aninferior anchor for the larynx.

Intrinsic Laryngeal Membranes

The intrinsic laryngeal membranes are more complexand are not quite as distinct as the extrinsic mem-branes. Figure 8-8 provides a schematic diagram of theorganization of the intrinsic membranes, while Fig-ure 8-9 provides an illustration of these membranesaccording to posterior and sagittal views of the larynx. Almost all of the intrinsic laryngeal membranesare a part of a single, continuous layer of broelastic

tissue called the elastic membrane . Nearly the entireinterior of the larynx is lined by this membrane. Theelastic membrane is divided into two components:the upper portion is referred to as the quadrangu-lar membrane and the lower portion is known as theconus elasticus .

ELASTIC MEMBRANE

Conus Elasticus Quadrangular Membrane

Medial and LateralCricothyroidLigaments

VocalLigaments

VentricularLigaments

AryepiglotticFolds

Inferior Superior

Figure 8-8 A schematic repre-sentation of the elastic membrane.




The quadrangular membrane is actually a pairedmembrane that originates superiorly along the lateralborders of the epiglottis, then continuing around theadjacent interior walls of the thyroid cartilage until theyterminate at the corniculate cartilages and medial sur-

faces of the arytenoid cartilages. This superior portionof the quadrangular membrane is known as the aryepi-glottic folds. As was mentioned in a previous section ofthis chapter, embedded within the aryepiglottic foldsposteriorly are the corniculate and cuneiform carti-lages. There may be muscle bers within the aryepi-glottic folds, but they tend to be poorly developed.From the aryepiglottic folds, the quadrangular mem-brane continues inferiorly until it terminates as a pair ofthickened ligaments called the ventricular ligaments .The ventricular ligaments course from the angle of thethyroid immediately below the epiglottic attachment to

the triangular foveae of the arytenoid cartilages. Recallthat the triangular foveae are found on the anterolateralsurfaces of the arytenoids in proximity to their apexes.Because of this arrangement, the two ventricular liga-ments approximate each other anteriorly (i.e., at theirthyroid attachment) but separate as they proceed pos-teriorly to the arytenoids. The ventricular ligamentsserve as the point of attachment for the ventricularfolds , more commonly referred to as the “false folds.”

The purpose of the conus elasticus is to bind the thy-roid, cricoid, and arytenoid cartilages. Inferiorly, thismembrane starts as the medial and lateral cricothy-

roid ligaments . The medial cricothyroid ligament canbe found at midline, running from the superior borderof the arch of the cricoid to the inferior border of thethyroid cartilage at the thyroid angle. The two lateralcricothyroid ligaments begin at the superior lateral

margins of the cricoid cartilage, then proceed into theinterior of the larynx, terminating immediately belowthe ventricular ligaments from the quadrangular mem-brane. At this superior margin, the lateral cricothyroidligaments attach themselves anteriorly to the thyroidcartilage just behind and below the thyroid notch ina region called the macula ava anterior . They thenproceed posteriorly to the vocal processes at the baseof the arytenoids. This superior margin of the conuselasticus is known as the vocal ligaments . The vocalligaments are the anchor for the true vocal folds.

Note that both the ventricular ligaments and vocal

ligaments originate at the inner aspect of the thyroidcartilage and then proceed back to the arytenoids.Both sets of ligaments converge at this anterior attach-ment but separate as they move posteriorly. Althoughthe course of the ventricular and vocal ligaments isparallel, the ventricular ligaments are superior to thevocal ligaments, terminating closer to the apices of thearytenoids as opposed to their bases. Subsequently,the ventricular folds are superior to the true vocal folds.

In summary, if you were to label the elastic mem-brane from its superior margin to its inferior margin,the landmarks would include the aryepiglottic folds,

Ceratocricoidligaments

Posteriorcricoarytenoidligament

Cricotrachealligament

Quadrangularmembrane

Thyrohyoidmembrane

Hyothyroidmembrane

Hyoepiglotticligament

Thyroepiglotticligament

Ventricularligament

Vocal ligament

Macula flava anterior

Conus elasticus

A BFigure 8-9 Various membranes of the larynx. A . Posterior view. (Modied with permission from Agur, A.M., Dalley, A.F. (2008).Grant’s atlas of anatomy (12th ed.). Baltimore, MD: Lippincott Williams & Wilkins.) B . Right sagittal view. (Modied with permissionfrom Anatomical Chart Company.)




ventricular ligaments, vocal ligaments, and nally themedial and lateral cricothyroid ligaments. The rsttwo landmarks are part of the quadrangular mem-brane and the remaining landmarks are part of theconus elasticus.

THE MUSCLES OF THE PHONATORY SYSTEM

The muscles of the phonatory system are classiedsimilarly to the laryngeal membranes. That is, musclesare classied as either extrinsic or intrinsic. Extrin-sic muscles have either their origins or insertionson a laryngeal cartilage, but the other attachmentis to a structure outside the larynx. Intrinsic muscleshave their origins and insertions within the carti-laginous connes of the larynx. An intrinsic musclemay reside between two different laryngeal cartilages(e.g., between the cricoid and arytenoid cartilages) orbetween the two partners of a pair (e.g., from the leftarytenoid to the right arytenoid).

With the extrinsic muscles, in most cases, one of theattachments is to the hyoid bone. Some of the muscles

come from anatomical structures superior to the hyoidand then insert somewhere along the superior marginof the hyoid. Others come from structures inferior tothe hyoid and then rise to attach to some point alongthe inferior margin of the hyoid. These muscles arereferred to as suprahyoid and infrahyoid muscles,respectively. A small number of extrinsic muscles

come from structures below the hyoid bone but donot insert onto the hyoid. Although these could beconsidered infrahyoid muscles, they are not typicallyclassied in that manner because they do not make anattachment to the hyoid. These few muscles will sim-ply be classied as miscellaneous extrinsic muscles.

Although the extrinsic membranes were presentedbefore the intrinsic membranes, the intrinsic muscles will be described rst in this section. As far as the physi-ology of the larynx is concerned, the intrinsic musclesplay a greater role than the extrinsic muscles, and forthis reason, the intrinsic muscles will be discussed rst.

It should be noted that all laryngeal muscles—intrinsic and extrinsic muscles alike—are paired. Although Table 8-1 provides the actions of the

TABLE 8-1

ORIGINS, INSERTIONS, AND ACTIONS OF THE INTRINSIC LARYNGEAL MUSCLES


Cricothyroid Anterolateral arch of the cricoid

Pars oblique into the anteroinferior cornu

of thyroid; pars recta

into the inner aspect ofthe lower margin of thethyroid lamina

With thyroid anchored, elevates cricoid; with cricoid

anchored, depresses thyroid;

increases the distancebetween the thyroid andarytenoid cartilages toincrease vocal fold tension

Lateral cricoarytenoid Anterolateral arch of the cricoid

Muscular process and anterior surface of the

arytenoid

Adducts the vocal folds

Oblique arytenoid Posterior muscular process and posterolateral

surface of arytenoid

Near the apex of the opposite arytenoid

Approximates the arytenoidsfor medial compression

Posterior cricoarytenoid Shallow depression of posterior cricoid lamina

Posterosuperior surface of the muscular process of

the arytenoid

Abducts the vocal folds by pulling the arytenoids

backward and outward

Superior thyroarytenoid Upper limit of thyroid notch

Muscular process of arytenoid

Tilts thyroid back to relax vocal folds; pulls muscular

processes forward to aid inmedial compression

Thyroarytenoid: muscularis

Angle of thyroid; posterior surface

Fovea oblonga and base of arytenoids

Primarily serves as a regulator of longitudinal tension, but

can also act as a vocal foldadductor

Thyroarytenoid: vocalis Angle of thyroid; posterior surface

Latero-inferior aspect of the vocal process of the

arytenoidTransverse arytenoid Lateral margin and

posterior surface of onearytenoid

Lateral margin and posterior surface of the

other arytenoid

Approximates the arytenoids for medial compression




Cricoidcartilage

Oblique arytenoid muscle

Arytenoid cartilage:Vocal process

Lateral cricoarytenoid muscle

Arytenoid cartilageMuscular process

Cricothyroid muscle

Vocalis muscle

Thyromuscularismuscle

Transversearytenoid muscle

Posteriorcricoarytenoid muscle

Superior view(Epiglottis removed)

Thyroid cartilage

Thyroarytenoidmuscle

Figure 8-10 The thyroarytenoid muscles. (Modied with permission from Anatomical Chart Company.)

laryngeal muscles, only a brief anatomical descriptionof each muscle will be provided in this section. Muscleaction will be discussed more fully in physiology sec-tion of this chapter.

Intrinsic Laryngeal Muscles

A brief summary of the origin, insertion, and actionof each intrinsic laryngeal muscle is provided in Table8-1. The intrinsic muscles include the thyroarytenoids ,posterior cricoarytenoids (PCAs) , lateral cricoarytenoids ,oblique arytenoids , transverse arytenoids , and cricothy-roids . The name of each of these muscles is a direct hintas to its origin and insertion.

Thyroarytenoid Muscles

The thyroarytenoid muscles course from the inneraspect of the angle of the thyroid cartilage back to thevocal processes and foveae oblonga along the bases of

the arytenoids (see Figure 8-10). In essence, the thy-roarytenoids make up the bulk of the vocal folds. Thesemuscles have two parts—a medial bundle (i.e., thyrovo-calis) that anks the vocal ligament and a lateral bundle(i.e., the thyromuscularis) that serves as the body of themuscle. During abduction , both portions of the thy-roarytenoids appear straight, but upon adduction , thethyromuscularis presents a somewhat twisted appear-ance. Because the vocal folds are composed primarilyof muscle tissue, they have the ability to contract. Theinteresting thing about the thyroarytenoids is the dual

function they play in phonation. The primary purposeof thyroarytenoid contraction is to increase vocal foldtension, but this muscle is also involved in decreas-ing vocal fold tension (this will be discussed in greaterdetail in the section Modications of Vocal Pitch). To alesser degree, the thyroarytenoids may also play a partin their own adduction.

According to Hirano (1974, 1981), the thyroarytenoidsconsist of ve layers of tissue (these layers are summa-rized in Figure 8-11). The epithelial layer (composed ofsquamous cells) is the most supercial of all the layersand assists in maintaining the shape of the vocal folds.The supercial layer of the lamina propria is soft and

Squamous epithelium

Superficial layer of thelamina propria

Intermediate layer of thelamina propria

Deep layer of thelamina propria

Vocalis muscle

Cover

Transition

Body

Superficial

Deep

Figure 8-11 A schematic representation of the layers of thethyroarytenoid muscles.




somewhat gelatinous in its consistency. This layer isresponsible for the mucosal wave that can be viewed when the vocal folds vibrate. The intermediate layer ofthe lamina propria is soft and rubbery due to the elas-tic bers that are found there. The fourth layer, the deeplayer of the lamina propria, is collagenous in consistency,giving it an appearance similar to cotton bers. Finally,

the vocalis muscle is composed of stiff, rubbery bers. AsFigure 8-11 indicates, the epithelial layer and superciallayer of the lamina propria are collectively referred to asthe cover of the thyroarytenoid muscles. The interme-diate and deep layers of the lamina propria are referredto as the transition. Finally, the vocalis muscle is consid-ered to be the main body of the thyroarytenoids.

Vocal fold length varies greatly from individual toindividual. However, on average, vocal fold length inadult males is in the range of 17 to 24 mm. For adultfemales, the range is between 13 and 17 mm. Natu-rally, the vocal folds of children are even shorter butbecome longer as they mature until they reach theadult size for their gender.

Lateral Cricoarytenoid Muscles

The origin of each LCA is the arch of the cricoid carti-lage in proximity to where the arch ends and the pos-terior quadrate lamina begins (see Figure 8-12). Theinsertion is the muscular process of each arytenoidcartilage. In this case, the point of origin is anteriorand inferior to the point of insertion, so contractionof the LCA will have just the opposite effect of thePCA. In other words, the LCA is an adductor muscle;its purpose is to assist in bringing the vocal folds tomidline. To a lesser degree, the LCA also assists inrelaxing the vocal folds.

Oblique and Transverse Arytenoid Muscles

The oblique and transverse arytenoid muscles origi-nate on one of the two arytenoid cartilages and theninserts onto the other. Because these two muscles areconned to the arytenoid cartilages, coursing from oneto the other, they are collectively referred to as the inter-arytenoid (IA) muscles (see Figure 8-12). The origin ofeach oblique arytenoid muscle is the posterior surface ofthe muscular process. The muscle then proceeds alongthe posterior surface to the opposite arytenoid carti-lage near its apex. This arrangement gives the obliquearytenoids an “X” appearance. You would be able tosee the “X” formed by these muscles because they aresupercial to the transverse arytenoid muscles.

The transverse arytenoid muscles originate at thelateral aspect of the posterior surface of one arytenoidcartilage and then course horizontally across the

posterior surface of the two arytenoids to the lateralaspect of the opposite arytenoid cartilage. Some of thedeeper bers continue around to the anterolateral sur-face to intermingle with bers of the thyroarytenoidmuscles. When the oblique and transverse arytenoidmuscles contract, they cause the two arytenoid car-tilages to approximate each other. Because the vocalfolds are attached to the vocal processes and foveaeoblonga, the net action is adduction of the vocal folds.Therefore, the IA muscles are classied as adductormuscles, along with the LCA described earlier.

Cricothyroid Muscles As their name implies, the cricothyroid muscles runbetween the cricoid and thyroid cartilages (see Fig-ure 8-13). The muscles are actually composed of twobundles, the pars recta and pars oblique . Both bun-dles have their origin at the anterior arch of the cri-coid, somewhat lateral to midline. The pars obliquebundle has its insertion along the anterior aspect ofthe inferior cornua of the thyroid cartilage. The parsrecta bundle inserts into the inner aspect of the infe-rior margin of the thyroid lamina.

Why You Need to Know In approximately half of the world’s population,there may be an additional muscle called thesuperior thyroarytenoid. This muscle originates atthe superior-most limit of the thyroid notch andproceeds posteriorly to insert onto the muscularprocess of the arytenoids. Upon contraction, thesuperior thyroarytenoids tilt the thyroid cartilageback, thereby shortening the distance between thethyroid cartilage and the arytenoid cartilages. Thisin turn creates a shortening of the vocal folds, whichrelaxes them.

Posterior Cricoarytenoid Muscles

The posterior cricoarytenoid muscles (referred to asthe PCA muscles) are illustrated in Figure 8-12. These

muscles originate at the shallow depressions imme-diately lateral to the vertical ridge on the posteriorquadrate lamina of the cricoid cartilage. They theninsert onto the muscular processes of the arytenoids.Because the origins of the PCAs are posterior andinferior to their insertions, contraction will cause themuscular processes of the arytenoids to rotate poste-rolaterally. Because the vocal folds are attached to thevocal processes and foveae oblonga of the arytenoids,the net action is abduction of the vocal folds. In fact,the PCA is the only abductor muscle in the larynx.




There is a space between the anterior arch of thecricoid and the thyroid cartilage. The relationshipbetween these two cartilages is similar to the visor onthe helmet of a suit of armor. When the cricothyroidmuscles contract, the thyroid tilts downward and forward and/or the cricoid tilts upward, somewhat simi-

larly to lowering the visor on the helmet. This changesthe angle between the thyroid and cricoid cartilagesand increases the distance between the interior aspectof the thyroid cartilage and the arytenoid cartilages.Because the vocal folds course between these twopoints, contraction of the cricothyroid muscles results

Transverse arytenoid(posterior view)

Oblique arytenoid(posterior view)

Lateral cricoarytenoid(lateral view)

Posterior cricoarytenoid(posterior view)

Interarytenoid

muscles

Muscularprocess

Transverse arytenoid muscle

Oblique arytenoid muscles

Lateral cricoarytenoid muscle

Posterior cricoarytenoid muscle

Interarytenoidmuscles

Posterior view

A BC D

Figure 8-12 The posterior and lateral cricoarytenoid muscles and the interarytenoid muscles. A . Posterior cricoarytenoid. B . Lateralcricoarytenoid. C . Oblique arytenoid. D . Transverse arytenoid. ( Top: Modied with permission from Anatomical Chart Company; A–D :Modied with permission from Agur, A.M., Dalley, A.F. (2008). Grant’s atlas of anatomy (12th ed.). Baltimore, MD: Lippincott Williams &Wilkins.)




in a lengthening of the vocal folds, thereby increasingtheir tension. As such, the cricothyroid muscles areclassied as tensor muscles.

Extrinsic Laryngeal MusclesThe extrinsic laryngeal muscles are subclassied aseither suprahyoid or infrahyoid muscles. Suprahyoidmuscles have one of their attachments superior tothe hyoid bone; infrahyoid muscles have one of theirattachments inferior to the hyoid bone. Upon con-traction, the net action of suprahyoid muscles is anelevation of the hyoid bone, and subsequently the larynx because the hyoid and larynx are coupled by thehyothyroid membrane. The net effect of contractionof the infrahyoids (and the miscellaneous muscles

mentioned later) is to depress or lower the hyoid bone

and larynx. The importance of these actions will bediscussed more fully in the section on physiology.

Suprahyoid Muscles

The suprahyoid muscles include the digastricus , sty-lohyoid ,mylohyoid , geniohyoid , hyoglossus , and genio-glossus . Table 8-2 provides a summary of the origins,

insertions, and actions of these muscles. Four of thesemuscles originate in the region of the mandible (i.e.,the jaw). From supercial to deep, these include thedigastricus (anterior body), mylohyoid, geniohyoid,and genioglossus. Supercial refers to muscles thatare closer to the surface of the skin. Deep then refersto muscles that are farther away from the surface ofthe skin, or closer to the base of the tongue inside theoral cavity in this case.

As its name indicates, the digastricus has twobellies—an anterior one and a posterior one (see Figure8-14). The anterior belly has its origin inside the lowerborder of the mandible. It then courses downward andbackward until it joins with the posterior belly in an inter-mediate tendon that penetrates the stylohyoid musclebefore inserting onto the lesser cornua of the hyoidbone. The posterior belly originates at the mastoid pro-cess , which is the rounded base of the skull immediatelybehind the ear, then courses downward and forward tomeet the anterior belly at the intermediate tendon. If thehyoid bone is anchored, contraction of the digastricus will assist in depressing the mandible (i.e., opening themouth). With the mandible xed, contraction will assist

in elevating the hyoid bone and larynx.

Cricoidcartilage

Thyroid cartilage

Pars recta

Pars oblique

Cricothyroidmuscle

Figure 8-13 The cricothyroid muscle. (Modied with permis-sion from Agur, A.M., Dalley, A.F. (2008). Grant’s atlas of anatomy (12th ed.). Baltimore, MD: Lippincott Williams & Wilkins.)

TABLE 8-2

ORIGINS, INSERTIONS, AND ACTIONS OF THE SUPRAHYOID EXTRINSIC LARYNGEAL MUSCLES


Digastricus: anteriorbelly

Inside lower border of mandible

Lesser cornua of hyoid bone

Elevates the hyoid bone or depresses the mandible

Digastricus: posterior belly

Mastoid process of temporal bone

Lesser cornua of hyoid bone

Genioglossus Mental symphysis of mandible

Lower bers to hyoid; upper bers to

inferior tongue

Primarily an extrinsic tongue muscle; it may also help

position larynx Geniohyoid Lower part of mental symphysis of mandible

Anterior corpus of hyoid With the mandible anchored, pulls the hyoid bone up and

forwardHyoglossus Corpus and greater

cornua of hyoidPosterolateral surface of tongue

Primarily an extrinsic tongue muscle; it may help position

larynx Mylohyoid Inner surface of body of

mandibleMidline raphe; posterior bers to hyoid corpus

Elevates the hyoid bone or depresses the mandible

Stylohyoid Styloid process of temporal bone

Junction of hyoid corpus and greater

cornua

Elevates the hyoid bone up and back




The stylohyoid muscle passes from the styloid pro-cess at the base of the skull to the junction of the cor-pus and greater cornua of the hyoid bone (see Figure8-14). Upon contraction, this muscle will draw thehyoid bone and larynx upward and backward.

The mylohyoid muscle is also illustrated in Figure8-14. It forms essentially the muscular oor of the oralcavity. Its origin is the mylohyoid line that runs alongthe inner surface of the corpus of the mandible. Fibersfrom each side of the mandible course downward andmedially until the two sides meet at the midline raphe .

The posterior-most bers along the midline raphe insertonto the corpus of the hyoid bone. When this musclecontracts, it will either elevate the hyoid bone and larynx or depress the mandible, depending upon whichanatomical structure is anchored and which is not.

The geniohyoid muscle originates at the lower por-tion of the mental symphysis of the mandible (i.e.,inside the chin) and then courses inferiorly to insertonto the anterior surface of the corpus of the hyoid bone(see Figure 8-15). Contraction of this muscle will resultin elevation of the hyoid bone in a forward direction.

Stylohyoid

Posterior belly of digastricus

Intermediate tendonof digastricus

Mylohyoid

Anterior belly of digastricus

Mylohyoid

Hyoid bone

Thyroid cartilage

Posteriorbelly of

digastricusIntermediatetendon

Anteriornteriorbelly ofelly ofdigastricusigastricus

Hyoid Hyoid Hyoid

Anteriorbelly ofdigastricus

Anteriornteriorbelly ofelly ofdigastricusigastricus

Anteriorbelly ofdigastricus

Midline rapheMylohyoid

Stylohyoid

A B CFigure 8-14 Suprahyoid muscles: A. digastricus, B. mylohyoid, and C. stylohyoid. ( Top: Modied with permission from Agur, A.M., Dalley, A.F.(2008). Grant’s atlas of anatomy (12th ed.). Baltimore, MD: Lippincott Williams & Wilkins; A–C : Modied with permission from Cael, C. (2009).Functional anatomy: Musculoskeletal anatomy, kinesiology, and palpation for manual therapists. Baltimore, MD: Lippincott Williams & Wilkins.)




Genioglossus

Geniohyoid

Mylohyoid

Hypoglossus

Hyoid bone

Sternohyoid

Superior belly of omohyoidSternocleidomastoid

Thyrohyoid

Posterior bellyof digastric

Stylohyoid

Geniohyoid

(mylohyoidcut to show)

Mylohyoid

Mylohyoidline

Hyoglossusyoglossus

Geniohyoid

GenioglossusHyoglossus

Hyoid

A BFigure 8-15 Suprahyoid muscles: A. geniohyoid, B. genioglossus, geniohyoid, and hyoglossus. ( Top: Modied with permission fromAgur, A.M., & Dalley, A.F. (2008). Grant’s atlas of anatomy (12th ed.). Baltimore, MD: Lippincott Williams & Wilkins; A, B: Modiedwith permission from Cael, C. (2009). Functional anatomy: Musculoskeletal anatomy, kinesiology, and palpation for manual therapists. Baltimore, MD: Lippincott Williams & Wilkins.)




The hyoglossus muscle is also illustrated in Fig-ure 8-15. It is a muscle primarily associated with thetongue, but it does have an indirect action upon thelarynx by way of the hyoid bone. Its origin is the cor-pus and greater cornua of the hyoid bone, and itsinsertion is along the sides and back of the tongue.This muscle is thought to inuence positioning of the

larynx in relation to tongue activity.The course of the genioglossus muscle is from theinner aspect of the mental symphysis of the mandibleto the tongue and hyoid bone (see Figure 8-15). As thegenioglossus runs in a posterior direction, upper bersinsert into the inferior regions of the tongue, whereaslower bers insert onto the corpus of the hyoid bone. Although this muscle is primarily associated with thetongue, it may play a part in positioning the larynx inmuch the same way as the hyoglossus muscle.

Infrahyoid Muscles

The extrinsic infrahyoid muscles are summarized inTable 8-3 according to their origins, insertions, andactions. The infrahyoids include the thyrohyoid , ster-nohyoid , and omohyoid muscles. The thyrohyoid musclescourse from the oblique lines of the thyroid cartilages tothe lower margin of the greater cornua of the hyoid bone(see Figure 8-16, top drawing and drawing C). Uponcontraction, the thyrohyoid muscles will either depressthe hyoid bone or elevate the thyroid cartilage, depend-ing on which of these two structures is anchored.

As can be seen in Figure 8-16 (top drawing anddrawing A), the sternohyoid muscles originate alongthe posterior aspect of the manubrium of the sternumas well as the medial aspect of the clavicle, then coursevertically to insert into the inferior border of the corpusof the hyoid bone. Contraction of these muscles resultsin depression (i.e., lowering) of the hyoid bone.

Similar to the digastricus muscles, the omohyoidmuscles consist of two bodies joined by intermediatetendons (see Figure 8-16, top drawing and drawing B).The inferior bellies of the omohyoid muscles have theirorigins along the superior borders of the scapulae. Thebers then course almost completely horizontally untilthey join bers of the superior bellies at the interme-diate tendons. The intermediate tendons are held inplace by tendinous slips that anchor onto the sternumand rst rib. From the intermediate tendons, bers ofthe superior bellies course vertically and somewhatmedially to insert into the inferior margin of the greatercornua of the hyoid bone. Although the omohyoidmuscles assist in preventing the neck region from col-lapsing during deep inhalation, they may also assist indepressing the hyoid bone.

Miscellaneous Extrinsic Muscles

Two muscles act upon the larynx in much the same way as the infrahyoid muscles, yet they are not clas-sied as infrahyoid because they have no attachmentto the hyoid bone. These are the sternothyroid and

TABLE 8-3

ORIGINS, INSERTIONS, AND ACTIONS OF THE INFRAHYOID AND MISCELLANEOUS EXTRINSICLARYNGEAL MUSCLES


Inferior pharyngeal constrictor a

Lower portion of tube which originates at

the base of the skull

Eventually becomes continuous with

the esophagus

Provides resonance characteristics for speech; may pull down on the

posterior quadrate lamina of thecricoid

Omohyoid: inferior belly

Upper border of scapula

Intermediate tendon Prevents the neck region from collapsing during deep inhalation;

may assist in depressing the hyoidbone

Omohyoid: superior belly

Intermediate tendon Lower border of greater cornua of

hyoidSternohyoid Posterior manubrium

of sternum andmedial clavicle

Lower border of corpus of hyoid

Depresses the hyoid bone; anchors the hyoid when the mandible is opened

against resistanceSternothyroid Posterior manubrium

of sternum and rstcostal cartilage

Oblique line of thyroid lamina

Depresses the thyroid cartilage

Thyrohyoid Oblique line of the thyroid lamina

Lower border of greater cornua of

hyoid bone

Depresses the hyoid bone or elevates the thyroid cartilage

a The lower portion of this muscle has some bers inserting into the posterior thyroid and cricoid cartilages.




A B C

Sternohyoid

Omohyoid (inferior)

Omohyoid (superior)

Digastricus (anterior)

Mylohyoid

Stylohyoid

Sternocleidomastiod

Trapezius

Geniohyoid

Omohyoid

Thyrohyoid

Sternothyroid

Sternum

Clavicle

Digastricus (posterior)

Sternohyoid

Omohyoidmohyoid(superior belly)superior belly)

Omohyoidmohyoid(inferior belly)inferior belly)Intermediatentermediate

tendonendon

Thyrohyoid

Omohyoid(superior belly)

Omohyoid(inferior belly)Intermediate

tendon

Figure 8-16 Infrahyoid muscles: A. sternohyoid, B. omohyoid, and C. thyrohyoid. (Modied with permission from Cael, C. (2009). Func-tional anatomy: Musculoskeletal anatomy, kinesiology, and palpation for manual therapists. Baltimore, MD: Lippincott Williams & Wilkins.)




inferior pharyngeal constrictor muscles (see Figures8-17 and 8-18, respectively). Table 8-3 provides sum-mary information relating to the origin, insertion, andaction of these two muscles.

The sternothyroid muscles originate along the pos-terior aspect of the manubrium of the sternum andthe cartilage of the rst rib. Their bers then travelvertically to insert into the lower border of the obliqueline of the thyroid cartilage. With the sternum and rstrib anchored, contraction of these muscles will resultin bilateral depression of the thyroid cartilage.

The inferior pharyngeal constrictor muscles makeup the lower part of the pharynx and are actuallyformed by a number of individual muscles that inter-mingle (these muscles will be discussed in more detailin Chapter 10). Some of the bers of these muscles

insert into the vertical ridge located at midline on theposterior quadrate lamina of the cricoid cartilage as well as the posterior borders of the thyroid cartilage.The action of these muscles assists in mediating theresonant characteristics of the vocal tone.

MUCOUS MEMBRANE

The entire laryngeal cavity is lined by a mucous mem-brane that is continuous with the mucous membranefound within the pharynx above and trachea below.

This membrane is tight and closely adheres to theepiglottis, aryepiglottic folds, and vocal folds, but ittends to be loose elsewhere within the larynx. Themucous membrane on the regions of the vocal folds

that approximate during phonation is composed ofsquamous epithelium. The mucous membrane thatlines the interior of the cricoid cartilage (referred to asthe subglottic space) is ciliated, similarly to the mucousmembrane of the trachea immediately below.

Thyrohyoid

Sternothyroid

Sternohyoid,reflectedinferiorly

Figure 8-17 Infrahyoid muscles: sternothyroid. (Modied with permission from Cael, C. (2009).Functional anatomy: Musculoskeletal anatomy, kinesiology, and palpation for manual therapists. Baltimore,MD: Lippincott Williams & Wilkins.)

Why You Need to Know Orlikoff and Kahane (1996) describe a laryngeal feedback system. Mechanoreceptors can be foundthroughout the joints, membranes, and musclesof the larynx. These specialized receptor cells are

thought to allow the brain to determine andmaintain the status of the larynx, making reexiveadjustments as necessary. To date, relatively little isknown about the specics of this feedback system.

NEURAL INNERVATION OF THEMUSCLES OF PHONATION

Table 8-4 provides a summary of the neural innerva-tion of select intrinsic and extrinsic muscles of thephonatory system. Four cranial nerves are involved in




Thyrohyoid membrane

Thyroid lamina

Cricothyroid muscle

Trachea

Inferior pharyngealconstrictor

Figure 8-18 Infrahyoid muscles: inferior pharyngeal constrictor. (Modied with permission fromAgur, A.M., Dalley, A.F. (2008). Grant’s atlas of anatomy (12th ed.). Baltimore, MD: Lippincott Williams& Wilkins.)

TABLE 8-4

NEURAL INNERVATION OF THE EXTRINSIC AND INTRINSIC LARYNGEAL MUSCLES

Muscle Innervation

Extrinsic Muscles

Digastricus (anterior belly) Trigeminal (cranial nerve V), mylohyoid branchDigastricus (posterior belly) Facial (cranial nerve VII), digastric branchGenioglossus Hypoglossal (cranial nerve XII)Geniohyoid Hypoglossal (cranial nerve XII), geniohyoid branchHyoglossus Hypoglossal (cranial nerve XII)Inferior pharyngeal constrictor Vagus (cranial nerve X); possibly spinal accessory (cranial nerve XI)Mylohyoid Trigeminal (cranial nerve V), mylohyoid branchOmohyoid Hypoglossal (cranial nerve XII) with C1–C3Sternohyoid Hypoglossal (cranial nerve XII) with C1–C3Sternothyroid Hypoglossal (cranial nerve XII) with C1–C3Stylohyoid Facial (cranial nerve VII), stylohyoid branch

Thyrohyoid Hypoglossal (cranial nerve XII) with C1 and C2Intrinsic Muscles

Cricothyroid Vagus (cranial nerve X), superior laryngeal nerveLateral cricoarytenoid Vagus (cranial nerve X), recurrent laryngeal nerveOblique arytenoid Vagus (cranial nerve X), recurrent laryngeal nervePosterior cricoarytenoid Vagus (cranial nerve X), recurrent laryngeal nerveSuperior thyroarytenoid Vagus (cranial nerve X), recurrent laryngeal nerveThyroarytenoid Vagus (cranial nerve X), recurrent laryngeal nerveTransverse arytenoid Vagus (cranial nerve X), recurrent laryngeal nerve




the process of phonation. These include the facial (VII),hypoglossal (XII), trigeminal (V), and vagus (X). Cranialnerves V, VII, and XII innervate the extrinsic muscles, whereas cranial nerve X innervates the intrinsics.

Innervation of the Intrinsic Muscles

All of the intrinsic laryngeal muscles receive theirmotor innervation from one of two branches of thevagus nerve (cranial nerve X). All intrinsic laryngealmuscles except the cricothyroids are innervated bythe recurrent laryngeal nerve . The cricothyroid mus-cles are innervated by the superior laryngeal nerve .

The recurrent laryngeal nerve gets its name fromthe fact that it takes the “scenic route” on its way to theintrinsic muscles of the larynx (see Figure 8-19). The

Vagus nerve

Superiorlaryngeal

nerves(external)

Left recurrentlaryngeal nerve

Aorticarch

Right recurrentlaryngeal nerve

Thyroidcartilage

Superior laryngeanerves (internal)

Inferior laryngealnerve

Subclavian artery

Figure 8-19 The superior and recurrent laryngeal nerves.

left recurrent laryngeal nerve passes under and aroundthe aorta on its way to the larynx, whereas the rightrecurrent laryngeal nerve passes under and aroundthe subclavian artery. Because the aorta is inferiorto the subclavian artery, the left recurrent laryngealnerve is a bit longer than the right recurrent laryngealnerve. However, there is no discernible effect on the

timing of neural impulses to the muscles these twonerves serve. By comparison with the recurrent laryn-geal nerves, the superior laryngeal nerves take a moredirect route on their way to the cricothyroid muscles.

Innervation of the Extrinsic Muscles

The suprahyoid muscles receive their innervation fromeither the facial (VII), hypoglossal (XII), or trigeminal(V) cranial nerve. The anterior belly of the digastri-cus and the mylohyoid muscles receive their motorsupply from branches of the trigeminal nerve. The

posterior belly of the digastricus and the stylohyoidmuscles are innervated by branches of the facialnerve. The geniohyoid, genioglossus, and hyoglossusmuscles all receive innervation from branches of thehypoglossal nerve.

The three infrahyoid muscles are innervated bybranches of the hypoglossal nerve along with branchescoming from various spinal nerves. The sternohyoidand omohyoid muscles are innervated by a branch ofthe hypoglossal nerve whose bers intermingle withbers from spinal nerves C1 through C3. The thy-rohyoid muscles are innervated by branches from thehypoglossal nerve that interdigitate with bers fromspinal nerves C1 and C2.

Finally, the inferior pharyngeal constrictor is inner-vated by the vagus nerve (cranial nerve X), with pos-sible contribution from the spinal accessory nerve(XI). The sternothyroid muscle is innervated by thehypoglossal nerve (XII) with contributions from C1,C2, and C3.

Why You Need to Know In rare instances, the laryngeal branches of thevagus nerve may be severed or damaged during necksurgery or because of an accident. This can resultin severe voice problems for the patient. Depend-ing on the extent of damage, the patient may nothave a voice at all, or the voice may sound dull andmonotonous due to the patient experiencing prob-lems in regulating pitch. The patient’s voice may bewhispery with diminished intensity. A more thor-ough discussion of the effects of vagus nerve damageon voice will be presented in Chapter 9.




THE LARYNGEAL CAVITY

Now that the larynx is complete with all the cartilages,connective tissue, and muscles, you will note that theinterior of the larynx is a tube with several spacesresiding within. If you were to look into the laryngealcavity, you would see the two ventricular folds and the

Epiglottis

Vocal fold

Aryepiglottic fold

Vocal process

Trachea

Ventricular fold

Cuneiform tubercle


Interarytenoid notch

Figure 8-20 The aditus laryngis with selected landmarks (the ventricular folds are superior to the true vocalfolds). (Modied with permission from Anatomical Chart Company.)

two true vocal folds extending into the space. The ven-tricular folds are superior to the true vocal folds (seeFigure 8-20). The “shelves” formed by the ventricularfolds and true vocal folds serve to divide the laryngealcavity into several regions.

Figure 8-21 provides a schematic organization ofthese regions. Starting at the very top of the larynx

Aditus laryngis

Vestibule

Ventricular fold

Ventricle

Vocal fold

Subglottic space

Rima glottis

Superior

Inferior

Figure 8-21 A schematic representation of the internal cavities of the larynx.




and making your way down, these include the adituslaryngis, vestibule, ventricle , and subglottic space .The aditus laryngis is the entryway into the laryngealcavity. It is bounded by the epiglottis anteriorly, thearyepiglottic folds laterally, and the arytenoid carti-lages posteriorly. Immediately below the aditus laryngis and immediately above the ventricular folds is

an open area called the vestibule. Between the ven-tricular folds and true vocal folds is a space that runshorizontally along the length of the two sets of folds.This space is called the ventricle. Finally, immediatelyinferior to the true vocal folds is a space correspond-ing to the interior of the cricoid cartilage. This space isreferred to as the subglottic space.

Although not really a space, there is a variable-sizedopening between the two true vocal folds known asthe rima glottis , or simply the glottis. Variable-sizedmeans that the width of the glottis can change depend-ing on what the vocal folds are doing. When the vocalfolds fully adduct, there is zero glottis—no openingbetween the vocal folds. During normal quiet veg-etative breathing, the vocal folds are in a somewhathalf-open position known as the paramedian posi-tion . In this case, the glottis is open but not quite as wide as it has the potential to be (for adult males, withthe vocal folds in the paramedian position, the glot-tis is approximately 8 mm at its widest point). Whena person yawns or starts to breathe heavily due tostrenuous exercise, the vocal folds abduct even more,beyond their paramedian position. In this scenario,

the glottis is at maximum width (for adult males, asmuch as 16 to 18 mm at its widest point).

The glottis is divided into two parts. The rst part isreferred to as the membranous glottis and the secondis the cartilaginous glottis. The membranous glottiscorresponds to the portions of the vocal folds thatare attached to the vocal ligaments (which are mem-

branous). This makes up approximately 60% of thelength of the glottis (approximately 15 mm in adultmales and 12 mm in adult females). The remaining40% of the length (i.e., the cartilaginous glottis) cor-responds to the vocal processes and foveae oblongaof the arytenoid cartilages (approximately 10 mm inadult males and 8 mm in adult females). The entirelength of the glottis then is approximately 25 mm inadult males and 20 mm in adult females.

Laryngeal Regions

The laryngeal cavity is typically divided into threeregions: the supraglottic, glottic, and subglotticregions. The supraglottic region involves all laryngealstructures above the level of the vocal folds (since thevocal folds form the glottis). This would include theaditus laryngis (i.e., epiglottis, aryepiglottic folds, andarytenoid cartilages), vestibule, ventricular folds, andventricle. As illustrated in Figure 8-22, the pyriformsinuses are posterolateral to the aditus laryngis. Thesesinuses are formed by the space between the superiorcornua of the thyroid and the arytenoid cartilages.

Epiglottis

Ventricular folds

Aryepiglottic fold

Cuneiform tubercle

Vocal folds

Pyriform sinus


Esophagus

Root of tongue(lingual tonsil)

Trachea

Vallecula

Medianglossoepiglottic fold

Figure 8-22 The vocal folds in the paramedian position along with selected landmarks.




Why You Need to Know For persons with swallowing disorders, food or drinkmay pocket within the pyriform sinuses because thepatient does not have the ability to propel the foodpast the larynx and into the esophagus. The patientmay choke or aspirate on the food or drink.

Why You Need to Know The Valsalva maneuver is also used by cardiologiststo assess the condition of the heart, and may also beused by persons experiencing tachycardia to slowdown their heart rate and/or lower their blood pres-sure. Otolaryngologists (ENTs) also know the utility

of a different form of the Valsalva maneuver as ameans of actively adjusting middle ear pressure(see Chapter 12).

The vocal folds and the glottis that is formed bytheir abduction make up the glottic region. Finally,the space below the vocal folds is known as thesubglottic space, and it corresponds to the sub-glottic region. The mucous membrane that linesthe interior of the subglottic space is composed ofciliated epithelial cells. The hairlike projections ris-ing from the mucous membrane continually beattoward the vocal folds. This helps move mucous and

inhaled debris (e.g., dust particles) toward the vocalfolds where it can be forcibly cleared by a reexivecough.

Physiology of the PhonatorySystem

The primary structure of the phonatory system, thelarynx, serves a couple of biological or primary func-tions. First, it acts as a protective mechanism for the

lower respiratory passageway. The larynx preventsforeign objects from getting into the trachea, bron-chi, and lungs. If by chance a foreign object did ndits way into the larynx, contact with the vocal folds would generate a cough reex to expel the foreignmatter. This is especially true during the process ofswallowing. When swallowed food or drink (referredto as a bolus ) approaches the larynx, the epiglottisand aryepiglottic folds constrict the aditus laryngisso that the bolus cannot enter the larynx. The bolusthen passes over the larynx posteriorly and into theesophagus. Anyone who has ever accidentally aspi-

rated swallowed water can certainly recall the violentcoughing that results!

The second biological function of the larynx is toserve as a valve during thoracic xation (also knownas the Valsalva maneuver ). During this procedure,expired air is trapped beneath the adducted vocalfolds, generating increased abdominal and/or tho-racic pressure. The increased pressure is used by aperson attempting to lift a heavy object, or by a per-son who may be straining to empty their bladder orrectum, or by a female giving birth.

The nonbiological or secondary purpose of thelarynx is to serve as the sound source for the humanvoice. It accomplishes this by offering variable resis-tance to airow coming from the lungs as expired air. As expired air is forced through the adducted vocalfolds, it sets them into vibration. The vibration of thevocal folds is the sound source for voice. It is this par-

ticular function of the larynx to which the remainderof this chapter will be dedicated. Before entering intoa thorough discussion of how the vocal mechanism works, you should be familiar with several basic con-cepts related to voice production.

BASIC CONCEPTS

Pure Tones and Complex Tones

Sound is produced by a variable disturbance of thepressure between molecules within a medium; in

most cases, the medium is air. When an object is setinto motion, it is said to vibrate (one complete backand forth vibration is called a cycle). The disturbanceof air molecules transfers energy, referred to as acous-tic energy. The acoustic energy travels from the sourceof the pressure disturbance from air molecule to airmolecule in a longitudinal wave to the hearing mech-anism of an animal or human where it is perceived.

If you have ever undergone an audiological evalu-ation or screening, you are no doubt familiar with thebeeping tones to which you were to respond. Thesetones are referred to as pure tones; that is, each tone

presented is a single, individual, discrete frequency . Fre-quency is the number of completed cycles of vibrationthat occur in one second (hence, cycles per second orcps). For example, an object (such as a tuning fork) thatproduces a 512 cps pure tone is completing 512 backand forth vibrations of its tines in one second. In other words, the vibrating tines of the tuning fork generate512 pressure disturbances per second. Not only does asound have frequency but it also has intensity . Intensityis the magnitude of energy carried along the sound waveand is measured in a unit known as the decibel (dB).




Frequency and intensity are physical measures,that is, they are constant and do not change becauseof humans’ perceptions. In speech science, we usethe measure of Hertz (Hz) to represent the number ofcycles per second, so an object vibrating at 1000 cps ismeasured as 1000 Hz. Humans, however, perceive fre-quency as pitch . Pitch is the psychological perception

of frequency and can change depending on people’sperceptions. A sound that is perceived as low in pitchhas a source that is vibrating at a slower rate than thesource of a perceived high-pitched sound. Similarly,intensity is a physical measure of sound pressure levelthat has a perceptual correlate— loudness .

There are relatively few things in our world thatproduce pure tones. Most sounds are complex tones .Complex tones are sounds resulting from two or morepure tones blended together. Through a process knownas Fourier analysis , a complex tone can be analyzedinto its pure tone components along with their indi-vidual intensities. The vocal tone (i.e., the sound cre-ated by vibration of the vocal folds) is a complex tonethat is composed of many frequencies; in other words,it includes a wide range of frequencies. The lowest fre-quency in this complex tone is referred to as the fun-damental frequency (abbreviated F 0). Although thevocal tone is a complex tone with a range of frequen-cies, we usually refer to it in terms of its fundamen-tal frequency instead of its range. The average adultmale has a fundamental frequency of approximately125 Hz, the average adult female has a fundamental

frequency exceeding 200 Hz, and children (regardlessof gender) have a fundamental frequency exceeding300 Hz.

The vocal tone is said to be rich in harmonics .Harmonics are created by many different modes ofvibration of the vocal folds. Fundamental frequencyis created by vibration of the entire length of the vocalfolds. However, not only does the entire length of thevocal folds vibrate, but sections along the vocal foldlength also vibrate, literally creating “vibrations withinvibrations.” For example, the two halves of each vocalfold also vibrate, and the frequency of vibration of

each of these halves is two times the fundamental.The relationship between frequency and length is aninverse one. As length gets shorter and shorter, fre-quency gets higher and higher. Therefore, since thereare two equal halves instead of a whole, each halfvibrates at twice the rate as the entire length. This isthe second harmonic (the rst harmonic is associ-ated with the entire length of the vocal folds, i.e., thefundamental frequency). Not only does each half ofthe vocal fold vibrate, but each third, fourth, fth,sixth, seventh, eighth, etc., also vibrates at a different

mode that is a multiple of the fundamental frequency.These would be the third, fourth, fth, sixth, seventh,eighth, etc., harmonics. As an example, if the funda-mental frequency is 100 Hz, the harmonics are 100 Hz(rst), 200 Hz (second), 300 Hz (third), 400 Hz (fourth),500 Hz (fth), 600 Hz (sixth), 700 Hz (seventh), 800 Hz(eighth), and so on. The human vocal tone on aver-

age can extend into as many as 20 or more harmon-ics although not all of them would likely be perceived. With each successive harmonic, vocal intensitytends to diminish at a rate of approximately 12 dBper octave until the higher-frequency harmonics areliterally imperceptible.

In music, you might recognize the term octave asa series of eight musical notes. In speech science, anoctave is dened as a successive doubling of frequency,usually in reference to the fundamental frequency.In the example above, the rst octave would be 100–200 Hz (200 Hz represents a doubling of the funda-mental frequency of 100 Hz). The second octave wouldbe 201–400 Hz (400 Hz being a doubling of 200 Hz),the third octave would be 401–800 Hz (800 Hz beinga doubling of 400 Hz), and the fourth octave wouldbe 801–1600 Hz (1600 Hz being a doubling of 800 Hz). Although the vocal folds can generate a large numberof harmonics (and therefore, octaves), vocal intensitydiminishes at the rate of 12 dB per octave. Becausethe highest frequencies are practically imperceptible,the average human being has an effective vocal rangeof approximately two to two and a half octaves. By

comparison, some humans have slightly greater vocalranges. Although this is not conrmed scientically,a quick search of the Internet reveals that singer RobHalford (from the heavy metal band Judas Priest) isreported to have a vocal range of approximately fouroctaves. Mariah Carey (no introduction needed!) and Annie Haslam (from the 1970s progressive rock bandRenaissance) are each reported to have a vocal rangeof ve octaves. Trained, professional singers may havea naturally wider vocal range than most humans, butthey also learn how to extend their vocal range tosome degree.

Subglottic Pressure

Vocal fold vibration requires a coordinated effortbetween release of the expired air stream from thelungs and adduction of the vocal folds. As the expiredair comes up from the lungs and approaches the larynx, the vocal folds adduct. Adduction of the vocalfolds creates an obstruction to the expired air so thatit becomes trapped below the vocal folds within thesubglottic space. As the expired air continues to build




below the vocal folds, it generates a certain amountof pressure against the inferior surfaces of the vocalfolds. This is known as subglottic pressure . As youshall see in the sections that follow, subglottic pres-sure is a crucial component in vocal fold mechanics.

Longitudinal Tension and Medial Compression

The larynx is capable of making two primary adjust-ments that regulate the vocal tone. These are longitu-dinal tension and medial compression . Longitudinaltension refers to the amount of tension that is gener-ated by changes in the length of the vocal folds. Any-one who has ever played with a rubber band knowsthat as the rubber band is stretched (i.e., as its length isincreased), its tension increases. The same holds truefor the vocal folds. Conversely, you could accuratelyassume that as the vocal folds are shortened, their ten-sion decreases. As the vocal folds lengthen and shorten,other changes are also occurring. Vocal fold lengthen-ing also results in a decrease in their cross-sectionalarea or mass. By the same token, shortening of thevocal folds results in increased cross-sectional area ormass. The relationship between cross-sectional areaand tension is an inverse one. As cross-sectional areaincreases, tension decreases, resulting in a lower fre-quency vocal tone. As cross-sectional area decreases,tension increases; the net result is a higher frequencyvocal tone. As you can no doubt deduce, changes invocal fold tension and mass have direct effects on the

frequencies that are produced when the vocal foldsvibrate. Keep in mind that although changes in cross-sectional area and tension are what are responsible forchanges in vocal tone frequency, the two are mediatedby changes in vocal fold length. Other than serving asthe mechanism for regulating cross-sectional area andtension, vocal fold length has essentially a negligiblerole in vocal tone frequency. For the most part, vocalfold length is a means toward an end.

Medial compression refers to the pressure that isgenerated by adduction of the vocal folds. In other words, medial compression could be thought of as the

“force of adduction.” Humans have the ability to reg-ulate the amount of compression between the vocalfolds from a very light contact to an excessive amountof compression. As medial compression increases, thevocal folds offer greater and greater resistance to sub-glottic pressure. The amount of subglottic pressurethat would be needed to overcome the resistance ofthe vocal folds when the vocal folds are making a lightcontact with each other is much less than the subglot-tic pressure that would be needed when the vocal foldsare adducted very tightly. Regardless of the amount of

medial compression, at some point, subglottic pres-sure will overcome the resistance of the vocal folds. Ifthere is minimal medial compression, then minimalsubglottic pressure will accumulate before the vocalfolds’ resistance is overcome. Because so little sub-glottic pressure is generated, a relatively small puff ofair will pass through the open vocal folds. Conversely,

when there is maximum medial compression, maxi-mum subglottic pressure will be necessary to over-come the resistance of the vocal folds. At the time thevocal folds are overcome, the massive subglottic pres-sure that had built up will be released as a relativelylarge puff of air. Essentially, the size of the puffs of air isassociated with vocal intensity. Small puffs of air (gen-erated by minimal medial compression) will result ina relatively low intensity vocal tone; large puffs of air will result in a vocal tone having greater intensity.

THE PROCESS OF PHONATION

Myoelastic Aerodynamic Theory of Phonation

Despite the advances of modern science, to this dateit is still not completely clear as to how the vocal foldsvibrate. Several theories have been posited over the years in an attempt to describe the process of pho-nation. Perhaps the most widely accepted theoryof phonation is the Myoelastic Aerodynamic The-ory (van den Berg, 1958). As its name indicates, thistheory is concerned with principles of muscle tissue

elasticity and aerodynamics. One would think that with all of the tools of modern science at our disposal,this theory would be a relatively recent one, but thetheory was actually proposed by two 19th centuryscientists—Helmholtz and Müller—and was furtherrened by van den Berg in the 1950s.

Central to this theory are the concepts subglotticpressure, elasticity, and Bernoulli effect . Subglotticpressure was dened earlier as the force of air uponthe inferior surfaces of the vocal folds when the vocalfolds are adducted and expired air is trapped belowthem. Being composed of muscle tissue, the vocal folds

have a certain elasticity; that is, they can be manipu-lated by external forces as well as internal mechanics.Finally, the Bernoulli effect states that when a gas orliquid ows through or around a constriction, veloc-ity of the gas or uid increases. The abrupt increasein velocity in turn results in a drop in pressure withinthe gas or uid relative to the walls of the constrictionthrough which it passes. The net result is a vacuumbetween the walls of the constriction. If you have everbeen on a freeway passing a tractor-trailer and gottenthe sensation that you are being “sucked” toward the




bigger vehicle, it was the Bernoulli effect that causedthat sensation. The differential in air velocity betweenthe two vehicles created a vacuum. Lower air pres-sure was generated by the tractor-trailer (which wascreating greater air velocity) and higher air pressure was generated by your car (which was creating lessair velocity). Air ows from regions of higher to lower

pressure, and hence your car was actually drawntoward the larger vehicle. It is also interesting to notethat the Bernoulli effect is integral to the mechanics ofight. The contour of an airplane wing is designed insuch a way that as air passes over and under the wing,velocity of air movement over the wing is greater thanunder the wing. This creates a drop in pressure abovethe wing by comparison with the pressure below it. Airbelow the wing creates “lift” as it attempts to equalizethe drop in pressure above the wing.

According to the Myoelastic Aerodynamic Theory, when the vocal folds are adducted, they create resis-tance to expired air coming from the lungs. Air pres-sure (in the form of subglottic pressure) then builds within the subglottic space. At some point, subglot-tic pressure will overcome the resistance of the vocalfolds. Because of their elasticity, subglottic pressure will force the vocal folds to separate creating a smallglottis. As soon as this occurs, subglottic pressureis released immediately as airow. The increase invelocity of the air as it passes through the glottis cre-ates a drop in pressure of the air relative to the medialborders of the vocal folds. The vocal folds are literally

brought back together by the vacuum that is createdby the increased velocity (i.e., the Bernoulli effect), as well as by the recoil pressure that is created by theirinherent elasticity. This entire sequence of events(buildup of subglottic pressure; subglottic pressureovercoming the resistance of the vocal folds; increasein velocity creating a vacuum that brings the vocalfolds back together again) results in one cycle of vibra-tion. For a vocal tone with a fundamental frequency of100 Hz, this entire cycle takes only 1/100 of a secondto complete. To look at it another way, there would be100 cycles of glottis open/glottis closed per second! At

such a fast rate, subglottic air does not ow throughthe glottis continuously but rather, small puffs orbursts of air pass through the glottis very similarly toNative American smoke signals.

By the description immediately above, it should beclear that also inherent to vocal fold vibration are thelaws of uid mechanics. You will recall from Chapter6 that when there is a difference in pressure betweentwo gradients, gases and liquids will always ow fromregions of greater pressure to regions of lesser pres-sure. When the vocal folds adduct for phonation,

expired air is trapped below the vocal folds, creatingsubglottic pressure. By the time the vocal folds areforced open, subglottic pressure is greater than theatmospheric pressure above the vocal folds (referredto as supraglottic pressure). As the vocal folds open,subglottic pressure is released and ows upwardthrough the glottis and vocal tract to equalize the

drop in supraglottic pressure.

Cover–Body Model

In recent decades, advances in computer-assistedmodeling and imaging techniques such as videostro-boscopy have allowed scientists to get a better lookat how the vocal folds vibrate. Among the pioneersin this area are Titze (1994, 2006) and Hirano et al.(e.g., Hirano, Kakita, Kawasaki, Gould, & Lambiase,1981; Hirano, Yoshida, & Tanaka, 1991). As a result ofhis studies involving computer-assisted modeling,Titze (2006) proposed a modication to the Myoelas-tic Aerodynamic Theory commonly referred to as theCover–Body Model.

Titze’s studies on vocal fold vibration (referred toas oscillations) lead him to believe that the Bernoullieffect alone could not account for how the vocal foldsmaintain their vibratory mechanics once phonationis initiated. That is, he discovered that the vocal foldshave the ability to continue oscillating even duringbrief periods when there is no energy source. TheBernoulli effect cannot account for this. Instead, Titze

found that the inherent structure of the vocal foldsplays a big part in their ability to maintain vibration.To understand how this happens, you should real-

ize that the entire masses of the vocal folds do notvibrate as a whole once subglottic pressure over-comes their resistance. In other words, the vocal foldsdo not separate from each other en masse . Rather, thevocal folds vibrate in a wavelike fashion from bottomto top. Figure 8-23 illustrates this concept. As you cansee in Figure 8-23A, the vocal folds adduct as expiredair comes up from the lungs, thereby generating sub-glottic pressure. At some point (see Figure 8-23B),

subglottic pressure overcomes the resistance of thevocal folds, and the lower parts of the vocal foldsare forced laterally by the pressure. At this point, thelower parts of the vocal folds are wider apart thanthe upper parts, and this creates convergent airow.The air continues upward and forces the upper partsof the vocal folds to move laterally (see Figure 8-23C). At the same time this is happening, the lower partsreturn to midline. Now the upper parts of the vocalfolds are wider apart than the lower parts. This cre-ates divergent airow. As illustrated in Figure 8-23D,




the upper parts of the vocal folds return to midlineand subglottic pressure once again exerts a forceupon their inferior surfaces. This process repeatsitself over and over again.

The vocal folds can be thought of as a mass-springsystem. According to Titze (1994, 2006), the body (i.e.,

thyroarytenoid muscle proper) is one mass, whereasthe cover (i.e., epithelium and supercial layer of thelamina propria) is composed of many masses fromthe bottom of the vocal folds to the top. All of themasses (cover and body together) are connected byvirtual springs, but their movements are independentof one other. This allows the masses within the coverto be displaced in a wavelike fashion from bottom totop, thereby creating regions of convergent and diver-gent airow through the glottis. This is referred to as avertical phase difference. Air pressure during regions

of convergent airow is greater than during regions ofdivergent airow. Titze contends that it is the asym-metry in pressures between convergent and diver-gent airow (i.e., the vertical phase difference) thatsustains the vocal folds’ oscillatory ability and not theBernoulli effect per se.

Adductedvocal folds

Adductedvocal folds

Subglotticpressure

Divergent air

Adductedvocal folds

Convergent air

Adductedvocal folds

Subglotticpressure

A B

C D

Figure 8-23 A schematic representation of vocal fold vibration (coronal view): ( A ) the vocal folds are ad-ducted and subglottic pressure exerts a force upon their lower surfaces; ( B) the lower portions of the vocalfolds separate creating convergent air; ( C ) the upper portions of the vocal folds separate as the lower portionsreturn to midline, thereby creating divergent air; and ( D ) the upper portions of the vocal folds return to midline.This cycle repeats itself ( A–B–C–D ), creating oscillations of the vocal folds.

Why You Need to Know A short section in this textbook cannot do justice tothe beauty of vocal fold vibration as described byTitze. For a more fascinating and in-depth look atvocal fold mechanics, you are encouraged to readTitze’s works—Principles of Voice Production (1994)and The Myoelastic Aerodynamic Theory ofPhonation (2006).




The Mechanics of Phonation

The Process

It is clear that phonation occurs when the vocal foldsare nearly or fully adducted. They cannot vibrate ifthey are overly abducted. This begs the question:How do humans adduct the vocal folds so that they

can phonate? Conversely, how do humans abduct thevocal folds so that they will stop phonating?In a single word, the answer is muscles. In two

words: intrinsic muscles. Recall from the discussionof the anatomy of phonatory muscles that some ofthem were classied as adductors, and one of them was classied as an abductor. The adductors are theLCA and the transverse and oblique arytenoids (col-lectively referred to as the interarytenoids, or IAs).The lone abductors are the PCAs.

As expired air passes from the lungs through thebronchi and up to the trachea, the LCA and IA mus-cles contract. Contraction of the IA muscles literallysqueezes the two arytenoid cartilages together (i.e.,adducts them). Because the vocal folds are attachedto the arytenoids at the vocal processes and foveaeoblonga, they too will be adducted. Simultaneous with IA contraction is LCA contraction. LCA contrac-tion causes the muscular processes of the arytenoidsto rotate medially, thereby pulling the vocal liga-ments downward and toward midline. Keep in mindthat the PCA ligaments restrict the amount of forwardand downward movement of the arytenoid cartilages when the LCA contracts. In summary, the net actionof the adductor muscles is to bring the arytenoidcartilages forward, medially, and downward. Thisaction causes the vocal folds to adduct. The adductormuscles can be contracted in varying degrees, whichmeans that humans have the ability to adjust theamount of medial compression between the vocalfolds.

Now that the vocal folds are adducted, they havethe capacity for phonation. As discussed earlier, theMyoelastic Aerodynamic Theory of phonation andCover-Body Model describe how this process takes

place. It should be noted, however, that during pho-nation, the arytenoids remain adducted by the IA andLCA muscles throughout the entire process. Vibra-tion of the vocal folds is not the result of continuousadduction and abduction of the arytenoid cartilages.For the most part, the arytenoid cartilages remainadducted during phonation. Vibration is the result ofsubglottic pressure overcoming the resistance of thevocal folds, and then the vocal folds’ natural recoiland a vertical phase difference bringing them backtogether again.

There does not need to be complete, absoluteadduction of the vocal folds to effect phonation. Bythe same token, not a lot of subglottic pressure is nec-essary to set the vocal folds into vibration. As littleas 2 to 3 cm H 2O is all the subglottic pressure that isneeded to set the vocal folds into vibration. For con-versational speech at approximately 60-dB intensity,subglottic pressure averages between 7 and 10 cmH2O. It increases to approximately 15 to 20 cm H 2O forloud speech, and even higher for high-intensity vocalactivity such as yelling or screaming.

How do we abduct the vocal folds, and under whatconditions do they abduct? Abduction of the vocalfolds is the result of a single pair of muscles—the PCAs.Contraction of the PCA muscles causes the muscular

processes of the arytenoids to rock upward and backward. This separates the arytenoid cartilages, therebyalso abducting the vocal folds. Keep in mind that theanterior cricoarytenoid ligaments restrict the amountof backward movement of the arytenoids. Obviously,abduction of the vocal folds is necessary for the indi-vidual to breathe, but the vocal folds also abduct peri-odically during vocal activity. The English languageconsists of approximately 41 speech sounds—24 con-sonants, 14 pure vowels, and three diphthongs. Thevast majority of these sounds are classied as voiced sounds, that is, they require vocal fold vibration. All of

the pure vowels and diphthongs are voiced, as well asmost of the consonants. Only nine consonant soundsare unvoiced (/p, t, k, f, s, ∫ , ™, h, t ∫ /). During speech, whenever a voiced sound is encountered, the vocalfolds adduct so that they can vibrate. They will remainadducted as long as there is a continuous stream ofvoiced speech sounds. As soon as an unvoiced speechsound is encountered, the vocal folds abduct so thatvocal fold vibration ceases. Upon encountering thenext voiced sound, the vocal folds adduct again to pho-nate. You should immediately gain an appreciation

Why You Need to Know As the vocal folds vibrate, a wave is created thattravels from their medial borders to their lateralmargins near to where the vocal folds are over-lapped by the ventricular folds. This is referred toas the mucosal wave (Berke & Gerratt, 1993; Hirano

et al., 1981). The rst two layers of the vocal folds(i.e., the epithelial layer and the supercial layer ofthe lamina propria) slide over the remaining threelayers as the vocal folds vibrate. The mucosal waveis used as a diagnostic tool. An absent or abnormalmucosal wave may signal a pathological condition.




for how rapidly the vocal folds must respond to thedemands of the sound system of a language!

Phases of Phonation

The process of phonation is divided into two phases—the prephonation phase and the attack phase . Therst phase is dened as the period of time during

which the vocal folds move from the paramedianposition to a nearly adducted or fully adducted posi-tion. The timing between the prephonation phase andexpiration of air is crucial. Mistiming between respi-ration and prephonation will likely result in aberra-tions of the attack phase.

The attack phase begins at the moment the vocalfolds are adducted and continues through the rstcycles of vibration. If timing between expiration andprephonation is optimal, the expired air will reachthe vocal folds at the same time the attack phasebegins. This is referred to as a simultaneous attack .By comparison, if air is released from the lungs beforethe vocal folds have adducted, there will be a certainquantity of air wastage through the glottis before thevocal folds begin vibrating. This is called a breathyattack , and the person who exhibits this attack willhave a breathy quality to their voice. On the oppositeend of the spectrum, if the vocal folds are adductedbefore air is released from the lungs and medialcompression is considerable, the person will exhibita glottal attack . The voice will sound very explosiveupon initiation of phonation.

mediated by adjustments in longitudinal tension.Changes in vocal loudness are mediated by adjust-ments in medial compression. In the paragraphs thatfollow, the mechanics of vocal pitch and intensity willbe discussed more fully.

Modications of Vocal Pitch

Humans have the ability to change their vocal pitchfrom a very low-pitched guttural sound (called glot-tal fry ) to a very high-pitched (i.e., falsetto ) sound.During conversational speech, vocal pitch constantlyvaries due to the changes in intonation that occur inrunning speech. Very seldom, however, will an indi-vidual use their highest and lowest vocal pitches dur-ing speech. Most humans tend to speak toward thelower end of their pitch range, about one-fourth ofthe way from the bottom of their pitch range to thetop. This is referred to as the person’s habitual pitch .During singing and other vocal activity, a wider pitchrange is typically used than during speech.

When the vocal folds are abducted, they are alreadyclose to their maximum length. During adduction then,the vocal folds shorten somewhat as they come to mid-line. The adjustments that occur to the vocal folds tocreate higher and lower pitches are accomplished rela-tive to this basic mechanic. With that said, your atten-tion is now turned toward the regulation of higher andlower vocal pitches, which is generally accomplishedthrough changes in longitudinal tension.

Regulation of Higher Pitch

From their habitual pitch level, humans have the abil-ity to create a range of higher pitches all the way tofalsetto. If one were to gradually increase his or herpitch from habitual to falsetto, the rst pitches wouldbe mediated by intrinsic muscle activity. As the indi-vidual proceeds to the highest pitches (nearing fal-setto), the limits of the intrinsic muscles would bereached so that certain extrinsic muscles would haveto be called upon.

Initially, higher pitch is mediated by the cricothy-

roid muscles, with possibly some additional contrac-tion of the thyroarytenoids and PCAs. The prevailingthought is that the cricothyroid muscles “load” thevocal folds for higher pitch by stretching them. Fine-tuning is accomplished by the vocal folds (i.e., thethyroarytenoids) themselves. The exact action thecricothyroids have on the pitch-changing mechanismcontinues to be debated to this day. Some scientistsbelieve that contraction of the cricothyroid mus-cles elevates the anterior arch of the cricoid towardthe thyroid cartilage immediately above while the

Why You Need to Know As will be discussed in Chapter 9, mistimingbetween the prephonatory and attack phases ofphonation can result in a voice disorder due tohypofunction or hyperfunction of the phonatorysystem. More times than not, these types of voicedisorders tend to be functional in nature, that is,there appears to be no known physical or neurologi-cal etiology for the problem.

MODIFICATION OF VOCAL TONEFREQUENCY AND INTENSITY

Humans have the ability to modify their voices. Theycan change their vocal pitch for the purpose of regu-lating prosody during speech or for the purpose ofsinging. Likewise, humans can vary the loudness oftheir voice from a barely audible whisper to a yellor scream. How do humans make these modica-tions to their voices? As was explained in an earliersection of this chapter, changes in vocal pitch are




thyroid cartilage remains essentially immobile. Oth-ers believe that contraction of the cricothyroid mus-cles causes the thyroid cartilage to tilt forward bydecreasing the distance between its inferior borderand the arch of the cricoid (in this case, the cricoidcartilage remains essentially immobile). Regardlessof which cartilage is actually acted upon, the result is

the same (recall the helmet visor analogy presentedearlier). Action of the cricothyroid muscles createsgreater distance between the interior of the thyroidangle and the vocal processes of the arytenoid car-tilages. Because the vocal folds are attached to thesetwo points, an increase in distance between these twopoints will result in a lengthening of the vocal folds. As the vocal folds lengthen, their cross-sectional areaor mass will decrease (i.e., the vocal folds will get thin-ner) and their tension will increase. The net effect isan increase in pitch. Fine adjustments are made tothe higher pitches by contraction of the muscle tis-sue within the vocal folds (i.e., the vocalis portion ofthe thyroarytenoid muscles). The PCAs play a minorrole in this mechanic by preventing the arytenoid car-tilages from tilting forward as the anterior structuresare displaced. Anterior movement of the arytenoids isalso limited by the PCA ligaments.

As pitch continues to increase toward falsetto, theintrinsic muscles will nally reach their limit. The vocalfolds will be stretched maximally so that additionalmuscle action will have to play a role in the high-est pitches. This muscle action comes from some of

the extrinsic laryngeal muscles—more specically,the suprahyoid muscles. The primary purpose of theextrinsic muscles is to provide support to, and main-tain the position of, the larynx. Secondary to this, thesuprahyoid muscles elevate the hyoid bone and larynx, while the infrahyoid muscles have the opposite effect.In terms of the production of the highest pitches, it isthought that when the suprahyoid muscles contractand the hyoid bone and larynx subsequently elevate,the result is increased tension of the conus elasticus,of which the vocal ligaments are a part. Indeed, if you were to look at your neck in a mirror during production

of your highest pitches, you would very likely see thethyroid prominence (i.e., Adam’s apple) move upwarddue to action of the suprahyoid muscles. Action ofthe suprahyoid muscles takes place in addition to theaction of the intrinsic muscles. The nal product is gene-ration of the highest pitches in the human vocal range.

Regulation of Lower Pitch

You would be correct in assuming that if stretch-ing of the vocal folds results in higher pitch, relaxingthem will result in lower pitch. When the vocal folds

are shortened, it results in an increase in their cross-sectional area with a concomitant decrease in ten-sion. These factors result in lower pitch. Recall fromthe discussion above that vocal fold lengthening isaccomplished by increasing the distance between theinterior of the thyroid angle (i.e., the anterior attach-ments of the vocal folds) and the vocal processes of the

arytenoid cartilages (i.e., the posterior attachments).Shortening of the vocal folds then requires that the dis-tance between the anterior and posterior attachmentsbe decreased. This is accomplished by contraction ofthe thyroarytenoid muscles themselves without sup-plemental contraction of any other intrinsic muscles. When the thyroarytenoids contract unopposed, theyliterally pull the thyroid cartilage back (the arytenoidcartilages remain stable during this action), therebyshortening the distance between the thyroid angleand vocal processes. The vocal folds basically “bunchup” on themselves. For 50% of the population that hasthem, the superior thyroarytenoid muscles performthe same function as the thyroarytenoids.

When you want to transition to your lowest pitches(i.e., glottal fry), additional muscle activity will benecessary. At this point, the vocal folds have beenshortened as much as possible by intrinsic muscleactivity so that the infrahyoid muscles must be calledupon to assist in reaching glottal fry. The infrahyoidmuscles depress the hyoid bone and larynx when theycontract (this can be seen by viewing yourself in themirror while producing very low pitches). Depression

of these structures results in a lessening of tensionon the conus elasticus, and subsequently the vocalligaments. As is the case with the highest pitches, thelowest pitches are produced by the combined actionof the appropriate intrinsic and extrinsic muscles.

Vocal Registers

As vocal pitch is varied from the lowest to the highestfrequencies, physiological changes occur to the vocalfolds. These are referred to as voice or vocal registers.Hollien (1972, 1974) identied three vocal registersduring speech production: (1) the pulse register that

is associated with the lowest frequencies in the vocalpitch range; (2) the modal register that is associated with the mid-frequencies of the vocal pitch range; and(3) the loft register that is associated with the highestfrequencies in the vocal pitch range.

In the pulse register, there are low frequency irregu-larly timed bursts of air through the glottis. The vocalfolds are compressed tightly and appear to be short,thick, and somewhat compliant. In some cases, theventricular folds may descend and nearly touch thevocal folds. The bulk of the vocal folds move very little




if at all; only the glottal margins appear to move in aoppy fashion. The infrahyoid muscles also contractto reduce tension on the vocal ligament. The result isa “bubbling” of air through the glottis. This bubblingsound contains very low frequencies, usually in therange of 50 Hz or less, and has been described as simi-lar to the sound of popcorn popping or bacon frying.

In the modal register (which is where conversationspeech occurs), the vocal folds have an upper andlower edge along the glottal margin and are still somewhat compliant. When air passes through the glottis,almost the entire vocal fold vibrates, starting with theinferior region and then spreading to the superiorregion. As pitch rises in the modal register, the vocalfolds become longer and stiffer, and thus become lesscompliant. At the highest pitches within the modalregister, the glottal margin appears as a single edge.The modal register accounts for the production of fre-quencies in the range of four to six octaves above thepulse register (roughly between 50 and 3200 Hz, butthis range varies widely from individual to individual).Not only is a wide range of frequencies possible in themodal register, but also a wide range of intensities isalso possible (approximately 40 to 110 dB). However,keep in mind that the highest frequencies will likelybe imperceptible because of the 12 dB per octave lossof energy.

In the loft register, the vocal folds become so stiffand tense that only their medial-most borders vibrateand the vertical phase difference (mentioned earlier)

is lost. There is only a single edge to the glottal margin.Because of the maximum tension that is produced, theanterior and posterior regions of the vocal folds barelymove, thereby reducing the effective vibrating area ofthe vocal folds so that very high frequencies are pro-duced. The suprahyoid muscles also contract to placeeven greater tension on the vocal ligament. The vocalfolds vibrate similarly to strings in this case. Frequen-cies in the loft register typically exceed 1000 Hz.

Modications of Vocal Loudness

Vocal intensity or loudness is a direct function ofchanges in the amount of subglottic pressure. Mini-mum levels of subglottic pressure will result in a voicethat has reduced intensity. Conversely, maximum levelsof subglottic pressure will create a voice having greaterintensity. As was mentioned earlier in this section ofthe chapter, when the vocal folds vibrate, they releasepuffs of air through the glottis. The number of puffs ofair that pass through the glottis per second is related tothe frequency of vibration. The size of the puffs, on theother hand, is related to vocal intensity. The laryngeal

adjustment responsible for regulating pitch is longitu-dinal tension. The laryngeal adjustment that regulatesvocal intensity is medial compression.

The more tightly the vocal folds are adducted duringphonation, the more resistance they offer to subglot-tic pressure. Under a condition of minimum medialcompression, minimum subglottic pressure will be

necessary to overcome the resistance of the adductedvocal folds. Because so little subglottic pressure hasbuilt up by the time the vocal folds are blown apart,relatively tiny puffs of air will pass through the glottis.The net result is a voice having minimal intensity.

On the other hand, under a condition of maximummedial compression, the requirement for sufcientsubglottic pressure to overcome the resistance of thevocal folds will be considerable. A very high level ofsubglottic pressure must be sustained to overcomethe medial compression created by the adductedvocal folds. When this resistance is nally overcome,relatively large puffs of air will pass through the glottis.The net result is a voice having maximum intensity.

Another way to increase vocal intensity is to pushmore air through the glottis. The force of this actionnot only creates more pressure below the vocal folds when they are closed but also faster airow through theglottis when the vocal folds separate. The faster airowcreates a greater drop in pressure between the vocalfolds, which in turn draws the vocal folds back towardthe midline faster and with greater force. When thevocal folds meet at midline, they become compressed

with greater force due to inertia. This leads to a longer“closed phase” during phonation, which in turn leadsto the opportunity for greater subglottic pressure tobuild up prior to the vocal folds being blown apartonce again. To illustrate this, compare the phonatorycycle during conversational speech to the phonatorycycle during speech marked by increased vocal inten-sity. During conversational speech, vocal intensity issuch that the vocal folds are open during 50% of thephonatory cycle, closing during 37% of the cycle, andclosed during 13% of the cycle. By comparison, dur-ing loud speech, the open phase accounts for 33% of

the phonatory cycle, the closing phase accounts for37% of the cycle, and the closed phase accounts forthe remaining 30%. In summary, airow appears to beused for intensity changes at low frequencies, whilemaximum medial compression (mediated by musclecontraction) appears to be the mechanism by whichgreater intensity is generated at higher frequencies.

A general rule of thumb is that vocal intensity willrise on the magnitude of approximately 8 to 12 dB witheach successive doubling of subglottic pressure. As wasstated earlier, subglottic pressure for conversational




speech at 60 dB is approximately 7 to 10 cm H 2O. Toincrease the intensity of speech to approximately 68to 72 dB, subglottic pressure would have to double toapproximately 14 to 20 cm H 2O. A yell or scream at 110dB would require subglottic pressure on the magnitudeof approximately 112 to 640 cm H 2O.

In the anatomy section of this chapter, you learned

that three muscles are classied as vocal fold adduc-tors. These are the LCAs and interarytenoids (i.e., theoblique and transverse arytenoids). Humans havethe ability to adjust the contraction of these muscles,thereby mediating medial compression.

The Relationship Between VocalTone Frequency and Intensity

For the most part, vocal intensity is regulated bymedial compression and its effect on subglotticpressure, while changes in vocal pitch are a result ofadjustments to longitudinal tension of the vocal folds.However, there are instances where adjustments tomedial compression may affect longitudinal tensionas well. Anyone who has ever raised the intensity oftheir voice in an abrupt and dramatic fashion hasprobably noted that their pitch increased as well. Thismay be due to one or both of two factors: (1) at greatervocal intensity, reexive tensing of the vocal folds mayoccur, and increased tension results in higher pitch;(2) with greater vocal intensity, increased subglot-tic pressure causes the vocal folds to adduct more

quickly, and the quicker timing of adduction resultsin an increase in pitch. Vocal pitch and intensity are used to mark the

suprasegmental aspects of speech production suchas intonation and stress. Intonation is mediated pri-marily by variations in vocal pitch, whereas stress ismediated by both pitch and intensity. This is accom-plished very rapidly throughout the stream of speech—on average, about one-tenth of a second. In that verybrief period of time, stress is generated by increasesin subglottic pressure on the magnitude of about2 cm H 2O along with slight increases in vocal pitch.

Increases in subglottic pressure are accomplished bycontraction of the muscles involved in medial com-pression (i.e., the lateral cricoarytenoids and IAs) as well as the internal intercostal muscles acting uponthe rib cage. Increases in pitch are accomplished bygenerating greater tension on the vocal folds throughaction of the cricothyroids and thyroarytenoids(vocalis portion).

Intonation, of course, would involve only the pitch-change mechanism. For example, for a rising intona-tion pattern (typically seen in questions that require

a “yes” or “no” response, such as “Are we going to thestore?”), there is approximately a 50-Hz increase inthe fundamental frequency of the vocal tone (Netsell,1973). We have a natural tendency to lower our pitchat the end of a breath group. This means that when we encounter an utterance that has a rising intona-tion, we must work against this natural tendency by

contracting the cricothyroid muscles.

Physiology of Other Forms of Vocal Activity

The foregoing discussion examined the physiologyof phonation primarily in reference to typical speechactivity. For other forms of vocal activity such asspeaking or singing in falsetto or whispering, thephysiology of phonation is a bit different. This nalsection of the chapter will briey describe the phona-tory physiology of falsetto and whisper.

Physiology of FalsettoRecall that falsetto involves the production of frequen-cies at the uppermost end of the vocal pitch range. Notonly is the rate of phonation affected, but the actualmanner of phonation changes as well. Although theretends to be some degree of overlap between the upperend of an individual’s modal register and the lower endof the loft register (where falsetto resides), there arelaryngeal adjustments made that are particular to fal-setto. During the production of falsetto, only the freemedial borders of the vocal folds make contact and

vibrate. The bulk of the vocal folds remain relativelyrm and stationary. The appearance of the vocal foldsis long, very stiff, and bowed. This results in a shortereffective vibrating area of the glottis, and hence higherfrequency vibration. The suprahyoid muscles alsoassist the process by creating greater tension on thevocal ligament when they contract. Increased tensionalso results in higher frequency vibration. The verticalphase difference is not at play during falsetto.

Physiology of Whisper

A whisper is not voiced; that is, the vocal folds do

not vibrate during this form of vocal activity. Duringnormal phonation, the arytenoid cartilages cometogether medially and the two vocal folds are parallelto each other along their entire length. During whis-per, however, the arytenoid cartilages do not comeinto contact with each other medially. Instead, theyare slightly abducted with their vocal processes con-verging medially (i.e., the arytenoids are “toed in”).This is accomplished by contraction of the lateralcricoarytenoids with little to no contribution fromthe IAs (Monoson & Zemlin, 1984; Solomon, McCall,




Trosset, & Gray, 1989). Such a conguration creates anopening in the cartilaginous region of the vocal folds,referred to as a glottal chink . If you were to look at thelength of the vocal folds from their adduction anteri-orly to their abduction posteriorly, it would resemblean inverted “Y.” As the person whispers, air passesthrough the glottal chink at a relatively rapid rate,

creating turbulence (the rate of airow during thenormal production of vowel sounds is approximately100 cc per second; for whisper, it is double this). Theturbulence of air as it passes through the glottal chinkis essentially what is perceived as the whisper.

Summary

This chapter provided a thorough description anddiscussion of the anatomy and physiology of thephonatory system. The phonatory system can beconsidered the motor or generator for vocal activity.

Phonation is accomplished by vibration of the vocalfolds and is mediated by intrinsic laryngeal muscleactivity. Phonation also involves changes in frequencyand intensity of the vocal tone. Changes in frequencyare mediated by adjustments to longitudinal tension, while changes in intensity are primarily the result ofadjustments to medial compression. Longitudinal

tension involves activity of intrinsic and extrinsiclaryngeal muscles. Medial compression is accom-plished by intrinsic muscle activity, and more speci-cally by contraction of the vocal fold adductors. Basicprinciples of voice production (e.g., complex tones,fundamental frequency, and harmonics) and otherforms of vocal activity (e.g., falsetto and whisper) werealso discussed. The following chapter (Chapter 9) willassist you in understanding how aberrations in pho-natory anatomy and/or physiology can result in dis-orders of voice. Then, Chapter 10 will show you howthe vocal tone is shaped and molded into the acousticphenomenon we recognize as human speech.



199

Knowledge Outcomes for ASHA Certication for Chapter 9• Demonstrate knowledge of the biological basis of the basic communication processes (III-B)

• Demonstrate knowledge of the etiologies of voice and resonance disorders (III-C)

Learning Objectives• You will be able to dene normal and disordered voices.• You will be able to explain the physiology of phonation (e.g., the Myoelastic Aerodynamic

Theory of phonation).• You will be able to explain how to clinically evaluate parameters of voice.• You will be able to describe some of the common voice disorders.• You will be able to explain clinical perspectives relevant to management of voice disorders.

CHAPTER 9

Pathologies Associated with the Phonatory SystemCHARLES L. MADISON


a- without; absence of a phonia

dys- abnormal; impaired dys phoniamyo- pertaining to muscles Myoelastic Aerodynamic Theory

-phonia sound; voice dys phonia

presby- pertaining to advanced age presby laryngis

puber- pertaining to puberty puber phonia

segment pertaining to phonemes (speech sounds) supra segment al

supra- above; overriding supra glottic

Introduction

In this chapter, an introduction to voice disorders will be presented by building on the anatomicaland physiological foundation offered in Chapter 8.The goal is to relate clinically relevant voice param-eters to the structure and function (i.e., anatomyand physiology) of the larynx in a way that willmake sense when the speech–language clinician, asa voice therapist, is faced with the responsibility of

evaluating and offering remedial options to clients with voice concerns. Clinicians learn the anatomy ofspeech production for the purpose of relating struc-ture to function as required to appropriately under-stand what they are hearing and how best to managevoice production for the most positive communica-tion outcome. However, there are clearly challengesto effective evaluation and management of voicedisorders. Deem and Miller (2000) noted four suchchallenges.



200 PART 4 THE PHONATORY SYSTEM

• There is no direct relationship between the per-ception of a voice disorder and the presence ofpathology.

• Social acceptance of voice problems creates asignicant challenge for the voice therapist.

• The patient’s level of motivation to restore vocalhealth will be related to the importance of thevoice in his or her profession.

• Terms used to describe voice disorders are oftenmisunderstood among professionals (p. 3).

In this chapter, these challenges will be addressed,although not completely resolved, as the principlesof voice production, voice perspective, and voiceparameters are discussed. The goal is to present anintroduction to voice that relates anatomy and physi-ology to normal voice, exceptional voice, and voicedisorders in a clinically relevant way.

Voice Production

Respiration, phonation, articulation, and resonanceare the underlying physiological processes of speechproduction. These processes are represented sche-matically in Figure 9-1 where air from the lungs causesvibration of the vocal folds (represented by the tun-ing fork) and thus a basic laryngeal tone (representedby the sine wave). Here, a simple tube represents thesupraglottic resonators, and the repeating waveform

at the right is a resulting vowel. The vowel wave couldbe that of any vowel, as the resonators serve to modifythe basic laryngeal tone (i.e., fundamental) into thedesired production.

As related to voice and voice disorders, the empha-sis in this chapter will be on phonation as driven byrespiration. Voice is the acoustic or audible result ofthe phonatory process or phonation . Sound is audi-ble vibration, and phonation is the physiological pro-cess that results in vocal fold vibration and thus voice.Phonation and respiration are inexorably linked inoral human communication. For vocal fold vibration

to occur, a driving force is necessary. In phonation,

the force is the air provided and controlled by thesubglottic respiratory mechanism. Movement of airis required. The phonatory process begins with clo-sure of the glottis , that is, the vocal folds moving tomidline. Subglottic air pressure increases to the pointthat it exceeds the resistance of the vocal folds. Thevocal folds are blown apart and air is released. Based

on the mass and elasticity of the vocal folds and theaerodynamic factors associated with air moving rap-idly through a narrow orice, the vocal folds return toa closed position and the process begins all over again(recall the discussion in Chapter 8 about the Myoelas-tic Aerodynamic Theory and Cover–Body Model).

This physical process of voice generation is theheart of the Myoelastic Aerodynamic Theory of pho-nation. Objects—including vocal folds—vibrate as afunction of their physical properties, mass, and elas-ticity. For example, some guitar strings are larger (i.e.,bigger in circumference) than others and thus havemore mass. The larger thicker strings produce a lowerpitched vibration than do the smaller thinner strings,and all strings produce a higher pitched vibration when made shorter and more taut by placing one’sngers on the frets. Analogous adjustments can bemade by human producers of voice. Although we donot adjust the length of the vocal folds by using ourngers, we are able to vary their length by adjustingthe relationship of the cricoid and thyroid cartilages,and we are able to vary the relative thickness/thin-ness of the vocal folds as well. It is the cricothyroid

muscles that are primarily responsible for this adjust-ment. Interestingly, the cricothyroids are the onlyintrinsic muscles of the larynx that are not innervatedby the recurrent laryngeal branch of the vagus nerve.The superior laryngeal branch of the vagus nerveserves the cricothyroid muscles, and thus insult to thesuperior branch might be suspected when a patient isunable to control vocal pitch.

The ability to make these changes in the mass andelasticity of the vocal folds affords us the opportunityto make incredible changes in the fundamental fre-quency perceived as pitch. The difference between the

vibratory energy source for a guitar and the human

Respiration Phonation Resonance Vowel

(subglottic) (glottic) (supraglottic) (output)

Figure 9-1 A schematic of the underlying processes of speech production.



CHAPTER 9 PATHOLOGIES ASSOCIATED WITH THE PHONATORY SYSTEM 201

voice producing mechanism is acknowledged. We donot pluck or strum the vocal folds. Instead, we forcesubglottic air past them to generate vibration. Thus, we must recognize the importance of the physicalproperties of the air movement (aerodynamics) inphonation. Once the physiological process of phona-tion is understood, normal voices, exceptional voices,

and disordered voices can be understood, appreci-ated, and managed. Voices that are appropriate forone’s age and gender, do not call undue or negativeattention to the speaker, or do not interfere with com-munication are considered normal. Some voices areconsidered exceptional because of their unique qual-ity or the masterful control exhibited by the speaker orsinger. Such voices are easily recognized and appreci-ated. They are exceptional in that they bring positiveattention to the speaker or singer. By contrast, disor-dered voices are ones that bring negative attention tothe speaker and/or interfere with communication.However, American society seems to have a liberaltolerance for voice differences, and thus noticeablevoice differences may not be viewed as disordered.Deem and Miller (2000) noted that this circumstancemay have an effect on patient motivation. Regardlessof whether voices are considered normal, exceptionalor disordered, the basic laryngeal anatomy is thesame as are the physiological processes that result inphonation and the physical principles that underliethem. Our understanding of voice normalcy, excep-tionality, or disorder is enhanced by our knowledge

of the anatomy and physiology and the physical prin-ciples of vocal fold vibration.

Perspectives

Several common pathologies of voice are summa-rized in Table 9-1. Voice disorders can be viewed fromseveral different perspectives, as speech–languagepathologists seek to better understand them andeffectively evaluate and treat them. In the discussionthat follows, voice disorders will be discussed from

the perspectives of the causes, prevalence, duration,and life span, then followed by an introduction tovoice that focuses on the parameters that dene it asnormal, exceptional, or disordered.

ETIOLOGY

Voice disorders are frequently discussed from an eti-ological perspective, a perspective intended to helpthe clinician better understand the cause or causes ofthe problem. Voice disorders are categorized as being

psychogenic (i.e., functional) or organic in origin. Psy-chogenic voice disorders can be further differentiatedas being subsequent to or a symptom of personalityand adjustment disorders; for example, stress, anxi-ety, or mental health conditions. Psychogenic voicedisorders can also be associated with personality typeand/or faulty voice habits. In fact, faulty voice hab-

its are most likely to be a factor in psychogenic voicedisorders. Vocal abuse, in one form or another, is theleading cause of voice disorders. By contrast, organicvoice disorders are viewed as a consequence of masslesions or neurogenic conditions.

A voice disorder is organic if it is caused by struc-tural (i.e., anatomic) or physiologic disease, either adisease of the larynx itself or by remote systemic ill-ness which alters laryngeal structure or function(Aronson, 1990). Aronson goes on to identify con-genital disorders, inammation, tumors, endocrinedisorders, trauma, and neurologic disease as organicetiological categories with voice consequences. Inter-estingly, psychogenic etiologies can result in organicpathologies, thus somewhat blurring the psycho-genic–organic etiological dichotomy. For example,vocal abuse is accepted as the etiological basis for thedevelopment of vocal nodules . The nodules—clearlymass lesions—are generally agreed upon to be a con-sequence of vocal abuse, which must be addressedclinically to alleviate the voice disorder. Althoughorganic in nature, vocal nodules (see Figure 9-2A),polyps (see Figure 9-2B), and contact ulcers (see Fig-

ure 9-2C) are often discussed as secondary patholo-gies consequent to abusive behavior, and thus aretypically classied as being psychogenic in origin.

However, alternative causal factors suggest thatboth psychogenic and organic causes can result inthe same pathology. Contact ulcers can result fromabusive behaviors, but they can also result fromgastroesophageal reux disease. Pannbacker (1992)noted the difculty in making a distinction betweenpsychogenic and organic voice problems. In essence,there are frequently psychogenic elements associ-ated with organic etiologies and psychogenic etiolo-

gies that result in organic factors. Pannbacker’s thesisis that voice disorder etiologies can be viewed on acontinuum ranging from psychogenic on one end toorganic on the other.

PREVALENCE

Another perspective from which to view voice disor-ders is that of prevalence. Some voice problems occurmuch more frequently than others. Six percent ofschool-aged children have been found to present with




TABLE 9-1

COMMON VOCAL PATHOLOGIES

Location Size Etiology Description Vocal Symptoms Management

Carcinoma of the larynx

(squamouscell, renalcell, mela-noma,sarcoma)

Variable Small (6 mm) to obstruc-

tive

• Unknown• Inhalation

of suspectedcarcinogens

Variable; not a well-dened

tumor

• Breathiness• Low pitch• Intermittent

aphonia• Diplophonia• Hoarseness

• Chemotherapy • Radiation• Surgery • Voice therapy

as part ofrehabilitation

Contact ulcers

Vocalpro cesses,typicallybilateral

Small to obstructive

• Adults 30 years

• Upper gastro-intestinaldisorders

Hyperemia leading to

sessile lesion;raised ulcer with inamedmargins

• Pain in the posteriorlaryngeal area when processesmove to close,e.g., swallowing


aphonia

• Voice therapy • Medical• Surgery (not

recommended)

Essential tremor of

the vocalfolds

N/A N/A • Adults 45 y ears• Central nervous

system disease,typically genetic

• Mild cases:vocal tremornoticeableon prolongedvowels

• Most severecases: vocaltremornoticeableon all vocalattempts

• Quavering intonation

• Phonationbreaks

• Rhythmictremor

• Laryngospasmsin severe cases

• Medication may result in someimprovement

• Voice therapy is of limitedvalue

Granuloma Vocalprocesses,usuallybilateral

Small to obstructive

• Surgicalintubation

• Esophagealreux

Pain associated with any

laryngealmovement(see contactulcers)

• Breathiness• Low pitch• Diplophonia• Mild dysphonia• Tension• Clunking

• Voice therapy • Reux

management• Surgery (not

recommended)

Interchordal cysts Surface of vocal folds,typicallyunilateral(if bilateral,unpaired)

6–12 mm • Obstruction of duct Fluid-lled sacs, usually sessile • Breathiness• Low pitch• Diplophonia

• Voice therapy • Surgical

Nodules Juncture of the anterior

1 3 andposterior2 3, typicallybilateral

Pinpoint to6 mm

• Vocal abuse• Hemorrhagic/

sudden onset• Thickened

epithelium/chronic

• Early ( 6months): soft,pink, normalepithelium

• Mature(6 months orlonger): whiteto yellow, rmepithelium

• Breathiness• Tension (early)• Pitch breaks• Hard attack on

initial vowels• Intermittent

aphonia• Diplophonia

• Vocal counseling • Voice therapy • Surgery (not

usuallynecessary)

Papilloma Vocal folds and sur-

roundingarea

6 mm • Viral Wart-like: raspberry

shape andtexture

• Breathiness• Low pitch• Tension• Aphonia• Hoarseness

• Chemotherapy • Surgery • Voice therapy




TABLE 9-1

COMMON VOCAL PATHOLOGIES (Continued)

Location Size Etiology Description Vocal Symptoms Management

Polyps (unilateral

or bilateral)

Laryngeal mucosa

Small (6 mm) to obstru-

ctive

• Airborneirritants:smoking,inhalation oftoxins, etc.

• Medications• Idiopathic

• Polypoiddegeneration:soft globularmass exhibitingmucoiddegeneration

• Pedunculated: with a peduncleor stalk

• Sessile: having no peduncle,attacheddirectly bya broadbase


aphonia• Diplophonia• Hoarseness

(wet or dry)

• Vocal counseling • Surgical

management• Postoperative

vocal rest• Postoperative

voice therapy

Spastic dysphonia

Larynx N/A Adults 30 years Adductor (most common)

or abductorspasms

• Erratic vocalfold spasms

• Voice therapy (guardedprognosis atbest)

• Counseling • Surgery

Vocal foldedema(laryngitis)

Arytenoids, vocal

processes tothe anteriorcommissure

Typically widespread

• Viral infection• Bacterial infection• Allergic reaction

Reddened, swollen

arytenoids,vocalprocessesand/or vocalfolds

• Breathiness• Intermittent

to completeaphonia

• Diplophonia• Hoarseness• Tension• Low pitch

• Controlledvocal use

• Medical• Vocal hygiene

counseling

Vocal fold paralysis

(unilateralor bilateral;abductor or

adductortype)

Relative to type and

position ofparalysis

N/A • Recurrentlaryngeal nervedamage causedby surgery,disease, or

trauma

Vocal fold immobility

or partialmobility

• Unilateralabductor:breathiness,low pitch,diplophonia

• Unilateraladductor:breathiness,diplophonia,low pitch,possibleaphonia

• Bilateralabductor:breathiness,fair vocalquality,obstructedairway, milddysphonia

• Bilateraladductor:vulnerableairway,aphonia

• Voice therapy • Surgery

Adapted from Wilson, F.B. (1990). A program of diagnosis and management for voice disorders . Bellingham, WA: VTI Voice Tapes, Inc.




chronically hoarse voices (Baynes, 1966), and 80% ofthat 6% were found to present with vocal nodules(Wilson, 1990). No other voice problem will approachthe prevalence of the hoarseness associated with vocalnodules as a focus of concern for speech–languagepathologists working in a school setting. Understand-ing the anatomical and physiological basis for thevoice quality associated with nodules is important ifthe clinician is to deal effectively with the evaluation

and management of them. Vocal nodules can beconsidered signicant because of the frequency with which they occur. Comparatively, papilloma (seeFigure 9-2D) is an example of a condition that affectsvoice, and occurs much less frequently than do vocalnodules, but it is no less important for the clinician tounderstand the anatomical and physiological conse-

quences of these mass lesions and his or her role inthe management of a child with papilloma.

DURATION

Some voice disorders present temporarily, usually asthe consequence of abuse or some short-lived andtreatable disease process. Edema of the vocal foldscan result in a voice quality characterized by breathi-ness and tension, similar to vocal nodules, thus mak-ing it difcult to identify the cause of the dysphoniabased on perceptual parameters alone. The anatomi-cal nature of the edema on one hand or vocal nod-ules on the other is different and the physiologicalconsequences of these conditions may be as well, butthe resulting voice may be quite similar, ranging frommild breathiness and tension to aphonia . This is anexample of the lack of direct relationship betweenhow a voice sounds and the presence of a particularpathology. With respect to duration, the dysphoniaassociated with edema may last only a few hours ora day or so, but similar voice characteristics resultingfrom the presence of nodules may require months of

vocal abuse management to eliminate.Other voice disorders can last a very long time or bepermanent. Spasmodic dysphonia is a progressive andoften permanent condition. Although symptomaticrelief is possible, in the vast majority of cases, patientsmust deal with the disorder for the rest of their lives.The loss of voice in the laryngectomee is clearly per-manent. Once the larynx is removed, the patient willnever phonate in the natural way as before the surgery.There are, of course, several alternative sound/phona-tion sources that will allow the laryngectomee to speak,but natural vocal fold phonation is permanently lost.

Upon abductionA

B Subglottic

C

D Juvenile Pedunculated

Sessile

Upon adduction

Figure 9-2 Various mass lesions of the vocal folds: ( A ) vocalnodules; ( B) polyp; (C ) contact ulcers; and ( D ) papilloma. (Re-produced with permission from CIBA Pharmaceutical Company,Summit, NJ; J. Harold Walton (Ed.), The larynx, W. Saunders, withillustrations by F.H. Netter, 1964.)

Why You Need to Know We live in marvelous times! Until relatively recently,undergoing a laryngectomy or having unsalvage-able trauma to the larynx meant the end of naturalspeech production. However, advances in the areasof bioengineering and organ transplantation maysoon change the way speech–language patholo-gists conduct their business—especially in regardto persons with profound voice disorders. The rst




LIFE SPAN

Finally, viewing and understanding voice disordersacross the life span also requires an understandingof the anatomical and physiological conditions thatresult in noticeable voice differences. Vocal nodulesfrequently result from the yelling and screaming thatchildren do, and papilloma is typically found in pread-olescent children when it does occur. The presbylaryn-

gis of the elderly client results in voice characteristicsfor which there may be structural and physiologicalexplanations—explanations inherent to the aging pro-cess and not typically associated with infancy, child-hood, or even young adulthood. It should be noted,however, that following their review, Boone, McFarlane,von Berg, and Zraick (2010) concluded that the voicecharacteristics of the elderly are more a function of dis-ease processes than of physiological deterioration.

In summary, regardless of perspective, when view-ing voice disorders it is imperative to be able to relatestructure and function of the voice producing mecha-nism to the affected parameters of voice. The voiceclinician will always be better prepared to understandthe disorder, to evaluate and monitor the voice, andto provide appropriate therapy and counsel if he/sheis able to relate the perceptual consequences of thecondition (i.e., the voice) to the structure and func-tion of the mechanism.

Parameters of Voice

The psychological parameters of voice—pitch, loud-

ness, quality, and exibility—are the perceptual char-acteristics of voice that dene it as either normal (i.e.,pleasing to the ear, not calling undue or negativeattention to the speaker, and not interfering with com-munication) or abnormal or disordered (i.e., dyspho-nic). Speech–language pathologists are faced with theresponsibility of describing and documenting voicesin terms of these parameters. When a clinician is ableto do so effectively, the voice problem will be wellunderstood, appropriate directions for therapy will beforthcoming, and treatment will likely be efcacious.

PITCH

In Chapter 8, pitch was dened as the psychologicalcorrelate of frequency. Pitch is primarily a functionof the basic laryngeal tone, or voice fundamental —the frequency at which the vocal folds open and close(or release puffs of subglottic air) per second. Stud-

ies have documented the habitual pitch of the voiceof various aged subjects. Thus, there is empirical evi-dence of habitual fundamental frequency as a func-tion of age. As noted in Chapter 8, there is individualvariation in vocal fold length from person to personas well as a signicant difference in the length of thevocal folds between adult males and females. The dif-ference in habitual pitch between males and femalesis evident in adults but not in children. In general,there is nearly an octave difference in habitual pitchbetween adult females and males, and females areable to achieve signicantly higher frequencies at theupper end of their pitch range than are their malepeers. Conversely, adult males are able to producelower frequencies at the lower end of their pitch rangethan are adult females. These gender-related dif-ferences are explainable and understandable when you consider the anatomical variance between adultfemale and male speakers such as overall laryngealsize, degree of the thyroid angle, and vocal fold lengthand mass. Therefore, from a clinical perspective, nor-mal pitch can be dened as a pitch that is appropri-ate for age and gender. Conversely, disordered pitch

occurs when the speaker loses age or gender identity.For example, an adult female has lost age identity ifshe answers the phone and is asked if the caller canspeak to her mother because the caller assumes fromher voice that she’s a child.

One of the most interesting, dramatic, and treat-able disorders of pitch is puberphonia , a condition in which an inappropriately high pitch—often falsetto —is used by males in their late teens or early adulthood.Puberphonia has the capacity to affect gender identityand surely calls undue and negative attention to thespeaker. Voices of somewhat high pitch, though not

as dramatically so as puberphonia, can cause con-cern on the part of the speaker, and occasionally theiremployer, and may have implications for employmentor promotions. It should be noted, however, that manytherapists remain cautious about trying to dramaticallyeffect pitch change in clients (puberphonia notwith-standing) for what might be termed “social” reasons.The concept that there is a habitual pitch that is best,and some might say healthiest, for each of us is dis-cussed often in the literature. Our most natural pitchis referred to as optimal pitch and is thought to be the

attempts at laryngeal transplantation have proven tobe successful for the most part. More incredible thanthis, though, is the recent advent of tissue engineering(i.e., creating complete organs from stem cells). Tissueengineering of the larynx has been accomplished suc-cessfully in animals. Just imagine how it will revolu-tionize the eld of speech–language pathology if tissueengineering can be rened for use with humans!




pitch at which our phonation producing mechanism ismost efcient. The idea that there is a pitch that is mostnatural for the anatomical and physiological featuresof our larynx runs deep among voice therapists even when they disagree about how to establish optimalpitch and may be reluctant to facilitate change to opti-mal pitch as a therapeutic goal. It may be best to think

of optimal pitch as the equivalent of habitual pitch forthe vast majority of healthy nonabusive speakers.Our discussion of pitch as a critical parameter of

voice production would not be complete withoutconsideration of vocal registers . The term vocal reg-ister refers to pitch ranges and to types of phonation,or ways in which the vocal folds function. Vocal reg-isters are laryngeal events that can be identied onphysical, acoustic, and perceptual bases and remindus of the incredible adaptability and exibility of thelaryngeal anatomy. These registers are ranges of vocalfrequencies that overlap but are perceptually distinct.The vocal register that we use most is referred to as themodal register and is important because it is associ-ated with the most common vibratory pattern of thevocal folds. Physiologically, when we phonate in ourmid-range or normal voice, our vocal folds present anupper and lower edge that vibrates along their entireanteroposterior length. As pitch increases, the vocalfolds are increasingly stretched and their thickness isdecreased. In the modal register, the frequency rangeis one and a half octaves or more and a wide inten-sity range (40 to 110 dB) is possible. The quality of the

modal register voice is considered rich, pleasing, andmellow. Normal vocal fold vibration is complex; as thepuffs of air are released through the glottis, the thy-roarytenoid muscle and the cover layers of the vocalfolds vibrate differentially.

By contrast, in the pulse register , phonation ischaracterized by low frequency irregularly occurringbursts. The vocal folds are thick, short, and tightlycompressed. The puffs of air may be individually per-ceived, and thus the phonation is referred to as glottal(or vocal ) fry , sounding similar to the sound of baconfrying. In the pulse register, vocal intensity is limited

and frequencies are in the range of 3 to 50 Hz. At theother end of the human phonation range, the highestfrequencies are produced in the loft register or falsettorange. In this mode of phonation, the vocal folds stiffento a single thin tense edge and only the free marginsvibrate. The vibration is primarily in the area of the junction of the anterior and middle thirds of vocal foldlength. Vocal fold movement is described as a simpleopening and closing with no phase effects or mucosal wave . The resulting voice is high pitched with restrictedintensity range and perhaps a breathy quality.

LOUDNESS

Loudness of voice is directly related to subglottic airpressure and is not a function of the mass and elas-ticity of the vocal folds as with pitch. To maintain aconstant loudness level, one must be able to main-tain constant air pressure below the glottis. The abil-

ity to maintain constant subglottic air pressure whileconstantly decreasing subglottic air volume is both aremarkable and achievable physiological ability formost people with a healthy respiratory and phonatorysystem. Controlled relaxation of the muscles of inspi-ration, including the diaphragm and intercostals, andsupport from the abdominal muscles is critical to themaintenance of constant subglottic air pressure.

Clinically, loudness is judged on the basis of itsappropriateness for the social or environmental situ-ation. For example, an individual having a personalone-to-one conversation with another person whobrings attention to himself by speaking in a voice thatis too loud for the situation may be perceived as havinga voice loudness problem. Conversely, a teacher whois so soft spoken that students have difculty hearingher lectures has a voice that is not loud enough for thedemands of the classroom.

The ability to maintain loudness control may becompromised in neurological conditions or in patients with degenerative neurological diseases. More oftenhowever, vocal loudness that is inappropriate for thesocial or environmental situation is a function of hear-

ing status. A person with a sensorineural hearing lossis likely to speak in a voice that is deemed too loudfor the situation. Because of this person’s inabilityto monitor the loudness of his own speech throughthe auditory system, he may speak in a voice that islouder than the situation requires. By contrast, a per-son experiencing a conductive hearing loss may speakin a soft voice—one considered not loud enough forthe situation. The conductive hearing loss diminishesthis person’s perception of ambient noise, thus mak-ing his voice sound louder to himself than it really is.In this case, the speaker has a tendency to reduce the

loudness of his voice to compensate for the increasedloudness he perceives. Regardless of whether theimpairment is sensorineural or conductive, hearingloss compromises a speaker’s ability to monitor hisvoice and the parameter of vocal loudness is affected.It should be noted that in neither foregoing case is theanatomy or physiology of the voice producing mecha-nism affected. Anatomy and physiology are also notaffected when diminished vocal loudness is attribut-able to psychological depression or to an excited (per-haps manic) psychological state, both of which are




possible. Finally, it should be noted that vocal loudnessmay be attributable to environmental and culturalinuences—for example, quiet soft spoken families orcultures verses louder, more verbally aggressive fami-lies or cultures. Again however, any noticeable differ-ences in vocal loudness that can be attributable toenvironmental or cultural differences are not a func-

tion of anatomical or physiological factors.

QUALITY

Voice quality, similar to the parameter of pitch andunlike loudness, is very much a function of anatomi-cal and/or physiological laryngeal factors. The pri-mary problem of dealing clinically with voice qualityis one of descriptive terminology. “Hoarse,” “harsh,”“breathy,” “tense,” “strident,” and other terms havebeen used to describe voice quality. The clinicianmust ask the following questions: (1) Which termsare the most relevant when diagnosing dysphonia?

(2) Which terms assist the clinician in relating struc-ture to function? And (3) Which terms help the cli-nician best plan for effective management? Wilson(1990) has suggested that a great deal can be under-stood and communicated about dysphonia by usingthe terms “breathiness” and “tension” as qualitydescriptors. Based on didactic and clinical experience,

breathiness and tension are descriptive terms of voicequality that relate well to the Myoelastic AerodynamicTheory of phonation, to the anatomical changes thataffect voice production, and to the relevant manage-ment of dysphonia.

Breathiness relates directly to phonatory inef-ciency. When the vocal folds are not vibrating in thenormal way or cannot adduct appropriately, theybecome inefcient and more air escapes than undernormal phonatory conditions. The excess air turbu-lence is perceived as a breathy voice quality. In ac-cid dysphonia , for example, the vocal folds do notapproximate normally (see Figure 9-3). The result is

Normal vocal fold symmetry

Paramedian

Median(adduction)

Abduction

A Left recurrent nerve paralysis(upon inspiration)

B

Uncompensated left recurrentnerve paralysis (upon phonation)

Compensated left recurrentnerve paralysis (upon phonation)

C D

Bilateral recurrent nerveparalysis (upon inspiration)

E

Figure 9-3 Normal vocal fold sym-metry and vocal fold paralysis: ( A ) normalvocal fold symmetry; ( B–E ) variouscongurations of vocal fold paralysis.(Reproduced with permission from CIBAPharmaceutical Company, Summit, NJ;

J. Harold Walton (Ed.), The larynx, W.Saunders, with illustrations by F.H.Netter, 1964.)




a breathy voice quality often described as weak, asit may be difcult for the speaker to produce a loudvoice because of reduced ability to increase subglot-tic air pressure. Most frequently, a left vocal fold isaccid and does not move to midline to approximate with the nonaffected fold, and thus there is no tensionperceived in the voice.

At this point, it is important to remember that ac-cid paralysis is associated with lower motor neuronand/or peripheral nerve damage. To illustrate this,consider the vagus nerve (cranial nerve X). The impor-tant branches of the vagus nerve for speech produc-tion are the pharyngeal branch, the superior branchof the laryngeal nerve (SLN), and the recurrent branchof the laryngeal nerve (RLN). Each of these branchesis paired, which provides bilateral innervation to thevelum and intrinsic muscles of the larynx. The pha-ryngeal branches of the vagus nerve provide motorinnervation to the soft palate. The SLNs serve the cri-cothyroid muscles and the RLNs innervate all of theother intrinsic muscles of the larynx. Recall that thecricothyroid muscles are involved in the regulation ofvocal pitch, while the other intrinsic laryngeal mus-cles mediate abduction and adduction of the vocalfolds as well as vocal pitch and intensity. These threebranches come off the vagus nerve in the followingorder (from superior to inferior): pharyngeal branch,SLN, and nally RLN.

The vagus nerve pathway is complex. Several fea-tures of voice can be affected depending on the extent

of vagus nerve involvement. In general, the higherthe damage to the vagus nerve, the more widespread(i.e., diffuse) the effect will be on the speech produc-tion mechanism. Conversely, the lower the damageto the vagus nerve, the less widespread (i.e., morefocal) the effect will be. For example, if the damage isabove the pharyngeal branch, not only will the velumbe affected but the intrinsic muscles of the larynx onthat side will also be affected because the SLN andRLN are below the level of the pharyngeal branch.The outcome of pharyngeal branch involvementlikely will be velopharyngeal incompetence and

hypernasality. Involvement of the RLN will be mani-fested in a diminished ability to abduct and adductthe vocal fold on the affected side; damage to the SLN will be manifested in a diminished ability to regulatevocal pitch, also on the affected side. On the otherhand, involvement of the intrinsic laryngeal muscles without involvement of the velum means that vagusnerve damage must be below the pharyngeal branchbut before either the SLN or RLN have branched off.Finally, when damage is even more peripheral—thatis, on the pharyngeal branch, SLN, or RLN alone—

only the structures innervated by that specic branch will be affected.

Recurrent laryngeal nerve paralysis is more com-mon on the left side than the right because of thelonger pathway of the left recurrent laryngeal nerve.The more common accid paralysis of the left vocalfold can result from trauma, surgery, or heart disease

although about one-third of the cases are idiopathic.Inability to adduct one or both vocal folds will result ina breathy voice quality. By contrast, in cases of excesstension in the voice, the vocal folds are extremely tenseand may spasm tightly. This type of voice is describedas spasmodic dysphonia and is considered the mostextreme type of hypertensive dysphonia. Tension isthe overwhelmingly predominant voice quality incases of spasmodic dysphonia.

It is possible, and actually quite common, to haveboth breathiness and tension as voice quality char-acteristics. Two common examples are edematous vocal folds and vocal nodules. Edematous vocal foldsoccur commonly as a result of vocal abuse. Yelling ata ball game or talking over noise at a party or otherpublic event can cause swelling of the vocal folds,thus changing their mass and elasticity and therebychanging their vibratory characteristics. The result isinefciency that allows excessive air to escape, andthus breathiness. Our natural tendency is to increaselaryngeal tension in an attempt to reduce breathiness.This same combination of breathiness and tension invoice quality is also common in cases of vocal nodules,

the most common discrete lesion of the vocal folds.The nodules, also referred to as singer’s, preacher’s, orteacher’s nodules, occur most often bilaterally on thefree margins of the vocal folds at the junction of theanterior and middle thirds. The callous-like bumps onthe folds cause them not to approximate in the normal way during phonation. Excessive air escapes, tensionis increased to compensate for the breathiness, andthe result is a breathy and tense voice quality.

SECONDARY CHARACTERISTICS

There are several secondary voice characteristics orfeatures that are frequently present in association witha breathy and tense dysphonic voice. Glottal or vocalfry is a low-pitched sound that can be attributed to aparalyzed vocal fold or vocal polyp. From an anato-mical and physiological perspective, it is important tounderstand that vocal fry can be the result of some-thing that is vibrating in addition to the vocal folds. When this occurs, two pitches may be heard and thisis referred to as diplophonia . The anatomical sourceof diplophonia is varied. It has been attributed to a




difference in the vibratory pattern of the two vocalfolds caused by paralysis of one fold or by a unilateralpolyp, as noted earlier. Other sources for diplopho-nia include aryepiglottic and ventricular fold vibra-tion occurring simultaneously with normal vocal foldvibration.

When coupled with breathiness and tension, vocal

fry contributes to what is often referred to as hoarse-ness or a hoarse voice quality. However, it shouldalso be recognized that vocal fry is used to describea mode of vocal fold vibration—the pulse register—that is not associated with dysphonia but is simplya different vibratory pattern from that of typicalphonation (i.e., the modal register) or falsetto (i.e.,the loft register). Other secondary phonatory char-acteristics may include pitch breaks and phonationbreaks . Pitch breaks are frequently associated withan abrupt shift from the typical (i.e., modal) registerto the loft register (i.e., falsetto). Interestingly, whensuch pitch breaks are controlled musically, they arereferred to as yodeling. Pitch breaks as secondaryvoice characteristic are likely associated with crico-thyroid function and may be attributable to superiorlaryngeal nerve damage.

Phonation breaks or aphonic periods are associ-ated with tense breathy voices, and are sometimesreferred to as intermittent whisper. It appears thatthe vibratory pattern of the vocal folds is interruptedsuch that voice (i.e., audible phonation) is stoppedbriey. This phenomenon is sometimes seen in cases

of advanced or well-developed vocal nodules. Insimilar voices, a variation on the phonation break isdelayed onset of phonation. In this case, the start ofphonation is delayed at the beginning of an utteranceand a brief period of aphonia or whispered speech isperceived prior to phonation beginning.

Other secondary features seen frequently in dys-phonic patients include noisy inhalation and inhala-tory laryngeal stridor . Both result from some degreeof airway obstruction. Noisy inhalation and laryngealstridor are audible features associated with severalvoice disorders. A paralyzed vocal fold could cause

audible air turbulence during inhalation as couldpapilloma or other laryngeal obstruction. Secondaryvoice characteristics are important for the voice clini-cian to note because they are features that add to theoverall impression of voice and are features that canbe explained by the anatomy and physiology of thevoice production mechanism. Secondary voice char-acteristics are closely associated with voice quality, ascontrasted with pitch, loudness, and exibility, andare important to document as part of the diagnosticand therapeutic process.

FLEXIBILITY

The nal voice parameter that denes normal andabnormal voice is exibility . As normal speakers, we expect, by both linguistic necessity and linguisticconvention, to have a degree of variation in our vocaloutput. Speech that is void of pitch and loudnessvariation is monotonous, probably void of affect, andinconsistent with cultural expectations. Stress, pause,and intonation in language are linguistic necessitiesif one is to communicate effectively. These features inlanguage can make a difference in meaning and whenthey do, they are referred to as suprasegmental pho-nemic elements. The rising intonation at the end ofquestions or the contrastive stress between the wordspro duce and pro duce affect the speaker’s meaning andperhaps the expectations for the listener. Even whenpitch, loudness, and intonational features of voice donot affect meaning in specic ways, they are impor-

tant to the communication of affect on the part of thespeaker. Speech delivered in a monotonous, com-puter-like manner is void of emotional tone or affect.In general, as listeners we nd such speech boring.The literal meaning of the message may be preservedbut the importance, urgency, or mood is lost.

Flexibility in speech is not a function of specicanatomical structures or physiological processes butis secondary to those anatomical features and physi-ological processes that are important to the control ofpitch and loudness. Clinically, a voice without appro-priate exibility can be described as lacking pitchand loudness variation and thus at and dull. At theextreme, a computer- or robot-like voice is conspicu-ously monotonous and lacking in emotional color. Although clinically monotonous voices are not nec-essarily robot-like, they can bring negative attentionto the speaker by the lack of conventional exibilityand affective communication. Cases where excessiveexibility is a voice liability are rare and are usuallyassociated with personality issues ranging from overdramatic and excited to psychotic.

Clinical Perspectives

Students in speech–language pathology—beginningclinicians if you will—are encouraged to develop aclinical perspective or fundamental framework toguide their approach to evaluation and therapy. Theproper perspective will help clinicians recognize theirlimitations, dene their role, and guide their effective-ness. The following are some perspective suggestionsfor consideration when dealing with voice disorders.




PERSPECTIVE 1: MEDICAL CLEARANCE

With respect to voice disorders, it is important to keepin mind that medical clearance is critical. Becausethere is no direct relationship between voice charac-teristics and specic laryngeal pathology, the cliniciancannot be certain of the cause of the voice disorder.Furthermore, it is outside the clinician’s scope ofpractice to diagnose laryngeal pathologies. Speech–language pathologists must avoid treating clients untilthe etiology of the voice problem has been conrmedand it is agreed that voice therapy is indicated. Treat-ing a dysphonic child, assuming the presence of vocalnodules when it is in fact papilloma that is present, isa critical error that must be avoided.

PERSPECTIVE 2: LISTENING

It might appear overly obvious or a trite admonition

to emphasize listening as a clinical perspective whenevaluating and treating voice disorders. After all, don’tclinicians instinctively listen to their clients? Yes, butvoice features can be subtle and confusing. Experiencesuggests that to be a good listener of voice parametersrequires training and practice. Student clinicians areurged to take advantage of available recorded mate-rials designed to help develop critical listening skillsfor primary and secondary vocal characteristics (e.g.,Boone et al., 2010; Dworkin & Meleca, 1997; Wilson,1990). Clinicians, as students or as practicing profes-sionals, should never hesitate to consult colleaguesabout what they are hearing in the voices of clients.Listen, listen again, and discuss what you are hearing.Discussion of what is heard, conrmation of what isheard, and arrival at possible consensus can only bein the best interest of the client.

PERSPECTIVE 3: DOCUMENTATION

Documentation of voice characteristics and dyspho-nic qualities is critical to quality referral, appropriatediagnosis, and effective management and treatment.

Careful description of pitch, loudness, quality, andexibility is valuable to the physician to whom the cli-ent is referred and helps to build a respectful profes-sional rapport. That same high quality professionaldescription will always remain as the permanentrecord of your analysis of the voice at the time. When your perception has been conrmed by the percep-tion of others, it is validated and thus respected. Inaddition, whenever possible, it is excellent practice tosupport your subjective perception of voice features with objective data.

It is acknowledged that in many settings, instru-mentation for voice analysis is not available, but when available should be used to the extent possibleto support perceptual judgments. Audio recordingsserve as a relatively permanent documentation ofthe voice at a particular point in time. They serve asa source of comparison for future voice samples and

can be used to garner the judgments of other profes-sionals at any time. Computer programs for voiceanalysis are excellent sources of objective data, par-ticularly on features related to pitch and exibility. Voice fundamental, habitual pitch, and pitch rangeare examples of features of phonation that can beeasily obtained with computer analysis. When com-puter analysis is not available, a pitch pipe or musi-cal instrument like a piano can help the clinicianestablish a reasonable estimation of several pitchfeatures. Loudness is highly subjective because it isa matter of appropriateness for the social situation.Computer programs provide some loudness docu-mentation, but the information obtained is disasso-ciated from the demands of the speaking situation. A simple sound level meter can be used in the com-munication environment, but that too is not likely tobe accessible to clinicians in the public schools. Thedocumentation of the quality of dysphonic voices isalso highly subjective. Although there are features ofcomputer analysis that relate to dysphonia, there isno substitute for the well-trained ear of the clinician. Again, audio recordings serve to preserve the voice

sample for later analysis and comparison and pro-vide a source of conrmation by others, thus validat-ing the perceptions of the clinician.

Why You Need to Know Several instruments are used today to obtain objec-tive data regarding the parameters of voice (i.e.,pitch, intensity, and quality). One such computer-based instrument is the Computerized Speech Lab(CSL) by Kay Elemetrics. The CSL is a hardware/ software package that includes such analyses asnasometry, real-time pitch analysis, and spectogra-phy. One particular software program—the Multi-dimensional Voice Prole, or MDVP—can be used toobjectively assess various parameters of vocal qual-ity. Although it is beyond the scope of this textbookto provide a detailed discussion of instrumentation, you are encouraged to read about the advances thathave been made in this particular area of speech– language pathology. Boone et al. (2010) provide agood primer in this area.




PERSPECTIVE 4: EMPHASIS

When writing diagnostic reports, SOAP notes , andother therapy documentation, the clinician is urged toplace appropriate emphasis on the most obvious andclinically relevant factors that characterize the voice. What stands out as most conspicuous in this voice? What is it about this voice that is within generallyacceptable normal limits, and what is not? Of thosefeatures that appear not to be within normal limits, which, if any, are dominant? Reporting with appropri-ate emphasis and clearly relating the salient features ofvoice to the basic parameters of pitch, loudness, qual-ity, and exibility will clarify clinical communication while providing a clear record of the client’s diagnosisand progress in therapy. Appropriate emphasis is par-ticularly important in the summary and recommen-dation sections of reports, where other professionalsare likely to rst get the “big picture” of the case.

PERSPECTIVE 5: COMMUNICATION

In all of what we do clinically, there is no substitutefor clear communication. Because voice cases almostalways involve interdisciplinary interaction, thespeech–language pathologist must be mindful of thelimits of their role and the nature of their contribu-tion. Although medical professionals are the mostlikely referral sources and referral recipients, schoolteachers, psychologists, and teachers of singing arealso likely professionals to whom referrals are madeand from whom referrals are received.

When communicating about voice disorders, thespeech–language pathologist must be careful not tomake a medical diagnosis or overstate the case in a waythat might be construed as a medical diagnosis. Theclinician should carefully describe the voice problem,support that description with as much objective andquantitative data as possible, identify the salient issuesfrom the case history, and clearly pose any questionsfor which he or she hopes to receive answers. The cli-nician can go so far as to say that the nature of the dys-

phonia and the notable features of the history areconsistent with the possible presence of vocal nod-ules, for example, but should present the case in a wayso as not to positively conrm the presence of nod-ules. The following is an example of how the commu-nication might be phrased:Dr. ENT:

CL is a 6-year-old male who was evaluated on Feb-ruary 28, 2007 and who presented with a dyspho-nia characterized by tension and breathiness that ismoderate in severity and is accompanied by phona-

tion breaks and intermittent aphonia. The dyspho-nia appears to have increased in severity over the pastsix months as reported by CL’s parents. They describehim as always having been an active child, prone tousing a loud voice inside, and being among the mostvocal in his play group outside. Yelling and screaminghave increased since he has been involved in organized

sports this year.CL’s voice and history are consistent with the possi-ble presence of vocal nodules, but he has not had vocal fold visualization or a medical examination relatedto his voice problem. Please advise as to the appropri-ateness of therapy to help CL understand and reducevocal abuse.

Respectfully,Ima Therapist

Summary

The intent of this chapter was to provide you with anunderstanding of how the anatomy and/or physiol-ogy of the phonatory system relates to various com-mon disorders of voice. Perhaps more so than any ofthe other systems involved in speech production (i.e.,the respiratory and articulatory systems), there is aclear relationship between laryngeal anomalies andexpected aberrations of voice. For example, increasedmass on the vocal folds created by mass lesions suchas vocal nodules, polyps, or papilloma will very likely

result in a lower pitch than normal. Should the masslesion invade the medial borders of the vocal folds, thevocal folds will not be able to approximate completelyduring phonation and the result will likely be mani-fested as a breathy voice quality. A differential in sizeor shape of bilateral lesions will likely cause the vocalfolds to vibrate asynchronously, and the result will bea harsh voice quality. In cases of spasmodic dyspho-nia, the laryngeal mechanism may spasm so severelythat the patient will exhibit a very labored vocal qual-ity known as a “strain-strangled” voice. Having a goodknowledge of the anatomy and physiology of thephonatory system will benet the clinician greatly inassessing and treating voice disorders.


At the beginning of Chapter 8, we described Destiny, a15-year-old high school student with diagnosed vocal nod-ules. Her history is clearly consistent with the medical diag-nosis. Singing can be and cheering often is a factor in the his-

tory of young women with vocal nodules. The quality of hervoice was described as hoarse with a degree of breathiness.




What is described as hoarseness (i.e., dysphonia) is veryoften a result of breathiness and tension, so the descriptionof Destiny’s voice is again quite consistent with the presenceof nodules. In Destiny’s case, her actual habitual pitch (asinstrumentally conrmed) was not reported but is likely tobe perceived as low because of her dysphonia. In fact, theentire history and description of her voice are consistentwith vocal nodules with the exception of pain on phona-

tion, which is less likely to be an associated symptom invocal nodules and more likely to be reported in associationwith contact ulcers. It is important to keep in mind, however,

that given the history and voice description, Destiny couldhave edematous vocal folds or, with the presence of pain onphonation, contact ulcers. Thus, the point is once again made

that we cannot conrm pathology with vocal characteristics.Medical diagnosis and clearance to proceed with therapyare necessary. The key to remediation of Destiny’s voice problem is toreduce vocal abuse. It is most likely that singing and cheeringare implicated as abusive activities, and it is also likely that

cheering is the more deleterious of the two. Does this mean that Destiny can no longer participate in these activities?Should complete vocal rest (i.e., no voice use) for a periodof time be recommended? The answer to both of thesequestions is no. In fact, complete and prolonged vocal restcan actually cause problems and will not solve the problemif—when voice use is resumed—vocal abuse continues. From a management perspective, it is recommended

that the clinician help Destiny to understand what vocalnodules are and what causes them. It is important for Des-

tiny to take responsibility for her situation and the manage-ment of it. She is not at fault or to blame for having nodules,but she will need to be an active participant in her vocalremediation. She is likely to wonder, “Why me?” There is no

explanation for why she has developed vocal nodules whileher friends who participate in the same activities have not.Although she should not feel guilty, she will have to acceptresponsibility for change, something that may not be easy ather age. Understanding that she need not give up activitiesimportant to her may be a great boost to her motivationfor change. Surgical removal of nodules is possible, but with-out change in vocal behavior (i.e., abuse reduction), nodulesare likely to recur. Identication of abusive behaviors is rec-ommended as a rst step. Cheering and singing are likely toemerge at the top of a list of abusive behaviors for Destiny,but social vocal habits with friends, communication style athome, and other vocal habits (e.g., laughing, throat clearing,hard glottal attack) could also be factors contributing to herproblem. Once a hierarchy is established, strategies can beexplored to manage the abusive behaviors. For example,while cheering, Destiny might either lip-sync the cheersor speak them without yelling. During practice, she mightrefrain from vocalizing the cheers and instead concentrateon the physical aspects of cheerleading. Also, if Destiny

were to “teach” others what she has learned about vocalabuse and its management, she might be able to help othersavoid similar problems in the future. In that way, she couldacknowledge her problem while helping others. While singing, she might reduce vocal intensity, limit sing-ing to only her modal register (i.e., mid-frequencies), limit

the amount of participation, and avoid singing loudly with the car radio or in the shower. If singing is a very importantactivity for Destiny, she might consider getting a teacher ofsinging to aid in the development of healthy singing tech-niques. Elimination of vocal nodules will take time, but theywill reduce in size and will eventually disappear throughelimination of vocal abuse.



PART 4 SUMMARYPart 4 (Chapters 8 and 9) provided you with a basic understanding of the anatomyand physiology of the phonatory system, along with some common pathologies asso-ciated with voice production. The primary structure of phonation—the larynx—is amusculocartilaginous structure that is supported by, and serves as a framework for,several muscle groups. The intrinsic laryngeal muscles are responsible for producingthe vocal tone and for mediating the pitch and loudness of that tone. The extrinsicmuscles are involved primarily in assisting pitch regulation. The process of vocal foldvibration was described according to the Myoelastic Aerodynamic and Cover-BodyTheories of phonation. The result of phonation is a complex tone that is rich in har-monic structure. In Chapter 9, you were introduced to a number of pathologies associ-ated with the phonatory system. A direct relationship was established between somecommon pathologies (e.g., mass lesions, vocal fold paralysis, spasmodic dysphonia)and the underlying anatomical and/or physiological anomalies associated with thosepathologies. In addition, Chapter 9 offered several perspectives for diagnosing andremediating vocal pathologies.

PART 4 REVIEW QUESTIONS 1. Name all of the cartilages that comprise the larynx. Which of these cartilages are

most important in the process of phonation? 2. Name the intrinsic and extrinsic membranes of the larynx and briey describe

each one’s purpose. 3. Name the intrinsic laryngeal muscles and briey describe how each of them

contributes to phonation. 4. Describe how the extrinsic laryngeal muscles contribute to laryngeal physiology.

What is the net effect of their contribution? 5. What are the contributions of the superior laryngeal nerve and recurrent laryn-

geal nerve to phonation? 6. From what cranial nerve do the superior and recurrent laryngeal nerves emerge?

What other cranial nerves are involved in the process of phonation? Describeeach one’s contribution.

7. What are the underlying physiological processes of voice production? Explaintheir interdependence.

8. Briey describe the Myoelastic Aerodynamic and Cover-Body Theories of pho-nation.

9. List and dene the components of a complex tone.

10. Dene medial compression and longitudinal tension. What is each one’s contri-bution to voice production?

11. Describe the phases of phonation. 12. How are pitch and loudness of voice controlled? 13. What is dysphonia, and how does it relate to the parameter of voice quality? 14. Name three voice disorders presented in Chapter 9 and describe the effects they

are likely to have on voice. 15. What is exibility of voice, and in what ways is it important in conversation? 16. Why is medical clearance important in voice disorder management for the SLP?

213



217


(III-B)• Demonstrate knowledge of the neurological basis of the basic human communication pro-

cesses (III-B)• Demonstrate knowledge of the acoustic basis of the basic human communication processes (III-B)

Learning Objectives• You will be able to describe the framework that supports the ar ticulatory/resonance system.• You will be able to recall the major anatomical structures of articulation and resonance and

their role in the process of speech production.

• You will be able to describe the muscles that mediate articulation and resonance.• You will be able to discuss the basic concepts involved in speech production as described by

Source-Filter Theory.

CHAPTER 10

Anatomy and Physiology of the Articulatory/Resonance System


alae wing-like processes depressor alae nasi

alaeque pertaining to a wing-like structure levator labii superior alaeque nasi

bucco- pertaining to the cheeks bucco pharyngeus

cerato- pertaining to a horn cerato pharyngeus

chondro- pertaining to cartilage chondro pharyngeus

cranius pertaining to the cranium epi cranius frontalis

crico- pertaining to the cricoid cartilage crico pharyngeus

epi- over or above epi cranius frontalis

genio- pertaining to the chin genio glossus

glosso- pertaining to the tongue glosso pharyngeal

-glossus pertaining to the tongue palato glossus

hyo- pertaining to the hyoid bone hyo glossus

incisivus pertaining to the incisor teeth incisivus labii inferior

labii pertaining to the lips levator labii superior

mylo- pertaining to the lower jaw mylo pharyngeus



CHAPTER 10 ANAT MY AND PHY I L Y F THE ARTI LAT RY RE NAN E Y TEM 219

The remainder of this chapter will be devoted to at oroug iscussion o t e anatomy an p ysio ogyof the articulatory/resonance system. It is expectedt at upon rea ing t is c apter, you wi e we versen the structure and mechanics of articulation and

resonance, an ow t ese processes wor toget er toroduce human speech. It should also be noted that

any of the structures that make up the articulatory/resonance system are a so invo ve in eg utition .Because speech–language pathologists work with

ersons aving swa owing isor ers, a iscussion othe anatomy and physiology of the swallowing mech-anism wi a so e presente in t is c apter.

Anatomy of the Articulatory/Resonance System

Three primary cavities form the vocal tract: pharyn-gea , ora , an nasa (see Figure 10-1). T e p aryngeacavity extends from the base of the skull to the cricoidcarti age o t e arynx. It as a vertica orientation. T eoral cavity extends from the lips and teeth anteriorlyo the palatoglossal arches posteriorly, and from thear an so t pa ate superior y to t e tongue in eri-

orly. Its orientation is horizontal. Finally, the nasal cav-ty actua y consists o two separate c am ers. T ese

chambers run horizontally from the nostrils anteri-

orly to the uppermost portion of the pharynx posteri-or y. Eac o t ese t ree primary cavities consists o anumber of anatomical structures and/or landmarks.

T e ora cavity is compose o severa anatomi-cal structures and landmarks. These include the lips,teeth, alveolar ridge, hard palate, velum , tongue, andman i e . Eac o t ese structures wi e escri e

in greater detail below. The nasal cavity includes thenose an two c am ers separate at mi ine y t enasal septum . Within each cham er is a series oan mar s t at wi e iscusse ater. Fina y, t e

pharyngeal cavity is rather unremarkable in terms ofstructures an an mar s ut is compose o an intri-cate and complex network of muscles that will be dis-cussed in a later section of this chapter.

T e voca tract t en consists primari y o t e o -owing structures: lips, teeth, alveolar ridge, hard

pa ate, ve um, tongue, man i e, ora cavity, nasacavity, and pharyngeal cavity. With the nasal and oralcavities eing oriente orizonta y an t e p aryn-geal cavity being oriented vertically, the vocal tractresembles a capital letter F.” In an adult male, thedistance between the vocal folds and lips is approxi-mately 17 cm. Five centimeters of this distance is theora cavity, wit t e remaining 12 cm eing t e engtof the pharynx.

Simi ar to many o t e anatomica structures o t erespiratory and phonatory systems, movement of the

achian tubeEus

elumV

alatoglossal arch

haryngo-epiglottic ol(marks boundary betweenoropharynx and laryngopharynx)

alatop aryngeal arc

Epiglottis

Esophagus

Trachea

Pharyngeal

cav ty

Nasopharynxropharynxaryngopharynx

Key

Nasal c vity

ard pala e

Oral c avity

Hyoidone

Figure 10-1 Sagittal view of the oral, nasal, and pharyngeal cavities. (Adapted with permission from Moore, K.L.,Agur A.M., Dalley, A.F. (2009). Clinically oriented anatomy (6th ed.). Baltimore: Lippincott Williams & Wilkins.)



220 PART 5 ANATOMY, PHYSIOLOGY, AND PATHOLOGY OF THE ARTICULATORY/RESONANCE SYSTEM

primary anatomical structures of the articulatory/resonance system are mediated by muscle activity.Therefore, this chapter will include a thorough dis-cussion of the muscles that assist in articulation andresonance. Many of these muscles have their insertionor origin on bones of the skull. During the process ofcommunication, facial expression may convey part of

the message. Muscles are involved in facial expression,and many of these muscles also have attachments tothe bones of the skull. Because of this, a discussion ofthe articulation/resonance system would not be com-plete without a description of the human skull. Oncethe human skull has been presented, the discussion will turn to the anatomical structures that make upthe oral, nasal, and pharyngeal cavities.

THE SKULL

Figure 10-2 shows several views of the human skull.Upon rst glance, the human skull appears to be astructure consisting of two parts: the skull proper andthe jaw bone. However, in actuality, the skull is a com-plex structure that consists of 28 bones that articulate with each other similarly to a three-dimensional jig-saw puzzle. Some of these bones are paired and oth-ers are singular. All of them can be categorized intoone of three groups: bones of the cranium , bones ofthe face, and miscellaneous bones. There are eightbones that comprise the cranium, the part of the skullthat houses the brain. These include the unpaired eth-

moid , sphenoid , frontal , and occipital and the pairedparietals and temporals . The facial portion of the skullis that part that corresponds to the recognized humanface. There are 14 bones that comprise the facial por-tion of the skull. These include the unpaired mandible and vomer and the paired maxillae , nasals , palatines ,lacrimals , zygomatics , and inferior nasal conchae .

Finally, the miscellaneous bones are six in num-ber and include a series of three tiny bones housed within each temporal bone of the cranium—the mal-leus , incus , and stapes —which are part of the hearingmechanism. These bones will be discussed at greater

length in Chapter 12 and therefore will not be dis-cussed in this chapter. Some anatomists include oneadditional bone under the miscellaneous category,resulting in a total of 29 bones for the skull. This is thehyoid bone which was discussed in detail in Chapter8. Anatomists who include the hyoid bone as one of29 do so because the hyoid is more intimately relatedto the tongue than to the larynx. However, becausethe hyoid does not articulate directly with any otherbones of the skull, it is not included here as a part ofthe skull. Having been discussed in more detail in

Chapter 8, the hyoid bone will not be described indetail here.

Gross anatomy of the skull will reveal several ana-tomical structures and landmarks. The orbits of theeye are prominent cavities where the eyeballs reside.Keeping to the analogy of a three-dimensional jigsawpuzzle, one will realize that the orbits are not com-

posed of one bone but actually are composed of partsof several bones, among them the ethmoid, frontal,lacrimal, maxillary, palatine, sphenoid, and zygomaticbones. Similarly, within the nasal cavity is a verticalpartition of bone. This partition is called the bonynasal septum, and it also is not a singular bone butactually composed of two bones: ethmoid (more spe-cically, the perpendicular plate) and vomer. Alongthe lateral walls of each chamber of the nasal cavityare three scrolls of bone known as the nasal conchaeor turbinates . The two upper conchae (superior andmedial) come from the ethmoid, whereas the low-ermost scroll is an independent bone—the inferiornasal concha. The three nasal conchae form smallchambers called meatuses. Returning to the exteriorof the skull, one will note several landmarks: the frons (forehead), occiput (posteriormost point of the skull),and vertex (superior tip of the skull). Along the sides ofthe skull, where the facial part ends and the craniumbegins, are depressions called temporae . These cor-respond to the temples when the soft tissue structuresoverlay the skull. Just lateral to and below each orbitis a prominent loop of bone called the zygomatic

arch, more commonly referred to as the cheekbone.The zygomatic arch is not a singular bone but ratheris created by parts of three bones: maxilla, temporal,and zygomatic.

If one were to remove the top of the skull by cuttingaround the circumference of the cranium, one wouldbe holding the calvaria or skullcap. By then remov-ing the brain from the cranium, one would note threemajor cavities within the oor of the cranium. Theseare the anterior , medial , and posterior cranial fossae .

On each side of the skull, immediately posteriorto where the mandible articulates with the skull, is

a small opening. This opening is the bony externalauditory meatus . Immediately behind and project-ing below each external auditory meatus is a roundedprotuberance called the mastoid process . Medial toeach external auditory meatus on the inferior surfaceof the skull is a sharp projection of bone known as thestyloid process . At the base of the skull between andbehind the styloid processes is a large hole. This holeis called the foramen magnum .

Finally, one will note that several jagged lines tra-verse the cranial part of the skull. These jagged lines



CHAPTER 10 ANATOMY AND PHYSIOLOGY OF THE ARTICULATORY/RESONANCE SYSTEM 221

A

B

Frontal bone

Coronal suture

Superior orbital fissure

Optic canal

Inferior orbital fissure

Vomer

Anterior nasal spine

Mandible

Mental foramen

Supraorbital notch

Supraorbital margin

Parietal bone

Temporal bone

Orbital surface

Zygomatic arch

Infraorbital foramen

Nasal bone

Inferior nasal concha

Nasal septum

Maxilla

Intermaxillary suture

Coronal suture

Frontal bone

Greater wing ofsphenoid bone

Glabella

Lacrimal bone

Nasal bone

Frontal processof maxilla

Infraorbital foramen

Anterior nasal spine

Maxilla

Mental foramen

Mental protuberance

Parietal bone

Temporal bone

Lambdoid suture

Occipital bone

Ear canal

Mastoid process

Styloid process

Zygomatic arch

Zygomatic bone

Mandible

Figure 10-2 Various views of the human skull. A . Anterior view. B . Lateral view. ( continued )




are known as sutures. There are four prominent sutures:coronal, sagittal, lambdoidal , and occipitomastoid . The

coronal and sagittal sutures are named in reference tothe planes in which they course. The lambdoidal sutureis named for the fact that it resembles the Greek letterlambda ( λ ). The occipitomastoid suture refers to theanatomical structures it joins together (i.e., the occipitalbone and mastoid processes of the temporal bones).

Facial Bones

Maxillae

The paired maxillae are illustrated in Figure 10-3. Thesebones make up the greater portion of the central face

just lateral to the nose and below the eyes and are sec-ond only to the mandible in size. The two maxillae fuse with each other at midline just below the nasal open-ing by way of the intermaxillary suture . This suturecontinues between the two upper central incisors andbetween the palatine processes of the maxillae. Imme-diately posterior to the upper central incisors is a smallopening called the incisive foramen . In very earlydevelopment, ne sutures that extend bilaterally fromthe incisive foramen to between the lateral incisors andcanines form a triangular region referred to as the pre-maxilla . In some animals, this is a separate bone, but in

humans the sutures are usually completely fused andtherefore the two halves of the premaxilla are counted

as part of the palatine processes of the maxillae.

C

Intermaxillary suture

Transverse palatine suture

Palatine bone (horizontal process)

Lateral pterygoid lamina

Medial pterygoid lamina

Ear canal

Styloid process

Temporal bone

Foramen magnum

Parietal bone

Inferior nuchal line

Incisive foramen

Palatine process (of the maxilla)

Zygomatic arch

Vomer

Mandibular fossa

Mastoid process

Occipital condyle

Condylar fossa

Occipital bone

Superior nuchal line

Figure 10-2 (Continued ) C . Inferior view. (Adapted with permission from Agur, A.M., Dalley, A.F. (2008). Grant’s atlas ofanatomy (12th ed.). Baltimore: Lippincott Williams & Wilkins.)

Why You Need to Know Sometimes in fetal development, the sutures of themaxillae fail to fuse properly, resulting in a condi-tion known as cleft palate. The cleft may involveonly the intermaxillary suture or may involve thesutures that dene the premaxilla. Cleft palate willbe discussed in greater detail in Chapter 11.

Each maxilla has a corpus (i.e., body) and a num-

ber of processes. In all, each maxilla articulates withnine other bones. These include the ethmoid, frontal,inferior nasal concha, lacrimal, the opposite maxilla,nasal, palatine, vomer, and zygomatic. Of note is thefrontal process that articulates with the frontal bone ofthe cranium and the zygomatic process that articulates with the zygomatic bone of the facial portion of theskull. Each maxilla also has an orbital process that cre-ates much of the inferior orbit of the eye. Immediatelybelow the orbit of the eye is a small opening called theinfraorbital foramen . Each maxilla has a number ofalveolar processes where the upper teeth are housed.




Frontal process

ygomatic process

termaxillary sutureInAlveolar proce ss

In raorbital oramen

Orbital process

A

ontal processFr

rbital process

gomatic processZ

fraorbital foramenIn

terior nasal spinA e

rpusC

B

Figure 10-3 he maxillae. A Anterior view. B . Lateral view. (Adapted with permission from Agur, A.M.,Dalley, A.F. (2008). rant’s atlas of anatomy (12th ed.). Baltimore: Lippincott Williams & Wilkins.)




Of particular note is a somewhat vertically orientedridge in the maxilla where the canine tooth resides(the third tooth from midline). Appropriately enough,this ridge is referred to as the canine eminence.

The palatine processes are noteworthy as theyform the anterior three-fourths of the hard palate. Thepalatine process of each maxilla fuses with its partner

to form most of the ceiling of the oral cavity and oorof the nasal cavity. On the nasal side of each palatineprocess is a small ridge called the nasal crest. The nasalcrests from both maxillae form a horizontally directedgroove where the perpendicularly directed vomerresides. The nasal crests continue in an anterior direc-tion and terminate as the anterior nasal spine.

Upon close inspection of the maxillae, one will notethat these bone are not solid but rather have a hol-low interior. These are called the maxillary paranasalsinuses , and they are the largest of all the paranasalsinuses. The maxillary paranasal sinuses are presentat birth.

Mandible

The mandible is more commonly referred to as the jaw bone and is illustrated in Figure 10-4. It is the larg-est of the facial bones of the skull. During embryonicdevelopment, the mandible starts as two halves joinedtogether at the mental symphysis which courses ver-tically, starting between the two lower central inci-sors. The mandible consists of an anterior corpusand two posterior rami (the mandibular rami). In the

region of the mental symphysis, the corpus extendsoutward forming the mental protuberance. The men-tal protuberance is bordered on each side by the men-tal tubercles. Along the superior margin of the corpusare dental alveoli for the lower teeth. Just lateral andsomewhat superior to each mental tubercle is a smallopening called the mental foramen. Also runningfrom each mental tubercle somewhat posteriorly andsuperiorly is an indistinct ridge called the obliqueline. On the inner (posterior) surface of the corpus is amore prominent ridge running horizontally from sideto side. This ridge is known as the mylohyoid line .

The mandibular rami arise at an angle that is approxi-mately 90 degrees to the corpus, although this angle mayvary somewhat from person to person. On the superiorborder of the mandibular rami are two processes. Theanterior process is called the coronoid process and theposterior process is referred to as the condylar process .The mandibular notch separates the coronoid processfrom the condylar process. The condylar process fromeach side articulates with the temporal bone of the skullto form the temporomandibular joint (TMJ) . This joint will be described in greater detail later.

Nasals

The paired nasal bones are illustrated in Figure 10-5.These bones form the bridge of the nose and lie medi-ally to the frontal processes of the maxillae. Althoughthey are rather small in size, they articulate with thefrontal bone, perpendicular plate of the ethmoid ,and maxillae as well as the septal cartilage . The twonasal bones are fused together at midline at the inter-nasal suture. A nasal foramen may also exist in one orboth bones.

Palatines

The paired palatine bones are somewhat “L” shapedand comprise the posterior one-fourth of the hardpalate as well as a portion of the oor and lateral wallsof the nasal cavity (see Figure 10-6). These bones alsohelp form the inferior orbits of the eyes. Of particu-lar note are the horizontal processes which form the

posterior portion of the hard palate. The anterior bor-der of each horizontal process is serrated to allow for astrong articulation with the palatine processes of themaxillae. The two horizontal processes when fusedform a posterior nasal spine. The posterior border ofthe horizontal processes is free and forms the point ofattachment for the velum. The palatine bones articu-late with each other as well as the ethmoid, frontal,inferior nasal conchae, maxillae, and vomer.

Lacrimals

The lacrimal bones are the smallest bones of thefacial portion of the skull (see Figure 10-7). They areso named because of their proximity to lacrimal (i.e.,tear) glands. In addition to forming a small portion ofthe medial orbits of the eyes, these bones articulate with the ethmoid, frontal, inferior nasal conchae, andmaxillae.

Zygomatics

The paired zygomatic bones are illustrated in Figure10-8. They help form a portion of the lateral and infe-rior walls of the orbits of the eye. Each bone consists

of a corpus and four processes: the frontosphenoidal;orbital; maxillary; and temporal, which describe theirattachments to other bones (the frontal, maxillae,sphenoid, and temporal bones). Of particular noteare the maxillary and temporal processes. Medially,the maxillary process of the zygomatic bone articu-lates with the zygomatic process of the maxilla. Lat-erally, the temporal process of the zygomatic bonearticulates with the zygomatic process of the tempo-ral bone. These articulations form the zygomatic arch, which is more commonly known as the cheekbone.




ental foramenM

Mylohyoid line

Posterior border

of ramus

ondylar process

C

A

Mental foramMental

protuberance

Angle ofmandible

Coronoidroc ss

Mandibularnotch

Condylarprocess

amus

Obliquene

Corpus

amus

Co pus

Figure 10-4 The mand . . . . . . ission from Agur, A.M.,Dalley, A.F. (2008). Grant’s atlas of anatomy (12th ed.). Baltimore: Lippincott Williams & Wilkins; B and C : Adapted with permission fromAnatomical Chart Company.)




Inferior Nasal Conchae

T e in erior nasa conc ae are i ustrate in Figure10-9. One of these bones is found in each of the twoc am ers ma ing up t e nasa cavity, more speci -cally making up the lowermost part of its lateral wall.T ese ones articu ate wit t e maxi a anterior y anthe palatine bones posteriorly. Along with the supe-rior and medial nasal conchae (which are part of theethmoid bone), the inferior nasal conchae are scrollsof thin one that are also referre to sometimes as thetur inate ones.

Vomer

The vomer is a somewhat quadrilaterally shaped bonet at comprises t e ower a o t e ony nasa sep-tum (the upper half of the bony nasal septum comesfrom the perpendicular plate of the ethmoid bone).Illustrated in Figure 10-10, the vomer resides in thehorizontally oriented groove created by the nasalcrests o t e maxi ae. In a ition to articu ating witthe maxillae, the vomer articulates with the palatine

ones e ow an t e perpen icu ar p ate o t e et -moid and the rostrum of the sphenoid bone above. Itsposterior or er is ree, ut its anterior or er articu-ates with the cartilaginous nasal septum.

Cranial Bones

Frontal

T e ronta one correspon s to t e ore ea regionand the anterior portion of the top of the cranium. Itis i ustrate in Figure 10-11. T e ronta one consists

of a squamous portion and an orbital portion. Thesquamous portion is t e arger o t e two an cor-responds to the forehead and anteriormost part ot e cranium. T e or ita portion correspon s to t esuperior orbits of the eye and the eyebrow region. Ininfancy, there may be a metop c suture that ivi est e ronta one into two a ves.

Medially between the orbits of the eyes is a frontalspine. Superior to t is spine, imme iate y etween t etwo eyebrows is a region called the labella . Lateral tot e g a e a are t e supraor ita margins. T ese mar-gins may be superimposed by either a supraorbitaloramen or notc . Wit in t e or ita sur aces are smaepressions in t e one ca e acrima g an ossae.

Tear glands are housed within these fossae. Finally,an opening exists etween t e or ita portions o t efrontal bone and below the frontal spine. This open-ing is re erre to as t e et moi a notc . In an intactskull, this notch is occupied by the ethmoid bone.

In a , t e ronta one articu ates wit 12 ones:the singular ethmoid and sphenoid and the pairedacrima s, maxi ae, nasa s, parieta s, an zygomat-

ics. T e posterior or er o t e squamous portion othe frontal bone articulates virtually along its entireengt wit t e two parieta ones.

Similarly to the maxillae, the frontal bone is alsoo ow in its interior. Two cavities are separate y a

thin bony septum, forming the paired rontal para-nasa sinuses . T ese sinuses are virtua y a sent at

irt . T ey start to eve op uring t e rst or second

year o i e ut o not u y orm unti pu erty.Parietals

T e parieta ones are i ustrate in Figure 10-12.The two parietal bones articulate with each other atmi ine so t at t ey orm essentia y t e roun eroof of the cranium. The parietal bones are shapedsomew at i e rectang es, meaning eac one as ourmargins and angles. The frontal margin is that parto t e parieta one t at articu ates wit t e ronta

one. The sagittal margin is that part of the parietalone that articulates with the other parietal bone. The

occipita margin is t e part o t e parieta one t atarticulates with the occipital bone, and, nally, thetempora margin is t at part o t e parieta one t atarticulates with the temporal bone.

T e articu ation etween t e two parieta s ta esplace along the sagittal suture. The articulation of theparieta ones wit t e ronta one ta es p ace a ongthe coronal suture. The parietal bones also articulate with the occipital bone along the lambdoidal suture.T e sagitta suture intersects t e corona suture ante-riorly and the lambdoidal suture posteriorly.

Internasal suture

Nasal foramenAnterior view

Figure 10-5 The nasal bones. (Adapted with permission fromAgur, A.M., Dalley, A.F. (2008). rant’s atlas of anatomy (12th ed.).Baltimore: Lippincott Williams & Wilkins.)




margin w ere t e occipita one articu ates witthe parietal bones and the mastoid margin wheret e occipita one articu ates wit t e tempora

ones. The point where the squamous part of theoccipital bone extends most posteriorly is called

t e inion or externa occipita protu erance. Run-ning transversely along the occipital bone wheret e squamous portion en s an t e asi ar portion

egins are two ridges called the superior and infe-rior nuchal lines.

T e asi ar portion o t e occipita one is moreremarka le in terms of lan marks. Most o vious is the

large hole in the basilar part called the foramen mag-num. The spinal cord passes through the foramen mag-num on its way own t e spina co umn. In t e anteriorregion of the foramen magnum and lateral to it are twoprom nent occipita con y es . T e occipita con y esare the points of articulation of the base of the skullto the rst cervical vertebra (C1, or the atlas). Anteriorto eac con y e is a ypog ossa cana . Anterior anmedial to the condyles is the pharyngeal tubercle , where the superiormost border of the pharynx attachesto the base of the skull. Finally, posterior to the condylesis a epression ca e t e con y ar ossa. Wit in t isossa is a small opening known as the condylar canal.

Temporals

The temporal bones comprise the sides of the cra-nium (see Figure 10-14). T ese ones consist otwo major parts and three subparts. The two major

Anterolateral view

Figure 10-7 The lacrimal bone. (Adapted with permission fromAgur, A.M., Dalley, A.F. (2008). rant’s atlas of anatomy (12th ed.).Baltimore: Lippincott Williams & Wilkins.)

A B

MaxillaryprocessMaxillaryprocess

Temporalprocess

Temporalprocess

Marginalprocess

Orbitalprocess

Frontalprocess

Frontalprocess

Figure 10-8 A . Anterior view.. B . Interior view. ( A : Adapted with permission from Agur, A.M., Dalley, A.F.(2008). Grant’s atlas of anatomy (12th ed.). Baltimore: Lippincott Williams & Wilkins.)




ortions of the temporal bones are the squamous andetrous portions. The squamous portion is smooth in

appearance and makes up the lateral, anterior, andsuperior portion o t e tempora one. O particu-ar note is t e zygomatic process, a an mar o t e

squamous portion that articulates with the temporalrocess o t e zygomatic one to orm t e zygomatic

arch, or cheekbone.

The petrous portion lies at the base of the skullbetween the sphenoid and occipital bones and can befurther divided into tympanic and mastoid sections.T e petrous portion gets its name rom t e act t att e one is very ar . Wit in t e tympanic section othe petrous portion reside the essential organs of hear-ing an a ance—t e coc ea an semicircu ar cana s.Posterior to the tympanic section is the mastoid section,

Perpendicular

plate of theethmoid

Inferiornasalconcha

Vomer

BA

Inferiornasalconcha

Medialpterygoid

lamina

Sellaturcica

Superior nasal concha

Frontalbone

Nasalbone

Middle nasal concha

Lacrimalbone

Palatine bone(horizontalprocess)

Palatineprocess of

maxilla

Figure 10-9 The inferior nasal conchae. A Sagittal view. B. Midsagittal view. (Adapted with permission from Anatomical ChartCompany.)

Perpendicular plateof the ethmoid

Crest ofnasal bone

Vomer

Palatine processof the maxilla

Palatine bone(horizontal process)

Nasalseptalcartilage

A

Rostrum ofsphenoid Palatine process

of maxilla

Vomer

Palatine bone

B

Figure 10-10 The vomer. A . Midsagittal view. B . Inferior view. (Adapted with permission from Agur, A.M., Dalley, A.F. (2008).Grant’s atlas of anatomy (12th ed.). Baltimore: Lippincott Williams & Wilkins.)




which includes the mastoid process. The mastoid sec-tion is not so i one ut rat er compose o numerousirregularly shaped cavities referred to as the mastoid aircells . In the inferior part of the mastoid section, theseair ce s are re ative y sma an iminis in size untiall that remains is one marrow. In the anterior ansuperior regions o t e mastoi section, t e air ce s areprogressively larger until they give way to the tympan can rum . T e upper imit o t e tympanic antrum is t etegmen tympanum , which is the roof of the tympaniccavity. T ese structures wi receive a more etai e is-cussion in C apter 12.

Two nal landmarks of note are the styloid pro-cess an t e man i u ar ossa . T e sty oi processroughly resembles a sharpened pencil tip. It is locatedin t e petrous portion o t e tempora one, poste-rior and inferior to the zygomatic process. The styloidprocess is t e point o attac ment o t ree musc es(styloglossus, stylohyoid, and stylopharyngeus) andtwo igaments (sty oman i u ar an sty o yoi ).The mandibular fossa is a depression located on theinferior surface of the temporal bone between thesty oi an zygomatic processes. T e con y ar pro-

cess of the mandible rests within this fossa formingt e temporoman i u ar joint (TMJ).

Ethmoid

T e et moi one is interesting in t at a t oug it isc assi e as a one o t e cranium, it a so contri utesto t e acia part o t e s u . T e et moi contri -utes to the orbits of the eyes and nasal cavity as wellas ma es up t e me ia portion o t e anterior cra-nial base. Figure 10-15 provides an illustration of this

one, w ic consists o ve parts: cri ri orm p ate,crista ga i , perpen icu ar p ate, an two et moi-

dal labyrinths . The cribriform plate is horizontallyoriente , w ereas t e crista ga i an perpen icu arplates comprise one piece that is oriented vertically(t e crista ga i rises a ove, w i e t e perpen icu arplate extends below the cribriform plate). The eth-moi a a yrint s are a so in erior to t e cri ri ormplate but have a lateral orientation.

T e cri ri orm p ate serves as a partition etweenthe nasal and cranial cavities (the nasal cavity is belowand the cranial cavity is above). It is perforated bysma openings. T e o actory nerve (crania nerve I)

Glabella

Supraorbital margin

Roof of orbital cavit y

Supraorbital notch

Zygomatic process

Anterior view

Figure 10-11 The frontal bone. (Adapted with permission from Agur, A.M., Dalley, A.F. (2008).Grant’s atlas of anatomy (12th ed.). Baltimore: Lippincott Williams & Wilkins.)




Sagittal suture

Parietal bones

Occipital bone

Lambdoid suture

Superior nuchal line

Inferior nuchal line

Mandible

Temporal bone

External occipital crest

Mastoid process

Occipital condyle

A

B C

Superiornuchalline

Inferiornuchalline

Foramenmagmun

Occipitalcondyle

Internaloccipital crest

Cerebellarfossae

Transversesulcus

Confluenceof sinuses

Basilarportion

Figure 10-13 The occipital bone. A . Posterior view. B . Interior superior view. C . Inferior view. (Adapted with permission from Agur,A.M., Dalley, A.F. (2008). Grant’s atlas of anatomy (12th ed.). Baltimore: Lippincott Williams & Wilkins.)




Zygomatic process

Ear canal

Mastoid process

Styloid process

A B

Squamousportion

Petrousportion

Internalauditorymeatus

Foramenmagnum

Squamousportion

Petrousportion

Figure 10-14 A . Lateral view. B . Internal superior view. (Adapted with permission from Agur, A.M., Dalley, A.F.(2008). Grant’s atlas of anatomy (12th ed.). Baltimore: Lippincott Williams & Wilkins.)

A B

Crista galli

Cribriform plate

Ethmoid air cells

Perpendicular plate

Cribriform plate

Crista galli

Ethmoid air cells

Middle concha

Superiorconcha

Figure 10-15 The ethmoid bone. A . Coronal view. B. Superior view. ( A and B1 : Adapted with permission from Anatomical Chart Company;B2 : Adapted with permission from Agur, A.M., Dalley, A.F. (2008). Grant’s atlas of anatomy (12th ed.). Baltimore: Lippincott Williams & Wilkins.)




of the super or or ta . The anterior marginsof the lesser wings articulate with orbital plates of thefrontal bone. The lesser wings come together at the jugum. Posterior to the jugum is the chiasmatic sul-cus w ic ouses t e optic c iasma w ere t e twooptic nerves (cranial nerve II) cross over after they

ave exite t e retina area o t e eye a s an passethrough the optic canals . Immediately posterior to thec iasmatic su cus is t e se a turc ca w ic ouses t epituitary gland.

The greater wings also extend laterally from thecorpus of the sphenoid. These wings contribute pri-marily to the orbits of the eyes as part of their supe-rior, lateral, and inferior walls. The lateral margins ot e greater wings articu ate wit t e zygomatic ones. At the point where the greater wings meet the corpuso t e sp enoi , t e pterygoi processes exten verti-cally in a downward direction.

Eac o t e two pterygoi processes is compose otwo laminae. These are the medial and lateral ptery-

Figure 10-16 The sphenoid bone. A Anterior view. B . Posterior view. C . Internal superior view. ( A : Adapted with permission fromAnatomical Chart Company; B : Adapted with permission from Oatis, C.A. (2008). Kinesiology (2nd ed.). Baltimore: Lippincott Williams& Wilkins; C : Adapted with permission from Agur, A.M., Dalley, A.F. (2008). rant’s atlas of anatomy (12th ed.). Baltimore: LippincottWilliams & Wilkins.)

Hamulus Medial

pterygoidlamina

Corpus Lesser wing Greater wing

Lateralpterygoidlamina

Pterygoid notch

Corpus Lesser wing Greater wing

Lateralpterygoid

lamina HamulusMedialpterygoid

laminaA B

C

Optic canal

Superior orbital fissure

Hypophyseal fossa

Posterior clinoid processDorsum sellae

Greater wing of sphenoid

Lesser wing of sphenoid

Anterior clinoid process




goid lamina, which are separated from each other bythe pterygoid notch. Along their anterior aspects, thepterygoid notches articulate with the palatine bones.The lateral pterygoid lamina is wider than the medialpterygoid lamina and serves as the point of articu-lation for the medial and lateral pterygoid muscles.The medial pterygoid lamina is more narrow and termi-

nates in a small hook-like structure called the hamulus .The corpus of the sphenoid is hollow. Two chamberscan be found within; these chambers are separated by athin midline septum creating a pair of sphenoid para-nasal sinuses . These sinuses are not present at birth,but rather start to form around the third year of life.The sphenoid paranasal sinuses, along with the frontal,ethmoid, and maxillary paranasal sinuses (mentionedin earlier sections), are lined with a membrane createdby a fusion of periosteum and mucous membrane (thismembrane is referred to as the mucoperiosteum ). Thelining of these paranasal sinuses is continuous with themucous membrane lining of the nasal cavity.

All of the paranasal sinuses drain into the nasal cav-ity proper. The sphenoid paranasal sinuses open intospaces above the superior nasal conchae. The fron-tal and maxillary sinuses open into the medial nasalmeatus, and the ethmoid paranasal sinuses open intothe superior and medial nasal meatuses.

nism , and muscles of facial expression will also beincluded here as part of the oral cavity. One will quicklyrealize that excluding the muscles of facial expression,these structures collectively make up the mouth. Themouth has both primary (i.e., biological) and second-ary (i.e., nonbiological) functions. In terms of biologi-cal function, the mouth serves as the conduit by which

the respiratory and digestive systems communicate with the external environment. As part of the diges-tive system, the mouth is used during the processes ofmastication (chewing) and deglutition (swallowing).The digestion of food begins in the oral cavity.

Cupid’s bow

Labiomental groove

Vermillionzone

Philtrum

Figure 10-17 Landmarks of the lips. (Adapted with permissionfrom Lippincott Williams & Wilkins’ Surface Anatomy Collection.)

Why You Need to Know Sinusitis is a condition where the mucous mem-

branes of the paranasal sinuses and nasal cavitybecome inamed. As the inammation continues,the paranasal sinuses may not be able to drain intothe nasal cavity. Mucous is then trapped within theparanasal sinuses, creating tenderness and pain. Ifthe condition is chronic, a surgeon may have to drilllarger holes (called windows) in the nasal cavity toallow the mucous to drain more freely.

In all, the sphenoid bone articulates with all ofthe other cranial bones of the skull as well as several

of the facial bones (maxillae, palatines, vomer, andzygomatics). This bone contributes to the orbits of theeyes as well as the nasal and pharyngeal cavities.

THE ORAL CAVITY

The oral cavity is the most active of the cavities involvedin speech production. It consists of several anatomicalstructures including the lips, cheeks, teeth, alveolarridge, hard palate, velum, tongue, and mandible. Thefaucial pillars , tonsils, velopharyngeal (V-P) mecha-

Why You Need to Know Although mothers often tell their children to breathethrough their nose, many tend to be “mouth breath-ers,” that is, they take in oxygen primarily throughthe mouth. The problem with such breathing is that

inhaled air is not moistened and heated quite as ef-ciently as it is when breathed in through the nose. Tosome degree, the nose also lters the air as it passesthrough on its way to the pharynx and beyond. Theoral cavity performs this task less effectively.

The nonbiological or secondary function of theoral cavity is to generate speech sounds and to modifythe pitch characteristics of the vocal tone through theprocess of resonance. These secondary functions willbe discussed in greater detail in the physiology sec-

tion of this chapter. In the paragraphs that follow, acloser inspection will be made of the individual struc-tures that comprise the oral cavity.

The Lips

The lips, or rima oris , are illustrated in Figure 10-17.The lips are composed of four layers of tissue; from




supercial to deep, these include the cutaneous, mus-cular, glandular, and mucous layers. Fat, in differingamounts depending upon the individual, may alsobe deposited within these layers. The cutaneous layeris simply skin. Deep to the cutaneous layer is a layerof muscle tissue. This muscle is the orbicularis oris ,a sphincter muscle that completely encircles the lips.

The orbicularis oris has a deep and a supercial layer.The deep layer consists of muscle bers arranged inconcentric rings, while the supercial layer receivesmuscle bers from other facial muscles (these mus-cles will be discussed later). The glandular layer con-tains labial glands that are similar to saliva glands instructure. Finally, the mucous layer of the lips is con-tinuous with the mucous membrane of the oral cav-ity and pharynx. On their inner (or lingual) surface,the lips are anchored at midline to the alveolar region(upper lip) and mandible (lower lip) by the superiorand inferior labial frenula (singular: frenulum).

A view of the external surface of the lips reveals sev-eral landmarks. The lips are darker in hue than the restof the face due to the transparency of the vermilion zone (this transparency is created by an abundanceof eleidin in the epithelium). The transparency of thevermilion zone allows the vascular tissue below tobe more prominently displayed. Running from theseptum of the nose to the middle of the upper lipare two vertically oriented ridges with a deep furrowbetween them. This furrow is called the philtrum .The philtrum terminates on the upper lip, creating a

midline depression that makes the upper lip appearlike an archer’s bow. Hence, the upper margin of theupper lip is referred to as Cupid’s bow .

The Cheeks

The cheeks, or buccae , are similar in structure to, andare continuous with, the lips. The external layer isskin (i.e., cutaneous), the innermost layer is a mucousmembrane, and muscular and glandular layers reside within. Several facial muscles (whose functions areto assist in mastication and to mediate facial expres-

sion) can be found in the muscular layer of the cheeks. Within the glandular layer reside ve or six glands cor-responding to the molar region of the teeth. Appropri-ately enough, they are referred to as the molar glands.Stenson’s duct (a part of the parotid salivary gland)also opens into the buccal region. Finally, a buccal fatpad may exist to some degree. In infants, this pad isquite prominent, but it tends to dissipate somewhatas the individual develops. The cheeks and lips, along with the gums and posterior teeth, form a secondarycavity within the oral cavity called the buccal cavity.

The Teeth

The complete set of teeth for an adult numbers 32, butfor a child, it is only 20. Obviously then, humans havetwo sets of teeth. The rst set that develops duringearly childhood is called the deciduous set (but is alsoreferred to by some people as the baby, milk, primary,or temporary teeth). These teeth eventually shed andare replaced by the permanent teeth. There are moreteeth in the permanent set because the maxillae andmandible have grown large enough to accommodatethe additional teeth.

Morphologically, there are four basic types of teeth:incisors, cuspids (also known as canines), premolars,and molars. Incisors are chisel shaped, allowing themto efciently cut and shear food. Cuspids are more tusk-like in appearance. This arrangement allows theseteeth to rip and tear. Finally, the premolars and molarsare at with broad surfaces; this makes them ideal for

crushing and grinding.A Typical Tooth

A typical tooth consists of several structures (see Fig-ure 10-18). Gross anatomy of the external surfacereveals a crown, neck, and root. The crown is the partof the tooth that can be seen (approximately one-third of the tooth). The root lies below the gum line

Crown

Neck

Root

Gingiva(gum)

Cementum

Pulp cavity

Dentin

Enamel

Peridontalligament

Apicalforamen

Figure 10-18 Anatomical structure of a typical tooth. (Adaptedwith permission from Anatomical Chart Company.)




and therefore cannot be seen (approximately two-thirds of the tooth). The neck is an ill-dened regionbetween the crown and root, generally at the gum line.The crown is covered by a very hard substance calledenamel (approximately 96% mineral by weight), whilethe root is covered by cementum (approximately 50%mineral by weight). The neck region corresponds to

the cementoenamel junction , where the enamelends and the cementum begins. The bulk of the solidportion of a tooth is referred to as dentin .

The tooth is anchored within its dental alveolus(tooth socket) by a periodontal ligament or mem-brane. The articulation of tooth and alveolus is a jointcalled a gomphosis . This type of joint holds the toothin its socket while allowing the periodontal ligamentto absorb the mechanical forces placed on the tooththrough chewing or other activity where the teethcome into contact with each other.

An internal view of a typical tooth will also reveal sev-eral landmarks and structures. The interior of a tooth ishollow, forming a pulp canal. The larger portion of thepulp canal is referred to as the pulp cavity . The pulpcavity is lled with dental pulp, specialized tissue that isrich in nerve endings and blood vessels. The nerve bersand blood vessels make their way into the pulp cavitythrough the apical foramen , which is actually at thebottom of the tooth root(s).

Depending on its type, a tooth can have any num-ber of surfaces. The contact surface of an incisor iscalled the incisal edge, but for the other teeth, it is

called the occlusal surface. The posterior surface(facing the oral cavity) is called the lingual surface, inreference to the tongue. The anterior surface of theincisors and cuspids is referred to as the labial sur-face in reference to the lips. For the premolars andmolars, this surface is called the buccal surface inreference to the cheeks. Finally, adjacent teeth haveapproximal surfaces. If one divides the upper andlower sets of teeth into left and right halves (i.e., start-ing at midline between the two central incisors), theapproximal surfaces will be classied as either mesial(facing toward the midline) or distal (facing away

from the midline). This means that the surfaces ofthe two central incisors that face each other are bothmesial surfaces.

The Development of Teeth

The life cycle of teeth involves four stages: growth, cal-cication, eruption, and attrition. During the growthstage, the tooth buds form along with the enamel anddentin. The enamel and dentin harden during thecalcication stage. These two stages take place whilethe teeth are still embedded within the maxillae and

mandible. The eruption stage takes place when theteeth begin to migrate into the oral cavity. This stagehas two substages: intraosseous and clinical. Dur-ing intraosseous eruption, the teeth make their waythrough the bony alveolar ridge. At this point, theteeth are still not completely calcied and the rootshave not fully formed. Through a process known as

resorption, specialized cells called osteoclasts breakdown the bone tissue within the alveolar ridge and theteeth migrate. Once the teeth have clinically erupted,osteoblasts reform the bone to create the alveoli.Clinical eruption is evidenced by the teeth cuttingthrough the gingivae . The nal stage, attrition, takesplace throughout life. As mechanical forces of chew-ing act upon the teeth, they wear down. However, theteeth still maintain their spatial relationships becauseeruption also continues throughout life.

The deciduous or primary teeth are 20 in numberbut do not all erupt at once. Eruption of the completedeciduous set takes approximately 14 to 18 months toaccomplish, although this can vary considerably fromchild to child. Typically, the rst teeth that erupt arethe lower central incisors. This takes place betweenapproximately 6 to 9 months of age. The upper centraland upper lateral incisors tend to be the next teeth toerupt, at approximately 8 to 10 months of age. Erup-tion then continues anteriorly to posteriorly until thesecond molars erupt at approximately 20 to 24 monthsof age. When all deciduous teeth have erupted, thechild will have 20 teeth: two upper central incisors;

two upper lateral incisors; two upper cuspids; twoupper rst molars; two upper second molars; two lowercentral incisors; two lower lateral incisors; two lowercuspids; two lower rst molars; and two lower secondmolars (see Figure 10-19A).

Before the complete permanent set of teeth comesin, there is a period of time when the child may havesome deciduous teeth and some permanent teeth.This is referred to as the mixed dentition stage. Thesame process that causes the deciduous teeth to eruptis responsible for eruption of the permanent teeth. Abony partition separates the deciduous teeth from the

permanent teeth below them. At the appointed time,osteoclasts resorb bone allowing the permanent teethto migrate. The deciduous teeth above are shed. Oncethe permanent teeth are in place, osteoblasts reformbone. The mixed dentition stage spans approximately6 years. It begins typically when the deciduous lowercentral incisors are shed at 6 to 8 years of age, andends when the deciduous second molars are shed atapproximately 10 to 12 years of age.

The permanent set of teeth begins to erupt withthe lower central incisors and upper and lower rst




molars at approximately 6 to 7 years of age. Eruptionthen continues for the anterior teeth (incisors and cus-

pids) and eventually for the posterior teeth (bicuspidsand molars). Eruption of the permanent teeth spansapproximately 11 to 19 years. The upper and lowerthird molars (also known as “wisdom teeth”) may noterupt until the individual is in his or her mid-20s.

When the complete permanent set has erupted,there will be 32 teeth, 12 more than were in the decid-uous set (see Figure 10-19B). Some permanent teethhave a deciduous partner, while some permanentteeth do not. The permanent teeth that have a decid-uous partner are referred to as successional teeth, whereas permanent teeth that do not have a decidu-

ous partner are called superadded teeth. The super-added teeth include two upper rst and two uppersecond bicuspids (also known as premolars), twolower rst and two lower second bicuspids, and twoupper and two lower third molars. Figure 10-19B illus-trates a complete permanent dental set. Each dentalarch (upper and lower) has 16 teeth with the left andright halves of each arch being mirror images of eachother. Each half arch has a central incisor, lateral inci-sor, cuspid, rst bicuspid, second bicuspid, rst molar,second molar, and third molar. The incisors, cuspids,

and bicuspids tend to have a single root although theupper rst bicuspids may have two roots. The lower

molars typically have two roots, but the upper molarstypically have three roots. The occlusal surfaces ofbicuspids and molars tend to be at by compari-son with the incisors and cuspids. The at surface ofthese teeth is divided into sections created by groovesalong the surface. These sections are called cusps. Asthe term implies, bicuspids have two cusps. The rstmolars typically have four cusps; the second molarsmay have three or four cusps; and nally the thirdmolars typically have three cusps.

A

B

Central incisor

Lateral incisor

Cuspid (canine)

1st Molar

2nd Molar

Upper

Lower

Upper

Lower

Central incisor

Lateral incisor

Cuspid (canine)

1st Premolar(biscupid)

2nd Premolar(biscuspid)1st Molar

2nd Molar

3rd Molar

Figure 10-19 The complete set of teeth. A . Deciduous teeth. B . Permanent teeth. (Adapted with permission from Anatomical ChartCompany.)

Why You Need to Know There is a relationship between the development ofthe teeth and development of speech. In general, the rst consonant sounds to emerge (at about 6 to 9months) are produced by either the lips (/p, m/) or thetongue and alveolar ridge (/t, d, n/). The rst primaryteeth (lower and upper central incisors and upper lat-eral incisors) emerge between 6 and 10 months. The20 primary teeth are in place by approximately 30months of age. The rst consonant sound to emergethat involves the teeth (and lower lip) is usually the /f/




Of some importance to speech–language patholo-gists are the spatial relationships of the teeth. A certainamount of maxillary overbite and overjet is normal.Because the maxillary arch is larger than the man-dibular arch, the anterior mandibular teeth (incisorsand cuspids) will rest inside of their maxillary coun-terparts when the jaw is closed (this is maxillary over-bite). The upper incisors are also angled a little moretoward the lips than the lower incisors, resulting in anormal degree of overjet.

Over 100 years ago, Angle (1899) proposed a systemfor classifying the relationship of the upper jaw to thelower jaw that is still used today. The reference pointfor this relationship is centric occlusion where themandible is central to the maxilla and there is com-plete occlusal contact of the upper and lower teeth(i.e., the jaw is “clenched”). Angle suggested threebasic types of occlusion (Class I occlusion and Class

I malocclusion are considered one type of occlusion, with Class II and Class III malocclusion viewed as theother two types). Class I occlusion, which is consid-ered normal, is evidenced by the cusps of the man-dibular (lower) rst molars resting ahead and insidethe cusps of the maxillary (upper) rst molars. Withthis normal prole, one can then describe three typesof malocclusion. With Class I malocclusion, the rstmolar relationship is intact, but some type of anomalyexists in the anterior region of the dental arch. WithClass II malocclusion, the cusps of the mandibularrst molars are behind and inside their counterparts

in the maxillary dental arch. The chin will appear tobe receding and the individual with this type of mal-occlusion will be said to have an “overbite.” Interest-ingly, almost half the world’s population has a Class IImalocclusion! With Class III malocclusion, the cuspsof the mandibular rst molars rest ahead of the maxil-lary rst molars, giving the chin the appearance that itis jutting out. A person with this type of malocclusionis said to have an “underbite.” Finally, in addition tothe overall occlusal relationship of the teeth, theremay be any number of teeth that are not positioned

properly. Any number of teeth may exhibit distoversion, infraversion, labioversion, mesioversion, supraversion , and/or torsiversion .

The Alveolar Ridge

The alveolar ridge is the bony part of the mandible

and maxilla where the alveoli (tooth sockets) reside.This ridge continues behind the upper and lower teethand is more prominent in the maxillary arch. A layer ofmucous membrane covers the bony ridge. This mucousmembrane is continuous with the membrane thatlines the rest of the oral cavity. The maxillary alveolarridge is more clinically important for speech–languagepathologists because it is the site of production of sev-eral of the consonant sounds in the English language.

The Hard Palate

The hard palate makes up the bony part of the ceilingof the oral cavity as well as the oor of the nasal cav-ity. As mentioned previously, it is not a singular bonebut instead is actually formed by the processes of fourbones. More specically, the anterior three-fourthsof the hard palate is formed by the palatine processesof the maxillae, whereas the posterior one-fourth isformed by the horizontal processes of the palatinebones. The palatine and horizontal processes fromthe left fuse with their partners on the right along theintermaxillary suture. At midline where the two hori-

zontal processes meet, the posterior nasal spine isformed. A palatal arch is created by the fact that thepalatine processes are thicker anteriorly and later-ally but thinner medially. This arch is highly variablefrom person to person and is somewhat dependentupon the status of the maxillary dental arch.

The maxillary alveolar ridge and hard palate are cov-ered with a mucous membrane. Immediately behind thealveolar ridge is a series of transversely oriented wrin-kles called rugae. Extending beyond the rugae along thelength of the hard palate is a midline raphe. The promi-nence of the rugae and midline raphe is also highly vari-

able from person to person. Finally, in approximatelyone-fth of the population, there may be a visible bulgeon the hard palate. This bulge is known as a torus palati-nus, which is typically an outgrowth of bone along theintermaxillary suture. The tissue surrounding the toruspalatinus is likely to have a bluish tint.

The Velum

The velum, or soft palate, is a three-layered struc-ture. The deepest layer is a palatal aponeurosis that

at around 30 to 36 months. This is followed by the /v/at around 48 months, and nally the two “th” sounds(where the tongue tip is placed between the upperand lower teeth) at around 54 to 60 months. Inciden-tally, when the primary upper and lower central andlateral incisors are shed at approximately 6 to 8½ years, some children may exhibit a bit of a regressionin the ability to produce the two “th” sounds correctly.These errors usually dissipate once the permanentcentral and lateral incisors are in place.




attaches onto the posterior free border of the hori-zontal processes of the palatine bones. This aponeu-rosis can be considered the “skeleton,” and along withother connective tissues, it makes up approximatelyone-third of the bulk of the velum. The intermediatelayer has muscle bers from several muscles. Laterally,muscle bers from the velum are continuous with the

muscles that comprise the superior pharyngeal con-strictor. Otherwise, the bulk of velar muscle tissue isconned to its mid-region. The supercial layer of thevelum is a mucous membrane that is continuous withthe rest of the oral cavity.

The muscles of the velum are summarized in Table10-1. When these muscles contract, they will elevate,lower, or tense the velum. The palatoglossus and

palatopharyngeus muscles serve to lower and relaxthe velum. The tensor veli palatini (TVP) muscle alsolowers the velum but tenses it as well. Finally, the leva-tor veli palatini (LVP) (which makes up the bulk of themuscular tissue of the velum) and the musculus uvu-lae raise the velum (see Figure 10-20 for views of thesemuscles). The actions of these muscles will be described

more fully when the V-P mechanism is discussed in thesection on physiology. At rest, the velum hangs downinto the upper posterior region of the oral cavity. Atmidline, one will see a singular structure known as theuvula . If you start at the uvula and move laterally, you will see two folds of mucous membrane along the sidesof the posterior oral cavity. These are the faucial pillars, which will be described in more detail below.

Palatoglossus

Levator veli palatiniTensor veli palatini

Palatopharyngeus

Musculus uvulae

Levator veli palatini

Epiglottis

Palatopharyngeus

B

A

Figure 10-20 Muscles of the velum. A . Posterior view. B . Sagittal view. (Adapted with permission from Tank,P.W., Gest, T.R. (2008). Lippincott Williams & Wilkins atlas of anatomy. Baltimore: Lippincott Williams & Wilkins.)




TABLE 10-1

ORIGINS, INSERTIONS, AND ACTIONS OF THE VELAR MUSCLES


Levator veli palatini Apex of petrousportion oftemporal boneand cartilaginous

framework of theauditory tube

Fibers interdigitate atthe velum

Primary velar elevator; raises thevelum up and back to close offthe nasal cavity from the oralcavity; may assist in triggering the

pharyngeal swallow reex

Musculus uvulae Nasal spines of thepalatine bones andadjacent palatineaponeurosis

Uvula of the velum Shortens and elevates the velum for astronger seal of the velopharyngealport than what the levator velipalatini can accomplish alone

Palatoglossus(glossopalatine)

Anterior surface ofvelum

Lateral tongue With tongue anchored, depressesvelum, but with not as much forceas the palatopharyngeus; mayassist in triggering the pharyngealswallow reex

Palatopharyngeus(pharyngopalatine)

Velum, pterygoidhamulus, andcartilage of theauditory tube

Superior cornu ofthyroid cartilageand lateral wall ofthe pharynx

Provides greater force than thepalatoglossus in lowering the velum;also pulls the velum backward; aidsin guiding the bolus to the lowerpharynx

Superior pharyngealconstrictor

Medial pterygoid plate,pterygomandibularraphe, mylohyoidline, lateral tongue

Medial pharyngealraphe

Assists the levator veli palatiniin creating greater seal of thevelopharyngeal port by pulling theposterior pharyngeal wall forward while pulling the lateral wallsinward

Tensor veli palatini Hamulus, spine,and angle of thesphenoid bone

Posterior border ofthe palatine boneand the connectivetissue andmusculature of the

velum

Unilateral contraction will pull thevelum to the side and slightlydownward; bilateral contraction will atten the velum and pull itdown slightly and increase tension

on the palatal aponeurosis; alsoopens the lumen of the Eustachiantube; may assist in triggering thepharyngeal swallow reex

The Tongue

The tongue is an intricate structure whose importancecannot be understated. Its biological functions are toserve as the primary organ of taste as well as to partici-pate in the processes of mastication and deglutition.Secondary to these functions is the formulation of

speech sounds. The tongue is the major structureresponsible for modifying the resonant characteristicsof the vocal tract and is also the primary articulator inthe production of many of the consonant sounds ofEnglish.

Gross Anatomy

Figure 10-21 provides an illustration of the grossanatomy of the tongue. The two primary parts of thetongue are the blade and root. The blade is that partof the tongue that is readily visible, while the root is

below the blade and cannot be seen easily. The bladeis further divided into a tip, blade, front, and back.If the tongue is pressed at against the ceiling of theoral cavity, the tip will rest against the anterior teeth,the blade will rest against the alveolar ridge, the front will rest against the hard palate, and the back will restagainst the velum. Running lengthwise down the cen-ter of the tongue is a furrow called the longitudinalmedian sulcus . Approximately two-thirds of the waydown the length of the dorsum of the tongue from itstip, the longitudinal median sulcus intersects with achevron-shaped landmark called the sulcus terminalis , which courses transversely and is perpendicular tothe longitudinal median ssure. At the point wherethe longitudinal median sulcus intersects the sulcusterminalis, a small pit known as the foramen cecum resides. At the posterior limit of the root of the tongue,




three slips of tissue arise and anchor the base ofthe tongue to the anterior (lingual) surface of the epi-glottis. These are the median and lateral glossoepi-glottic folds . Between the median glossoepiglotticfold and each of the lateral glossoepiglottic folds aresmall depressions called valleculae . The surface of thetongue has somewhat of a rough appearance. This isdue to the presence of papillae all over the surface of

the tongue anterior to the sulcus terminalis. There arefour types of papillae: liform, fungiform, simple, and vallate . The papillae house the taste buds whichare the essential organs for the sense of taste.

The posterior one-third of the tongue is smoother inappearance than the anterior portion. Several mucousglands are found here along with lymphoid tissueknown as the lingual tonsil. Anteriorly on the under-surface of the tongue, you will note a vertically orientedslip of mucous membrane that courses from the infe-rior surface of the tongue to the oor of the oral cavity.This is the lingual frenulum .

The outer surface of the tongue is a mucous mem-brane that is continuous with the covering of all other

structures in the oral cavity. On the inferior surface ofthe tongue, the mucous membrane is relatively thin.It is thick, loose, and freely movable in the region pos-terior to the sulcus terminalis. Anterior to the sulcusterminalis, the mucous membrane is thin and closelyadheres to the underlying muscle tissue. The mucousmembrane consists of a basement layer of connec-tive tissue called the corium . The corium is dense andsomewhat felt-like in consistency. It can be thought ofas the “skeleton” of the tongue.

The Tongue as a Muscular Hydrostat

The bulk of the tongue is composed of muscle tissue.Some of the muscles are housed completely withinthe tongue itself and are referred to as intrinsic mus-cles. Other muscles originate on anatomical struc-tures outside the tongue but attach to some part of thetongue (and hence are known as extrinsic muscles).Other than the hyoid bone and the corium, there isrelatively little skeletal support for the tongue. Instead,the tongue has the ability to change its shape and posi-tion without diminishing its volume in the process. Assuch, the tongue acts like a uid-lled structure that is

Median glossoepiglottic fold

Epiglottis

Foramen cecum

Root of tongueSulcusterminalis

Vallate

Simple

Longfiliform

Fungiform

Apex (tip)

Body of tongue

Vallecula

Lateral glossoepiglottic fold

Lingual tonsil

Palatoglossal arch

Longitudinal median sulcusLingualpapillae

Figure 10-21 Gross anatomy of the tongue and surrounding structures. (Adapted with permissionfrom Tank, P.W., Gest, T.R. (2008). Lippincott Williams & Wilkins atlas of anatomy. Baltimore: LippincottWilliams & Wilkins.)

Why You Need to Know At one time or another, you may have heard anotherperson say something to the effect that “that person istongue tied.” Obviously we do not possess the abilityto tie our tongues into knots! The term “tongue tied”generally means that the person is having difcultyspeaking. In fact, the individual may have a lingual frenulum that is too short so that it may not providethe tongue the mobility to approximate the alveolar

ridge, hard palate, and/or velum. This indeed couldvery likely cause imprecise or incorrect articulationof speech sounds that require the tongue to movetoward the ceiling of the oral cavity.




TABLE 10-2

ORIGINS, INSERTIONS, AND ACTIONS OF THE INTRINSIC TONGUE MUSCLES


Inferior longitudinal Hyoid bone and rootof the tongue

Apex of the tongueand styloglossus

Primarily works to depress the tonguetip, but also assists in shortening,protruding, and retracting the tongue,and moving the tip from side to side

Superior longitudinal Submucous broustissue of thetongue root andthe median brousseptum

Edges of the tongueand the brousmembrane

Primarily works to elevate the tonguetip, but also assists in protruding andretracting the tongue, relaxing thelateral margins of the tongue, andmoving the tip from side to side

Transverse Median brousseptum

Submucous broustissue at thelateral margins ofthe tongue

Primarily works to narrow and elongatethe tongue, but also assists inrelaxing the lateral margins of thetongue and elevating the posteriorpart of the tongue

Vertical Mucous membraneof the dorsum ofthe tongue

Lateral and inferiorsurfaces of thetongue

Primarily works to atten the tongue,but also assists in protruding thetongue and creating a longitudinalgroove along the middle of the tongue

incompressible. Of course, the tongue is not lled withuid but instead is composed of muscle tissue. Thisarchitecture is referred to as a muscular hydrostat (Kier & Smith, 1985; Smith & Kier, 1989).

The corium of the tongue provides the leverage foreight muscles (four intrinsic and four extrinsic) to playoff each other to effect the movements the tongue iscapable of making (Miller, Watkin, & Chen, 2002). As it

changes its shape and position, inward displacementin one area of the tongue results in outward displace-ment of another area, thereby preserving the tongue’svolume. The hydrostatic property of the tongue allowsit to perform a myriad array of movements includ-ing bulging, centralizing, curling, attening, groov-ing, lateralizing, pointing, protruding, retracting, andmoving from side to side, among others.

The intrinsic tongue muscles include the following:inferior longitudinal , superior longitudinal , transverse ,and vertical . Table 10-2 summarizes the origins, inser-tions, and actions of these muscles, while Figure 10-22

provides illustrations of them. It should be noted thatthe intrinsic muscles are all considered paired becauseof the presence of a vertically oriented cavity within thetongue called the brous midline septum . Fibers of thesuperior longitudinal muscles are conned primarily tothe mid-region of the tongue, while the inferior longi-tudinals can be found more laterally. The bers of bothof these muscles course along the length of the tongue. As the terms transverse and vertical imply, these twomuscles have bers that are arranged in the transverseand vertical planes. Upon inspection of Table 10-2, you

will observe that the intrinsic muscles are responsibleprimarily for rened tongue movements and postures(e.g., elongating, attening, narrowing, shortening).

Why You Need to Know The two halves of the interior of the tongue also receiveindependent neural innervation and blood supply.In neurological disorders where half of the tongue isaffected (i.e., unilateral paralysis), the unaffected halfwill still function properly. A clinical sign of unilateralparalysis of the tongue is deviation of the tongue to theparalyzed side when the patient is asked to stick outthe tongue. This is because the unaffected muscles willoverbalance and mechanically turn the tongue to theside of least resistance—the paralyzed side.

The extrinsic muscles are responsible for gross pos-turing of the tongue. These muscles include the genio-glossus , styloglossus , palatoglossus , and hyoglossus . The

origins, insertions, and actions of these muscles aresummarized in Table 10-3. The palatoglossus was men-tioned as a muscle of the velum (refer back to Figure10-20). The remaining extrinsic muscles are illustratedin Figure 10-23. Being an astute student, you will notethat all of these muscles have the term “-glossus” (refer-ring to the tongue) as the second half of their name.The rst half of the name refers to the other structureto which the muscle is attached (e.g., “genio-” = chinor inside of the mandible; “stylo-” = styloid process;“palato-” = velum; “hyo-” = hyoid bone).




The genioglossus has anterior and posterior musclebers. This muscle makes up the bulk of the tonguetissue. It is the largest and strongest of all tongue mus-cles. The styloglossus is an antagonist of the genioglos-sus (i.e., its action is the opposite of the genioglossus).The palatoglossus (also referred to sometimes as theglossopalatine) has three functions: (a) it pulls thevelum down; (b) it elevates the posterior portion ofthe tongue; or (c) it does both. Which action is per-formed is dependent upon which structure (tongue

or velum) is anchored, or upon both structures beingfree to move.

The hydrostatic interplay between and amongthe intrinsic and extrinsic muscles allows for intri-cate posturing and maneuvering of the tongue. Thesuperior longitudinal is responsible for elevating thetongue tip while the inferior longitudinal performsthe opposite function. The transverse muscle nar-rows the tongue. Tongue protrusion is accomplished

primarily by contraction of the posterior bers of thegenioglossus; however, this muscle contracting alone will simply cause the tongue to hang downward as itprotrudes. The superior longitudinal, inferior longi-tudinal, and vertical muscles assist in protrusion bypointing the tongue tip and narrowing the tonguebody. Retraction of the tongue is effectuated primarilyby the anterior bers of the genioglossus. The supe-rior and inferior longitudinals shorten the tongue as itretracts and the hyoglossus depresses the sides of thetongue during retraction. If you wanted to retract thetongue all the way back into the pharynx (as in swal-

lowing), you would contract the styloglossus muscle.Movement of the tongue from side to side is accom-

plished by contraction of the superior and inferiorlongitudinals. The two muscles on the right actingtogether will turn the tongue tip to the right. Similarly,simultaneous contraction of the superior and inferiorlongitudinals on the left will turn the tongue tip to theleft. Depression of the body of the tongue is accom-plished by contraction of the genioglossus (medialportion of the tongue) and hyoglossus (lateral edgesof the tongue). To elevate the posterior tongue, con-traction of the palatoglossus muscle is necessary. The

Superior longitudinal

Transverse and vertical

Inferior longitudinal

Vertical fibers

Longitudinalfibers

A

BFigure 10-22 The intrinsic tongue muscles. A . Coronal view.B . Sagittal view. (Adapted with permission from Tank, P.W., Gest,T.R. (2008). Lippincott Williams & Wilkins atlas of anatomy. Baltimore:Lippincott Williams & Wilkins.)

Tongue

Styloglossus

Genioglossus

Mandible

Hyoglossus

Hyoid bone

Figure 10-23 The genioglossus, styloglossus, and hyoglossusmuscles. (Adapted with permission from Tank, P.W., Gest, T.R.(2008). Lippincott Williams & Wilkins atlas of anatomy. Baltimore:

Lippincott Williams & Wilkins.)




TABLE 10-3

ORIGINS, INSERTIONS, AND ACTIONS OF THE EXTRINSIC TONGUE MUSCLES


Genioglossus Superior mental spine ofthe posterior mandibularsymphysis

Upper corpus of thehyoid, some to thedorsum of the tongue,and some to the upper

pharynx

Posterior bers assist in protrudingthe tongue tip and relaxing thelateral margins of the tongue;anterior bers retract the tongue;

contraction of the entire muscledepresses the medial portion ofthe tongue and assists in creatinga longitudinal groove along themiddle of the tongue

Hyoglossus Greater cornu and corpusof hyoid

Lateral submucoustissue of posteriortongue

Depresses the sides of the tongue;assists in retracting the tongue

Palatoglossus Anterior surface of velum Lateral tongue Assists in elevating the posterior partof the tongue

Styloglossus Styloid process of temporalbone

Lateral area of dorsumof tongue

Assists in retracting the tongue bypulling it toward the pharynx forswallowing

transverse muscle assists the palatoglossus by bunch-ing up the back of the tongue.

If you wanted to create a longitudinal groove alongthe middle of the tongue, you’d have to contract thegeniohyoid and vertical muscles. To create a shallowgroove, you’d contract only a part of the geniohyoid.Contraction of the entire geniohyoid would create adeep groove. Finally, relaxation of the lateral edges ofthe tongue is accomplished by contracting the poste-rior bers of the genioglossus as well as the superior

longitudinal and transverse muscles. You no doubtare getting the impression that the tongue is capableof rened movement and posturing, and this requiresa sophisticated dance between and among the intrin-sic and extrinsic tongue muscles!

The Mandible

The mandible (illustrated in Figure 10-4) was describedin detail along with the other bones of the skull. Inthis section, instead of describing the mandible, we will examine more closely the joint that is created by

the articulation between the mandible and temporalbone of the skull. As was mentioned earlier in thischapter, this is referred to as the temporomandibular joint (TMJ).

The Temporomandibular Joint

The TMJ is formed specically by the articulation of thecondylar process of the mandible with the mandibularfossa of the temporal bone. The mandibular condyleonly indirectly articulates with the mandibular fossabecause it is separated from it by the articular meniscus.The parts of the condyle and mandibular fossa that

actually articulate with each other are covered by abrocartilage. This deviates from typical joint archi-tecture because most bones that articulate with eachother are padded with hyaline cartilage. The primarydifference between hyaline cartilage and brocarti-lage is that the latter is devoid of vascular tissue. Thisis important for the TMJ because blood vessels wouldbe crushed by the action of the TMJ during chewingand vocal activity if the articular surfaces were lined with hyaline cartilage. Finally, the entire TMJ is encap-

sulated by a membrane called the articular capsule.The condyle is held in place by a series of ligaments.These include the temporomandibular (or lateral),sphenomandibular, and stylomandibular ligaments.

The TMJ is classied as a ginglymoarthrodial joint.This type of joint allows for a hinge-like movement with some limited gliding. In actuality, there are twoTMJs but if functioning properly the two act as a sin-gle bilateral unit. The joint is set in such a way thatthe mandible is able to move vertically (i.e., openingand closing), anteroposteriorly (i.e., protruding andretracting), and transversely (i.e., from side to side).

All these three dimensions of movement take placeto some degree during chewing and speaking.

Why You Need to Know TMJ dysfunction syndrome can severely restrict one’sability to utilize the mandible for chewing or speechpurposes. Symptoms may include facial pain andspasm, reduced mandibular movement, and noisesin the joint. Treatment may include surgery or theuse of an orthodontic prosthesis to reduce grindingof the teeth.




Mandibular MovementsThe primary movement of the mandible is elevationand depression. When the mandible is elevated, themouth is closed. By the same token, when the man-dible is depressed, the mouth is open. Two sets ofmuscles are responsible for these movements, andthey are referred to as the mandibular elevator andmandibular depressor muscles. Tables 10-4 and 10-5provide summary information about the elevator anddepressor muscles, respectively.

The mandibular elevator muscles include the

masseter , medial (or internal ) pterygoid , and temporalis .The masseter and temporalis muscles are illustratedin Figure 10-24, and the medial pterygoid is illus-

trated in Figure 10-25. The masseter has both inter-nal and external bers. Although it is a relatively slowmuscle, it is the most powerful of all muscles of mas-tication. The temporalis is a quicker muscle whoseaction is snapping. The medial pterygoid along withthe masseter are referred to as the mandibular slingmuscles because they suspend the mandible in placealong with the mandibular ligaments mentioned inthe previous section.

The mandibular depressor muscles include thedigastricus , mylohyoid , geniohyoid , and lateral (or

external ) pterygoid . The rst three of these muscles were described in Chapter 8 as suprahyoid laryngealmuscles, but they also have the ability to pull the man-

TABLE 10-4

ORIGINS, INSERTIONS, AND ACTIONS OF THE MANDIBULAR ELEVATOR MUSCLES


Masseter (externalbody)

Anterior portion ofzygomatic arch

Angle and lateralsurface of themandibular ramus

Along with the medial (internal)pterygoid straps the mandibleto the skull; primarily closes andretracts the jaw; may assist in

lateral jaw movement

Masseter (internal

body)

Posterior and

medial portion ofzygomatic arch

Upper half of ramus

and lateral surfaceof coronoid processof the mandible

Medial (internal)pterygoid

Pterygoid fossa andmedial surface oflateral pterygoidplate

Inner surface of theramus and angle ofthe mandible

Along with the masseter, straps themandible to the skull; primarilyelevates the mandible; assists inprotruding the mandible

Temporalis Entire temporal fossa Anterior border ofthe ramus andcoronoid processof the mandible

Primarily elevates the mandible;assists in retracting the mandibleand moving the mandible laterally

TABLE 10-5

ORIGINS, INSERTIONS, AND ACTIONS OF THE MANDIBULAR DEPRESSOR MUSCLES


Digastricus (anteriorbelly)

Inside lower border ofmandible

Lesser cornua of hyoidbone

With the hyoid anchored, primarilydepresses mandible; anteriordigastricus assists in retracting themandible

Digastricus (posteriorbelly)

Mastoid process oftemporal bone

Lesser cornua of hyoidbone

Geniohyoid Lower part of mentalsymphysis ofmandible

Anterior corpus ofhyoid With the hyoid anchored, primarilydepresses mandible; assists inretracting the mandible

Lateral (external)pterygoid

Lateral greater wingof sphenoid andlateral pterygoidplate

Pterygoid fossa onthe anterior neck ofmandibular condyle

Primarily depresses the mandible;bilateral contraction assists inprotruding mandible; unilateralcontraction will assist in lateralmandibular movement (i.e., agrinding action)

Mylohyoid Inner surface ofcorpus of mandible

Midline raphe;posterior bers tocorpus of hyoid

With the hyoid anchored, primarilydepresses mandible; assists inretracting the mandible




dible down. The lateral pterygoid muscle is illustratedin Figure 10-25 along with the medial pterygoid sothat you can see the relationship between them. Thedigastricus, geniohyoid, and mylohyoid muscles areillustrated in Figure 10-26.

As was mentioned in the section above, the man-dible not only has the ability to raise and lower but canalso protrude, retract, and move from side to side. Thesame muscles that elevate and depress the mandible

are responsible for these movements. Anteroposteriorand transverse movement of the mandible is depen-dent upon which of these muscles is contracting at agiven time. Mandibular protrusion is dependent uponsimultaneous contraction of the medial and lateralpterygoid muscles. Retraction is mediated by simul-taneous contraction of the posterior bers of the tem-

poralis and the anterior belly of the digastricus as wellas the mylohyoid and geniohyoid muscles. Finally,transverse (i.e., lateral) movement is dependent uponsimultaneous contraction of the lateral pterygoid andthe posterior portion of the temporalis. Imagine howintricate the interplay of muscular contraction must beto effect the rotary movements of the mandible that areseen during chewing and to a lesser extent, speaking!

Other Structures of the Oral Cavity

Faucial PillarsThe faucial pillars can be seen quite clearly when youopen your mouth and examine the back of your oralcavity in a mirror. As a reference point, at midline ofthe ceiling along the posterior limit of the oral cavityis the uvula, the singular bulb-like structure at the ter-minus of the velum. If you start at the uvula and followeither side along the back of the oral cavity, two foldsof skin will become apparent on each side. These foldsare the anterior and posterior faucial pillars. Although you will see only the mucous membrane of these folds, within them are muscle bers. The anterior faucial

Temporalis

Masseter(internal fibers)

Masseter(external fibers)

Figure 10-24 The masseter and temporalis muscles. (Adaptedwith permission from Scheumann, D.W. (2002). The balanced

body: A guide to deep tissue and neuromuscular therapy (2nd ed).Baltimore: Lippincott Williams & Wilkins.)

Lateral pterygoid

Medial pterygoid

A BFigure 10-25 The medial and lateral pterygoid muscles. A . Lateral view. B . Posterior view. ( A : Adapted with permission fromScheumann, D.W. (2002). The balanced body: A guide to deep tissue and neuromuscular therapy (2nd ed). Baltimore: LippincottWilliams & Wilkins; B : Adapted with permission from Anatomical Chart Company.)




pi ars ouse ers o t e pa atog ossus musc es. T eposterior pillars contain bers from the palatopharyn-geus muscles. As such, the anterior pillars are some-times referred to as the palatoglossal folds, while theposterior pillars are known as the palatopharyngealo s. A space—t e ons ar ossa —exists etween

these two fol s.

Tonsils

At t e posterior imits o t e ora cavity are a seriesof lymphoid masses called tonsils. These masses arearranged somewhat in a circle and are therefore referredo as Waldeyer’s ring . One of these masses was men-

tioned in the section on the tongue: the lingual tonsil.T is tonsi , oun at t e ase o t e posterior ongue,is the oor of Waldeyer’s ring. The lateral walls of thering are create y t e pa atine tonsi s. T ese arehoused within the tonsillar fossae between the ante-

rior and posterior faucial pillars. Some of the tonsillarossae sti remains imme iate y superior to t e pa -

atine tonsils. This space is called the supratonsillarossa . Fina y, t e cei ing o Wa eyers ring is orme y the pharyngeal tonsil, or adenoids. The adenoids

are oun a ong t e posterior p aryngea wa in t eregion of the velum.

Being lymphoid tissue, the tonsils are responsible forg ting in ection. As acteria are intro uce into t eoral and pharyngeal cavities, the tonsils trap as mucho t e inva ers as possi e so t at t e upper respira-tory tract will remain healthy. However, sometimes,t e tonsi s ecome in ame an in ecte . T is is usu-ally evident by pus accumulating in the supratonsillarossae. Because t e p aryngea ostium (opening) o

t e Eustac ian tu e is proxima to t e a enoi s, anyinfection of the adenoids may reux into the Eusta-c ian tu e an t roug it enter t e mi e ear cavity.

Mylohyoid

Mylohyoid

Hyoid bone

Geniohyoid Mandible

Posterior belly ofthe digastricus

Anterior belly ofthe digastricus

A

B

Hyoid boneFigure 10-26 The digastricus, geniohyoid, and mylohyoidmuscles. A . Anterior-inferior view. B . Posterior-superior view.

Why You Need to Know Chronic hypertrophy (swe ing) of the adenoids mayresult in obstruction of the nasopharynx, which inturn may resu t in mouth breathing and denasa -ity of the voice. The individual’s speech will sounddu , especia y for the nasa consonants /m/, /n/,and / /. Words like “mom,” “nice,” and “song” willsound like “bob,” “dice,” and “sog.” At some point, thedoctor may decide to perform a “T & A” procedure— removal of the tonsils and adenoids.

Velopharyngeal Mechanism

Most of the structures of the velopharyngeal (V-P)mec anism, or port, were escri e in t e sectionon the velum. The V-P mechanism is responsible forregu ating t e communication etween t e ora annasal cavities. This is important for both digestive andspeec unctions, as wi ecome evi ent w en t e V-P mechanism is revisited later in this chapter in thesection on p ysio ogy. T e V-P mec anism consists othe velum and posterior pharyngeal wall. When thevelum is raised to approximate the posterior pharyn-gea wa , t e V-P port is c ose . Separation etweenthe velum and posterior pharyngeal wall meanst at t e V-P port is open. T e musc es t at me iatemovement of the velum (refer back to Table 10-1) areinvo ve in V-P mec anics.

In some individuals, a bulging of the posteriorp aryngea wa , ca e Passavant’s pa , may exist toassist the velum in approximating the posterior wall othe pharynx. Whether Passavant’s pad actually existsis a topic o e ate among anatomists. Some e ieveit does not, while others believe it does. Still others




Muscles of Facial Expression

A thorough discussion of the oral cavity would not becomplete without at least mentioning the muscles ofthe face. Not only do humans communicate primar-ily through an acoustic signal (i.e., speech), they alsocommunicate through facial expression. Further-more, the production of some speech sounds requires

contraction of at least some of the facial muscles.Therefore, this nal section of our journey throughthe oral cavity will provide you with an overview of themuscles that mediate facial expression.

The orbicularis oris , which was described in thesection concerning the lips, is the reference point formost of the muscles of facial expression. Many of themuscles listed in Table 10-6 make their insertion intoits supercial layer from various angles. Five muscles(depressor labii inferior , levator labii superior , leva-tor labii superior alaeque nasi , zygomatic major , andzygomatic minor ) approach the orbicularis oris from

an oblique direction above or below. Two muscles,the buccinator and risorius , insert into the orbicu-laris oris from a horizontal direction. Three muscles(depressor anguli oris , levator angli oris , and mentalis )course in a perpendicular fashion toward the orbicu-laris oris before inserting into it. The incisivus labiiinferior and incisivus labii superior are not true lipmuscles, but they course in a direction parallel to thelength of the orbicularis oris. The remaining muscles(corrugator , epicranius frontalis , orbicularis oculi ,and platysma ) are supplementary muscles of facial

expression. Many of these muscles are illustrated inFigure 10-27.

All of these muscles act as a unit to mediate facialexpression. The full gamut of facial expressions canbe represented by contraction of any number of thesemuscles. This includes blinking and winking the eyes;raising and lowering the eyelids; pursing the lips;frowning; and smiling. Indeed, these expressions canbe accomplished with varying intensity (e.g., a “gen-tle” frown versus a “heavy” frown). A closer inspec-tion of Table 10-6 will reveal the complexity of muscleactivity that is involved in facial expression.

THE NASAL CAVITY

When one thinks of the nose, the rst thing thatcomes to mind is breathing or smelling. If you believethat these are the only functions of the nose, you’dbe in error. The nose—or more specically the nasal

cavity—plays an important role in speech produc-tion. This function will be described in more detail inthe section on physiology; for now, we will turn ourattention to the anatomical structures of the noseand nasal cavity. The nasal cavity begins at the noseand terminates in the region of the nasopharynx ,immediately above the velum and anterior to theposterior pharyngeal wall. The structures that willbe discussed in this section include the nose, nasalseptum, nasal conchae and meatuses, and mucousmembrane.

Buccinator

Levator labiisuperior

Orbicularis oris

Mentalis

Platysma

Depressoranguli oris

Depressorlabii inferior

Zygomatic:

MajorMinor

BuccinatorRisorius

Epicraniusfrontalis

Corrugator

Orbicularis oculi

Figure 10-27 Selected muscles of facial expression. (Adapted with permission from Cael, C. (2009). Functional anatomy: Musculosk-eletal anatomy, kinesiology, and palpation for manual therapists. Baltimore: Lippincott Williams & Wilkins.)



TABLE 10-6

ORIGINS, INSERTIONS, AND ACTIONS OF THE MUSCLES THAT MEDIATE FACIAL EXPRESSION


Buccinator Pterygomandibular raphe,lateral surface of thealveolar process of themaxilla, and the mandiblein the region of the thirdmolars

Muscle bers of both theupper and lower lips

Compresses the lips and cheeks againstthe teeth and draws the corners ofthe mouth outward

Corrugator Superciliary arch of thefrontal bone Skin above the medialarch of the eyebrows Pulls the eyebrows downward andinward, thereby wrinkling the skin ofthe forehead between the eyes

Depressor angulioris

Oblique line of themandible

Orbicularis oris at theangle of the mouthand the upper lip

Depresses the angle of the lip andassists in compressing the upper lipagainst the lower lip

Depressor labiiinferior

Oblique line of themandible near themental foramen

Orbicularis oris of thelower lip

Pulls the lower lip downward andoutward

Epicraniusfrontalis

Epicranial aponeuroses Skin of the forehead nearthe eyebrows

Raises the eyebrows and causes the skinon the forehead to wrinkle horizontally

Incisivus labiiinferior

Mandible in the region ofthe lateral incisor teeth

Orbicularis oris at theangle of the mouth

Pulls the corner of the mouth inwardand downward

Incisivus labiisuperior

Maxilla immediately abovethe canine teeth

Orbicularis oris at theangle of the mouth

Pulls the corner of the mouth inwardand upward

Levator angulioris

Canine fossa of the maxilla Upper lip and angle ofthe lower lip

Pulls the corner of the mouth upwardand assists in closing the mouth bypulling the lower lip upward

Levator labiisuperior

Lower margin of the orbitof the eye, maxilla, andzygomatic bone

Upper lip between thelevator anguli oris andlevator labii superioralaeque nasi

Elevates and everts the upper lip

Levator labiisuperioralaeque nasi

Frontal process andinfraorbital margin ofthe maxillae

Lateral cartilages ofthe nose and theorbicularis oris

Elevates the upper lip

Mentalis Incisive fossa of the

mandible

Skin of the chin Elevates, protrudes, and everts the

lower lip, and wrinkles the skin of thechinOrbicularis oculi Nasal process of the frontal

bone, frontal processof the maxilla, andpalpebral ligament

Lateral palpebral raphe Closes the eyelids, draws tears from thelacrimal glands into the eyes

Orbicularis oris Near midline on theanterior surfaces of themaxilla and mandible

Mucous membrane ofthe margin of the lipsand raphe with thebuccinator

Closes the mouth and puckers the lips

Platysma Skin over the lower neckand upper lateral chest

Inferior border of themandible and skin overthe lower face and angle

of the mouth

Depresses and wrinkles the skin of thelower face and mouth; aids in theforced depression of the mandible

Risorius Fascia of the massetermuscle

Skin of the corner of themouth and musclebers of the lower lip

Pulls the mouth angle outward

Zygomatic major Anterior surface of thezygomatic bone,immediately lateral to thezygomatic minor muscle

Orbicularis oris of theupper lip and skinof the corner of themouth

Pulls the angle of the mouth upwardand outward

Zygomatic minor Anterior surface ofthe zygomatic bone,immediately medial to thezygomatic major muscle

Orbicularis oris of theupper lip

Elevates the upper lip




As illustrated in Figure 10-28, the nose can be dividedinto several parts. These include the root, bridge, dor-sum, apex, base, nares, and columella nasi. The rootof the nose corresponds to the point where the nasalbones articulate with the frontal bone. The bridge isthat part of the nose that corresponds to the nasalbones. Extending from the nasal bones is cartilage;the dorsum is this part of the nose. The apex (or tip) is

the part of the nose that protrudes furthest from theface. The base is the bottom of the nose where it joinsthe face above the upper lip. Along the base are twoopenings called the anterior nares, which are morecommonly referred to as nostrils. The anterior naresare separated by a partition called the columella nasi.The columella nasi is simply a continuation of thedorsum to the base of the nose.

The outer lining of the nose is epithelial tissue (i.e.,skin). Underlying the mucous membrane are sev-eral cartilages that give the nose its shape (see Figure10-29). The septal cartilage is a vertically oriented

partition that extends outward from the nasal oriceat midline. It not only serves as the dorsum of thenose but also completes the nasal septum that sepa-rates the nasal cavity into two chambers. Its poste-rior attachment is the bony nasal septum. Recall thatthe bony nasal septum is formed by the perpendicu-lar plate of the ethmoid (the superior part) and thevomer (the inferior part). The lateral nasal cartilagesmake up the sides of the nose, while the alar carti-lages (major and minor) complete the frameworkby assisting in the formation of the nares. The lateral

nasal cartilages articulate with the septal cartilage andthe nasal bones. The alar cartilages articulate with thelateral nasal cartilages.

Superimposed upon the nasal cartilages are severalmuscles that assist in the process of breathing and toa lesser extent play a role in facial expression. Table10-7 summarizes the muscles of the nose in termsof their origins, insertions, and actions. Figure 10-30illustrates these muscles, which include the anteriornasal dilator , depressor alae nasi , levator labii supe-rior alaeque nasi , nasalis , posterior nasal dilator , and

Root

Dorsum

Ala

Apex

Nasal septum

Naris

Bridge

Base

Figure 10-28 Landmarks of the nose. (Adapted with permis-sion from Lippincott Williams & Wilkins’ Surface AnatomyCollection.)

Septal nasal cartilage

Lateral process

Accessory nasal cartilages

Lateral crus of major

alar cartilage

Medial crus of majoralar cartilage

Figure 10-29 Nasal cartilages. (Adapted with permission fromAgur, A.M., Dalley, A.F. (2008). Grant’s atlas of anatomy (12th ed.).Baltimore: Lippincott Williams & Wilkins.)

Nasalis

Nasalis

Procerus

Depressoralae nasi

Nasaldilator

Figure 10-30 Selected muscles of the nose.




TABLE 10-7

ORIGINS, INSERTIONS, AND ACTIONS OF THE MUSCLES OF THE NOSE


Anterior nasal dilator Lower edge of the lateralnasal cartilage

Deep tissue of the skin thatcovers the nasal alae

Dilates the nostrils

Depressor alae nasi Incisive fossa of themaxillae

Lower region of thecartilaginous nasal

septum and adjacent alaeof the nose

Depresses the alae of thenose which constricts the

nostrils

Levator labii superioralaeque nasi

Frontal process andinfraorbital margin ofthe maxillae

Lateral cartilages of the noseand the orbicularis oris


Nasalis Superior and lateral tothe incisive fossa of themaxillae

An aponeurosis of theprocerus muscle as wellas an aponeurosis of thenasalis from the oppositeside

Depresses the cartilages ofthe nose, which narrowsthe nostrils

Posterior nasaldilator

Nasal aperture of themaxillae and adjacentsesamoid cartilages

The skin of the inferior andposterior alar cartilages


Procerus Lower nasal bones andupper lateral nasalcartilages

Skin of the lower foreheadbetween the eyebrows Depresses the medialangle of the eyebrow and wrinkles the skin over thebridge of the nose

procerus . With the exception of the procerus, thesemuscles serve to either dilate or constrict the nostrils.

The interior of the nasal cavity consists of two cham-bers separated by the nasal septum. The open spaceimmediately inside the anterior nares is the vestibule

(children stick their nger here when “picking theirnose”). Along the lateral walls of each chamber arethree scrolls of bone that extend into the cavity spaceand form longitudinal channels along the length ofthe nasal cavity. The scrolls of bone are the superior,medial, and inferior nasal conchae or turbinates. Youmay recall from a previous discussion in this chap-ter that the superior and medial nasal conchae comefrom the ethmoid, while the inferior nasal conchae isan independent bone.

The longitudinal channels formed by the conchaeare the nasal meatuses. As there are three conchae,there are three meatuses in each chamber. Referredto as the superior, medial, and inferior meatuses, theycorrespond to their like-named conchae. Each meatus

lies below its corresponding concha. The lateral walls ofthe nasal cavity also contain the openings through which the paranasal sinuses drain into the nasal cavity.

The ceiling of the nasal cavity is composed primarilyof the cribriform plate of the ethmoid. The cribriformplate is perforated so that bers from the olfactorynerve (cranial nerve I) can pass into the nasal cavity.The posterior limit of the nasal cavity opens into theuppermost region of the pharynx—the appropriatelynamed nasopharynx. The nasal cavity communi-cates with the nasopharynx via the posterior nares, orchoanae .

The interior of the nasal cavity is covered by amucous membrane. As with the rest of the respira-tory passageway, the mucous membrane is ciliated.That is, tiny hairs project from the surface of themucous membrane. A thin layer of mucous blan-kets the interior of the nasal cavity. This protectiveblanket traps organisms and contaminants. The ciliacontinually sweep the mucous and trapped invad-ers toward the nasopharynx. Eventually, the pollutedmucous makes its way down the throat and into thestomach.

Why You Need to Know Many people have a “deviated” septum from traumato the nose (e.g., being hit in the nose while boxing)or disease. This means that the cartilaginous por-tion of the nasal septum is bent so that it deviates toone side instead of remaining midline. The devia-tion is usually to the left. A deviated septum canpose problems for a person in terms of breathingthrough one nostril or drainage of mucous on oneside of the nose.




THE PHARYNGEAL CAVITY

The pharyngeal cavity is more commonly referred toas the throat, although it actually extends all the wayto the base of the skull superiorly and to the esopha-gus inferiorly (refer back to Figure 10-1). Its composi-tion is similar to that of the velum; it has a basement“skeleton” known as the pharyngeal aponeurosis ,an intermediate layer of muscle tissue, and nally asupercial layer of mucous membrane.

Pharyngeal Aponeurosis

The pharyngeal aponeurosis is a funnel-shaped sheetof connective tissue that originates at the base ofthe skull, and more specically, the pharyngeal tuber-cle of the occipital bone (immediately anterior to theforamen magnum), petrous portion of the temporalbone, cartilage of the Eustachian tube, and medialpterygoid lamina of the sphenoid. In an adult male,this tube is approximately 12 cm in length. The great-est width of the pharynx is approximately 4 cm andthe greatest depth is approximately 2 cm. This is atthe superior end of the tube, at the base of the skull.The pharynx then narrows considerably until by thetime it terminates at esophagus, it has a width of onlyapproximately 2½ cm and virtually zero depth (i.e.,the anterior and posterior pharyngeal walls touch

each other and do not separate until food or drinkpasses through on the way to the esophagus).

Pharyngeal Muscles

The pharyngeal aponeurosis is superimposed by mus-cle tissue. The muscular pharynx is highly complex.

Muscles interdigitate to such an extent that it is dif-cult to parse out the individual muscles. Therefore,the muscular layer of the pharynx is typically dividedinto three overlapping regions referred to as the supe-rior, medial, and inferior constrictor muscles. Each ofthe constrictor muscles consists of between two andfour individual muscles. In addition to the constric-tor muscles, secondary muscles also play a role inpharyngeal mechanics. Table 10-8 provides summaryinformation for the pharyngeal muscles. The constric-tor muscles are illustrated in Figure 10-31. The supe-rior pharyngeal constrictor consists of four muscles:buccopharyngeus , glossopharyngeus , mylopharyngeus ,and pterygopharyngeus . The medial pharyngeal con-strictor consists of two muscles: ceratopharyngeus and chondropharyngeus . The inferior pharyngealconstrictor consists of two muscles: cricopharyngeus and thyropharyngeus . Although the superior pharyn-geal constrictor is the most complex of the constrictormuscles, it also is the weakest. All three of the constric-tor muscles inuence the volume of the pharyngeal

Middle pharyngeal constrictor

Inferior pharyngeal constrictor

Esophagus

Superiorpharyngealconstrictor

Hyoid

Thyroid cartilage

Cricoid cartilage

A Esophagus

Pharyngeal raphe

Middle pharyngealconstrictor

Stylopharyngeus

Cricopharyngeal partof inferior constrictor

Superior

pharyngealconstrictor

B

Inferior pharyngealconstrictor

Figure 10-31 The pharyngeal muscles. A . Lateral view. B . Posterior view. (Adapted with permission from Moore, K.L., Agur. A.M.,Dalley, A.F. (2009). Clinically oriented anatomy (6th ed.). Baltimore: Lippincott Williams & Wilkins.)




TABLE 10-8

ORIGINS, INSERTIONS, AND ACTIONS OF THE PHARYNGEAL MUSCLES


Inferior constrictor:CricopharyngeusThyropharyngeus

Thyroid cartilage,cricoid cartilage,inferior cornu ofhyoid bone

Medial pharyngealraphe and theesophagus

Assists in swallowing and vocalresonance by reducing the cross-sectional area of the pharyngeallumen in the laryngopharyngeal

region (by forward movement of theposterior pharyngeal wall and medialmovement of the lateral pharyngeal walls in a sphincter-like fashion)

Middle constrictor:CeratopharyngeusChondro -pharyngeus

Greater and lessercornua of hyoidbone

Medial pharyngealraphe; bers overlap with inferior bersfrom the superiorconstrictor andsuperior bers of theinferior constrictor

Performs a similar function as theinferior constrictor except the actionis conned to the oropharyngealregion

Palatopharyngeus(pharyngopalatine)

Soft palate, pterygoidhamulus, and thecartilage of theauditory tube

Superior cornu of thethyroid cartilageand lateral wall ofthe pharynx

With the velum stabilized, the upperbers assist the superior constrictorin drawing the lateral pharyngeal walls medially; lower bers elevatethe pharynx and larynx

Salpingopharyngeus Inferior border ofthe medial aspectof the cartilage atthe orice of theauditory tube

Blends withbers of thepalatopharyngeusmuscle

Pulls the lateral walls of the pharynxupward and inward, therebydecreasing the width of the pharynx

Stylopharyngeus Medial side of thebase of the styloidprocess

Between the superiorand middleconstrictors

Pulls upward on the pharynx anddraws the lateral walls even morelaterally, thereby increasing the width of the pharynx; pulls upwardon the pharynx and larynx

Superior constrictor: Buccopharyngeus Glossopharyngeus Mylopharyngeus Pterygopharyngeus

Medial pterygoidplate,pterygomandibularraphe, mylohyoidline, lateral tongue

Medial pharyngealraphe

Performs a similar function as theinferior and middle constrictorsexcept the action is conned to thenasopharyngeal region

tube. When bilateral contraction of these musclesoccurs, they act as a sphincter that serves to narrowthe pharyngeal lumen. This action has implicationsfor swallowing and vocal resonance.

pharyngopalatine), salpingopharyngeus , and stylopha-ryngeus muscles also play a part in pharyngeal mechan-ics. The palatopharyngeus muscle was described earlieras a velar depressor, but some of its bers blend withbers of the pharynx. This muscle shortens the distancebetween the velum and pharynx, thereby narrowing the

posterior faucial pillars. With the velum stabilized, thepalatopharyngeus assists the superior constrictor indrawing the lateral pharyngeal walls medially, therebynarrowing the pharyngeal lumen. The salpingopharyn-geus muscle also assists in narrowing the pharyngeallumen. When it contracts, it pulls the lateral walls of thepharynx upward and inward, thereby decreasing the width of the pharynx.

The stylopharyngeus has the opposite effect on thepharynx as the constrictors, palatopharyngeus andsalpingopharyngeus. This muscle elevates the pharynx

Why You Need to Know Of particular importance is the cricopharyngeusmuscle which is part of the inferior constrictor. Inmany cases of laryngectomy (removal of the larynx,usually due to cancer), a portion of the cricopharyn-geus is preserved, if possible. The cricopharyngeuswill serve as the laryngectomee’s sound source for“voicing” by vibrating as air is forced across it.

Although not part of the pharyngeal constrictorcomplex, the palatopharyngeus (also known as the




and pulls the lateral walls even more laterally, thereby widening the pharyngeal lumen. This muscle, along with the palatopharyngeus, also elevates the pharynx and larynx, which is an action necessary in swal-lowing.

Mucous Membrane

The supercial layer of the pharynx is a mucousmembrane that is continuous with the mucous mem-brane of the oral cavity, larynx, and esophagus. Inthe uppermost region of the pharynx, the membraneconsists of columnar ciliated epithelium. In the lower(i.e., oral and laryngeal) regions, the membrane con-sists of stratied squamous cells. Clusters of mucousglands lie immediately beneath the mucous mem-brane. These clusters are more numerous around theorice of the Eustachian tube than elsewhere in thepharynx.

Pharyngeal Regions

As illustrated in Figure 10-1, the pharynx is dividedinto three regions: the nasopharynx, oropharynx , andlaryngopharynx . The nasopharynx is superior to thevelum and extends from the choanae to the posteriorpharyngeal wall. This part of the pharynx containsseveral landmarks. These include the torus tubarius ,pharyngeal ostium of the Eustachian (auditory) tube,adenoids, and pharyngeal bursa. The torus tubariusis a comma-shaped ridge in the lateral walls of thenasopharynx. It is composed of two muscles lyingbeneath the mucous membrane: the salpingopalatine(anterior portion) and salpingopharyngeus (posteriorportion). The ostium of the Eustachian tube residesunder the curved part of the torus tubarius. The ade-noids are found along the posterior pharyngeal wall,superior to the velum. Finally, the pharyngeal bursais a groove in the mucous membrane that runs verti-cally at midline from the adenoids to the base of theskull.

By comparison with the nasopharynx, the oro- and

laryngopharynges are relatively void of landmarks.The oropharynx extends from the velum superiorlyto the hyoid bone inferiorly. The laryngopharynx thenextends from the hyoid bone superiorly to the adituslaryngis inferiorly.

NEURAL INNERVATION

Because all structures of the vocal tract are in the headand neck, you might surmise correctly that cranialnerves will be responsible for innervating the mus-

cles of the velum, tongue, mandible, face, nose, andpharynx. Table 10-9 summarizes the neural innerva-tion of most of the muscles that were discussed in thischapter. In total, half of the 12 cranial nerves serve thestructures of the face and the oral, nasal, and pharyn-geal cavities. These include the trigeminal (cranialnerve V), facial (VII), glossopharyngeal (IX), vagus (X),

spinal accessory (XI), and hypoglossal (XII) nerves. All of the muscles of the velum are innervated bythe vagus nerve except the tensor veli palatini (TVP), which is innervated by the trigeminal. The musculusuvulae, palatoglossus, and palatopharyngeus mayalso be innervated by the spinal accessory nerve.

All of the intrinsic muscles of the tongue are inner-vated by the hypoglossal nerve. The same is true for allof the extrinsic tongue muscles except the palatoglos-sus, which is innervated by the vagus and possibly thespinal accessory nerve.

The mandibular elevator muscles are all inner-vated by the anterior trunk of the mandibular branchof the trigeminal nerve. Three cranial nerves inner-vate the mandibular depressor muscles. The anteriorbelly of the digastricus, the lateral pterygoid, and themylohyoid muscles are innervated by the trigeminalnerve. The posterior body of the digastricus is inner-vated by the facial nerve. Finally, the geniohyoid mus-cle is innervated by the hypoglossal nerve.

All three pharyngeal constrictor muscles receivetheir innervation from the vagus nerve. The spinalaccessory nerve may also be involved, but its role in

the innervation of these muscles is not as clear as thevagus. This is also true of the palatopharyngeus andsalpingopharyngeus muscles. The only exception topharyngeal innervation is the stylopharyngeus muscle, which is innervated by the glossopharyngeal nerve.

The muscles of the nose and face are not includedin Table 10-9. However, as a general rule, the mus-cles of the nose and face receive motor innervationfrom the facial nerve. The skin, glands, and other softtissues receive primarily sensory innervation fromthe trigeminal nerve. Although virtually all musclesof the nose and face are innervated by the facial nerve,

they receive their innervation from various branchesof the nerve. For example, the stylohyoid musclereceives innervation from the stylohyoid branch ofthe facial nerve. The corrugator, frontalis, and orbic-ularis oculi muscles are innervated by the temporalbranch, and the last of these three muscles also isinnervated by the zygomatic branch. The buccinator,procerus, and orbicularis oris muscles are innervatedby the buccal branch of the facial nerve. Finally, theplatysma muscle receives innervation from the man-dibular and cervical branches of the facial nerve.




Physiology of the Articulatory/Resonance System

In this section, we turn our attention to the physiol-ogy of the articulatory/resonance system. First, you will learn the mechanics that are involved in speechproduction. Related to this is a discussion of how thevocal tone produced by the vocal folds is shaped andformed into the acoustic signal we recognize as humanspeech. Finally, because dysphagia is an importantarea of clinical practice in speech–language pathol-ogy, you will be provided the basic mechanics of mas-tication and deglutition.

THE MECHANICS OF SPEECH PRODUCTION

When one comes to an understanding of the mechan-

ics of speech production, one begins to appreciate thecomplexity of the event. A typical human producesconversational speech at a rate of approximately175 words per minute. This equates to approxi-mately 20 speech sounds per second. To be able toproduce speech at such a rapid rate, the structuresthat make up the vocal tract must work coopera-tively and in synchrony. This involves the coordi-nated effort of l iterally hundreds of neural impulsesand muscle contractions. Although it is not the pur-pose of this text to provide you a thorough descrip-

TABLE 10-9

INNERVATION OF SELECT MUSCLES OF THE ARTICULATORY/RESONANCE SYSTEM

Muscle Innervation

Mandibular Muscles

Elevator MusclesMasseter (internal and external branches) Trigeminal (cranial nerve V), anterior trunk of mandibular branchMedial (internal) pterygoid Trigeminal (cranial nerve V), anterior trunk of mandibular branchTemporalis Trigeminal (cranial nerve V), anterior trunk of mandibular branch

Depressor MusclesDigastricus Anterior belly—trigeminal (cranial nerve V); posterior belly—facial

(cranial nerve VII)Geniohyoid Hypoglossal (cranial nerve XII)Lateral (external) pterygoid Trigeminal (cranial nerve V), mandibular branchMylohyoid Trigeminal (cranial nerve V), mylohyoid branch

Tongue MusclesExtrinsic MusclesGenioglossus Hypoglossal (cranial nerve XII)Hyoglossus Hypoglossal (cranial nerve XII)

Palatoglossus Vagus (cranial nerve X); possibly spinal accessory (cranial nerve XI)Styloglossus Hypoglossal (cranial nerve XII)

Intrinsic MusclesInferior longitudinal Hypoglossal (cranial nerve XII)Superior longitudinal Hypoglossal (cranial nerve XII)Transverse Hypoglossal (cranial nerve XII) Vertical Hypoglossal (cranial nerve XII)

Velar MusclesLevator veli palatini Vagus (cranial nerve X)Musculus uvulae Vagus (cranial nerve X); possibly spinal accessory (cranial nerve XI)Palatoglossus Vagus (cranial nerve X); possibly spinal accessory (cranial nerve XI)

Palatopharyngeus Vagus (cranial nerve X); possibly spinal accessory (cranial nerve XI)Tensor veli palatini Trigeminal (cranial nerve V)

Pharyngeal Muscles All pharyngeal constrictor muscles Vagus (cranial nerve X); possibly spinal accessory (cranial nerve XI)Palatopharyngeus Vagus (cranial nerve X); possibly spinal accessory (cranial nerve XI)Salpingopharyngeus Vagus (cranial nerve X); possibly spinal accessory (cranial nerve XI)Stylopharyngeus Glossopharyngeal (cranial nerve IX)




tion of speech production, a basic discussion of thephysiology of the articulatory/resonance systemshould drive home the complexity of human vocalcommunication.

In the foregoing section on the anatomy of the vocaltract, you may have realized that some structures are

relatively benign in terms of their contribution toarticulation and resonance, while other structuresplay a more active role. Some structures are immov-able, whereas others are moveable due to muscle con-traction. In the sections that follow, a brief description will be provided for each of the structures that com-prise the vocal tract: lips, teeth, alveolar ridge, hardpalate, velum, tongue, mandible, and pharynx.

In the sections that follow, you will be presentedthe vowels and consonants that make up the soundsystem of the English language. There are 26 letters ofthe alphabet, but approximately 43 speech sounds in

English. Because there are more speech sounds thanalphabet letters in English, speech–language patholo-gists use a special character set to represent each ofthe speech sounds. This character set comes fromthe International Phonetic Alphabet (IPA). The IPAuses alphabet letters to represent some of the speechsounds but relies on special characters to representothers. Table 10-10 provides a list of the English vowelsand consonants and the IPA characters that are usedto represent them. As you read the sections below, if you encounter an IPA character you are not familiar

with, simply consult Table 10-10 to see how that par-ticular sound is pronounced.

The Lips

The lips are composed of the orbicularis oris muscles.The orbicularis oris muscles, in turn, serve as the

insertion for several facial muscles. The buccinator,depressor anguli oris, depressor labii inferior, inci-sivus labii inferior, incisivus labii superior, levatoranguli oris, levator labii superior, levator labii supe-rior alaeque nasi, mentalis, risorius, zygomatic major,and zygomatic minor muscles all act upon the lips inone fashion or another. These muscles work togetherin various combinations to mediate a wide range oflip movements during vocal activity. One particularmovement seen in speech production is lip round-ing. This is accomplished primarily through actionof the orbicularis oris muscles, which act in a sphinc-ter-like manner when they contract. Lip rounding isnecessary for the production of certain vowel sounds(e.g., /u/ and /o /) as well as the consonant sound/w/. Lip rounding and protrusion results in elon-gation of the oral cavity, which in turn changes theresonant properties of the vocal tract. Lip protrusionis accomplished by simultaneous contraction of thedepressor labii inferior, levator labii superior, menta-lis, and zygomatic minor muscles.

The lips are also involved in the production of otherconsonant sounds referred to as bilabials. As the term

TABLE 10-10

VOWELS AND CONSONANTS OF ENGLISH AND THE IPA CHARACTERS THAT REPRESENT THEM

Vowels Consonants

Character Example Character Example Character Examplei beet p pig cheapI bit b big jeepe I, e bait t too m miceε bet d due n niceæ bat k Kate sing u boot g gate j yell

book f face w wello , o boat v vase r rake

bought s Sue l lakea yacht z zoo ῳ bird θ thinә mother ð then∧ but ∫ shock

about measure

aI

nice h how a cow I oil




implies, the two lips come into contact with each otherduring the production of these sounds, which includethe /p/, /b/, and /m/. You can see right away that thelips are actively involved in speech production.

The Teeth

The teeth are involved in speech production to a cer-tain extent, although their contribution to the processis more benign than the lips or other structures of theoral cavity. With the exception of the lower set of teethduring mandibular movement, the teeth are immov-able. However, the teeth are involved in the produc-tion of some speech sounds such as the linguadentalconsonants / θ / and /ð/ (referred to as the soft andhard “th” sounds, respectively) and the labiodentalconsonants /f/ and /v/. As the name implies, lingua-dental consonants are produced by placing the tonguetip between the upper and lower teeth. By the sametoken, labiodental sounds are produced by compress-ing the upper teeth onto the lower lip. In either case,the teeth do not initiate the production of the conso-nant but rather serve as the secondary articulators(the tongue and lips are the primary articulators).

The Alveolar Ridge

One may recall from the discussion in the anatomysection of this chapter that the alveolar ridge is thebony part of the upper and lower gums where thetooth sockets reside. They are covered by a layer ofmucous membrane. In terms of speech produc-tion, the maxillary alveolar ridge deserves mention.Being benign in terms of its contribution to speechproduction, it serves as the secondary articulator ofconsonant sounds referred to as alveolar sounds. Thetongue is the primary articulator in the production ofthese sounds, which includes the /t/, /d/, /s/, /z/, /l/,and /n/. For some people, the /r/ sound may also beproduced in the region of the alveolar ridge.

The Hard Palate

The hard palate is also a benign structure and there-fore serves as a secondary articulator in the produc-tion of some speech sounds. In some cases, the tip ofthe tongue approximates the anteriormost part of thehard palate (at its juncture with the alveolar ridge).This includes the consonants / ∫ /, / /, / /, and / /.The /r/ may also be produced in this region by somepeople. One consonant sound in English is a truepalatal sound—the /j/. In this case, the blade of thetongue articulates with the bulk of the hard palate.

The Velum

Being composed partly of muscular tissue, you cansurmise that the velum is an active structure in speechproduction. It is the secondary articulator for the pro-duction of the velar consonant sounds /k/, /g/, and/ /. In these cases, the back of the tongue elevates toapproximate the velum. However, in speech produc-tion, the primary purpose of the velum is to assist inregulating oral/nasal resonance. Along with the pos-terior pharyngeal wall, the velum does this as part ofthe V-P mechanism or port.

When the V-P port is open, some of the vocal toneis diverted into the nasal cavity to resonate there whilethe remainder of the vocal tone resonates in the oralcavity. When the V-P port is closed, the nasal cavity issealed off from the oral cavity so that all of the vocaltone passes into the oral cavity to resonate. This mech-anism is very important because in English, all speech

sounds are produced through oral resonance exceptfor three consonants. These three are referred to as thenasal consonants and include the /m/, /n/, and / /. You will note that these three sounds were presentedabove. That is, the /m/ is a bilabial consonant, the /n/is an alveolar consonant, and the / / is a velar conso-nant. What distinguishes these three sounds from allthe others is that not only is there resonance takingplace in the oral cavity but in the nasal cavity as well.The resonance of part of the vocal tone within the nasalcavity gives these three sounds a distinctive nasal qual-ity or “twang.” This is referred to as nasal murmur .

For the V-P port to be open so that nasal resonancecan occur for the /m/, /n/, and / /, the soft palate mustbe depressed. You will recall that the V-P mechanismacts in a sphincter-like fashion so that the velum doesnot lower like a door on a hinge but rather separatesfrom the posterior pharyngeal wall. The musclesthat are responsible for depressing the velum are thepalatoglossus and palatopharyngeus muscles, and toa lesser extent possibly the tensor veli palatini (TVP)muscles. Any time one of the nasal consonants isencountered in conversational speech, these muscles

must contract to depress the velum and open the V-Pport. All the other speech sounds in English requiresome degree of V-P closure.

The degree of V-P closure during speech variesaccording to the phonetic context. Obviously, the V-Pport is open considerably for the nasal consonants.However, V-P closure is not necessarily complete forthe production of nonnasal speech sounds. There is adegree of V-P opening for the low vowels (/ ε/, / æ/, / /,/a/) although not as much as for the nasal consonants.Similarly, there is a smaller degree of V-P opening for




the high vowels (/i/, / I/, /u/, / /) than the low vow-els, and even greater closure of the V-P port for theoral consonants than either the low or high vowels.The degree of V-P closure is greatest for the plosives(/p/, /b/, /t/, /d/, /k/, /g/) than other speech soundsbecause these require the greatest intra-oral air pres-sure for production. The V-P port must be closed to

allow you to generate the intra-oral pressure that isnecessary for production of the plosives. V-P port clo-sure is accomplished by contraction of the levator velipalatini (LVP) and musculus uvulae muscles.

From the foregoing discussion, you can see that V-P closure does not have to be absolute to effectuatethe proper balance between oral and nasal resonance.Moll (1962) estimated that normal speakers exhibit14% opening of the V-P port during production of theisolated /i/ vowel, 37% opening for the / a / vowel, andas much as 38% V-P opening for the / æ/ vowel. Accord-ing to Raphael, Borden, and Harris (2007), no appar-ent nasality is perceived during speech if the velumcomes within 2 mm (approximately 20 mm 2 of openarea) of the posterior pharyngeal wall. On the otherhand, there is a denite perception of nasality once thevelum exceeds 5 mm (approximately 50 mm 2 of openarea) of distance from the posterior pharyngeal wall.

When you consider the rapidity of human speechand the relatively random nature in which the nasalconsonants are dispersed throughout a person’sspeech, you will quickly realize that more criticallyimportant is the timing of V-P opening and closure.

Poor timing of the V-P mechanism may result in animbalance between oral and nasal resonance. To drivehome the point, recall that the average rate of speechis approximately 175 words per minute (roughly 20speech sounds per second). The duration of an Englishnasal sound is approximately 70 msec and the durationof other speech sounds may be somewhat longer (e.g.,vowels) or shorter (e.g., plosives) than that. You shouldhave no problem appreciating how quickly the velummust move to provide the proper balance between oraland nasal resonance at such high rate of speech.

The Tongue

The tongue is the primary articulator during the pro-duction of most consonant sounds and is also theprimary structure responsible for the production ofvowel sounds. The tongue is involved in the produc-tion of 18 of the 24 consonant sounds in the Englishlanguage (the consonants that are produced withouttongue involvement are the /p/, /b/, /m/, /f/, /v/, and/h/). In the case of the linguadental consonants (/ θ /and /ð/), the tip of the tongue is placed between theupper and lower teeth. For the alveolar consonants(/t/, /d/, /s/, /z/, /n/, /l/, and for some people /r/),the tip of the tongue comes into proximity with themaxillary alveolar ridge. In the case of the palatal con-sonants (/j/, / ∫ /, / /, / /, / /, and for some people/r/), the blade and/or front of the tongue articulates with the hard palate. Finally, for the velar consonants(/k/, /g/, and / /), the back of the tongue raises to

approximate the velum. Although the /w/ sound isconsidered by many to be a bilabial sound, the backof the tongue may also come into proximity with thevelum during its production.

The tongue is also involved in the production of allof the vowel sounds. In English, there are 14 monoph-thongs (also known as pure vowels) and ve diph-thongs . A more thorough discussion of the acousticqualities of the vowels will be presented in the sec-tion below. For now, you are referred to Figure 10-32.This gure illustrates what is commonly known as thevowel quadrilateral. The left side of the quadrilateralrepresents the anterior region of the oral cavity (i.e.,the lips and alveolar ridge). The right side representsthe posterior region (i.e., the velum and pharynx). You will note two dimensions: horizontal and vertical.

Back

Front

High

Low

i

e

u

o

a

c

v

e

æ

I

C e n t r a l

MidVerticaltongue

placement

Horizontal tongueplacement

Figure 10-32 The vowel quadrilateral showing the result ofvertical and horizontal tongue placement within the oral cavity.(Adapted with permission from Raphael, L.J., Borden, G.J.,Harris, K.S. (2006). Speech science primer (5th ed.). Baltimore:Lippincott Williams & Wilkins.)

Why You Need to Know When the degree and/or timing of V-P closure areadversely affected, the result may be a conditionof hypernasality or denasality. With hypernasality,there is too much nasal resonance during the pro-duction of nonnasal speech sounds. With denasality,there is not enough nasal resonance during the pro-duction of /m/, /n/, and / /. Some structural anoma-lies that may result in poor oral/nasal resonancewill be discussed in Chapter 11.




The horizontal dimension represents protractionand retraction of the tongue within the oral cavity.That is, the tongue is able to move toward the lips,toward the pharynx, or any point between the two. Theterms front, central, and back are used to indicate therelative position of the tongue horizontally. The ver-tical dimension represents movement of the tongue

toward the oor of the oral cavity, toward the ceiling(i.e., hard palate), or any point between the two. Theterms high, mid, and low are used to indicate the rela-tive position of the tongue vertically. The vowel soundsare classied then, according to these two dimensions.For example, the /i/ vowel is classied as a high frontvowel. This means that the tongue tip and blade moveforward and up toward the alveolar ridge. In the case ofthe /a/ vowel, the tongue moves backward and downtoward the lower oropharynx. All monophthongs areclassied in this manner.

The diphthongs are single vowel sounds consist-ing of a blending of two monophthongs produced ina rapid fashion. In other words, the tongue rapidlytransitions from its placement for one vowel (the on-glide) to the placement for a second vowel (the off-glide). For example, the diphthong / I/ is produced when the tongue initiates its placement for the vowel/ / (low and toward the back of the oral cavity) andthen moves rapidly to the articulatory position for the/ I/ vowel (high and toward the front of the oral cavity).This process occurs so rapidly that acoustically weperceive a singular vowel sound.

Naturally, muscle activity is necessary for allowingthe tongue to move to the various regions of the oralcavity to produce most of the consonants and all ofthe vowel sounds. Recall in the previous section thattongue muscles are classied as either extrinsic orintrinsic. The extrinsic muscles are responsible forgross positioning of the tongue within the oral cav-ity. For example, the hyoglossus muscles and anteriorbers of the genioglossus muscles retract the tongue while posterior bers of the genioglossus musclesprotrude the tongue. The palatoglossus and styloglos-sus muscles elevate and retract the back of the tongue.

Finally, the hyoglossus muscles along with the entiregenioglossus muscles depress the tongue within theoral cavity.

The intrinsic tongue muscles are responsible formaking ne adjustments to the tongue but also assistin positioning the tongue within the oral cavity. Theinferior longitudinal and superior longitudinal mus-cles shorten the tongue. However, the inferior longitu-dinal muscles can also pull the tongue tip downwardand the superior longitudinal muscles can also raisethe tongue tip upward. The transverse muscles nar-

row and elongate the tongue, while the vertical mus-cles atten it. These muscles allow the tongue to moverapidly within the oral cavity, which is essential forspeech production. The tongue tip is able to producemore than eight repetitive movements per second(e.g., “tah-tah-tah-tah . . . ”)! This makes the tongue avery efcient articulator.

The Mandible

The mandible or lower jaw is also actively involved inspeech production. Its movements are accomplishedby way of the temporomandibular joints (TMJs). As was mentioned in an earlier section of this chapter,although there are two TMJs, they act as a unit whenelevating and depressing the mandible. Mandibu-lar elevator (i.e., masseter, medial pterygoid, andtemporalis) muscles close the mouth by raising themandible, and mandibular depressor (i.e., digastri-cus, geniohyoid, lateral pterygoid, and mylohyoid)muscles open the mouth by depressing the mandible.Not only does the mandible move in a vertical dimen-sion (i.e., opening and closing), but it can also movein an anteroposterior, lateral, and rotary fashion.These actions are accomplished through differentialcontractions of the elevator and depressor muscles.Seldom does the mandible completely close duringspeech production. Movement of the mandible dur-ing vocal activity is approximately 7 to 18 mm verti-cally and 2 to 3 mm anteroposteriorly. You will note

that as one produces the front (/i/, / I/, /e/, / ε/, / æ/)and back (/u/, / /, /o/, / /, /a/) vowels from high tolow position, mandibular depression becomes greaterand greater. Like the tongue, the mandible is alsocapable of rapid repetitive movements. On average,the mandible can produce approximately 7.5 repeti-tive movements (e.g., “pah-pah-pah-pah . . .”) persecond. This makes the mandible capable of handlingthe demands placed upon it by speech production.

The Pharynx

The pharynx is a funnel-shaped tube that courses fromthe base of the skull to the esophagus. It is typicallydivided into three regions: the nasopharynx, oropharynx, and laryngopharynx. The pharynx houses a com-plex array of muscles collectively referred to as thesuperior, middle, and inferior constrictor muscles. Interms of speech production, the pharynx is somewhatstatic, that is, it does not appear to contribute signi-cantly to the production of speech sounds. However,being a cavity, it does have resonant properties (andthe same can be said of the oral and nasal cavities as




well, although the contribution of the nasal cavity isalso static while the oral cavity is highly dynamic).The action of the constrictor muscles appears to bemore important in swallowing than in the productionof speech.

The Integration of Oral Structures

It should be emphasized that the lips, mandible,tongue, velum, and pharynx do not perform isolatedmovements. That is, movements of these structuresare interrelated and integrated to an extent. For exam-ple, the mandible is coupled to the tongue and lowerlips and teeth. It assists these structures in meetingtheir articulatory contacts with other anatomicalstructures. The velum, tongue, and faucial pillars alsoseem to act as an integrated unit. Stimulation of thelarynx, palate, or pharynx will cause the tongue toprotrude, and stimulation of the anterior oral region will result in tongue retraction.

Finally, the width of the pharyngeal lumen can alsobe inuenced by the epiglottis, tongue, and velum.The oral and pharyngeal cavities are coupled by thesestructures. For example, upward movement of thetongue, downward movement of the velum, andmedial movement of the palatoglossal arches willcause a reduction in the coupling between the oraland pharyngeal cavities. Therefore, you should becognizant of the fact that the articulators do not per-form their tasks in a serial order; rather, their move-

ments are often dependent upon the movements ofother structures.

ACOUSTICS, ARTICULATION,AND RESONANCE

With the anatomy and physiology of the vocal tractdescribed, it is now time to turn your attention to howthe anatomy and physiology act to shape the vocaltone into an acoustic signal we perceive as humanspeech. Recall from Chapter 8 that the human larynxis capable of producing a complex tone that is rich

in harmonic structure. Humans possess the abilityto vary the vocal tone in its frequency and intensity. Variations in vocal frequency are evident in the into-national patterns that are used during conversationalspeech.

The vocal tone is simply a buzzing sound. Thestructures that are superior to the larynx (i.e., thestructures that make up the vocal tract) are respon-sible for transforming the vocal tone into speech. It isthe purpose of this section of the chapter to describethe transformation process. It is beyond the scope of

this chapter to offer a detailed and thorough accountof articulation and resonance (that can be accom-plished through a basic course in speech science).The purpose of the foregoing discussion then is toprovide you with a very basic understanding of theseprocesses.

Basic Principles of Acoustics

Before the transformation process can be described, you must have an understanding of some basic con-cepts related to acoustics. First, you must understandthe concept of resonance. In general, resonance issimply a response to an outside force. The responseis typically vibration. When something resonates, itvibrates. The object that vibrates is called a resonator . When a resonator is acted upon by an outside force, itresponds to that outside force by vibrating. Practicallyeverything on this planet vibrates and has its ownnatural resonant frequency . When an outside forcematches a resonator’s natural resonant frequency, itvibrates at its greatest amplitude and is said to be “inresonance.” Anyone who has ever placed their lipsover the mouth of an empty bottle and blown into ithas witnessed resonance. When the force of exhaledair reaches the natural resonant frequency of thebottle, the bottle responds by vibrating at its greatestamplitude. The result is a loud sound.

The vocal tract is similar in structure to a bottle ortube that is closed at one end (i.e., the vocal folds) and

open at the other (i.e., the lips). If an outside force actsupon the vocal tract, it will resonate. However, becauseof the placement of the tongue and other anatomicalstructures, the vocal tract can be partitioned into aseries of chambers, each one having its own naturalresonant frequency that responds to the outside forceacting upon it. In the case of the vocal tract, what isthe outside force? Quite simply, the outside force isthe vocal tone being generated by the larynx. As thevocal tone passes through the vocal tract, it sets theair within the vocal tract into vibration, resulting inresonance within the partitioned chambers. Which

frequencies resonate depends upon the volumes ofthese chambers.

There is a predictable relationship between cham-ber volume and resonance. This relationship can beeasily demonstrated by using the same bottle men-tioned above. If you blow with enough force into theempty bottle, the result will be a loud sound of rela-tively low frequency. However, if you ll the bottlehalfway with water and then blow into it, the loudsound is now relatively higher in frequency. By llingit halfway with water, you have lessened the effective




vibrating volume of the bottle. In other words, thevolume of the bottle is smaller. Therefore, the rela-tionship between volume and frequency is an inverseone. As volume decreases, frequency increases andvice versa.

Returning to the vocal tract you may quickly sur-mise that its partitioned chambers can be adjustedin terms of their volumes; the result then would bechanges in the natural resonant frequencies of thosechambers. In other words, humans have the abilityto manipulate and change which frequencies of thevocal tone will resonate. As such, the vocal tract canbe thought of as an acoustic lter . Depending on

vocal tract conguration, certain frequencies of thevocal tone will resonate while other frequencies willlose energy or dampen.

In fact, large bands of frequencies will resonateat any given time. These bands are called formants . When the partitioned cavities of the vocal tract reso-nate, several formants are produced. The rst for-mant (F 1) is the band of lowest frequency; the secondformant (F 2) is the next higher frequency band; thethird formant (F 3) is composed of even higher fre-quencies, and so on. Formants can be seen clearlyon a spectrogram—the output of a spectrograph, an

electronic instrument that analyzes sound accordingto frequency and intensity. Figure 10-33 provides aspectrogram showing the vowels /i/, /a/, and /u/. Theformants are the dark horizontal bars. The darknessof the bars indicates that they are of relatively greatamplitude (in other words, they are in resonance). The“thickness” of the bars shows that the formants are not just individual frequencies but bands of frequencies.

A distinction should be made between periodicsounds and aperiodic sounds . When a sound is gen-erated, it creates waves of acoustic energy. If the waves

repeat themselves consistently and predictably overtime, the result is a periodic sound. If, however, the waves emanate in a random fashion so that there isno discernible pattern to their behavior, the result isan aperiodic sound. The vocal tone is a periodic, com-plex tone. An example of an aperiodic sound is noise(e.g., a hissing sound). When the vocal tract is rela-tively open (i.e., very little constriction exists along itslength), the acoustic signal that is produced is peri-odic. However, when an obstruction or constrictionexists anywhere along the vocal tract, the result willbe a sound that is aperiodic. Periodicity of sound willbe described in more detail below.

Finally, one should understand the differencebetween voiced and unvoiced speech sounds. When asound is voiced, it means that the vocal folds are vibrat-ing and generating a vocal tone during its production.In contrast, the vocal folds do not vibrate during theproduction of unvoiced sounds; this means that thereis no vocal tone being generated during the produc-tion of unvoiced sounds. In English, all vowel soundsare voiced. Fifteen of the 24 English consonant soundsare voiced. This means that the voiced consonants willhave some degree of periodicity because of the vocaltone being generated as they are being articulated.

Articulation and Resonance

The purpose of this section is to provide you with abasic understanding of how articulation and reso-nance results in the transformation of the vocal toneinto an acoustic signal recognized as speech. In 1960,Gunnar Fant developed the Acoustic Theory of SpeechProduction to describe how vowels are produced.Over the years, his theory has become more widelyknown as the Source-Filter Theory (see Figure 10-34).

F r e q u e n c y

Time

/ i / / a / / u /

F 1

F 2

F 3

F 1

F 2

F 3

F 1

F 2

F 3

Figure 10-33 A spectrogram showing the formants for the vowels /i/, /a/, and /u/. (Adapted withpermission from Raphael, L.J., Borden, G.J., Harris, K.S. (2006). Speech science primer (5th ed.). Baltimore:Lippincott Williams & Wilkins; Courtesy of Kay Elemetrics.)




there is a peak at 500 Hz, another at 1500 Hz, andanother at 2500 Hz. The peak at 500 Hz representsthe natural resonant frequency for the rst formant,the peak at 1500 Hz represents the natural resonantfrequency for F 2, and the peak at 2500 Hz representsthe natural resonant frequency for F 3. It should benoted that although Figure 10-34 shows only one

example of a transfer function, there are actuallymany transfer functions—each one associated with adifferent conguration of the vocal tract. If the con-guration of the vocal tract is changed even mini-mally (e.g., by tongue movement), a different transferfunction will result, that is, the resonant characteris-tics of the vocal tract will change and a differentsound will emerge.

As the vocal tone makes its way through the vocaltract, it is passed through the lter and the transferfunction modies the vocal tone so that the result-ing spectrum resembles both the source and the l-ter. The harmonic structure of the vocal tone remainsintact, but instead of a steady and gradual decrease inamplitude from the lower to higher frequencies, thereare amplitude peaks superimposed upon the vocaltone by the transfer function. These peaks correspondto the format frequencies of the transfer function. Thevarious speech sounds in a language are created bychanging the lter (i.e., vocal tract conguration),thereby changing the transfer function. The sourcefunction remains relatively the same; it is the trans-fer function that causes a change in speech sound. In

other words, each speech sound has its own transferfunction created by a different conguration of thevocal tract.

Vowels

According to the Source-Filter Theory, vowels are pro-duced simply by changing the conguration of thevocal tract, which is accomplished primarily by place-ment of the tongue. As you may recall from an earliersection of this chapter, vowels are classied as frontto back and high to low. These terms describe whatthe tongue is doing during vowel production. Shifting

the position of the tongue changes the congurationof the vocal tract, which in turn sets up changes inresonance. In other words, formant frequencies canbe adjusted by the position of the tongue. Althougheach vowel in English has several formants, only therst two (F 1 and F 2) are of critical importance for dis-criminating most of the vowel sounds.

The rst format (F 1) is affected primarily by tongueheight. Movement of the tongue toward the ceilingof the oral cavity (as for the high vowels) will resultin a lowering of frequencies associated with F 1, and

1000 2000 3000

500 1500 2500

30

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10

0 R e l a

t i v e a m p

l i t u d e

( d B )

R e l a t i v e a m p

l i t u d e

( d B )

30

20

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0

1000 2000 3000

30

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l a t i v e a m p

l i t u d e

( d B )

SOURCE FUNCTION(Vocal Tone)

TRANSFER FUNCTION(Resonances of Vocal Tract)

OUTPUT (Product of Source and Transfer Functions)

Frequency (Hz)

Figure 10-34 The source and transfer functions of Source-Filter Theory, with resulting output (a vowel sound). (Adaptedwith permission from Raphael, L.J., Borden, G.J., Harris, K.S.(2006). Speech science primer (5th ed.). Baltimore: LippincottWilliams & Wilkins.)

As its more common name implies, speech produc-tion is a result of two components—a source and alter. Anatomically, the source is the vibrating vocal

folds while the lter is the vocal tract. As illustrated inFigure 10-34, when the vocal folds vibrate, they createa complex tone that is rich in harmonics (as illus-trated by the vertical lines in the top-most graph).These harmonics diminish in intensity for the higherfrequencies. The vocal tone produced by the vibrat-ing vocal folds is referred to as the source function.The vocal tract, as a lter, causes certain bands of fre-quencies to resonate. As shown in the middle graphof Figure 10-34, this is referred to as the transfer func-tion. The peaks you see are formants. In the graph,




movement of the tongue toward the oor of the oralcavity will result in a rise in frequencies associated with F 1. The second formant (F 2) is affected primarilyby the anterior-to-posterior placement of the tongue. As the tongue moves in an anterior direction (as forthe front vowels), the frequencies associated with F 2 rise, and as the tongue moves in a posterior direction,

the frequencies associated with F 2 lower.To understand this, you should consider that thetongue essentially divides the oral cavity into twochambers, one anterior to the position of the tongueand the other posterior to it. The rst formant is associ-ated with resonance within the chamber that is poste-rior to the tongue and the second format is associated with resonance within the chamber that is anterior tothe tongue. If the tongue is moved toward the ceilingof the oral cavity, the chamber posterior to the tongue will enlarge, thereby causing the frequencies associ-ated with F 1 to lower. If one moves the tongue forward(i.e., towards the lips), it causes the anterior chamberto become smaller, thereby resulting in a rise in fre-quencies associated with F 2 (remember the relation-ship between chamber volume and frequency).

To illustrate, consider the vowels /i/ and /a/, whichare high-front and low-back vowels, respectively. Forthe vowel /i/, the tongue moves forward and towardthe ceiling of the oral cavity. For the vowel /a/, thetongue moves backward and toward the oor of theoral cavity. One would expect then that F 1 for the vowel/i/ would be lower than F 1 for the vowel /a/ because

the tongue is in a higher position for /i/. Similarly, one would expect that F 2 would be higher for /i/ than for/a/ because the tongue has a more anterior placementfor /i/ than for /a/. Indeed, the average F 1 frequencyfor an adult male is 270 Hz for /i/ and 730 Hz for /a/;the average F 2 frequency is 2290 Hz for /i/ and 1090Hz for /a/ (see the formant comparisons for thesevowels in Figure 10-35). All the other vowel sounds are

a result of changes in formant frequencies brought onby changes in tongue height and advancement. Witheach change in tongue height and/or advancement, adifferent lter is created and hence, a different trans-fer function is created as well. Each vowel has its ownacoustic spectrum.

Consonants

The production of consonant sounds differs fromthat of vowels. Although some consonants resemblevowels in terms of their spectral properties, most ofthem do not look much like vowels. In general, vowelsounds are produced by relatively little constrictionanywhere along the vocal tract. In other words, thevocal tract tends to be open. Most of the consonants,on the other hand, are produced by creating either acomplete obstruction or a narrow constriction somewhere in the vocal tract.

In the physiology section of this chapter, you learnedthat consonants are classied according to the place where they are created. Bilabial consonants are pro-duced by the lips; labiodental consonants by the lipsand teeth; linguadental consonants by the tongue andteeth; alveolar consonants by the tongue and alveolarridge; palatal consonants by the tongue and hard pal-ate; velar consonants by the tongue and soft palate;and nally the one glottal consonant by the open vocalfolds. Consonant sounds are also classied accordingto the manner in which they are created.

Plosives (also known as stops) are produced by cre-

ating a complete obstruction of the expired breathstream so that intra-oral air pressure builds up behindthe obstruction. The air pressure is then releasedabruptly, creating an explosive sound. The plosivesinclude the /p/, /b/, /t/, /d/, /k/, and /g/ sounds. Forthe /p/ and /b/, the obstruction is at the lips (recallthat they are classied as bilabial sounds). For /t/ and/d/, the obstruction is at the alveolar ridge. Finally,for /k/ and /g/, the obstruction is at the velum. Theabrupt release of air pressure results in a spike ofacoustic energy that is aperiodic. The /b/, /d/, and /g/sounds are voiced, so there is at least a small degree of

periodicity associated with the vocal tone during theproduction of these consonants.

Fricative consonants are produced by creating anarrow constriction somewhere in the vocal tract.Instead of completely obstructing the breath stream,the breath stream is forced through the narrow con-striction, thereby creating turbulence or friction. Thefricatives are the largest class of consonants accord-ing to manner of production in English. They includethe /s/, /z/, /f/, /v/, / θ /, /ð/, / ∫ /, / /, and /h/ sounds.The turbulence created by these sounds results in a

270 730

2290 1090

/ i / / a /

F 1

F 2

/ i / / a /

F 1

F 2

Figure 10-35 Comparison of formants for the vowels /i/ and/a/ for an adult male. (Adapted with permission from Raphael, L.J.,Borden, G.J., Harris, K.S. (2006). Speech science primer (5th ed.).Baltimore: Lippincott Williams & Wilkins.)




before the swallow is initiated). The posterior tongueis raised by the palatoglossus muscles to preventfood from being forced into the pharynx. With assis-tance from the hard palate, the tongue forms a bolus of appropriate size so that it can be passed into thepharynx and eventually the esophagus. Masticationinvolves the elevator and depressor muscles of the

mandible, the intrinsic and extrinsic muscles of thetongue, and the muscles of the lips and cheeks. While the food is being chewed, the individual

must breathe through the nose. To be able to do so,the palatoglossus muscles must contract to lower thevelum and establish communication between thenasal and pharyngeal cavities. You will note that duringthe oral preparatory phase, the palatoglossus performsa dual function—lowering the velum while raising theback of the tongue.

Oral Phase

The oral, or buccal, phase is the rst true stage of swal-lowing. In this phase, chewing stops. With the bolusprepared, activity shifts to the transport of the bolusto the pharynx. The posterior tongue lowers while theanterior tongue elevates toward the hard palate. Thetongue then retracts in a posterior direction to squeezethe bolus back toward the pharynx. The muscles ofthe lips and cheeks remain contracted to narrow theoral cavity to facilitate bolus transit. As the bolusapproaches the oropharynx, the back of the tongueand uvula elevate primarily through contraction of the

palatoglossus and styloglossus muscles. This actionseals the nasopharynx to prevent the bolus from beinginjected into it. Muscles of the lips, face, tongue, anduvula are involved in the oral phase of swallowing,requiring neural innervation from the trigeminal (V ),facial (VII), and hypoglossal (XII) cranial nerves. Theglossopharyngeal (IX) cranial nerve provides sensorybers to the tongue. Once the bolus makes contact with the faucial pillars, the oral phase terminates andthe pharyngeal phase begins. At this point, swallow-ing becomes involuntary, as the autonomic nervoussystem takes primary control of the process.

Pharyngeal Phase

As the bolus enters the oropharynx, the velum elevatestoward the posterior pharyngeal wall, primarily by con-traction of the levator veli palatini (LVP) muscles. Themuscles making up the superior constrictor contract,thereby narrowing the faucial pillars to prevent thebolus from being ejected into the oral cavity. As thisis taking place, the hyoid bone and larynx elevate andmove anteriorly through action of the suprahyoidmuscles. The anterior and superior positioning of the

larynx relaxes the cricopharyngeus muscles, whichrelaxes the upper esophageal sphincter (UES) at theupper end of the esophagus. The epiglottis passivelyseals the aditus laryngis while the vocal folds adductto seal the lower respiratory passageway. The bolus isforced down the pharynx by contraction of the con-strictor muscles. As it approaches the epiglottis, the

bolus divides into two masses that are then forcedaround the larynx and through the pyriform sinuses inpreparation of entry into the esophagus. The massesmeet again at the UES and are forced by the inferiorconstrictor into the esophagus. Breathing ceases dur-ing the second it takes for the bolus to be transportedthrough the pharynx to the esophagus. The pharyn-geal phase involves neural innervation from four cra-nial nerves: trigeminal (V); vagus (X); spinal accessory(XI); and hypoglossal (XII).

Esophageal Phase

Esophageal transit time is approximately 10 to 20 sec-onds. Once the bolus enters the esophagus, the cri-copharyngeus muscles contract to seal the UES. In theupper third of the esophagus, the constrictor musclesforce the bolus down until the striated muscles give way to involuntary muscles. Peristalsis and gravitycontinue to push the bolus of food toward the stom-ach. As the lower esophageal sphincter is approached,it relaxes and the bolus is emptied into the stomach. Atthe same time the bolus enters the esophagus, the larynx and velum lower to allow respiration to resume.

The vagus (X) cranial nerve appears to be mostactively involved in the esophageal phase of swal-lowing. For the upper one-third of the esophagus,the vagus nerve has more of a direct role by innervat-ing the voluntary muscles bers found there. For theremainder of the esophagus, the vagus plays more ofa modulatory role as the autonomous nervous systeminnervates the smooth muscle bers in this region.

Why You Need to Know Treatment for swallowing disorders includes com-pensatory swallowing strategies, dietary modications, exercises to improve muscle function,medications and/or surgery, and neuromuscularelectrical stimulation. The last treatment optioninvolves stimulation of paralyzed muscles withelectric current to trigger a swallowing response. Thespeech–language pathologist is an integral memberof the dysphagia team. If you are interested in thetopic of neuromuscular electrical stimulation, anexample of research in this area can be found inBaijens, Speyer, Roodenburg, and Manni (2008).



269

Knowledge Outcomes for ASHA Certication for Chapter 11• Demonstrate knowledge of the etiologies of articulation disorders (III-C)

• Demonstrate knowledge of the characteristics of articulation disorders (III-C)• Demonstrate knowledge of the etiologies of swallowing disorders (III-C)• Demonstrate knowledge of the characteristics of swallowing disorders (III-C)

Learning Objectives• You will be able to describe how a knowledge of articulatory phonetics can assist you in

understanding the various pathologies that may affect the ar ticulatory/resonance system.• You will be able to discuss the etiology and characteristics of cleft lip and palate and other

craniofacial anomalies, and how these anomalies may adversely affect ar ticulation andresonance.

• You will be able to dene velopharyngeal incompetence and provide examples of pathologicalconditions that may result in this disorder.

• You will be able to evaluate how ar ticulation and resonance may be adversely affected bycranial nerve damage.

• You will be able to recite some of the differences between apraxia of speech and dysarthria.• You will be able to discuss how apraxia of speech and dysarthria affect the ar ticulatory/

resonance system.• You will be able to describe several progressive and nonprogressive neurological pathologies

and how their characteristics may adversely affect articulation and resonance.

• You will be able to differentiate the different types of hearing impairment and describe howhearing impairment may adversely affect speech production.

CHAPTER 11

Pathologies Associated with the Articulatory/Resonance System


acro- peak acro cephalosyndactyly arthro- pertaining to the joints arthro -ophthalmopathy

cardio- pertaining to the heart velo cardio facial syndrome

cephalo- referring to the head acro cephalo syndactyly

cranio- referring to the head or skull cranio facial anomaly

dactyl- pertaining to the ngers acrocephalosyn dactyl y

dermal pertaining to the skin ecto dermal

dys- abnormal dys ostosis



270 PART 5 ANATOMY, PHYSIOLOGY, AND PATHOLOGIES OF THE ARTICULATORY/RESONANCE SYSTEM

A Brief Review of Articulationand Resonance

ARTICULATORY PHONETICS

As you learned in Chapter 10, the vocal tract com-prises the articulatory/resonance system. The vocaltract consists of three cavities (i.e., nasal, oral, andpharyngeal) and several anatomical structures.These include the lips, teeth, alveolar ridge, hard

palate, velum, tongue, and pharynx. As the vocaltone passes through the vocal tract, it is molded andshaped into the various speech sounds of a languageby action of these structures.

To understand how the articulatory/resonancesystem can be affected by pathologies, you must rsthave a basic understanding of articulatory or physi-ological phonetics—the study of the sounds of a lan-guage in regard to the physiological movements thatare necessary to produce them. You were introducedto articulatory phonetics in Chapter 10. Although weprovided a brief description of articulatory phonetics

in that chapter (especially as it related to the move-ments that are required of the various articulators),it is probably not a bad idea to reintroduce the topic(in condensed form) at the beginning of this chapterso that you will have a point of reference in terms of“normal” articulation and resonance when the disor-ders are presented later in this chapter.

It should be mentioned that it is not within thescope of this textbook to provide you a comprehensivediscussion of articulatory phonetics. Our purpose inincluding this discussion is simply to provide you the

basic framework behind articulation and resonance. As such, the discussion will focus on the productionof individual speech sounds and not on connected(or conversational) speech. For example, the effects ofcoarticulation on connected speech will be reservedfor a course in speech science and therefore will notbe presented in this chapter. Only a brief overview ofbasic articulatory phonetics will be provided here.

You should make the distinction between articu-lation and resonance . Articulation involves the accu-

racy, direction, and timing of the movements of thevocal tract structures to produce speech sounds. Res-onance involves modication of the vocal tone as aresult of forced vibration as the tone passes throughthe cavities of the vocal tract. Both processes (i.e.,articulation and resonance) occur simultaneously,resulting in the production of speech sounds.

Refer to Table 11-1. This table provides a classi-cation of the consonant sounds in the English lan-guage. Consonant sound production can be classiedaccording to the place and manner of articulation, as well as whether or not the vocal folds vibrate during

their production. Place refers to where the articulatorsgo during consonant production, while manner refersto how the consonant sound is actually produced. Asthe term implies, bilabial means two lips. Consonantsclassied as bilabial are produced at the lips. Labio-dental refers to the lips and teeth. Interdental means“between the teeth.” Alveolar refers to the alveolarridge; palatal refers to the hard palate; velar refers tothe soft palate; and glottal refers to the glottis.

In terms of manner, plosive sounds are created bycompletely occluding the expired breath stream and


ecto- outer ecto derm

ectro- congenital absence of ectro dactyly

-gnathia a condition of the jaw micro gnathia

hemi- partial hemi paresis

hyper- an excessive amount of hyper nasality micro- abnormally small micro gnathia

ophthalmo- pertaining to the eyes ophthalmo pathy

-osis a condition dysost osis

ost- pertaining to bone(s) dys ost osis

-pathy a pathological or diseased condition ophthalmo pathy

syn- together (i.e., fused) syn dactyly

velo- pertaining to the velum, or soft palate velo pharyngeal



CHAPTER 11 PATHOLOGIES ASSOCIATED WITH THE ARTICULATORY/RESONANCE SYSTEM 271

then releasing it abruptly, resulting in an explosive typeof sound. Fricative sounds are produced by creatinga narrow constriction that the expired breath streamis forced through or around, creating turbulence or afriction type of sound. Affricates are a combination ofplosives and fricatives. First, a complete obstructionis created in the vocal tract, but the obstruction gives way rapidly to a constriction that the breath stream isforced through. The nasal consonants are produced inmuch the same way as voiced plosives, but there is theadded feature of resonance within the nasal cavity dueto the opening of the velopharyngeal (V-P) port duringtheir production. Opening of the V-P port allows some

of the breath stream to be diverted to the nasal cav-ity while the balance of the breath stream continuesthrough the oral cavity. Glides are consonant soundsthat are somewhat similar to diphthongs. There isa rapid transition from one articulatory position toanother that creates these sounds (i.e., the /w/ and/j/). Finally, the /r/ and /l/ sounds are given the name“liquid” because like liquid (e.g., water), they changedepending on the context in which they are produced(i.e., as water changes its shape and form dependingon the container in which it is poured, the liquid con-sonants also change their shape and form depending

on what other speech sounds are produced adjacentto them).

Finally, 9 of the 24 consonant sounds are pro-duced without vocal fold vibration. In Table 11-1, you will note that in several of the cells there are twoconsonants separated by a comma. In each of thesecases, the consonant on the left is an unvoiced con-sonant; in other words, the vocal folds do not vibrateduring their production. The consonant on the rightof the comma is voiced. All of the single consonantsin Table 11-1 are voiced with the exception of the /h/

sound, which is the only unvoiced consonant thatdoes not have a voiced partner. As a nal word, itshould be noted that resonance is involved in con-sonant production (especially for the nasals, glides,and liquids), but consonant production is more aresult of breath stream obstruction or constrictionthan resonance.

The tongue is involved in the production of three-fourths of the consonant sounds. The consonantsounds that do not require involvement of the tongueare the bilabials (/p/, /b/, and /m/), labiodentals (/f/and /v/), and the fricative /h/. The bilabials are pro-duced by compressing the upper and lower lips. The

labiodentals are produced by compressing the upperteeth onto the lower lip. The /h/ sound is producedby forcing air through the open glottis, creating tur-bulence at the level of the vocal folds. As far as all ofthe other consonants (i.e., alveolars, interdentals,palatals, and velars) go, the tongue works with thealveolar ridge, teeth, hard palate, or velum to producethe consonant. In the case of the interdentals (the “th”sounds / θ / and /ð/) for example, the tongue tip isplaced behind or between the upper and lower teeth.From this example, you should be able to determinehow the other consonants are produced. The /w/

sound is interesting because it has two simultaneousplaces of articulation. Note as you produce the /w/sound (as in “wood”) that your lips round as the bodyof the tongue moves up toward the soft palate.

There are eight cognate pairs of consonants inEnglish. For these cognate pairs, both the place andmanner of articulation are identical. The only differ-ence between the two sounds in each pair is that oneis produced without vocal fold vibration, whereasthe other is produced simultaneously with vocal foldvibration.

TABLE 11-1

TRADITIONAL (PLACE/MANNER) CLASSIFICATION OF ENGLISH CONSONANT SOUNDS

Place of Production

Manner of Production

Bilabial Labiodental Interdental Alveolar Palatal Velar GlottalPlosive p, b t, d k, g Fricative f, v θ , ð s, z , h Affricate ,

Nasal m nGlide (w) j w Liquid l r

Note : All of the characters above represent their corresponding sounds, except the following:θ soft “th” as in breath ð hard “th” as in breathe “sh” as in shoe “zh” as in measure “ch” as in chew “j” as in jury “ng” as in sing j “y” as in yellow




Vowel sounds are typically classied accordingto where the tongue is placed within the oral cavity.Tongue placement can be accomplished within thevertical and horizontal dimensions. Vertical place-ment is referred to as tongue height. Horizontal place-ment is referred to as tongue advancement. Bothheight and advancement of the tongue determinevowel sound production. Vowel sounds are not dif-ferentiated according to the unvoiced/voiced schemebecause all vowels are produced with vocal fold vibra-tion (hence, they are all voiced).

Referring to Table 11-2, you can see that tongue

height is described using such terms as high, mid,and low. A high vowel is produced by elevation ofthe tongue toward the ceiling of the oral cavity. Bythe same token, a low vowel is produced by lower-ing the tongue toward the oor of the oral cavity. Interms of tongue advancement, the terms front, cen-tral, and back are used. Front vowels are produced byplacing the tongue in the vicinity of the teeth. Backvowels then are produced by placing the tongue inthe vicinity of the soft palate and pharynx. When you combine both tongue height and advancement, you get a wide range of possible tongue positions.For example, the /i/ vowel (as in the word “heat”) isclassied as a high front vowel because the tongueis placed in a position that approximates the alve-olar ridge. The /æ/ vowel (as in the word “cat”) isalso produced by placing the tongue in an anteriorposition, but the tongue is also placed at the oor ofthe oral cavity. As one produces the front and backvowels from high to low, the mandible also lowersa bit more and more. You can test this out your-self. Say the words “beat,” “bit,” “bait,” “bet,” and“bat” in succession. Make a mental note of what the

tongue and mandible are doing when you say these words (you are producing the front vowels in suc-cession from high to low). It should be noted thattongue height and advancement function to createthe various vowel sounds by modifying the resonantcharacteristics of the oral cavity. With each changein placement of the tongue, the oral cavity becomesa different resonator and thus, a different vowelsound is produced (recall the Source-Filter Theorydescribed in Chapter 10).

The tongue is also the primary structure involvedin the production of diphthongs (/ a I/ as in “nice”;

/ a / as in “how”; / I/ as in “boy”). However, in thecase of the diphthongs, the tongue rapidly shiftsfrom the articulatory position for one vowel tothe articulatory position for a second vowel. Notethe characters that are used to represent the diph-thongs. Go back to Table 11-2 and you can see whichtwo vowels are involved in the production of eachdiphthong. Take the / a / diphthong. This soundis produced by having the tongue first assume theposition for the / a / vowel and then rapidly transi-tioning the tongue to the position for the / / vowel.Note that in this case, the shift is from a low backvowel to a high back vowel, and indeed, / a / isproduced by shifting from a low tongue positionto a high tongue position. The advancement of thetongue remains back throughout the productionof / a /. In the case of / a I/ and / I/, both tongueheight and advancement change. Both of thesesounds start with a low back tongue position butthen move quickly to a high front tongue position.Shifts from one articulatory position to anothercreate a gliding acoustic quality that is distinctiveof the diphthongs.

TABLE 11-2

CLASSIFICATION OF ENGLISH VOWEL SOUNDS ACCORDING TO TONGUE HEIGHT AND ADVANCEMENT

Tongue Advancement

T o n g u e

H e

i g h t

Front Central Back–Central Back

High i I u

High–mid e oMid Low–mid Low æ a

Key: i see bird u moonI hit teacher woulde cake mud o boat red about bought

æ sad a mop




RELATING ARTICULATORY PHONETICSTO DISORDERS OF ARTICULATIONAND RESONANCE

Why should you be concerned with this crash coursein articulatory phonetics? The answer is simple. If youunderstand how speech sounds are produced, thatis, which anatomical structures are involved and thephysiological processes that play a part in articula-tion and resonance, you can easily determine howaberrations in structure and/or function will affectthe production of speech sounds. Many articulationand resonance disorders have an anatomical, neuro-logical, or physiological etiology. It is the relationshipbetween these etiologies and the resulting articula-tion and/or resonance disorder to which we now turnour attention.

Pathologies Affecting Articulationand Resonance

DEFINITIONS AND ORGANIZATIONOF DISORDERS

Before we begin an extended discussion of the rela-tionship between anatomical and physiologicalimpairments and articulation/resonance disorders, we must begin with some basic denitions. First andforemost, you should understand the distinction

between an articulation disorder and a phonologi-cal disorder . An articulation disorder results from“[i]ncorrect production of speech sounds due tofaulty placement, timing, direction, pressure, speed,or integration of the movement of the lips, tongue,velum, or pharynx.” (Nicolosi, Harryman, & Kresheck,2004, p. 21) In other words, an articulation disorderis a physical impairment of the ability to correctlymove and position the articulators for the correct pro-duction of speech sounds. A phonological disorder,on the other hand, not only involves incorrect pro-duction of speech sounds but also involves violations

of the rules that govern the speech sound system. Infact, it is typically the violations of underlying rulesthat results in speech sound errors. To put it another way, phonology is one component of language; artic-ulation is one component of phonology. Therefore, aphonological disorder is a broader disorder than anarticulation disorder. It is not within the scope of thistextbook to discuss phonological disorders but ratherto help you see the relationship between abnormalanatomy and/or physiology and articulation/reso-nance disorders.

A distinction also needs to be made between anorganic disorder and a functional disorder . Anorganic disorder (whether articulation, language,voice, or any other communication disorder) can betraced back to an observable etiology such as a bio-chemical aberration, genetic variation, illness, injury,or neurological impairment. By contrast, a functional

disorder exists in the absence of any known or observ-able organic pathology. In the case of articulation, adisorder may exist simply due to the habituationof faulty motoric patterns (i.e., the child habituallymakes incorrect placements of the articulators). Afunctional articulation disorder may also be referredto as a developmental articulation disorder becausethe errors tend to occur during childhood during thedevelopmental period. It is not within the scope ofthis chapter to discuss functional disorders becauseof the fact that no known anatomical or physiologicaletiology is apparent. We will instead turn our atten-tion to articulation disorders of an organic nature.

For the remainder of this chapter, you will beacquainted with a variety of organic disorders thatmay result in impaired articulation and/or resonance.These organic disorders will be discussed in relationto their underlying etiology—structural, neurological,and sensory. Structural disorders involve aberrationsof anatomy such as cleft lip and/or palate. The etiol-ogy of neurological disorders is within the nervoussystem. Neurological disorders include nerve dam-age (especially to the cranial nerves), motor speech

disorders , and other neurological disorders affect-ing the central and/or peripheral nervous systems.Motor speech disorders affect the proper executionof movements that are necessary for correct speechproduction and include apraxia of speech (AOS) anddysarthria. Other neurological disorders may includeprogressive neurological disorders (e.g., amyo-trophic lateral sclerosis [ALS], multiple sclerosis [MS])or nonprogressive neurological disorders (e.g., cere-bral palsy [CP]). Finally, sensory disorders involveimpairments of sensory systems that are essential forproper articulation and resonance. These include the

auditory, tactile , and kinesthetic systems. The discus-sion of sensory disorders that takes place later in thischapter will only focus on the auditory system.

It must be emphasized that you should not betoo overly concerned with the classication schemementioned above. There are other ways of classifyingimpairments that affect the articulatory and resonancesystems. It should also be noted that within the clas-sication system mentioned earlier, there is consider-able overlap. For example, AOS will be discussed as amotor speech disorder although it could just as easily




be discussed as a neurological disorder. Similarly, nervedamage (e.g., trauma) could be viewed as a structuraldisorder although it will be discussed here as a neuro-logical disorder. Your focus then should not be on howimpairments are classied but rather on the relationshipbetween these impairments and the potential articula-tion and/or resonance disorders that may result. That

said, let us turn our attention to these impairments.

STRUCTURAL DISORDERS THAT MAYAFFECT ARTICULATION AND RESONANCE

Perhaps, the most obvious structural disorder that will likely have a detrimental effect on articulationand resonance is cleft lip and palate. Similarly, thereare several other craniofacial anomalies that mayalso manifest themselves as deviations of articulationand/or resonance. In the case of structural disorders,the probability that articulation and resonance will

both be adversely affected is high.

Cleft Lip and/or Palate

Cleft lip and palate are among the most common con-genital anomalies (American Cleft Palate-Craniofacial Association and Cleft Palate Foundation, 1997). Theincidence of clefting differs according to race. Cleft lip with or without cleft palate occurs in approximately onein 1000 live births among Caucasians; approximately1.7 in 1000 live births among Asians; approximately3.6 in 1000 live births among Native Americans; and 1in 2500 live births among African Americans (Harold,2009). In Chapter 10, you learned that the two max-illary bones fuse together medially at the intermaxil-lary suture. A cleft occurs when the maxillary bonesdo not fuse between the eighth and twelfth weeks ofembryonic development. There are several classica-tion schemes for cleft lip and palate, but these are notimportant for the purpose of this discussion. As youcan see in Figure 11-1, clefts may involve the upper

lip only (referred to as cleft lip); the hard palate only

BA

C D

Figure 11-1 Various types of cleft. A . Cleft lip only. B . Cleft palate only. C . Unilateral cleft lip and palate. D . Bilateral cleft lip and palate.(Modied with permission from Anatomical Chart Company.)




(referred to as cleft palate); the upper lip and hard pal-ate (referred to as cleft lip and palate); or the upper lip,hard palate, and velum (referred to as complete cleftlip and palate). Clefts of the prepalatal region (i.e., thelip and alveolar ridge) can be unilateral or bilateral.

Possessing an understanding of the anatomy of thelips, teeth, hard palate, and velum, you should be able

to surmise that a cleft will likely have an adverse effecton articulation and/or resonance. Clefts of the lipand/or alveolar ridge without involvement of the hardor soft palate may result in some articulation errorsdue to the likelihood that the individual’s dentitionis adversely affected. Similarly, a cleft of the lip mayaffect the individual’s ability to round the lips for the/w/ consonant or the vowels that require lip rounding(mainly several of the back vowels). However, there will probably not be a problem with resonance as thehard and soft palates are essentially intact.

When the hard palate and/or velum are involved,both articulation and resonance may be detrimentallyaffected. From the standpoint of articulation, a cleft ofthe hard or soft palate may prevent the individual frombeing able to generate sufcient intraoral air pres-sure to produce the pressure consonants —primarilythe plosives and affricates, but also the fricatives toa lesser extent. The individual’s productions of theplosives, fricatives, and affricates may be distorted, weak, or absent. From the standpoint of resonance,a cleft of the hard and/or soft palate will compromisethe integrity of the oral and nasal cavities. There will

not be a separation between the oral and nasal cav-ity, so a portion of the breath stream may pass unim-peded into the nasal cavity and resonate there. Theresult is a condition known as hypernasality , a reso-nance disorder in which nonnasal speech sounds (allof the vowels and diphthongs and all but three of theconsonants in English) may become heavily nasal-ized. The air that passes into the nasal cavity, if undersufcient pressure, may also create turbulence as itexits the nostrils, creating nasal air emission. In themore extreme cases of cleft lip and palate, the indi-vidual typically develops compensatory strategies in

an attempt to produce the pressure consonants andto reduce hypernasality. Of these, the glottal stop andpharyngeal fricative are commonly used to substi-tute for the plosives and fricatives, respectively. Thepharyngeal fricative (which is produced by creatingturbulence of the breath stream in the pharynx) doesnot occur in English, not even for persons who havean intact speech sound system. The glottal stop alsois not recognized as an English speech sound, but itis used in certain linguistic contexts by persons whohave an intact speech sound system (e.g., in saying the

word “curtain,” we seldom enunciate the /t/ sound;instead, we substitute a glottal stop and pronouncethe word as “ker-n” with a very slight pause betweenthe two syllables). The difference between a person with an intact speech sound system and an individual who has a cleft palate is that the glottal stop tends tobe pervasive in the speech of the individual with cleft

palate.It should be noted that many children with cleft pal-ate also have chronic bouts of conductive hearing loss . As you may recall from Chapter 10, the Eustachian (orauditory) tube runs from the middle ear cavity to thenasopharynx. In the case of cleft palate, food or drinkthat is swallowed may be injected into the nasopharynx because of the opening created by the cleft. If thefood or drink gets injected into the Eustachian tube,it can lead to middle ear infections, known as otitismedia . The result could be a conductive hearing loss.The hearing loss could also adversely affect speechproduction (this will be discussed more fully below).

Other Craniofacial Anomalies

Cleft lip and palate is classied as a craniofacialanomaly because the structures of the skull and facedeviate from what would be considered normal anat-omy. Although trauma to the face and/or skull couldcertainly result in an anomaly, we typically thinkof craniofacial anomalies as having a genetic etiol-ogy. There are literally hundreds of genetically basedcraniofacial anomalies or syndromes. Many of thesesyndromes have little effect on speech production,but there are many that may have an adverse effecton speech. Cohen and Bankier (1991) estimated thatthere are nearly 350 syndromes in which orofacialclefting is a characteristic. It is outside the scope ofthis textbook to provide an exhaustive discussionof these syndromes; instead, you will be exposed toa small sample of craniofacial syndromes that mayaffect speech sound production.

Why You Need to Know Many craniofacial syndromes have a genetic etiol-ogy. The etiology is typically autosomal, meaningthat chromosomes other than those that determinegender and sexual characteristics are affected.In some cases, the syndrome can be traced backthrough the family history. These are known as familial cases. When new mutations of the syn-drome occur, they are referred to as sporadic. Theproportion of cases that are familial versus sporadicdiffers from syndrome to syndrome.




Apert Syndrome

Apert syndrome, or acrocephalosyndactyly , is a cran-iofacial anomaly that occurs in approximately one

of every 100,000 live births (Gorlin, Cohen, & Levin,1990). As the more technical name implies, persons with this disorder exhibit two prominent features—an unusually peaked head and webbed ngers and/or toes (see Figure 11-2). This disorder primarilyaffects the mandible and maxilla, and the face may beat or concave. There may be unusual deformities ofthe palate, including clefts. The pharynx tends to beshallow, which may result in a compromised airway.Hearing loss is common. In terms of speech produc-tion, there could be numerous speech sound errorsdue to several factors: compromised integrity of the

velopharyngeal mechanism ; malformed oral struc-tures; and hearing impairment.

Crouzon Syndrome

Crouzon syndrome (technically referred to as cranio-facial dysostosis ) is similar to Apert syndrome but isless severe. It occurs more often than Apert syndrome,in approximately 1 of every 25,000 live births (Gorlinet al., 1990). The webbing of the ngers and toes thatis seen in Apert syndrome is not seen in craniofacialdysostosis. However, the premature fusion of cra-

nial bones seen in Apert syndrome is also seen here. Additional facial features typically seen in Crouzonsyndrome are widely spaced eyes, shallow orbits, abeak-like nose, and a attened nasal bridge. The shal-low orbits make the eyes appear as if they are pro-truding (see Figure 11-3). In terms of oral structures,the person with Crouzon syndrome will have a smallmaxilla and a shorter nasopharyngeal space. Kreiborg(1981) found that cleft lip and/or palate are rare butnot impossible in this syndrome. If clefting doesoccur, you can expect deviations in oral–nasal reso-nance. Similarly, malformation of oral structures maybe manifested by a variety of articulation errors.

Ectrodactyly-Ectodermal

Dysplasia-Clefting SyndromeEctrodactyly-ectodermal dysplasia-clefting syn-drome —or simply EEC syndrome—is primarily man-ifested by “lobster-claw” deformities of the hands andfeet, a paucity of body hair, dry skin, and missing ormalformed nails and teeth. In the case of the handsand feet, one or more central digits may be missing(i.e., ectrodactyly), giving the appearance of claws. Themalformation of teeth and nails, sparse hair, and dryskin (due to the absence of sweat glands) is known asectodermal dysplasia. As you can see from the name

A

B

C

Figure 11-2 Apert syndrome. A . Typical facial features seen in the syndrome. B . Syndactyly of thengers. C . Syndactyly of the toes. ( A : Modied with permission from Gold, D.H., Weingeist, T.A. (2001).Color atlas of the eye in systemic disease. Baltimore, MD: Lippincott Williams & Wilkins; B: Modied withpermission from Strickland, J.W., Graham, T.J. (2005). Master techniques in orthopedic surgery: The hand (2nd ed.). Philadelphia, PA: Lippincott Williams & Wilkins; C : Image provided by Stedman’s [Dr. Barankin’sCollection].)




of the syndrome, clefting is also a prominent charac-teristic. Cleft lip and palate occur in approximatelythree-fourths of cases of EEC syndrome. A conduc-tive hearing loss (due to anomalies of the middle earbones—malleus, incus, and stapes) occurs in justunder one-third of cases of this disorder. If a cleft doesexist, the individual will likely have difculty in gener-

ating sufcient intraoral air pressure to produce thepressure consonants. There may also be hypernasal-ity with concomitant nasalization of nonnasal speechsounds. Dental anomalies and other oral variationsmay result in numerous speech sound errors. Theindividual with EEC syndrome may engage in com-pensatory articulatory strategies.

Pierre Robin Sequence

Pierre Robin sequence is technically not a syndromebecause a genetic defect does not appear to be the eti-ology of the disorder. During fetal development, themandible fails to grow properly so that the tongue isprevented from descending into the oral cavity. Thetongue remains high in the oral cavity, preventing thepalatal shelves from elevating and fusing. The result isa cleft palate, usually U or V shaped. In addition to acleft palate, the individual with Pierre Robin sequence will exhibit habitual posterior displacement of the

tongue into the pharynx, which in turn may causeupper airway obstruction and swallowing problems.Further decits may be exhibited in the digits, ears,eyes, and heart. Pierre Robin sequence may occur inisolation but is just as likely to be one component of abroader craniofacial anomaly (see Figure 11-4).

Stickler Syndrome

An example of a syndrome that includes character-istics of Pierre Robin sequence is Stickler syndrome,or congenital progressive arthro-ophthalmopathy .Many of the signs of Pierre Robin sequence are mani-

fested in this syndrome, with added pathology of the joints (e.g., arthritis, skeletal abnormalities) and visualsystem (e.g., astigmatism , cataracts , detached reti-nas, and severe myopia ). Once again—as with othercraniofacial anomalies involving clefting—the cleft will likely create problems in oral–nasal resonance. Insevere cases, unusual articulatory strategies may be

Figure 11-3 Typical facial features seen in Crouzon syndrome.Note the protruding eyes, beak-like nose, and a attened nasalbridge. (Modied with permission from Gold, D.H., Weingeist, T.A.(2001). Color atlas of the eye in systemic disease. Baltimore,MD: Lippincott Williams & Wilkins.)

A B

Figure 11-4 Pierre Robin sequence. A . Lateral view of the facial features typicallyseen in the sequence. Note the micrognathia. B . Cleft palate in an individual with thesequence. ( A : Reprinted with permission from Sadler, T.W. (2006). Langman’s medicalembryology (10th ed.). Philadelphia, PA: Lippincott Williams & Wilkins. Courtesy ofDr. R.J. Gorlin, Department of Oral Pathology and Genetics, University of Minnesota.B: Reprinted with permission from Chung, E.K. et al. (2006). Visual diagnosis in pediatrics (1st ed.). Philadelphia, PA: Lippincott Williams & Wilkins. Courtesy of Ellen Deutsch, MD.)




used to compensate for the inability to generate suf-cient intraoral air pressure and/or to reduce hyper-nasality and nasal air emission.

Velocardiofacial Syndrome

Perhaps, the most frequently occurring craniofacialsyndrome of which clefting is a characteristic is velo-

cardiofacial syndrome (Peterson-Falzone, Hardin-Jones, & Karnell, 2001). As the name of this syndromeimplies, the soft palate, heart, and structures of theface are typically involved. Individuals with this disor-der tend to have cardiac problems and atypical facialfeatures such as a prominent nose, long face, retrudedchin, and unusually small head (known as micro-cephaly). Of primary concern to the speech–languagepathologist is the involvement of the velum. It mayhave a cleft or there may be congenital velopharyn-geal incompetence due to a soft palate that is so shortthat it cannot approximate the posterior pharyngeal wall to provide proper balance between oral andnasal resonance. In either case, the likely outcome will be hypernasality. The nonnasal speech sounds(i.e., all English speech sounds except the /m/, /n/,and / /) may be highly nasalized. The individual mayalso exhibit compensatory articulatory substitutionssuch as the glottal stop and pharyngeal fricative.

Other Structural Anomalies

Velopharyngeal Incompetence Not Related toCraniofacial Anomalies

Velopharyngeal incompetence may occur congeni-tally in the absence of craniofacial anomalies. Thiscondition results from a soft palate that is too short

so that it cannot approximate the posterior pharyn-geal wall in the region of the nasopharynx or froma nasopharyngeal space that is too deep or wide toallow the soft palate to gain an adequate seal. In termsof speech production, the result of velopharyngealincompetence is similar to what you would expectfor cleft palate—hypernasality. However, not all casesof velopharyngeal incompetence are a result of anunderlying craniofacial anomaly. Some structuralvariations not associated with a particular syndromemay result in velopharyngeal incompetence. Forexample, the individual may simply have a hard pal-ate that is too short. This may cause an otherwise nor-mal velum to have an anterior displacement that doesnot allow it to approximate the posterior pharyngeal wall. On the other hand, the hard palate may be nor-mal, but the velum may be too short. In many of thesecases, the muscles that mediate movement of the softpalate may insert into the hard palate instead of theanterior portion of the soft palate. Finally, in somecases, there may be neurological damage to eitherthe nerves or muscles that control movement of thevelum so that it cannot elevate to meet the posteriorpharyngeal wall (this condition will be discussed inmore detail below). No matter the underlying cause,the result will be velopharyngeal incompetence and with that a likelihood of improper balance betweenoral and nasal resonance.

Glossectomy

According to the American Cancer Society (2004), thereare approximately 30,000 new cases of oral cancer inthe United States each year. Of these cases, nearly7500 involve cancer of the tongue. The incidence thenis approximately 2.5 per 100,000 population annu-

ally. The primary causes of oral cancer (and cancer ofthe tongue) are long-term alcohol and tobacco use. Although cancer of the tongue is fairly uncommonby comparison to other cancers, its effects can bedevastating. In the most severe cases, the individual with tongue cancer will require a total glossectomy .Removal of all of the tongue will have a negative effecton speech production and swallowing.

As you have learned, the tongue is involved in theproduction of all of the vowels and diphthongs and75% of the consonant sounds in English. It is also an

Why You Need to Know Not included in this formal discussion of cranio-

facial anomalies, but worth mentioning, is Downsyndrome. This syndrome is neither a craniofa-cial disorder nor a structural disorder as denedhere. However, it is an autosomal genetic disorderresulting from a condition known as trisomy-21 ,the presence of an extra 21st chromosome. Theprimary characteristic of Down syndrome is intel-lectual impairment, but other characteristics tendto be present such as almond-shaped eyes, shortlimbs, poor muscle tone, and protruding tongue.This syndrome is mentioned here because speechproduction errors tend to occur in persons hav-ing this syndrome. Speech may be characterized asimprecise, sluggish, or slurred (Gordon-Brannan &Weiss, 2006). Omissions of nal consonants in wordsare also common (Kumin, 1998; Stoel-Gammon,1998). By comparison with the craniofacial anoma-lies described here, in the case of Down syndrome,speech sound errors do not appear to be a result ofstructural deformity. Finally, chronic ear infectionsand a conductive hearing loss may create furtherdisturbances in speech production.




TABLE 11-3

THE INFLUENCE OF CRANIAL NERVES ON SPEECH PRODUCTION AND SWALLOWING

Cranial Nerve Innervates Whose Action Is ToNumber Name

V Trigeminal Digastricus (anterior belly) Lower the jaw Lateral pterygoid Lower and protrude the jaw Masseter Raise and retract the jaw

Medial pterygoid Raise the jaw Mylohyoid Lower the jaw Temporalis Raise and retract the jaw Tensor veli palatini Lower and tense the soft palate

VII Facial Buccinator Compress the lips against the teethDepressor anguli oris Compress the upper lip onto the

lower lipDepressor labii inferior Pull the lower lip downward and

outwardDigastricus (posterior belly) Lower the jaw Incisivus labii inferior Pull corner of the mouth inward and

downwardIncisivus labii superior Pull corner of the mouth inward and

upward

Levator anguli oris Pull the corner of the mouth and lower lip upward

Levator labii superior Raise the upper lipLevator labii superior

alaeque nasiRaise the upper lip

Mentalis Protrude and turn the lower lip outwardOrbicularis oris Close the mouth and pucker the lipsRisorius Pull the mouth angle outwardZygomatic major Pull the mouth angle upward and

outwardZygomatic minor Raise the upper lip

IX Glossopharyngeal Stylopharyngeus Assist in swallowing and vocal resonance X Vagus Levator veli palatini Raise the soft palate

Musculus uvulae Raise the soft palatePalatoglossus Lower the soft palate and raise the back

of the tonguePalatopharyngeus Lower the soft palate and assist in

swallowing and vocal resonancePharyngeal constrictors Assist in swallowing and vocal resonanceSalpingopharyngeus Assist in swallowing and vocal resonance

XI Spinal accessory Musculus uvulae Raise the soft palatePalatoglossus Lower the soft palate and raise the back

of the tonguePalatopharyngeus Lower the soft palate and assist in

swallowing and vocal resonanceSalpingopharyngeus Assist in swallowing and vocal resonance

XII Hypoglossal Geniohyoid Lower the jaw

Genioglossus Protrude the tongue tip and retract and lower the tongueHyoglossus Retract and lower the tongueInferior longitudinal Shape the tongueStyloglossus Raise the tongue in a posterior

directionSuperior longitudinal Shape the tongueTransverse Shape the tongue Vertical Shape the tongue




or neuropathy are dependent upon which nerves areaffected and the location where the damage is focused.In general, the higher up one goes toward the brainand brainstem, the more diffuse (i.e., widespread)the damage will be. By the same token, the lower onegoes toward the periphery, the more focal (i.e., limited)the damage will be. In the paragraphs that follow, you

should keep in mind that the discussion pertains todamage to the lower motor neuron (LMN) as opposedto the upper motor neuron (UMN). Signs and symp-toms of cranial nerve damage differ considerablydepending on whether the damage is in the centralnervous system or peripheral nervous system. Theeffects of UMN damage on articulation and resonance will be discussed in more depth in the later section onprogressive neurological disorders. Regardless of whichcranial nerve is affected, the primary signs of LMNdamage may include fasciculations, accid paralysis ,loss of reexes, muscle atrophy , and weakness.

Damage to the Trigeminal Nerve

Although there are many possible etiologies of trigem-inal nerve damage, one neuropathy specic to thisnerve that is worth mentioning is trigeminal neuralgia, which is also known as tic douloureux. It is the mostfrequently occurring of all neuralgias. The cause of thisdisorder is not fully understood, but it is thought that itmay be due to degeneration of the trigeminal nerve orby pressure placed upon it by inammation or someother source. The primary symptom of trigeminal

neuralgia is a sharp, cutting sensation on one side ofthe face, usually in the area of the jaw. In some cases,the disorder may mimic the symptoms of dental dis-ease. In younger people, there may be concern that thesymptoms could be an early sign of multiple sclerosis(MS). The pain can last from several minutes to severalhours at a time, and it can be triggered by such activi-ties as smiling, chewing, blowing the nose, or brush-ing the teeth. The disorder may come and go in someindividuals but may be more chronic in others. Duringperiods of severe pain, the individual may experiencedifculty in chewing or speaking.

According to Table 11-3, the trigeminal nerve is pri-marily responsible for innervating the muscles thatraise and lower the jaw. This action is necessary formastication as well as speaking. Only one other cranialnerve is involved in jaw movement—the facial nerve, which innervates the posterior body of the digastri-cus to assist in lowering (i.e., opening) the jaw. Thetrigeminal nerve also innervates the tensor veli pala-tini muscle, which assists in lowering the soft palate,but the majority of muscles that mediate movementsof the soft palate are not innervated by the trigemi-

nal nerve. Therefore, damage to the trigeminal nerve will have a detrimental effect on an individual’s abilityto open and close the jaw, and a lesser effect on theability of an individual to lower the soft palate. Howmuch ability is diminished depends on whether thedamage is unilateral or bilateral. If the damage is uni-lateral, the jaw will deviate to the side of the damage

when the individual is instructed to open or close the jaw. If the damage is bilateral, there may be completeinability to open and close the jaw, thereby impedingthe individual from chewing and also affecting speechproduction. The effect on speech production willinvolve primarily oral resonance (see what happensto the resonance of your voice when you speak with your jaw being closed or opened very wide). From anarticulatory standpoint, the inability of the individualto close the jaw may affect production of the bilabials(i.e., /p/, /b/, /m/), interdentals (i.e., / θ / and /ð/), andlabiodentals (i.e., /f/ and /v/). Because of the func-tional relationship between the tongue and mandible,high anterior speech sounds (e.g., the alveolars andhigh front vowels) may be affected to a lesser extent.

Damage to the Facial Nerve

Bell’s palsy is a neuropathology that is associated withthe facial nerve (see Figure 11-5). It is the most com-mon cause of facial paralysis and is always unilateral.

Figure 11-5 A child with Bell’s palsy (facial nerve pathol-ogy) on the right side of her face. Note the drooping of the eyeand corner of her mouth on the right. (Modied with permis-sion from Bickley, L.S., Szilagyi, P. (2003).Bates’ guide to physicalexamination and history taking (8th ed.). Philadelphia, PA: LippincottWilliams & Wilkins.)




The etiology is unknown although it is thought that avirus (e.g., herpes simplex) may be behind the disor-der. For most sufferers, the condition is only tempo-rary, typically lasting 3 to 8 weeks on average. However,for approximately 16% of persons who develop Bell’spalsy, the condition may become chronic. The pri-mary symptoms of this disorder include altered sense

of taste; difculty speaking; drooling from the mouthon the affected side; drooping of the ipsilateral eyelidand corner of the mouth; dryness or excessive tearingof the affected eye; and a heightened sense of hearingon the affected side.

As shown in Table 11-3, the facial nerve primarilyinnervates the muscles that mediate facial expres-sion, although it also innervates the posterior bellyof the digastricus, which assists in lowering the jaw.However, as you know from the forgoing discussionof the trigeminal nerve, jaw movement will morelikely be affected adversely by cranial nerve V dam-age. The bad news is that the facial nerve is the onlycranial nerve that innervates the facial muscles, sothere is no neural redundancy to serve as a protec-tive mechanism. As is true for the trigeminal nerve,unilateral damage will not affect speech productionor swallowing as adversely as bilateral damage will. Inthe case of Bell’s palsy, damage is always unilateral,so speech production and swallowing may be onlymildly affected. Other forms of facial nerve damagecan be bilateral.

Not all facial muscles are involved in speech pro-

duction. For this discussion, we are only interestedin the muscles that mediate movement of the lips.These include the buccinator, depressor anguli oris,depressor labii inferior, incisivus labii inferior andsuperior, levator anguli oris, levator labii superior,levator labii superior alaeque nasi, mentalis, orbicu-laris oris, risorius, and zygomatic major and minor.The net action of these muscles is to compress, evert,round, and pucker the lips as well as pull the cor-ners of the mouth laterally, upward, and downward.Some of these actions are necessary for speech pro-duction and swallowing. In the case of speech pro-

duction, inability to compress or round the lips mayadversely affect production of the bilabials (i.e., /p/,/b/, /m/) and labiodentals (i.e., /f/ and /v/) as wellas the rounded speech sounds (i.e., /w/, /u/, / /, /o/,/ /, / / and / /).

In terms of swallowing, you know from Chapter 10that the lips compress to prevent the bolus from exit-ing the mouth as the tongue forces the bolus towardthe pharynx. Therefore, damage to the facial nervemay disrupt the swallowing process. Depending onthe severity of the problem, food and drink may eject

from the mouth as the individual attempts to swallow.The individual may also exhibit drooling from one orboth sides of the mouth.

Damage to the Glossopharyngeal Nerve

From Table 11-3, you can see that the glossopharyngealnerve is involved minimally in the processes of reso-

nance and swallowing. This nerve innervates only onemuscle involved in these processes—the stylopharyn-geus. This muscle plays a part along with several othermuscles to dilate, elevate, relax, and tense the pharynx. Since several other muscles are also involved inthese actions, damage to the glossopharyngeal nervealone will likely have a minimal effect on resonance orswallowing. The vagus nerve, and possibly the spinalaccessory nerve as well, would have to be damagedalong with the glossopharyngeal nerve for there to beany measurable effect on resonance or swallowing.

Damage to the Vagus and Spinal Accessory Nerves When it comes to the head and neck region, there isan almost inexorable link between the vagus and spi-nal accessory nerve. A controversy exists as to whetherthe spinal accessory nerve really innervates any of thehead and neck muscles independently of the vagusnerve. Therefore, you will note in Table 11-3 that allof the muscles listed under the spinal accessory nerveare also listed under the vagus nerve. The vagus nervedoes innervate some muscles that the spinal acces-sory nerve clearly does not—the levator veli palatini

and all of the pharyngeal constrictor muscles. Thediscussion that immediately follows will focus onthe vagus nerve, but keep in mind that for some ofthe structures mentioned later, the spinal accessorynerve may also be involved.

From Chapter 8, you learned that the vagus nerveplays a major role in phonation via the recurrent andsuperior laryngeal nerves. However, the vagus nervealso innervates several muscles that are integral inmediating movements of the pharynx, soft palate, andtongue. This nerve innervates the muscles that raisethe soft palate as well as two of the three muscles that

lower it (the third muscle—the tensor veli palatini—isinnervated by the trigeminal nerve). The vagus nervealso innervates one muscle that assists in raising theback of the tongue. Finally, the vagus nerve innervatesseveral muscles that mediate pharyngeal movements(the only exception is the stylopharyngeus muscle, which is innervated by the glossopharyngeal nerve).Clearly, the vagus nerve is the primary source of inner-vation for the muscles of the soft palate and pharynx.It plays a lesser role in the innervation of the musclesthat mediate tongue movement. Therefore, damage




to the vagus nerve is more likely to affect the soft pal-ate and pharynx.

The site of nerve damage is very important inunderstanding which structures will be affected. Almost immediately upon exiting the base of the cra-nium, the inferior ganglion of the vagus nerve gives offthree important branches along its journey through

the neck. Most superior of these is the pharyngealbranch. Below the pharyngeal branch, the vagus givesoff the superior laryngeal nerve, and nally below thatthe recurrent laryngeal nerve. If damage occurs at thelevel of the inferior ganglion, then all structures belowthat point will be affected, including the soft palate,pharynx, and larynx. If the damage is below the level where the pharyngeal branch comes off the vagusnerve, then the damage will be conned to the larynxsince the nerve is still intact at the level of the pha-ryngeal branch (remember this mantra: “the higherup the lesion, the more widespread the damage”). Ifdamage is conned to the pharyngeal branch alone,then the larynx will not be affected but the soft palateand pharynx will.

That said, if the pharyngeal branch of the vagusnerve is damaged, the result will likely be diminishedmovement of the soft palate and pharynx (see Fig-ure 11-6). As you recall, the soft palate is part of thevelopharyngeal mechanism. If the soft palate cannotraise and lower properly, the result will be improperoral–nasal resonance. An individual with paralysis ofthe soft palate will likely have some degree of hyper-

nasality. The hypernasality will be more pronouncedif there is bilateral damage because both sides willbe paralyzed and the soft palate will not be able to

elevate at all. In the case of unilateral damage, theuvula will still be able to elevate on one side, so atleast some degree of velopharyngeal closure can beaccomplished.

Why You Need to Know Having the patient produce a staccato “ah” is adiagnostic test to determine where damage to thevagus nerve is occurring. If upon producing a stac-cato “ah” there is no movement of the soft palate atall, you can expect that there is bilateral damage tothe vagus nerve. If upon producing a staccato “ah”the soft palate deviates to one side, then the damageis likely unilateral. In the case of unilateral damage, you can determine which side is affected by observ-ing the uvula. The uvula will move to the unaffectedside. This is because the muscles on the unaffectedside are still able to contract, and thereby will “pull”

the soft palate to that side. Figure 11-6 depicts vagusnerve damage on the patient’s right side.

In terms of swallowing, an inability to raise thesoft palate may cause the bolus to be injected intothe nasopharynx when it is forced into the pharynxby the tongue. Collection of food or drink within thenasopharynx may set the stage for bacteria to travelup the Eustachian tube and into the middle ear,potentially resulting in otitis media.

Similarly to the soft palate, the pharynx plays a rolein resonance and swallowing. Therefore, paralysis ofthe pharyngeal muscles may adversely affect theseprocesses. In the case of resonance, the voice maysound “mufed” or not as crisp as you would expect.In the case of swallowing, the lack of motility withinthe pharynx may prevent the bolus from being passedinto the esophagus. Instead, the bolus may pocket inthe inferior pharynx, most notably within the pyri-form sinuses. In severe cases, aspiration of the bolusinto the larynx can occur.

Damage to the vagus nerve (and to a lesser degreethe spinal accessory nerve) will probably not have asnegative an effect on articulation as it may on reso-nance and swallowing. The soft palate and pharynxare not actively involved in the articulation of speechsounds. The vagus nerve does innervate one extrin-sic tongue muscle (the palatoglossus), but the actionthat this muscle performs on the tongue can also beaccomplished by the styloglossus muscle, which isinnervated by the hypoglossal nerve. Production ofback consonants and vowels (i.e., /k/, /g/, / /, /u/,/ /, /o/, / /, and / a /) may be affected somewhat, but

Failureto rise

Deviatedto left

Figure 11-6 Hemiparesis of the soft palate due to right vagusnerve damage. The soft palate will deviate to the opposite sideduring the production of staccato “ah.” (Modied with permis-sion from Bickley, L.S., Szilagyi, P. (2003). Bates’ guide to physicalexamination and history taking (8th ed.). Philadelphia, PA: LippincottWilliams & Wilkins.)




in most cases the individual will still be able to pro-duce these sounds.

Damage to the Hypoglossal Nerve

With the exception of the innervation of the geniohyoidmuscle, the hypoglossal nerve’s role is almost exclu-sively associated with movements of the tongue (seeFigure 11-7). This nerve innervates all of the intrinsicmuscles of the tongue as well as all of the extrinsictongue muscles except the palatoglossus (which, as you have just learned, is innervated by the vagus andpossibly even the spinal accessory nerve). Clearly,damage to this cranial nerve is going to have serious

consequences for the primary structure of articula-tion and oral resonance.

Articulation, chewing, resonance, and swallowing will all be affected adversely by damage to the hypo-glossal nerve, especially if the damage is bilateral. Ashas been mentioned several times, the tongue is theprimary articulator, playing a role in the productionof three-fourths of the consonant sounds in English(the non -tongue–inuenced consonants are /p/, /b/,/m/, /f/, /v/, and /h/). In addition, the tongue is theprimary structure involved in oral resonance for allof the vowels and diphthongs. For the processes ofchewing and swallowing, the tongue also plays animportant role. During deglutition, the tongue helpsshape and form the bolus as it is being chewed. Dur-ing swallowing, the tongue is responsible for “squeez-ing” the bolus back along the ceiling of the oral cavity,eventually forcing it through the oropharyngeal isth-mus and into the pharynx. Just think of how adversely

affected an individual’s ability to chew, speak, andswallow would be if he had bilateral damage to thehypoglossal nerve!

Motor Speech Disorders

As you learned in Chapter 5, a motor speech disorderis the result of a neurological impairment in whichmotor planning, programming, neuromuscular con-trol, or the execution of speech is adversely affected(Duffy, 2005). The more common etiologies of thiscondition are cerebrovascular accident (i.e., stroke),

degenerative disease, traumatic brain injury, and neo-plasm. Two neuropathologies are classied as motorspeech disorders: apraxia of speech ( AOS) and dysar-thria . As you will learn in reading the paragraphs thatfollow, one of these disorders—dysarthria—in manycases is the result of cranial nerve damage and there-fore the discussion of dysarthria is highly related to theforegoing discussion on cranial nerve damage. How-ever, keep in mind that the discussion above centeredon the likely outcome of isolated cranial nerve dam-age, and specically damage that is more peripherally

Figure 11-7 Hemiparesis of the tongue due to right hypoglos-sal nerve damage. The tongue will deviate to the affected sideduring protrusion. (Modied with permission from Campbell,W.W. (2005). DeJong’s the neurologic examination (6th ed.).Philadelphia, PA: Lippincott Williams & Wilkins.)

Why You Need to Know Similarly to the vagus nerve and the soft palate, youcan determine whether hypoglossal nerve damageis unilateral or bilateral, and if unilateral, whichhypoglossal nerve is affected. In this case, ask thepatient to stick her tongue out. If she cannot do thistask at all, the damage is likely bilateral. If, how-

ever, she can stick out her tongue but it deviates toone side of the mouth, the damage is unilateral.Which side the tongue deviates tells you whichhypoglossal nerve is damaged. The tongue will devi-ate to the side of the damage. This is because unilat-eral damage to the genioglossus muscle means thatonly half of it is contracting—the half that causesthe tongue to move toward the opposite side. Thetongue will move away from the intact genioglossus,that is, toward the “bad” side. Figure 11-7 depictsdamage to the right hypoglossal nerve.




based. In the majority of cases of dysarthria, severalcranial nerves may be involved or the damage maybe more diffuse as the site of lesion tends to be morecentral.

To the untrained observer, AOS and dysarthria mayappear to be very similar disorders. However, to aspeech–language pathologist, the difference between

the two is more obvious. Table 11-4 provides a sum-mary of some of the differences between AOS and dys-arthria. First and foremost, the site of lesion is differentbetween the two. AOS is a central nervous systemdisorder with damage originating in the language-dominant cerebral hemisphere (for most people, theleft hemisphere). In some cases of dysarthria, dam-age also occurs at the level of the cerebral cortex, butin most cases, the damage is subcortical, bulbar (i.e.,brainstem), cerebellar, and/or peripheral. Anothernoteworthy difference between the two is the fact that AOS tends to be conned to the articulatory system,

whereas dysarthria tends to affect every aspect ofspeech production including respiration, phonation,articulation, and resonance. In the case of dysarthria,the patient looks like he has a motor disorder. Finally,differences exist between the two types of motorspeech disorder in terms of (1) the speech sounds thattend to be in error; (2) the types of articulation errorsthat are exhibited; (3) the consistency of articulationerrors; and (4) the effect of increasing linguistic contexton the patient’s speech. These differences in speechproduction will become more apparent in the follow-

ing sections. You should realize, however, that withineach of the two motor speech disorders, there tends tobe quite a bit of variability from person to person. Twopersons having a diagnosis of AOS or dysarthria mayexhibit a different set of articulation errors. Becauseof this, the discussion below will not focus on specicarticulation errors but on generalities.

As a nal note, it should be mentioned that thespeech–language pathologist tends to see a largenumber of persons who have had a stroke who exhibita motor speech disorder along with swallowing dif-culties. Estimates of the prevalence of dysphagiaamong persons who have had a stroke range from 25%to 70% (Howden, 2004; Mann, Hankey, & Cameron,2000; Marik & Kaplan, 2003; Martino, Foley, Bhogal,et al., 2005; Paciaroni, Mazzotta, Corea, et al., 2004;Schelp, Cola, Gatto, Goncalves da Silva, et al., 2004).Disturbances in any or all of the phases of the swallowcan occur (e.g., aspiration, ejection of food outside

the mouth or into the nasopharynx, inability to formthe bolus or transport it to the oropharynx, pocket-ing of the bolus in the pyriform sinuses). Because ofthe high prevalence of dysphagia in persons who havehad a stroke, swallowing therapy is likely to be a com-ponent of a comprehensive intervention plan.

Apraxia of Speech

AOS is a central nervous system disorder. As was pre-viously mentioned, the focus of neuropathology is inthe language-dominant cerebral hemisphere. Rarely

TABLE 11-4

DIFFERENTIATING BETWEEN APR AXIA OF SPEECH AND DYSARTHRIAFeature Apraxia of Speech Dysarthria

Neuropathology Cortical, in the language-dominant hemisphere

Cortical, subcortical in either hemisphere, and/or peripheral

Nonverbal oral movements Range of movement and strength are typically normal

Range of movement and strength are typically impaired

Speech sounds in error Consonants; vowels may or maynot be affected Typically, consonants and vowels are affectedTypes of articulation errors Distorted sound substitutions,

omissions, and transpositionsDistortions and omissions of speech sounds

Consistency of articulation errors Variable with periods of error-free speech production

Consistent and predictable with no periods of error-free speech production

Automatic versus volitional speech Automatic speech can be errorfree

Automatic and volitional speech are equally affected

Effects of utterance complexity Utterances with greater complexity usually elicit more errors

Errors occur regardless of utterance complexity

Oral/nasal resonance Resonance is rarely affected With involvement of the velum, there will likely be improper balance

between oral and nasal resonance

Phonation Phonation is rarely affected Phonation is often affectedRespiration Respiration is rarely affected Respiration may be affected




that when it comes to speech production, these neu-ropathies include some type of dysarthria. Indeed, thedisorders described and discussed in this section arethe neurological disorders; the speech disorder (i.e.,dysarthria) is just one characteristic of the broaderneurological disorder.

Progressive Neurological Disorders

To see the wide range of symptoms and signs that existfrom disorder to disorder, we will compare three well-known progressive neurological disorders: ALS, MS,and Parkinson’s disease. The three differ in terms ofneurological involvement, symptoms, and the speechcharacteristics that are typically exhibited.

ALS, or Lou Gehrig’s disease, is a fatal neuropathyin which the motor neurons—both upper and lower—degenerate, resulting in diminished or lost voluntarymuscle activity. As the disease progresses, muscles nolonger receive neural impulses, so they become para-lyzed and wither away (see Figure 11-8). The etiologyis unknown. ALS is slightly more common in men thanin women, usually occurring between the ages of 40and 60 years. In the United States, approximately oneperson per 250,000 will develop ALS. Early symptomsof ALS include general weakness followed by twitch-ing, cramping, or stiffening of affected muscles usuallyin an arm or leg. In the later stages of the disease, themuscles of the respiratory system are affected to thepoint that the individual will likely die of respiratory

failure or pneumonia. Because both the upper andlower motor neurons are affected, ALS is a central and peripheral nervous system disease. In Chapter 5, youlearned that an outcome of UMN damage is spastic-ity, whereas an outcome of LMN damage is accidity.If you think about this in relation to the speech mech-anism, you may correctly surmise that ALS results in

mixed dysarthria of the accid and spastic types. Aber-rations in activity for the muscles of the speech produc-tion mechanism will result in speech that exhibits thefollowing signs: hypernasality with nasal air emission,imprecise articulation of consonants, slow speakingrate, and vowel distortions. Problems in swallowingare also common, especially in the later stages of thedisease. There is, however, a wide range of specicsymptoms from person to person (Duffy, 2005).

MS is an autoimmune disorder in which the per-son’s immune system attacks the central nervoussystem. The myelinated axons of neurons lose theirmyelination; this process prevents neurons in thebrain and spinal cord from communicating with eachother by interrupting a neuron’s ability to conduct neu-ral impulses to other neurons (see Figure 11-9). Thebreakdown of myelin creates scar tissue (i.e., sclerosis)

Figure 11-8 A patient with amyotrophic lateral sclerosis. Notethe atrophy of muscles in his arms. (Modied with permissionfrom Campbell, W.W. (2005). DeJong’s the neurologic examination (6th ed.). Philadelphia, PA: Lippincott Williams & Wilkins.)

Cell body

Axon

Dendrites

Myelin sheath

Nodes of Ranvier

Plaque

DemyelinationAxon terminals

Figure 11-9 Illustration of the demyelination and scarring thatoccur in multiple sclerosis. (Anatomical Chart Company.)




along the axon. “Multiple” refers to the fact that demy-elination can occur in several places within the centralnervous system—brainstem, cerebellum, cerebrum,and spinal cord. MS occurs more often in womenthan in men. Its onset is usually between the ages of20 and 40 years, although cases have been known tooccur in persons older than 40 years. Approximately

140 to 150 persons per 100,000 develop the disease.The specic etiology is unknown, but some believethat its origin may be viral. Symptoms of this diseaseinclude chronic fatigue, sensory disturbances (e.g.,burning, itching, numbness, and tingling), and visualproblems (e.g., double vision, decreased color per-ception, and reduced visual acuity). Because demyeli-nation can occur in several places within the centralnervous system, the resulting dysarthria can be dif-cult to predict. In many cases, there is no dysarthriaat all. For those cases where dysarthria is present,the most common type is mixed with characteristicsof the ataxic and spastic types (which would seem toindicate that the cerebellum and UMNs are affected).If the cerebellar system is involved, the distinguishingspeech characteristic is imprecise articulation result-ing in slurred speech due to poor motor coordination.The person will sound as if she is intoxicated. “Over-shooting” of the tongue (possibly due to the spastic-ity) as it attempts to make articulatory contacts is alsofairly common in persons who have MS.

Similar to MS, Parkinson’s disease is also a cen-tral nervous system neuropathy. The site of lesion is

within the basal ganglia in the subcortical regions ofthe cerebral hemispheres. Diminished production ofthe neurotransmitter dopamine results in decreasedstimulation of the motor cortex by the basal ganglia, which results in the following symptoms: bradykinesia, masked facies , muscle rigidity with diminished rangeof motion, shufing gait, stooped posture, and tremors(see Figure 11-10). By comparison with other progressiveneurological diseases, Parkinson’s disease is fairly com-mon, occurring in approximately 350 to 400 persons per100,000. In the United States, there are nearly twice asmany men than women with Parkinson’s disease. Tox-

ins and head trauma (such as what a boxer like Muham-mad Ali might experience in his career) are thought tobe two etiologies. For many persons with Parkinson’sdisease, the etiology is idiopathic . Primarily because ofthe bradykinesia, the most common articulation andresonance problems are imprecise consonants (due toarticulatory undershooting) and hypernasality. Verbaloutput is also characterized by difculty in initiatingspeech, quick rushes of unintelligible speech (usuallymumbled), and palilalia . Swallowing problems are alsocommon in persons with Parkinson’s disease.

Tremor

Masklike facialexpressionStooped

posture

Rigidity

Arms flexed atelbows and wrists

Hips and kneesslightly flexed

Tremor

Short,shuffling steps

Tremor

Figure 11-10 Clinical signs seen in a patient with Parkinson’sdisease. (Modied with permission from Timby, B.K., Smith, N.E.(2003). Introductory medical–surgical nursing (8th ed., p. 626).Philadelphia, PA: Lippincott Williams & Wilkins.)

Why You Need to Know One pathological condition worth noting here ismuscular dystrophy (MD). It was not included inthe main discussion because technically it is nota neurological disorder. Instead, it is a musculardisorder that affects approximately 15 to 20 personsper 100,000. There are several forms of musculardystrophy; some affect both males and females whileothers (e.g., Duchenne MD) affect males almostexclusively. Muscular dystrophy can occur at almostany age, and the severity of symptoms varies acrosstype of MD. Symptoms, however, are chronic, diffuse,and progressive. Although the nervous system typi-cally is not affected by MD, the signs and symptomsof the disorder are similar to what you’d see in manyof the degenerative disorders that affect the ner-vous system. If the structures of the vocal tract areaffected, you can expect to see speech (i.e., dysar-thria) and swallowing difculties.




Nonprogressive Neurological Disorders

Cerebral palsy (CP) (see Figure 11-11) is one of themost common nonprogressive neurological disor-

ders and is the most common developmental motorimpairment (Best, Bigge, & Sirvis, 1994; Love, 2000).Cerebral palsy is a result of injury to the central ner-vous system (i.e., the brain) before, during, or soonafter birth (Dillow, Dzienkowski, Smith, & Yucha,1996; Hardy, 1994; Love, 2000). The annual incidenceof the disorder is approximately 2 to 2.5 per 1000 livebirths. There are several types of cerebral palsy. Themost common is spastic CP, with approximately 50%of all cases being of this type. The athetoid type makesup approximately 20% of cases, and the ataxic typeoccurs in approximately 10% of cases. The remaining

20% of cases involve mixed types of cerebral palsy.Disturbances in speech production may involve the

respiratory, phonatory, articulatory, and resonancesystems (Bishop, Brown, & Robson, 1990; Dillow et al.,1996; Hardy, 1994; Love, 2000). Persons who have spas-tic CP may exhibit reduced vital capacity that resultsin inadequate breath support for speech (in termsof both phonation and articulation). They may alsohave a degree of hypernasality due to velopharyngealincompetence. Speech production tends to be slowand laborious, with imprecise articulation especially

for the affricates and fricatives (Love, 2000). Persons with CP of the athetoid variety may exhibit rapid andirregular breathing, and some may even engage inreverse breathing . The effect of athetosis on phona-tion can be quite severe, rendering the person aphonicin the worst cases, and in less severe cases, phonationmay be strained and strangled. Poor mobility of the

soft palate will result in hypernasality. During articu-lation, you may observe a person with athetoid CPengaging in exaggerated jaw movements but severelylimited tongue movements. These processes will likelyresult in distortions of the consonants and vowels(in the case of the latter, tongue height is usually notaffected but tongue advancement is). Finally, speechcharacteristics of persons with ataxic CP are similarto what you would expect for ataxic dysarthria due tothe incoordination of muscle activity. These includeshallow inspiration and lack of expiratory control;imprecise consonants and vowels; inconsistent soundsubstitutions and omissions; and poor rhythm andreduced prosody of speech. Oral–nasal resonance, onthe other hand, tends to be unaffected.

SENSORY DISORDERS THAT MAY AFFECTARTICULATION AND RESONANCE

There are several sensory impairments that may havean adverse affect on articulation and/or resonance.These include auditory, kinesthetic, and tactile dis-orders. Of these, only auditory disorders (i.e., hearing

impairment) will be presented as an example of howsensory disorders may affect the processes of articu-lation and resonance.

Hearing Impairment

A nal anatomical/physiological correlate to speechsound disorders is hearing impairment. In Chapters12 and 13, you will learn more about the auditory sys-tem and disorders that have an impact upon a per-son’s ability to perceive sound. For this section, you will see the connection between the auditory and

speech production systems.The relationship between hearing impairment

and articulatory and resonance disorders cannotbe overstated. For persons without hearing impair-ment, speech production is monitored through sev-eral modalities, including the auditory, tactile, andkinesthetic modalities. The auditory channel is theprimary means by which we monitor our speech. Forthose of us who have normal hearing, we are keenlyaware of what our voices sound like. To illustrate this,record your voice as you speak. As you are speaking,

Figure 11-11 A child with cerebral palsy. (Modied withpermission from Weber, J., Kelley, J. (2003). Health assessment innursing (2nd ed.). Philadelphia, PA: Lippincott Williams & Wilkins.)




make note of what your voice sounds like. Then, playback the recording. No doubt you will notice that itdoes not sound quite the same as when you hear yourvoice “live.” This is because when we speak, our voicesare fed back to us through two auditory channels—air conduction and bone conduction . As your voiceleaves your lips, it is transmitted through the air back

to your ears (just like it does for anyone else who isnear you). However, in addition to receiving feedbackin this channel, you are also hearing your own voicethrough the forced vibrations of your skull as youspeak (of course, other people around you do not hear your voice in this manner). When you listen to yourvoice on a recording, you are only hearing it throughair conduction; you lose the bone conduction chan-nel. In other words, when you listen to your voice on arecording, you are essentially hearing it the same wayeveryone else does. The point in mentioning this isthat proper operation of our auditory system is criti-cal to our ability to monitor our speech. You can wellimagine that a hearing loss, if severe enough, preventsan individual from monitoring his voice. If he cannotmonitor his voice, how is he going to know whether thespeech sounds he is producing are accurate? There isstill tactile and kinesthetic feedback, but these modali-ties are secondary to the auditory modality. Loss of theauditory modality will likely have a signicant nega-tive impact on the speech production system.

Hearing impairment is described in terms of itstype, conguration, and severity. Of particular inter-

est are four types of hearing impairment: central,conductive, mixed, and sensorineural . A conduc-tive loss involves the outer and/or middle ears. Forsome reason, acoustic energy is not being transmittedeffectively to the inner ear. This type of hearing loss isreversible. For example, if the etiology is otitis media, itis a relatively simple matter to clear up the infection bya course of antibiotics. Once the infection is cleared,hearing returns to normal. Similarly, if there is damageto the tiny bones of the middle ear (i.e., the ossicles),this can also be addressed through reconstructive sur-gery. Hearing will then return to normal, essentially. A

sensorineural hearing loss, on the other hand, is per-manent. In this case, the hair cells within the cochlea(which are necessary to convert mechanical energyfrom the middle ear into a neural impulse to be sent tothe brain via the acoustic nerve) are irreversibly dam-aged, or the acoustic nerve has some form of pathol-ogy. A mixed hearing loss has both a conductive anda sensorineural component. The conductive loss canbe corrected, but the sensorineural loss will remain.Finally, a central hearing loss refers to poor auditoryreception as a result of central nervous system dam-

age. The hearing mechanism (i.e., outer ear, middleear, inner ear, and acoustic nerve) is essentially intact,but the neural signal does not make its way to theauditory cortex because of brain damage.

Hearing loss is also described according to its levelof severity. Terms such as “mild,” “moderate,” “severe,”and “profound” are often used to describe how severe

the hearing loss is. Conguration refers to the extentof the hearing loss in terms of the sound frequenciesthat are most affected by the loss. For example, a per-son could have a high frequency hearing loss, a low fre-quency hearing loss, or a sloping hearing loss (whichmeans that the severity is worse as the frequencies gethigher). When it comes to hearing impairment andits effect on speech production, the more severe theloss, the more likely the speech sound system will beadversely affected. Also, you can expect that a hearingloss in the mid-frequencies (i.e., 500, 1000, 2000, and4000 Hz) will have a greater affect on speech produc-tion than other frequencies because the vocal toneconsists of these mid-frequencies.

The speech production system may be affectedby a hearing loss alone or by a hearing loss that is acomponent of another anomaly that affects speech.In a previous section of this chapter, you learned thatconductive hearing loss is often associated with cleftpalate. Because the hard and/or soft palate is compro-mised, food or drink is susceptible to being injectedinto the nasopharynx, and from there, bacteria maydevelop and pass from the Eustachian tube into the

middle ear cavity. Otitis media may be the nal out-come. In fact, children with cleft palate (or otherdisorders where the velopharyngeal mechanism iscompromised) tend to have recurring bouts of otitismedia. You should be able to imagine how these recur-ring infections and the conductive loss they bring canaffect a child’s speech sound system, especially if theinfections occur often during the speech developmentperiod (approximately the rst 6 to 8 years of life).

Approximately 1450 persons per 100,000 are deaf.Each year, approximately 1 infant in 1000 will beborn with a profound hearing loss. The term “deaf”

is used to denote a person whose sense of hear-ing is essentially nonfunctional. In other words, thehearing loss is likely to be sensorineural (or central),profound, and pervasive across the entire frequencyrange. Deafness can be congenital or acquired. Someof the most common etiologies are infections, meta-bolic disorders, neurological disorders, prematurity,toxins, trauma, tumors, and vascular disorders. If theimpairment is acquired after the period of speechdevelopment, there may be some deterioration ofspeech sound production and oral–nasal resonance,




but for the most part the speech production system will be minimally affected. On the other hand, if theimpairment is congenital or acquired before or dur-ing the period of speech development, you can expecta greater negative impact on the speech productionsystem. In this case, there may be numerous speechsound errors involving the consonants, diphthongs,

and vowels (in fact, the child may have a phonologicaldisorder). Speech sound errors are typically substitu-tions and omissions (the latter typically occurring fornal consonants in words; Abraham, 1989). Othererrors may include (1) an inability to distinguishbetween oral and nasal consonants; (2) frequent sub-stitutions of plosives for fricatives and liquids; (3) aninability to distinguish between voiced and unvoicedconsonants; and (4) neutralization of vowels (i.e., thefront and back vowels tend to be produced more cen-trally like the schwa / /).

Oral–nasal resonance will also be affected. Persons with profound hearing impairment tend to exhibita vocal quality known as cul-de-sac resonance . Thevoice of a person who exhibits cul-de-sac resonance will sound “at” or “mufed.” Denasality is also com-mon in persons with profound hearing impairment.There may also be poor coordination between respi-ration and phonation, resulting in diminished vocalintensity, aberrant stress and intonational patterns,and unusual syntactic phrasing.

Summary In this chapter, you learned the effect that pathologiesof the vocal tract have on the speech production sys-tem (i.e., the processes of articulation and resonance). A wide range of pathologies may affect speech soundproduction and oral–nasal resonance. These includestructural disorders, neurological disorders, andsensory disorders. Structural disorders include cleftlip and palate, other craniofacial anomalies such as Apert syndrome, and other structural anomalies suchas velopharyngeal incompetence and glossectomy.

Neurological disorders were further classied intothree groups: cranial nerve damage, motor speechdisorders, and other neurological disorders. Motorspeech disorders include AOS and dysarthria. Youlearned that other neurological disorders can be clas-sied as either progressive or nonprogressive. Pro-gressive disorders include ALS, MS, and Parkinson’sdisease. Cerebral palsy was discussed as an exampleof a nonprogressive neurological disorder. Finally,hearing impairment was presented as an exemplarof sensory disorders. These disorders have varying

effects on an individual’s ability to produce speechsounds (consonants, diphthongs, and vowels) and/or to regulate proper oral–nasal resonance. The pur-pose of this chapter was to instill within you an appre-ciation of the importance of knowing the anatomyand physiology of the articulatory/resonance systemand how pathological conditions may affect speech

production and swallowing.


In Chapter 11, you learned some of the characteristics ofPierre Robin syndrome. You know that it is classied as acraniofacial anomaly. Of primary interest to you are thesigns you observed during your evaluation: micrognathia,cleft palate, and glossoptosis. You know that micrognathiameans an abnormally small jaw and you also know thatglossoptosis is an abnormal downward or backward place-ment of the tongue. With your knowledge of the articu-latory/resonance system and articulatory phonetics, youknow there is a strong likelihood that Aidan’s untreated cleftpalate will adversely affect oral–nasal resonance. Your ob-servations indicate that he does indeed have hypernasalitywith nasal air emission. The micrognathia and glossoptosis

together may have a negative impact on Aidan’s ability toproduce certain speech sounds. As you know that his ha-bitual tongue placement is too far back, you suspect thathe will have difculty in using the tongue to produce theanterior speech sounds. Aidan’s cleft palate is also going tohave a negative impact on his speech production, as the ex-cessively diverted air into the nasal cavity will prevent Aidanfrom generating sufcient intraoral air pressure to produce

the pressure consonants—plosives, fricatives, and affricates.Upon administering the Goldman-Fristoe Test of Articulation,your suspicions are supported. Aidan exhibited numerousarticulation errors, especially in regard to the pressure con-sonants. Although the Goldman-Fristoe does not specically

test vowel sounds, you informally observed that Aidan’sproductions of the vowels were characterized by pervasive,heavy nasalization; you also noted that he experienced greatdifculty in producing the front vowels. Aidan’s medical his-

tory noted that he had frequent bouts of otitis media. Yoususpect that the middle ear infections were coming frombacteria that were created by food and drink being injectedinto the nasopharynx during swallowing. The primary focus of intervention should be to repair

the cleft palate. You predict that by having his cleft palaterepaired, several positive outcomes will result: (1) the hy-pernasality of his voice will decrease or possibly even beeliminated; (2) intraoral air pressure will be restored so thatAidan can produce the pressure consonants; and (3) theear infections and the conductive hearing loss they createwill be dramatically reduced in frequency and number. Once

the cleft has been repaired, your focus will be to assist Aidanin acquiring the correct productions of the speech soundshe had in error.



PART 5 SUMMARYThis part provided a thorough description and discussion of the articulatory andresonance system and the pathologies that may affect the integrity of this system. InChapter 10, you learned that the articulatory/resonance system is composed of thevocal tract, which includes the oral, nasal, and pharyngeal cavities and the structuresfound within them. These include the lips, teeth, tongue, mandible, alveolar ridge,hard palate, velum, nasal cavity, and pharynx. You learned about the velopharyn-geal mechanism and how its function is very important in swallowing and regulatingoral-nasal resonance. Finally, you were introduced to the Source-Filter Theory thatdescribes how the vocal tone that is produced by the vocal folds is shaped and formedinto speech sounds.

Chapter 11 provided you a thorough discussion of structural, neurological, and sen-sory pathologies and how they may affect swallowing and speech sound productionand/or resonance. Structural problems such as cleft lip and palate or glossectomy canadversely affect the production of many speech sounds and can also affect oral-nasalresonance in a negative manner. Neuropathies also affect an individual’s ability toaccurately produce speech sounds or to regulate oral-nasal resonance by paralyzing

muscles that are necessary for articulation and resonance. Finally, you learned thathearing impairment can also affect articulation and resonance. In general, the moresevere the hearing impairment, the more adversely the speech production system willbe affected. This is because as hearing impairment becomes more severe, the indi-vidual receives even less feedback from the auditory system to allow her to monitorthe accuracy and quality of her speech output.

PART 5 REVIEW QUESTIONS 1. Describe the bones of the skull (facial and cranial) and recall as many of the pri-

mary landmarks as you can for each bone. 2. What is meant by the term “muscular hydrostat” as a descriptor of the architec-

ture and function of the tongue? 3. Describe the architecture of the velum. How is the architecture of the velum

similar to the architecture of the pharynx? List the muscles of the velum andpharynx and explain what they do when they contract.

4. Discuss how the mandibular depressor and elevator muscles can mediate an-teroposterior and lateral movements of the jaw.

5. What are the four phases of mastication and deglutition? Describe each phase inas much detail as you can.

6. Explain how Source-Filter Theory accounts for the production of English vowelsounds. 7. How are English vowel sounds classied? What terms are used to describe tongue

advancement and tongue height? 8. How are consonants classied? Explain what the terms “place” and “manner”

mean. 9. What is velopharyngeal incompetence? Name three pathological conditions in

which velopharyngeal incompetence may be an issue. 10. Compare and contrast apraxia of speech and dysarthria.

292




11. Explain how damage to each of the following muscles can have an adverse effecton speech production: trigeminal; facial; glossopharyngeal; vagus, spinal acces-sory; hypoglossal.

12. Dene “progressive” and “nonprogressive” neurological disorders. Give an ex-ample of each one and describe how the disorder may affect speech production.

13. How might a sensory disorder like hearing impairment affect speech produc-tion? What would likely result in a more severe articulation disorder—congenitalimpairment or acquired impairment after the developmental years? Why?



Anatomy,Physiology, andPathology ofthe Auditory/Vestibular System

PART 6





processes (III-B)• Demonstrate knowledge of the acoustic basis of the basic human communication processes

(III-B)

Learning Objectives• You will be able to generalize the anatomical terms used in the study of aural anatomy and

physiology.

• You will list and describe the anatomical structures of the conductive auditory mechanism.• You will list and describe the anatomical structures of the inner auditory mechanism.• You will list and describe the anatomical structures of the vestibular mechanism.• You will be able to explain the physiological function of the conductive auditory mechanism.• You will be able to explain the physiological function of the inner ear in terms of audition and

balance.

CHAPTER 12

Anatomy and Physiology of the Auditory/Vestibular System

297


audio- related to hearing audio gram

aur-/auri- pertaining to the ear aur al; auri cular

bi-/bin- two bi lateral; bin aural

contra- opposite side contra lateral

dB decibels 60 dB

deci- one-tenth deci belHz hertz, cycles per second 1000 Hz

inter- between inter aural

intra- within intra cellular

ipsi- same side ipsi lateral

mV millivolts 80 mV

ohms unit of resistance 41.5 ohms

os-/osseo-/osteo- bone osseo us labyrinth



298 PART 6 ANATOMY, PHYSIOLOGY, AND PATHOLOGY OF THE AUDITORY/VESTIBULAR SYSTEM

Clinical Teaser—Introduction

A 50-year-old father of three, ages 15, 12, and 9, was recentlyseen by an audiologist for a diagnostic evaluation havingbeen referred by his physician for some very disturbingepisodes of dizziness. The rst incident took him somewhatby surprise in that he was driving and looking over hisshoulder to change lanes. When he turned his head back tocenter he became so vertiginous that he had to pull overand just sit quietly until the sensation passed, approximately30 minutes later. He proceeded to drive home but con-

tinued to suffer from nausea and lightheadedness upon head turning for the rest of the evening. He reported unsteadi-ness for the following several days. The next incident waseven more eventful and his symptoms seemed to localize

to his right ear. Approximately 30 minutes prior to the initiation of the dizziness, his right ear “just closed off” andstarted roaring. Then the vertigo and nausea began, this

time to the point that he actually vomited. By the nextmorning, he was feeling better. His ear had stopped roaringand it seemed to “open up” but again he had some residualunsteadiness for several days. He did note though that when

he goes to sleep at night he can hear a slight noise in hisright ear he had not noticed before.

The patient’s overall medical condition is good exceptfor some spring hay fever symptoms and the need to loseapproximately 40 pounds. The patient states that cola,pizza, and popcorn with lots of butter and salt are hisdownfall. His initial audiometric evaluation was unremarkable ex-cept for a slight low-frequency hearing loss in his right ear.He was counseled to return for a repeat test when he is hav-ing ear symptoms to document any measurable changes. The patient did return one week later with the pres-ence of a roaring in his right ear and residual unsteadi-ness from a vertiginous episode the day prior. His rightear hearing thresholds had dropped further in the lowfrequencies to a mild-moderate level. In light of theprogression of his loss and continued symptoms, it wasrecommended that he be referred to an otologist fora medical evaluation and treatment and return to theaudiologist for balance testing. Are there any terms or concepts in the above case study

that are unfamiliar to you? As you read the rst chapter in this unit, pay attention to the anatomy and physiology thatmay be per tinent to this case. You will revisit this case at the

end of the second chapter in this part.


oto- relating to the ear oto scope

retro- beyond retro cochlear

-scopy to look into oto scopy

uni- one uni lateral

Pa micropascals 20 Pa

Introduction

This unit on the anatomy and pathology of the ear was written by a clinical audiologist who has workedfor years with physicians identifying hearing disor-ders. However, it took the labor of teaching studentsthe subject of anatomy, physiology, and pathology to

really appreciate the effect one has on the other. Thiseffect is so signicant that instruction on the physiol-ogy of the auditory system has been blended into theinstruction on anatomy in this chapter, as opposed toseparating the two topics as has been done in the otherchapters in this book. Also within this chapter are Why You Need to Know boxes that contain brief discussionson relevant pathologies, although a more thoroughdiscussion of pathologies will follow in Chapter 13.

You may be interested in the anatomy of the earfrom the perspective of a future speech-languagepathologist (SLP) or audiologist. Not only will the

hearing mechanism be discussed in this chapter, butinformation will also be provided on the primary,basic function of the human inner ear—the balancesystem. The hearing function of our ear gets the mostattention and has a critical purpose for us humans;however, the balance system provides the necessaryinformation to keep us upright and oriented in relation

to gravitational forces. Hearing is critical to humans inthat it is necessary for the acquisition of our oral com-munication. We still lack complete understanding ofboth functions of the ear. This chapter will provide you with the basics of both hearing and balance.

An impairment of the hearing mechanism whetherfrom injury, disease or genetics, often causes a commu-nication problem. Failure to identify hearing loss early inlife, no matter the etiology, can have detrimental effects.These effects are seen as delays in speech and languageacquisition, difculties in academic performance, andmaladjustment in social emotional development.




points on the XY graph as the lower frequencies (below500 Hz) and the higher frequencies (above 5000

Hz) require more sound pressure to become audibleto our ears. Amazingly, the frequency range to whichthe human ear is most sensitive is approximately thesame range as many of our speech sounds (i.e., 125 to8000 Hz). Can one assume that the speech sounds used

in spoken language were selected to take advantage ofthe frequency range over which our ears are most sen-sitive? Later in this chapter, there will be a detailed dis-cussion of the physiology of the ear that accounts forthe increased sensitivity at a select frequency range.

Outer ear Middle ear Inner ear Neural pathway

Figure 12-1 Overview of the entire ear with the four anatomical divisions. (1) The outer ear gath-ers the acoustic pressure wave and directs it to the ear canal. (2) The middle ear acts on the acousticpressure wave mechanically, contributing by vibrating against the uid-lled inner ear. (3) The uid of theinner ear hydromechanically stimulates the specialized structures of hearing transforming the energyto the electrical stimulation received by the neural bers. (4) The neural pathway carries the electricalenergy to the brain, so that the processes of hearing and balance are accomplished. (Reprinted withpermission from Anatomical Chart Company.)

Why You Need to Know You are at an electronics store, primed to spend your hard earned dollars on a state-of-the-artsound system. The salesperson is touting the vari-ous features of each, selling you on the fact that a

particular stereo has a frequency response rangeup to 30,000 Hz. You are not impressed. You knowthat the salesperson’s pitch is nothing but hype.

You read this chapter before going to the electronicsstore, so you know that the upper end of the stereo’s frequency range is beyond the capacity of the typi-cal human ear to perceive. You know that any fre-quency above 20,000 Hz will be completely lost onhumans. You realize that your pet is going to be theonly member of your household who will be able to fully appreciate the entire frequency range of yournew stereo system (a dog’s hearing range extendsto 60,000 Hz and a cat’s range extends to 85,000Hz). You are not willing to spend several hundreddollars on a stereo system only an animal can fullyappreciate—even if the animal is your beloved pet!

Anatomy and Physiology of theAuditory and Vestibular Systems

Anatomically, the hearing mechanism can be dividedinto four parts: outer ear , middle ear , inner ear , andneural pathway (see Figure 12-1). The primary struc-



CHAPTER 12 ANATOMY AND PHYSIOLOGY OF THE AUDITORY/VESTIBULAR SYSTEM 301

tures of the outer ear include the pinna (or auricle )and the external auditory meatus (EAM, or ear canal ).The middle ear consists of the tympanic membrane (TM; commonly known as the eardrum , which formsthe boundary between the outer and middle ears),ossicles (malleus, incus , and stapes ; collectively knownas the ossicular chain ), Eustachian (or auditory )

tube , and the middle ear cavity (a space). The innerear includes the cochlea , vestibule , and semicircularcanals . Finally, the neural pathway includes the vestib-ulocochlear nerve (cranial nerve VIII), which consistsof the combined cochlear and vestibular branches asit courses through different levels of the brainstem.

The four parts of the auditory system provide theirown particular contribution to the pressure wave cre-ated by a sound source that is ultimately “heard” bythe individual. A pressure wave consists of a repeatingpattern of high- and low-pressure regions (relative toatmospheric pressure) moving through a medium. Thestructures of the ear basically function as an energytransducer converting pressure waves into the elec-trical energy transmitted to the brain for processing.The outer ear acts on the pressure wave by gathering itinto the system. The middle ear then acts on the wavemechanically completing its contribution by vibratingagainst the uid-lled inner ear. The uid within theinner ear hydromechanically stimulates the specializedstructures of hearing transforming their energy to theelectrical stimulation needed by the neural bers. Theneural bers carry the electrical energy to the central

centers for audition so that hearing can take place.

STRUCTURES OF THE AUDITORYCONDUCTIVE SYSTEM

The anatomical structures of the outer and middle earare known as the conductive auditory system as theyserve to conduct the acoustic signal to the sensoryand neural receptors (i.e., the cochlea and cochlearbranch of cranial nerve VIII).

Outer Ear

Pinna and EAM

The pinna or auricle is the most obvious anatomicalstructure, and is usually what most people think of when a person says the word “ear” (see Figure 12-2).The framework of the pinna is made of cartilage, knownas the auricular cartilage . There are several musclesthat attach the pinna to the head, reverting back toother mammals that turn their ears to localize sound.Most humans have no motor control of these muscles,but there are exceptions. (Every family seems to haveone elder relative who likes to entertain small children

by voluntarily wiggling their ears.) The helix is the out-ermost portion of the auricular cartilage that curvesto form the ear’s cupped shape. Darwin’s tubercle is acartilaginous protuberance which presents as a thick-ening on the helix. The tubercle is dominantly inher-ited but still may or may not be visible. This tubercle isseen as a “throwback” to the higher primates (hence

the term Darwin in the name). The helix itself endsinferiorly to form the lobule (or earlobe ). The lobuleis the most common site for ear piercing as it is com-posed of tough connective tissue lacking the rmnessand elasticity of cartilage. The lobule has a large bloodsupply, serving to help warm the ears in cold climates.The earlobe contains many nerve endings and forsome people is an erogenous zone. Earlobes elongateslightly with age (and gravity). Human earlobes maybe detached (free) or attached. We have our relativesto thank for this characteristic. Free or detached lobesare dominantly inherited and attached earlobes are

inherited through recessive gene transmission. Theantihelix is another prominent ridge and ends inferi-orly to form the antitragus which serves to form thelower border of the concha bowl . The tragus is a apof cartilage on the anterior wall of the ear canal. Press-ing on the tragus serves nicely to close off the canalto dampen unwanted sound. There are no two pinnasalike; even differences exit between the two pinnas ofthe same individual. It is one part of the aural anatomythat can be easily examined and studied.

The EAM (or ear canal) is continuous with the car-tilage of the pinna to about one-third of its depth, but

Helix

Scaphoidfossa

Darwin’stubercle

Triangularfossa

Crus ofhelix

Cymbaconcha

Externalacousticmeatus

Tragus

Antitragus

Cavumconcha

Intertragicnotch

Lobule

Antihelix

Crura ofantihelix

Conchabowl:

Figure 12-2 Structure of the human pinna (auricle) with per-tinent landmarks. (Reprinted with permission from AnatomicalChart Company.)




then turns to bone for the remaining two-thirds of itsdepth (the bone is the temporal bone of the skull).The pinna and EAM reach adult size by about 9 to12 years of age. The location of the pinna in relation tothe other features of the head is very predictable (seeFigure 12-3). Moderate deviations of the relationshipbetween the pinna and other facial structures maysignal a congenital disorder or syndrome.

The human ear is a paired organ; one benet of thisis in the localization of a sound source. For example,

acoustic pressure waves directed toward the right ear will have greater amplitude, contain a broader fre-quency spectrum, and reach the right ear sooner thanthe same wave traveling around the head to the leftear opposite from the source. These interaural differ-ences alert the brain and allow humans to locate thesource of a sound. The shape of the pinna also acts as adirectional microphone. Sounds arriving from behindare dampened slightly compared to sounds that hitthe pinna directly from the front. This effect helps usseparate the signal from a background sound.

The pinna with the help of the concha bowl (refer

back to Figure 12-2) collects and directs the acoustic waves down the EAM. The meatus is basically a tube with the tympanic membrane (TM) being the internal,closed end. Therefore, the ear canal acts as a closedtube resonator having its own resonant characteristics.Remembering your high school physics class, certainfrequencies will get either enhanced or dampened.The length of the ear canal is approximately 2.5 cm or25 mm in adults and its diameter of approximately 7mm will amplify the incoming acoustic wave as muchas 20 dB at 2500 Hz. In all, with the addition of the res-

onance of the concha bowl, there is a 5 to 20 dB boostof the incoming acoustic wave in the frequency rangebetween 1500 and 7000 Hz.

The pinna and the EAM also have a nonacousticfunction. The depth and curvature of the ear canal (asomewhat irregular “S” shape) serves to protect theTM from direct injury. However, small children have

been known to place beans, beads, and other various“treasures” down the ear canal.The ear canal has a self-cleaning function. It is lined

with epithelial skin cells. In the ear canal, the skindoes not slough off like our other skin cells; instead,the skin migrates along the canal to the entrance fromthe depth of the eardrum to be sloughed off to theoutside. This is called epithelial migration . The outerone-third of the canal is also where cerumen or ear wax is produced. Cerumen, a yellowish-brown, waxysubstance is the normal product of sebaceous glands(i.e., sweat glands) secreting their oily substance ontothe cilia, the ne hairs located at the entrance to thecanal. Together they protect the canal by repelling water and expelling the dead skin cells. Cerumen isalso slightly acidic, which discourages the growthof bacteria and fungi that would otherwise grow inthe warm moist environment of the ear canal. Forthe most part, cerumen build-up is not a problem. Thedead skin migrates to the entrance of the ear canal.The action of the cilia, plus the mechanical action of the jaw during talking and chewing, serves to massagethe cerumen out of the canal. Impaction of cerumen

is typically caused by one’s attempt to mechanicallyclean the canal with a cotton-tip applicator or otherominous tool (your grandmother was correct whenshe told you not to place anything smaller than yourelbow down your ear canal). To inspect for cerumenone performs otoscopy using an otoscope . The “S”curve of the canal will need to be straightened out. Thisis accomplished by pulling the helix up and back. This will direct the light of the otoscope down the canal forvisualization of its contents and the eardrum.

Middle Ear

Tympanic Membrane

The TM (or eardrum) denes the border between theouter and middle ear (see Figure 12-4). It is a true mem-brane in that it is very thin, having a very small mass. Ahealthy TM is a relatively transparent, pearl-gray allow-ing the observer to identify several structures behind itin the middle ear. Its thinness and small mass make itvery mobile, yet it is also very sturdy. The TM resides atan approximate 55 ° angle at the end of the ear canal. Itis slightly taller than it is wide and is concave in shape

Figure 12-3 The location of the pinna in relation to the otherfeatures of the head. Note the alignment of the pinna with thecanthus (corner) of the eye. (Reprinted with permission fromNettina, S.M. (2001). The Lippincott manual of nursing practice (7th ed.). Baltimore, MD: Lippincott Williams & Wilkins.)




so that its center is displaced medially, toward thestructures of the middle ear cavity. For most of its cir-cumference, the TM ts in a small sulcus in the bony wall of the EAM called the annular or tympanic sulcus .Since the outer ring of the TM is xed into the sulcus,not all of the surface of the TM can vibrate. The effec-tive vibrating area of the TM is approximately 55 mm 2.

The TM consists of three layers. The central brouslayer of the TM accounts for its sturdiness. This cen-tral or intermediate layer is comprised of radial andcircular bers held together by connective tissue, and

sandwiched between the two remaining layers. Theoutermost (i.e., lateral) layer consists of a thin epithe-lium that is continuous with the lining of the ear canal.The innermost or medial layer is a mucous mem-brane that is continuous with the lining of the middleear cavity. The bers of the intermediate (i.e., middle)layer are found mostly throughout the TM except ina small superior portion. Because of the sparsenessof the bers in this superior region, it is referred to asthe pars accida . The remaining brous portion ofthe TM is known as the pars tensa . The pars accidais not acoustically active, but serves to equalize pres-

sure by moving outward when the air in the middleear cavity is compressed by inward movement of thepars tensa, serving in essence as a relief valve.

Otoscopy is the primary means of inspecting theTM. Visualized on a healthy TM are the tiny blood ves-sels that course its surface. Another landmark seen when performing otoscopy is the cone of light , whichis the reection of the otoscope light due to the con-cavity of the TM. The cone of light will be presentat approximately 5 o’clock for the right ear and7 o’clock for the left. Many physicians use the pres-

ence or absence of the cone of light to aid in their diag-nosis of middle ear disease. In cases of disease due topoor ventilation of the middle ear cavity, the TM tendsto displace medially or inward due to the negativepressure within the middle ear cavity. This typicallycauses the cone of light to be absent during otoscopy. When there is an absence of the cone of light, manyphysicians will report that the eardrum looks “dull.”

Pars tensa (A)

Cone of light (B)

Umbo (F)

Manubrium ofmalleus (E)

Pars flaccida (H)

Long processof incus (G) Lateral process

of malleus (D)

Pars tensa (A)

Annularligament (C)

C

A

A B

B

F

E

D

H

G

Figure 12-4 The tympanic membrane (TM) or eardrum. A . Artist’s rendition of a “normal” TM. (Reprinted with permissionfrom Tank, P.W., Gest. T.R. (2008). Lippincott Williams & Wilkins atlas of anatomy . Baltimore: Lippincott Williams & Wilkins.)B . A “normal” TM ( in vivo) with visible landmarks. Using otoscopy, the observer should be able to identify several structures thatlie behind a healthy TM. (Reprinted with permission from Moore, K.L., Agur, A. (2002). Essential clinical anatomy (2nd ed.).Philadelphia: Lippincott Williams & Wilkins.)

Why You Need to Know Poor ventilation from Eustachian tube dysfunc-

tion results in negative pressure within the middleear cavity. The pars accida region of the TM maybecome displaced inward. When this conditionbecomes problematic, the physician must attemptto equalize the negative pressure within the middleear cavity to the more positive atmospheric pres-sure. This is done by placing a pressure equaliza-tion (PE) tube in the TM. The pars tensa is theregion where these tubes are placed because of itsability to retain the PE tube for a relatively longperiod of time. The epithelial tissue of the eardrumwill eventually grow under the tube and expel it from the surface. The TM can spontaneously perfo-rate from infection or be perforated from trauma.It can usually heal itself from small perforationsbut when a large perforation typically does not healon its own, a surgical procedure called a tympano-plasty can be performed. The middle ear is natu-rally sealed off from water exposure, so when a TMperforation allows water (and the bacteria thataccompany it) to enter the middle ear space, it canlead to an increased risk of middle ear infection.




Ossicular Chain

Portions of the ossicles can be identied through thetransparent TM during otoscopy. The cavity medial tothe TM is called the middle ear cavity or space. Located within the space is a chain of three linked bones. Col-lectively they are referred to as the ossicular chain,or ossicles (see Figure 12-5). These three bones areamong the smallest in the entire human body; one canplace all three bones on the surface of a dime and stillhave room to spare! As one proceeds medially from theTM, the rst and largest bone in the chain is called themalleus which is approximately 9 mm in length. Dur-

ing otoscopy, one can see the long process of the mal-leus, called the manubrium . The manubrium appearsas an opaque whitish streak behind the TM coursingdownward at about one o’clock in the right ear and 11o’clock in the left. The manubrium is rmly attached tothe medial surface of the TM. It is the manubrium thatdraws the TM inward toward the middle ear space giv-ing the TM its concave shape. The most depressed partof this concavity is named the umbo . In addition tothe manubrium, there are two projections off the mal-leus called processes. They are the anterior and lateralprocesses, named for the location of their anatomicaldirections. The lateral process is in the anterosuperiorquadrant of the TM, and appears as if it is “pointing” atthe observer when seen through a healthy, transpar-ent TM. The anterior process cannot usually be visual-ized with otoscopy. The pars tensa and pars accidaappear to be divided by a fold, known as the malleolarfold , running along the upper portion of the TM. Thisfold is created by an anterior attachment of a ligamentband to the anterior process of the manubrium and aposterior attachment of a ligament band to the lateralprocess of the manubrium.

The second bone in the ossicular chain is the incus.

It weighs slightly more than the malleus but is shorter,being approximately 7 mm in length. Using otoscopy,only a portion of the incus, its long process , can bevisualized through a healthy transparent TM. Thelong process hangs down parallel to the manubriumand the short process of the incus projects posteri-orly. The body of the incus and the bulky head of themalleus cannot be seen while performing otoscopy.They are suspended above the level of the TM in theuppermost region of the middle ear cavity called theepitympanic recess , or attic . The head of the mal-leus and body of the incus articulate with each other,forming the malleoincudal joint . There appears to beonly limited range of motion of this joint.

The third and most medial bone in the ossicularchain is the stapes. The stapes is not only the smallestof the three bones that comprise the ossicular chain,but is also the smallest bone in the human body, at amere 3.5 mm in length. The angle of the stapes, along with its distance medially from the TM, makes it invis-ible to the otoscope. The head of the stapes articulates with the lenticular process of the incus, forming theincudostapedial joint .

The neck of the stapes bifurcates to become theanterior crus and posterior crus . The two crura form

Head of malleus

Neck of malleus

Anterior processof malleus

Lateral processof malleus

ManubriumHead of stapes

Incudostapedial joint

Lenticular process

Posterior crus of stapes

Anterior crus of stapes

Footplate of stapes

Long process of incus

Short process of incus

Body of incus

Malleoincudal joint Figure 12-5 The ossicles withpertinent landmarks. Located inthe middle ear space, the malleus,incus, and stapes are collectivelyreferred to as the ossicular chain.(Reprinted with permission fromTank, P.W., & Gest, T.R. (2008).Lippincott Williams & Wilkins atlasof anatomy . Baltimore: LippincottWilliams & Wilkins.)

Why You Need to Know Chronic middle ear disease or traumatic injurycan fairly easily disrupt the incudostapedial joint,causing a disarticulation. This condition results in amoderate loss in the conduction of sound to the innerear. Surgeons may attempt to repair the integrity ofthe chain by reconstructing the damaged ossicles.




an arch in their attachment to the base, which is calledthe footplate . The footplate of the stapes inserts intothe oval window and is sealed by the elastic annularligament in much the same way as the TM is held inplace within the tympanic sulcus. The annular li gamentrmly holds the footplate in place while still allowingfor efcient vibration within the oval window.

The bones of the ossicular chain are suspendedby ligaments attached to strategic places within the walls of the middle ear cavity. These attachments takeplace in most anatomical directions: lateral, anterior,superior, and posterior. The ligaments are designed tosuspend the ossicular chain without interfering withits vibratory efciency.

Stapedius and Tensor Tympani Muscles

Two important striated muscles attach themselves totwo of the three ossicles. The stapedius tendon insertsonto the neck of the stapes, hence its name. The body

of the stapedius muscle is deeply embedded in bonearising from the posterior wall of the middle ear cavity;only its tendon emerges from a bony projection, the pyramidal eminence , to attach to the stapes. The sta-pedius muscle is innervated by its own branch of thefacial nerve (cranial nerve VII). The muscle serves tocontract in response to sudden loud sounds. Muscleaction rotates the stapes in a posterior direction. Thetensor tympani tendon enters the middle ear cavityfrom the anterior wall. Similarly to the stapedius mus-cle, the body of the tensor tympani muscle is housed within a bony canal so that only its tendon enters themiddle ear space. The tendon of the tensor tympanimuscle attaches to the neck of the malleus. The tensortympani is innervated by the trigeminal nerve (cranialnerve V). When this muscle contracts, it pulls the mal-leus in an anteromedial plane reducing the range ofmotion of the TM. The dual action of stapedius and ten-sor tympani contraction (termed the acoustic reex )serves to stiffen the ossicular chain, thereby reduc-ing the admittance of the acoustic signal particularlyfor lower frequency sounds. Therefore, contraction ofthese muscles is theorized to be a protective mecha-

nism for the cochlea by preventing the stapes fromexcessively vibrating in the oval window (to be dis-cussed later). However, for most humans the responsetime for this action is too slow to prevent hearing dam-age from exposure to sudden, excessive sound (e.g., ashotgun blast or a recracker exploding).

Middle Ear Cavity

The middle ear cavity is an air-lled space lined with amucous membrane. It is located in the petrous por-tion of the temporal bone of the skull and is approxi-mately two cubic centimeters (2 cm 3) in volume. Themiddle ear cavity is surrounded on all sides by boneexcept its lateral wall, which houses the TM. It is bestknown for housing the ossicles but has numerous

other signicant landmarks. The space as a whole ismore hourglass-shaped than cube-shaped as shownin Figure 12-6. It is taller than it is wide, with a narrow-ing in the middle and a wider space inferiorly andsuperiorly. The wide upper space of the cavity is knownas the epitympanic recess or attic. As mentioned ear-lier, the epitympanic recess is where the head of themalleus and the body of the incus reside.

For the purpose of examination, the middle earcavity will be referenced by its walls in the variousanatomical directions. The entire lateral wall of thecavity is occupied by the TM. By removing the lateral

wall, the remaining contents of the middle ear cavitycan be examined. Along the posterior wall in the areaof the epitympanic recess is the aditus . The aditus isthe passageway that leads to the air cells within themastoid process of the temporal bone of the skull. Theair in the middle ear cavity communicates throughthis passageway with the mastoid air cells. The pur-pose of the air cells is simply to lessen the weight ofthe head, since the temporal bone is not solid. If thepetrous portion of the temporal bone was solid, thehuman head would weigh several ounces more than

Why You Need to Know Audiologists measure the intensity level that triggersthe acoustic reex contraction by monitoring the

change in the admittance of the stimulus. On average,it takes 85 dB SPL to elicit a contraction of the stape-dius muscle (Gelfand, 1984). The presence or absenceof the stapedius reex contraction is an indirect mea-sure of the integrity of both the cochlear nerve (cranialnerve VIII) and facial nerve (cranial nerve VII) atthe level of the lower brainstem (Borg, 1973). Theintense acoustic stimulus must travel the reex arcintact through the cochlear nerve, along the auditorypathway to the level of the superior olivary complex to communicate with the nuclei of the facial nerve, sothat the stimulus will trigger a response from the sta-pedius muscle. There are several pathological lesionsthat can interrupt the normal acoustic reex circuit.For example, a lesion on cranial nerve VII or VIII canelevate the intensity level necessary for contraction oreliminate the muscle contraction altogether. Audi-ologists utilize a special instrument for testing the

acoustic reex, called an immittance meter .




Tympanic membrane

Tympanic(annular) sulcus

AnteriorPosterior

Roundwindow

Facial nerve

Lateralsemicircular canal

Facial nerve canal

Jugular vein

Eustachiantube

Stapes footplatein oval window

Promontory

Tensor tympani

AnteriorPosterior

A

BFigure 12-6 The middle ear cavity. Its contents are referenced by its walls in the various anatomical direc-tions. Illustrated are four views of the middle ear cavity. A . The tympanic membrane (TM) comprises the lateralwall. Looking into the ear canal, some structures of the middle ear cavity can be viewed through the transparentTM. (Reprinted with permission from Tank, P.W., Gest, T.R. (2008). Lippincott Williams & Wilkins atlas of anatomy. Baltimore: Lippincott Williams & Wilkins.) B . A view of the medial wall of the cavity with the TM, malleus, and incusremoved. (Reprinted with permission from Tank, P.W., Gest, T.R. (2008). Lippincott Williams & Wilkins atlasof anatomy. Baltimore: Lippincott Williams & Wilkins.) ( continued )




Chorda tympaninerve

Facial nerve

Incus

Malleus

Bony canal fortensor tympani

Tendon oftensor tympani (cut)

Eustachian tube

Typmanic membrane

D

Prominence of lateralsemicircular canalFacial nerve

Aditus to mastoid antrum

Prominence of canalfor facial nerve

Canal of tensortympani muscle

Stapedius tendonPyramidal eminence

Tympanicmembrane

Tendon oftensor tympani

Chorda tympani

Malleus

Epitympanic recess

Incus

Stapes

C

Stapes (removed)

Figure 12-6 (Continued ) C . Coronal section of the cavity facing the posterior mastoid wall. (Modied with permission from Moore,K.L., Dalley, 0A.F., Agur, A.M. (2009). Clinically oriented anatomy (6th ed.). Baltimore: Lippincott Williams & Wilkins.) D . Inside the middleear cavity looking laterally at the tympanic membrane. (Reprinted with permission from Tank, P.W., Gest, T.R. (2008). Lippincott Williams& Wilkins atlas of anatomy. Baltimore: Lippincott Williams & Wilkins.)




it does. Another signicant landmark on the posterior wall just below the level of the aditus is the pyramidaleminence of the stapedius muscle.

The inferior or jugular wall (i.e., the oor) of themiddle ear cavity is relatively unremarkable. It con-sists of a thin plate of bone which separates thetympanic cavity from the jugular bulb that lies just

beneath its surface. The superior wall, also called thetegmental wall or roof, is not known for any speciclandmark but is signicant in that only a thin plateof bone separates the middle ear cavity from the cra-nial cavity where the brain resides. Severe or chronicinfection in the middle ear space could lead to anabscess in this wall resulting in an infection invadingthe brain. From studying the areas surrounding themiddle ear cavity, it is obvious that complications ofrecurrent untreated infection can result in mastoidi-tis or brain abscess.

The remaining walls of the middle ear space havenumerous relevant landmarks. The anterior wall isnoted for the orice (i.e., entrance) of the Eustachiantube (ET) . The ET orice is bone that is continuous with the middle ear wall but the ET terminates inthe nasopharynx as cartilage. This structure will beexamined more thoroughly later. Parallel to the ETruns the tensor tympani muscle. The tensor tym-pani muscle and the orice of the ET are separatedby a thin curved projection or process of bone calledthe cochleariform process . The tendon of the tensortympani passes over this process as it exits the ante-

rior wall on its way to attach to the malleus, and indoing so it gains a little leverage when contracting theossicles. Running along the outside of the anterior wall is a portion of the carotid canal.

Within this area of the middle ear space, the facialnerve is housed in a bony canal. The canal runs fromthe anterior wall superior to the cochleariform pro-cess, then curves across within the medial wall andturns downward to exit deep into bone on the poste-rior wall. In this immediate area are three branches ofthe facial nerve. Two of the three deserve mention: thestapedial branch and the chorda tympani branch.

The chorda tympani conveys taste sensation from theanterior two-third of the tongue. It traverses the mid-dle ear cavity between the long process of the incusand the manubrium of the malleus. The stapedialbranch innervates the stapedius muscle. When otolo-gists perform ear surgery, they are careful to identifythe facial nerve canal as well as the branches of thefacial nerve. Surgeons try not to disturb the chordatympani although it can tolerate being displacedsomewhat during a procedure. The patient may expe-rience some odd metallic taste sensations during post-

operative recovery. The facial nerve canal is strictlyavoided during any surgical procedure. If the facialnerve is disturbed, the patient can suffer permanentfacial weakness or paralysis.

The medial wall, also known as the labyrinthine wall , contains landmarks related to the inner ear. Mostnotable is the oval window. The oval window separates

the air-lled middle ear cavity from the uid-lledcontents of the inner ear. The footplate of the stapesrests in the oval window in an anteroposterior orien-tation and is held in place by the annular ligament.There appears to be a greater degree of attachment ofthe footplate anteriorly than posteriorly. As mentionedpreviously, although the footplate is held in place bythe annular ligament, it does not adversely affect thevibratory action of the ossicular chain onto the oval window. The vibratory action appears to be more likea swinging gate rather than a plunger motion.

Why You Need to Know The stapes may become attached or “xed” to thesurrounding bone by abnormal bone growth. Thebone growth is not life threatening and often the onlysymptom is a roaring tinnitus and a resultant hear-ing loss. The condition, known as otosclerosis , is typi-cally identied using audiometry and immittancemeasures . The bone growth can be removed and aprosthetic device can be used to “replace” the stapes,thereby restoring the integrity of the ossicular chain.

A second structure leading to the inner ear (speci-cally the cochlea) is also located along the medial wallof the middle ear cavity. It is the round window . Theround window separates the middle ear cavity from thescala tympani , a duct within the cochlea. The round window is covered by a exible membrane. Vibra-tion of the stapes in the oval window compresses theuid within the cochlea, thereby creating a wave. Theinward movement of the stapes footplate is allowedbecause the round window membrane yields to theuid wave by bulging toward the middle ear cavity.

Between the oval and round windows is the promon-tory , a distinctive bulge in the wall created by the rst(i.e., basal) turn of the cochlea on the other side.

Superior to the oval window is the bony promi-nence of the lateral or horizontal semicircular canalof the vestibular system. The prominence is seen as abulge on the medial wall. The prominence is thin andcan be eroded with severe chronic middle ear diseasecausing infection to invade the vestibular system.The facial nerve canal (discussed earlier) runs acrossthe medial wall to exit on the posterior wall. It runs




between the lateral semicircular canal prominenceand the oval window.

Contained within the middle ear space are all theattachments that serve to suspend and balance theossicles. There are eight in all. Three ligaments sus-pend the malleus: superior, anterior, and lateral mal-leolar ligaments. The tendon of the tensor tympani

muscle also serves to suspend the malleus. The mal-leus is attached laterally to the TM. The incus is sus-pended in place by the posterior and superior incudalligaments. The stapes is suspended in the oval windowby the annular ligament and is also suspended by thetendon of the stapedius muscle. These attachmentsbalance the ossicles so that the rotational axis is verynear to the center of gravity (CoG). This arrangementallows the TM and ossicular chain to operate as a unit.The TM and ossicles initiate and cease vibration syn-chronously.

Eustachian Tube

The orice of the ET was mentioned as a landmark within the anterior wall of the middle ear cavity. It was named for the Italian anatomist and physicianEustachius who lived in the mid-1500s. The ET isthe passageway leading from the nasopharynx (justabove the soft palate in proximity to the uppermostregion of the pharynx) to the anterior wall of themiddle ear cavity. The ET opens to replenish the airin the middle ear cavity. For the middle ear to func-

tion optimally, the ET must equalize the air pressure within the middle ear and the “atmospheric” air pres-sure that inhabits the ear canal and impinges uponthe eardrum. Atmospheric pressure can vary greatly.For example, air pressure is much lower on Pike’s Peakin Colorado than in New Orleans, a city that is pre-dominantly below sea level. The ET allows humans to withstand these great variances in air pressure so thatthe hearing mechanism will function properly.

The middle ear portion of the ET (i.e., the orice) isopen and xed within the temporal bone. As one pro-ceeds toward the nasopharynx, the bone gives way

to cartilage (approximately one-third of its length isbone, with the nal two-thirds being cartilage). Wherethe bone transitions into cartilage, the ET becomesquite narrow in a region called the isthmus . The car-tilaginous portion of the ET normally remains closedat rest and opens by the action of two muscles—thelevator veli palatini and the tensor veli palatini .

The ET is approximately 35 mm (3.5 cm) in length inadults. The adult ET is angled downward and forwardto set at about a 45 ° angle. In children the tube is in amore horizontal position. As the child’s head grows, it

elongates and migrates into a more vertical position.The ET terminates in the nasopharynx where it is sur-rounded by lymphoid tissue known as the adenoids .

Why You Need to Know Based on work by researchers such as Brodsky andKoch (1993), it has been demonstrated that theadenoids can contribute to recurrent or chronic eardisease as they can harbor a chronic infection. Thetissue swells as it reacts to bacteria or other patho-gens. In children who have suffered multiple upperrespiratory infections (URIs), the adenoids are oftenvery large. The enlarged lymphoid tissue may blockthe nasopharyngeal opening of the Eustachian tube(ET). Since the ET passageway is lined with mucousmembrane, a URI can also cause inammationof the mucosa leading to further obstruction. Aninamed ET cannot open, and therefore cannot

equalize the air pressure within the middle ear tooutside atmospheric air pressure. The air pressurein the middle ear space then becomes negative bycomparison to outside air pressure. The negativeair pressure will cause the mucous membrane thatlines the middle ear cavity to secrete uid. The uid lls the middle ear space, negatively impacting theossicular chain by adversely affecting its ability tovibrate. A temporary conductive hearing loss is avery likely outcome of this condition.

The levator veli palatini and tensor veli palatini wrap around the cartilaginous portion of the ET. Thetwo muscles serve a dual purpose in that they assist inopening the cartilaginous ET as well as act upon thesoft palate (i.e., velum). It is not known exactly howthe muscles open the ET but many anatomists believethat the tensor veli palatini is responsible for dilation whereas the levator veli palatini pulls the cartilage ina medial direction along with the uvula.

When the ET opens, atmospheric air rushes throughto replenish the middle ear space. The ET can be forcedto open by the valsalva maneuver , but natural open-

ing of the ET takes place during yawning, swallowing,chewing or talking. At the same time the ET dilates,the soft palate is raised (primarily by the action of thelevator veli palatini) to block or separate the nasal cav-ity from the oral cavity. The raising of the soft palateshields the ET from food or drink in the oral cavityso that they are not injected into the nasal passageway and out of the nose and/or into the middle earcavity via the ET. The raising of the soft palate closes offventilation from the oropharynx and ensures that onlynasally inhaled air passes through to the middle ear.




Transformer Action of the TMand Ossicular Chain

It was previously discussed how the ear canal iscapable of amplifying an incoming pressure wave.Once again, thanks to physics, we will see how the

TM and the ossicular chain work together to furthercontribute to the amplication of the acoustic sig-nal. The purpose of the TM and ossicular chain is totransform the acoustic pressure waves that hit theTM into mechanical energy that in turn can be usedto set up hydraulic pressure waves within the innerear. When this transformer action takes place, the

net result is amplication of intensity of the incomingsignal of approximately 27 dB. While the middle ear istransforming the acoustic waves to uid waves, it isovercoming the resistance of the outside air to the u-id-lled inner ear. Because air and uid have differentdensities, there is an impedance mismatch betweenthe two mediums. Physics teaches us that for energyto ow with the least resistance (i.e., impedance) orthe least amount of energy loss, it must ow continu-ously through a similar medium. Air functions at aresistance of 41.5 ohms and cochlear uid at a resis-tance of 161,000 ohms, representing a differentialratio of 3880:1 (Wever & Lawrence, 1954). Obviously,the impedance properties of these two media are verydifferent. If the ear had no way of matching theseresistances (i.e., making the differences smaller), onlyone-tenth of 1% of the sound carried on the air pres-sure wave would pass to uid, whereas the remain-ing 99.9% would be reected back through the outerear. Therefore, one of the primary functions of theossicular chain is to act as a mechanical transformer.It accomplishes this in three very distinct ways: areaadvantage, curved membrane buckling , and lever

action .The area advantage is the largest contributor to thetransformer action of the middle ear.

As illustrated in Figure 12-7, one way to increasepressure is to decrease the area that the force is beingdistributed across ( pressure force/area ). The effec-tive vibrating area of the TM is 55 mm 2, whereasthe area of the oval window by comparison is about3.2 mm 2. This means that the area of the TM is 17 timeslarger than the area of the oval window. By focusingall the acoustic energy from the TM to a smaller area

Smaller area

Force ofTM vibration

Figure 12-7 The large vibratingarea of the tympanic membrane inrelation to the smaller vibrating areaof the oval window (pressureforce/area). (Modied with per-mission from Emanuel, D.C.,Letowski, T. (2007). Hearing science. Philadelphia: Lippincott Williams& Wilkins.)

Why You Need to Know Years ago, surgeons looked for a way to surgicallyrepair a poor functioning Eustachian tube. Allattempts failed. It did not appear that correction ofnegative middle ear pressure could be accomplishedby surgical intervention. Surgeons then began to

examine other ways in which negative middle earpressure could be alleviated. Pressure equalization(PE) tubes were rst developed to assist combatpilots in equalizing middle ear pressure. They arenow commonplace for children who suffer fromchronic Eustachian tube dysfunction. Complica-tions from middle ear disease occur less frequentlynow because the surgeon can bypass the dysfunc-tional ET by placing PE tubes through the tympanicmembrane to equalize pressure via the ear canal.

Why You Need to Know Chronic patulous (i.e., open) Eustachian tubes cancause a patient severe difculty. The patulous tubeacts as a sound conduit, directing our own vocaliza-tions and breathing up into the middle ear cavity.Patients have an awareness of these sounds (knownas autophonia ) as well as an awareness that theirtympanic membranes are vibrating with inhala-tion and exhalation (Mencher, Gerber, & McCombe,1997). This can be very disconcerting to thepatient. This condition may result from dramatic

weight loss or chronic use of decongestants. Histori-cally, physicians have not been very successful atrelieving patients’ symptoms.




(the oval window), pressure is increased considerably.The 17:1 size differential of the TM to the oval win-dow translates into an increase of acoustic pressure ofabout 25 dB (Bekesy, 1960).

The second variable in transformer action is curvedmembrane buckling, as illustrated in Figure 12-8.The TM does not vibrate as a whole unit. Instead, itvibrates in segments, with those portions that are leastanchored being more readily set into vibration. Thesegments of the TM closer to the annular sulcus andthe manubrium are more resistant to displacement.

The force displacing the TM is distributed in multiplesegments rather than being displaced in one largesegment. This action serves to increase pressure.

The last impedance matching function is accom-plished by the ossicular chain acting as a class 1lever. As Figure 12-9 shows, the efciency of a leveris increased when the pivot point is placed closerto the load being displaced. In this case the longleg of the lever is the manubrium, the pivot pointis the malleoincudal joint, the long process of theincus is the shorter section of our lever, and the loadbeing displaced is the stapes in the oval window. Inthe end, only a slight amount of pressure placed onthe manubrium is necessary to yield an increase inpressure at the oval window. This lever action effectadds an additional gain of 2 dB to the acoustic sig-nal (Wever & Lawrence, 1954). With all three trans-former variables acting together, the result is a gainof approximately 27 to 30 dB for the incoming signal. Any disease process or injury that might disrupt evenone of these events will result in a signicant loss ofhearing by adversely affecting the transformer actionof the middle ear.

STRUCTURES OF THE INNEREAR LABYRINTH

The inner ear is also referred to as the labyrinth because of its maze-like complex structure. It con-tains the end organs of two sensory systems: the ves-tibular system and the auditory system.

The inner ear is housed deep in the petrous portionof the temporal bone of the skull. As Figure 12-10 illus-trates, the inner ear itself is divided into three sections:(1) the cochlea of the auditory system, (2) the vestibuleof the vestibular system, and (3) the semicircular canals

Manubrium

Tympanic (annular) sulcus

Figure 12-8 Curved membrane coupling. The tympanic mem-brane vibrates in multiple segments.

F o r c e o

f T M

v i b r a

t i o n

A

B

D

C

Figure 12-9 The simple lever action advantage of the ossicularchain. A . Longer leg (manubrium). B . Fulcrum or pivot point(malleoincudal joint). C . Shorter leg (long process of incus).

D . Mass (stapes footplate in the oval window).

Vestibule

Cochlea

Round window

Oval window

Semicircular canals:Superior (anterior)Lateral (horizontal)Posterior

Cochlea

Auditory system

VestibuleSemicircular canals

Vestibular system

Figure 12-10 The two systems and the three sections of theinner ear. (Reprinted with permission from Tank, P.W., Gest, T.R.(2008). Lippincott Williams & Wilkins atlas of anatomy. Baltimore:Lippincott Williams & Wilkins.)




of the vestibular system. The entire inner ear, whetherthe vestibular system or the auditory system, is housed within a bony (osseous) labyrinth or capsule. Con-tained within the bony labyrinth is a chambered mem-branous, epithelium-lined channel. The membranouslabyrinth ts within the bony labyrinth and follows its

contours. This is mostly true for the vestibular system.However, as seen in Figure 12-11, the channels withinthe cochlea have a slightly different orientation. All ofthe channels found within both the bony and mem-branous labyrinths are lled with uid.

The two uids of the inner ear are perilymph andendolymph . Each uid has its own distinct chemis-try. Perilymph lls the channel formed between theouter wall of the membranous labyrinth and the inner wall of the bony labyrinth. Perilymph resembles thechemistry of extracellular uid, being high in sodium(Na ) and calcium (Ca ) and low in potassium (K ).Endolymph, the uid within the membranous laby-rinth, has a high potassium (K ) content and lowsodium (Na ) and calcium (Ca ) concentration. Theendolymphatic uids of the membranous labyrinthof the vestibular and auditory systems are intercon-nected by a series of ducts forming one continuousendolymph lled system—the ductus reuniens andanother small diversion, the endolymphatic sac . Theendolymphatic sac lies in a bony niche within the cra-nium. Nowhere do the endolymph and the perilymphuids of the two labyrinths communicate with oneanother.

Structures of the Vestibular System

Vestibule

The vestibule is the central egg-shaped cavity of theinner ear. The vestibule lies medial to the middleear, having the oval window as its lateral border. Sus-

pended within the perilymph is the vestibule’s mem-branous labyrinth. Within the membranous labyrinthare two end organs known as the utricle and saccule .

The saccule lies on the medial wall and is continu-ous with the cochlea. The utricle is the larger of thetwo and is continuous with the semicircular canals.The semicircular canals open into the utricle by wayof ve openings. The posterior and anterior semicir-cular canals share one opening at the common crus .Figure 12-12 shows a cutaway of the utricle and sac-cule exposing the receptor end organ called the mac-ula . The two maculae are oriented so that they are atright angles to each other. The macula of the utricleresponds to horizontal stimulation and the maculaof the saccule responds to vertical stimulation. Themajor role then of the utricle and saccule is to keepthe body vertically oriented with respect to gravityand linear acceleration.

The maculae contain biological sensors calledhair cells . Each hair cell is innervated by afferentnerve bers. The hair cells convert the stimulationfrom gravitational or linear forces into a synapse with the nerve bers that ultimately make up thevestibular portion of the vestibulocochlear nerve

Bony labyrinth

Endolymph duct

Endolymphatic sac

Scalatympani

Scalavestibuli

Cochlearduct

Saccule

Utricle

Membranous ampullaeSemicircular ducts: Superior

Posterior Lateral

Ductusreuniens

Common crus

Helicotrema

Endolymph

Membranouslabyrinth

Perilymph

Bony

labyrinth

Perilymph

Bony labyrinth

Perilymph

Membranous labyrinth

Endolymph

Vestibular system

Auditory system

Figure 12-11 The relationship of the bony labyrinth and the membranous labyrinth channels throughout the inner ear. The smallviews depict how the membranous labyrinth ts within the bony labyrinth of the vestibular system and how within the cochlea themembranous channel is pulled to one side with attachments to the bony labyrinth. These attachments divide the bony labyrinth into twosections, one above and one below the membranous labyrinth. (Reprinted with permission from Tank, P.W., Gest, T.R. (2008). LippincottWilliams & Wilkins atlas of anatomy. Baltimore: Lippincott Williams & Wilkins.)




(cranial nerve VIII). Hair cells are so named becausecilia project from their cell bodies. These stereocilia can number between 50 and 100 per hair cell. Theyproject from the cell body and are ordered to angleby height. There is one particularly tall cilium (calledthe kinocilium ) located on the perimeter of each haircell. Whether or not a hair cell is excited depends on

which direction its stereocilia are stimulated. Whenthey are bent toward the kinocilium the ring rateincreases and bending away from the kinociliumdecreases the ring rate to the vestibular nerve. Thelineup of hair cells within each macula is arrangedso that they lie in different directions. A single sheetof hair cells can detect motion forward and back andside to side. The maculae can therefore cover anymotion in a horizontal or vertical plane. The maculaestructure consists of a cluster of hair cell bodies withtheir stereocilia embedded in an epithelial gelatinousmembrane called the otolithic membrane . Situatedon top of the otolithic membrane are tiny calciumcarbonate crystals called otoconia . The hair cells arestimulated when linear acceleration in any direc-tion causes a weighted shift of the otoconia on theotolithic membrane mass. The otoconia provide theinertia, and the otolithic membrane mass drags onthe hair cells. Sudden changes in gravity such as tak-ing a fast elevator ride with a sudden stop at the topor even rapid acceleration in a sports car followedby a sudden stop will cause an individual to expe-rience this reaction. However, once you are moving

at a constant speed, again as in a car, the otolithscome to equilibrium and you no longer perceive themotion until you come to a stop.

Semicircular Canals

Arising from the utricle are three loops referred to asthe semicircular canals. The three semicircular canalsare oriented to different anatomical positions: poste-rior, anterior (i.e., superior), and lateral (i.e., horizon-tal). They are oriented spatially at right angles to eachother which allow them to respond to angular headmotion (e.g., head rotation). Each canal plane is per-

pendicular to the other canal directions, comparableto the relationship of two right angle sides and theoor of a cube. The canals on each side operate simul-taneously as if joined with the canals on the oppositeside of the head. The right posterior canal and the leftanterior canal, the right and left lateral canals, andthe left posterior and right anterior canals respondas a unit. Therefore, head rotation in any direction will stimulate a response from the appropriate pairedstructure. Each semicircular canal opens into the ves-tibule by a bulb-like expansion called an ampulla. Fig-ure 12-13 shows a cross section of the ampulla and its

Macula ofutricle

Macula of saccule

Otolithicmembrane

Otoconia

Hair cellbody

Supportingcells

Vestibularnerve fibers

Stereocilia

Direction forexcitation

Utricular macula

Saccular macula

A

B

C

Kinocilium

Figure 12-12 Structure of the vestibule of the inner ear. A . Thebony vestibule cut away to reveal the utricle and saccule. B . Struc-ture of the macula. C . Orientation of the macula within the utricleand saccule. (Reprinted with permission from Bear, M.F., Connors,B.W., Paradiso, M.A. (2006). Neuroscience exploring the brain (3rded.). Baltimore: Lippincott Williams & Wilkins.)




contents. Housed within the ampulla and lying per-pendicular to the long axis of the canal is the recep-tor end organ called the crista ampullaris . The cristacontains the vestibular hair cells and supporting cells.The stereocilia of the hair cells extend into a gelati-nous mass resembling a semipointed cap, called thecupula . When the head rotates in an angular motion,

ow of endolymph within the membranous labyrinthlags behind, pushing on the cupula and causing thestereocilia to bend. When the stereocilia bend in theappropriate direction toward the kinocilium, the cellbodies respond and send information via the vestibu-

lar branch of the vestibulocochlear nerve to the brain. When the stereocilia are pulled by endolymph owin a direction away from the kinocilium, there is anabrupt reduction in the information sent to the nervebers. Therefore, with head motion, the cupulae ofthe paired canals (e.g., the right anterior and left pos-terior) are displaced in a push–pull direction so that

one side is always being excited whereas the otheris always being inhibited. The push–pull informa-tion equals out and the signal is accepted. Dizziness,the inappropriate sensation of motion, is the brain’sresponse from an imbalance of the push–pull system.

Endolymph

AmpullaCupula

Stereocilia

Vestibularnerve fibers

Hair cells

B

Cupula

Stereocilia

Direction of movement

Supportingcells

C

A

Flow oflow ofendolymphndolymph

Flow ofendolymph

Haircell body

Nervefibers

Crista ampullarisFigure 12-13 Cross section of the ampulla (with the semicircular canals oriented to different anatomical directions). A . Each canalopens into the vestibule by a bulb-like expansion called an ampulla. (Reprinted with permission from Anatomical Chart Company.)B . Cross section view of the ampulla with the receptor end organ crista ampullaris exposed. (Reprinted with permission from Bear, M.F.,Connors. B.W., Paradiso, M.A. (2006). Neuroscience exploring the brain (3rd ed.). Baltimore: Lippincott Williams & Wilkins.) C . Endolymphow pushing on the crista. (Reprinted with permission from Anatomical Chart Company.)




Vestibular Nerve Pathway

The afferent nerve bers projecting from the vestibu-lar end organs collect to form Scarpa’s ganglion . Fromthis ganglion, the vestibular nerve courses throughthe internal auditory canal (IAC) (or meatus) of thetemporal bone to enter the brainstem at the pons-medullary junction , a deep groove that separates thepons from the medulla . This is the point of transitionfrom the peripheral vestibular system to the centralstructures of vestibular input. The central structures

consist of four major nuclei: the superior, medial, lat-eral, and descending. The adaptive process of the cen-tral vestibular system takes place in the cerebellum. Its job is to monitor and integrate vestibular, somatosen-sory and visual sensory input and make conscious andunconscious corrective motor adjustments.

Maintenance of the center of gravity (CoG) issensed by the integration of three systems—visual,vestibular, and somatosensory—and not one senseis solely responsible for the information. Visual inputis responsible for recognizing the horizon, and there-

fore needs an external reference for its sensations. Vestibular input is the result of an internal referenceto the sense of weight (gravity) on the macula dur-ing a resting position of the head. The somatosensoryinput gains information from an internal reference bythe orientation of one body part to another throughthe position and tone of skeletal muscles and the

pressure on the soles of the feet from a rm surface.There is no exact combination from the contributionof the three input systems. When there is an absencein either visual or somatosensory information, thevestibular system is utilized. The vestibular systemcan function independently of the two as its primaryinterest is controlling head and eye position. The vestibulo-ocular reex (VOR) is a reexive eye move-ment that stabilizes vision during head movement byproducing an eye movement in the direction oppositeto the head movement. (This reex is what allows usto read while jogging on the treadmill.) The semicir-cular canals detect the head rotation, which triggersa compensatory movement of the eyes. The VOR doesnot depend on visual acuity and works in total dark-ness or when the eyes are closed.

Why You Need to Know Benign paroxysmal positional vertigo (BPPV) isthe most common type of vertigo. Patients report aspinning sensation when lying down, rolling overin bed, bending down or looking up. Estimatesindicate that at least 20% of all patients who present

to the physician complaining of vertigo have BPPV(Foroehling et al.,1991). The disorder may result from an age-related degeneration of the mecha-nism. In individuals under the age of 50, it is moreoften associated with head trauma and is rarelyseen in children. For whatever reason, a few of theotoconia from a macula detach from the otolithicmembrane and are free to oat in the endolymphusually resting in the ampulla of the posteriorsemicircular canal. A change in head position cre-ates movement of the endolymph and the oatingotoconia. Their presence adds to the density of the

endolymph ow resulting in stimulation of thecupula which will, in turn, increase the neuronal ring rate of that canal and result in an exagger-ated perception of movement. It is believed that thesymptoms will subside if the otoconia can be coaxedback to the macula from where they came. This isattempted through a series of positioning maneu-vers called canalith repositioning treatment (CRT).For evidence-based practice on BPPV and canalithrepositioning treatment, refer to Froehling et al.(2000).

Why You Need to Know Vestibular rehabilitation therapy (VRT) is balanceretraining through physical therapy. As discussed inthe text, the maintenance of one’s balance involvesintegration from multiple systems; therefore, suc-cessful VRT requires a careful and thorough evalua-tion to identify the specic area(s) of weakness. Theexercises will target the particular decit(s) andretraining will take advantage of neural mecha-nisms in the brain for adaptation, plasticity, andcompensation. An audiologist will be involved in theevaluation of balance and hearing and maybe evenretraining therapy as VRT is within the audiologist’sscope of practice (as well as the scope of practice ofoccupational therapists and physical therapists).

Why You Need to Know Motion sickness is a result of the visual and soma-tosensory systems sensing different information. Thevisual system perceives motion but the somatosen-sory cannot conrm the motion; therefore, confu-sion of the integrated signal takes place. When thereis confusion in the interpretation, it is the vestibularsystem that contributes to the maintenance of thecenter of gravity for balance.




Structures of the AuditorySensory-Neural System

The anatomical structures of the cochlea and thecochlear nerve are known as the sensory-neural sys-tem as it houses the ne receptors that must sense andchange the acoustic signal into the neural informa-tion transmitted to the brain for the process we thinkof as hearing.

Cochlea

The cochlea is the inner ear organ of audition. Whilethe outer and middle ears comprise the mechanismfor conducting sound to the cochlea, the cochlea isthe mechanism that changes the acoustic signal intothe neural impulses that are transmitted to the brainfor the process we think of as “hearing.”

The cochlea is no larger in size than a pea but isamazing in its function. It is so complex that we donot completely comprehend its physiology and is soembedded in the dense temporal bone that access forthe purpose of research is very difcult. The cochlea’sposition in the head is oriented so that the apex isanterior and slightly lateral within the head pointingtoward the cheekbone. The bony labyrinth resemblesa snail’s shell coiled around itself between 2½ and 2 5 8 times before reaching its apex. The cochlea is 5 mmin height; at its base, it is 9 mm in width and taperstoward the apex. Figure 12-14 shows a cross sectionof the cochlea and its contents. The porous, perfo-

rated bony core of the cochlea is called the modiolus . The cochlea wraps around the modiolus from baseto apex. The perforated modiolus accommodates theblood vessels and nerve bers leading off from thehair cells. In its design, the modiolus adds protectionto the essential blood vessels supplying the cochleaand nerve bers also coursing through its center.

Housed within the bony labyrinth is its membra-nous channel known as the scala media (also knownas the cochlear duct ). The scala media conforms tothe shape of the bony cochlea so that it is also coiled.Uncoiled, the scala media measures approximately

25 to 35 mm in length. In looking at a cross section,the scala media does not oat within the perilymphof the bony labyrinth but rather a large section of thescala media is attached to the lateral wall of the bonycapsule. There are connections to the medial wall as well, dividing the interior of the cochlea into thirds.The boundaries of the scala media completely sepa-rate the bony labyrinth into two channels. Perilymphlls the space above and below the scala media. Thetwo bony channels surrounding the scala media meetat the apical end of the bony labyrinth with a small

opening at the apex called the helicotrema . Thisopening allows perilymph to be continuous through-out the bony channel even though there is a division.The upper channel is called the scala vestibuli andthe oval window forms its point of origination. Thelower channel is called the scala tympani and theround window is its point of termination.

There are two, less emphasized, uid pathways thatlead off from the inner ear structures. One leadingaway from the vestibule is the vestibular aqueduct(VA). Contained within the VA is a membranous saccontaining endolymph. The other aqueduct, termedthe cochlear aqueduct (CA), leads away from thebasal turn of the scala tympani only a few millimetersfrom the round window to the subarachnoid space ofthe brain. The CA contains perilymph since it origi-nates at the scala tympani. A commonly accepted viewabout the CA is that it allows transfer of perilymph tocerebrospinal uid (CSF). Perilymph has essentiallythe same chemical composition as CSF.

Why You Need to Know Enlarged vestibular aqueduct syndrome (EVAS) is identied as an inner ear bony malforma-tion causing a bilateral (and usually) progressivesensorineural hearing loss. The specic etiology isunknown, however, it appears to be the result of agene mutation but environmental factors have alsobeen suspected. The effect is that the membranoussac containing endolymph is much larger than nor-mal. EVAS is diagnosed by high-resolution radio-logical scans that show the enlarged aqueduct.

The scala media contains the receptor end organof hearing, the organ of Corti (see Figure 12-14). Thelateral wall of the scala media is attached to the bonylabyrinth by the spiral ligament . The medial or modi-olar attachment of the scala media is the osseousspiral lamina . The spiral lamina consists of two thinplates of bone. There is a space between the two lay-

ers of the lamina where the nerve bers course and iscalled the habenula perforata .

Joining the spiral lamina is the basilar membrane(BM) ( also known as the cochlear partition ). The spi-ral ligament reaches out to meet the BM, completingthe oor. The organ of Corti rests on the membrane.The spiral ligament, a band of exible connective tis-sue, afxes the BM to the lateral wall of the bony laby-rinth. When displaced, the membrane pivots at thepoint where it attaches to the spiral lamina. Togetherthe BM and the spiral lamina run the entire length of




Cochlearbranch of thevestibulocochlearnerve (VIII)

Spiral ganglion

Spiral lamina

Scala vestibuli

Scala media(cochlear duct)

Modiolus

Spiral ganglion

Spiral lamina

Scala vestibuli

Scala tympaniBasilar membrane

Organ of Corti

Stria vascularis

Scala media(cochlear duct)

Reissner’smembrane

Tectorialmembrane

Inner hair cells

Tectorial membrane(drawn transparently sothe structures beneathcan be viewed)

Stereocilia

Outer hair cells

Hensen’s

cells

Basilarmembrane

Nervefibers

Inner/outerpillar cells

Deiter’scells

Cells ofclaudius

A

B

C

Spirallimbus

Spiral ligament

Scala tympani

Oval window

Tunnelof Corti

Figure 12-14 Cross section of the cochlea. A . Coiled around the bony core the cochlea protects its nerve bers. B . The mem-branous labyrinth divides the bony labyrinth into two sections: the scala vestibuli above and the scala tympani below. The scalamedia houses the receptor end organ of hearing. C . The structures of the organ of Corti rest on the basilar membrane. (Reprintedwith permission from Gartner, L.P., Hiatt, J.L. (2009). Color atlas of histology (5th ed.). Baltimore: Lippincott Williams & Wilkins.)




the cochlea, separating the scala media from the scalatympani. The cochlea and spiral lamina are wider at thebase than the apex, whereas the BM (cochlear parti-tion) runs just the opposite, being narrower at the baseand wider at the apex. Because of this arrangement,the BM is under considerable tension at the base but isrelatively accid at the apex. The physical characteris-

tics of the BM play a critical role in the process of audi-tion allowing for passive tuning of the high frequenciesat the base and low frequencies at the apex.

Reissner’s membrane forms the superior wallof the membranous labyrinth. It projects obliquelyacross the scala media to attach to the lateral wall ofthe duct. This attachment serves to separate the scalamedia from the scala vestibuli above. The stria vascu-laris extends along the lateral wall of the scala mediafrom Reissner’s membrane to the basilar membrane.The stria vascularis is a highly vascularized layer ofepithelium thought to produce and maintain thechemical balance of the ions (in particular potassium) within the endolymph of the scala media.

Organ of Corti

The organ of Corti, named for the Italian anatomistCorti during the mid-1800s, is the end organ for hear-ing and rests on the BM. Acoustic energy that wastransformed into mechanical energy by the middleear will be further transformed into electrochemicalneural information by the organ of Corti. The basicstructure includes two types of sensory cells and many

supporting cells. Supporting cells include the inner and outer pillar cells . The arrangement of the pillarcells is in rows which are wide apart at their base andmerge together at their apices dening the triangulararea called the tunnel of Corti , which is lled with itsown uid called cortilymph . The base for the pillarcells is on the BM and is broad and supportive.

On the modiolar (i.e., medial) side of the pillar cellsis a single row of sensory inner hair cells (IHCs) . Onthe lateral side of the pillar cells are three rows of sen-sory outer hair cells (OHCs) . The IHCs and OHCsare held in place by a complex network of supporting

cells. The structure and arrangement of Deiters’ cells cradle the base of the OHCs and send phalangeal pro-cesses to the surface to intermesh forming the roofof the organ of Corti. The tight meshwork is knownas the reticular lamina . It forms a tight seal to theendolymphatic space. Hensen’s cells are tall colum-nar cells adjacent to the last row of Deiters’ cells. TheHensen’s cells also lend their support to the OHCsand support the tectorial membrane . Claudius’ cells are cube-shaped cells that rest on the BM and ll thespace between Deiters’ cells and the base of the stria

vascularis (Claudius, Deiters, and Hensen were 19thcentury German anatomists). The Claudius cells alsoadd strength to the BM. The spiral limbus is a moundof connective tissue that rests on the spiral lamina. Itprovides the medial attachment for Reissner’s mem-brane and the tectorial membrane.

The tectorial membrane is not really a membrane,

but rather a gelatinous ap composed of collagen andproteins (Steel, 1983). The membrane projects radiallyacross the organ of Corti. It has the capability of pivot-ing from its medial attachment to the spiral limbus. Itsfunction is to provide the mechanical shearing (pushor pull) of the stereocilia of the OHCs. The stereociliaof the OHCs, particularly in row 1, are embedded in itsinferior surface. It is signicant to note that the IHCsare not embedded in the tectorial membrane. Endo-lymph lls the space between the tectorial membraneand the reticular lamina. As seen in Figure 12-15, thedifferent hinge points for the tectorial membrane andthe BM lend to the mechanical stimulation of theOHCs. The IHCs are disturbed by the drag imposedon them from the surrounding uid.

Basilarmembrane

Stereocilia

Displacement force ofbasilar membrane

Outer haircells

Stereociliabending

Tectorial membrane

Reticularlamina

Inner haircell

Pivot point for tectorial membrane

Spirallamina

Turbulent flowof endolymph

Figure 12-15 The action of the tectorial and basilar mem-branes on the outer hair cells. The inner hair cells are stimulatedby the turbulent ow (i.e., drag) of the endolymph. (Reprintedwith permission from Bear, M.F., Connors, B.W., Paradiso,M.A. (2006). Neuroscience exploring the brain (3rd ed.). Baltimore:Lippincott Williams & Wilkins.)




The two types of receptor hair cells, inner and outer,are different from each other in several physical ways.The IHCs are “ask” or “tear drop” shaped whereasthe OHCs bodies are more cylinder or test tube like inshape. The single row of IHCs numbers approximately3500 cell bodies and the three to four rows of OHCsnumber approximately 12,000 to 13,000 cell bodies

(Retzius, 1884, as cited in Hudspeth, 1989). Geisler(1998) discovered that the length of the OHCs variesdepending on its location along the tuned BM. As onecould anticipate, the hair cells are shorter at the baseof the BM than the hair cells arranged along the low-frequency tuned apex of the BM. Tilney, Tilney, andDeRosier (1992) reported that the stereocilia project-ing from the apical surface of the auditory hair cellsare organized into bundles and rows of graded lengths.Both the IHC and OHC bundles lack the tall kinocil-ium seen with the vestibular hair cells. The pattern ofthe stereocilia bundle on the IHCs forms a shallow “U”shaped row, whereas the pattern of the stereocilia bun-dle on the OHCs resembles a “W” or “V.” Stereocilia ofboth cell types are shorter and more numerous at thebase of the cochlea than they are at the apex. Maxi-mum numbers seen at the basal end reach approxi-mately 150 per cell body. The number of stereociliatapers off toward the apical end of the cochlea, wherethere are approximately 65 to 70 per OHC. The shorterstereocilia are linked laterally ensuring that when theyare disturbed, they move more or less as a unit.

The IHCs and OHCs function very differently. The

IHCs selectively respond to the various frequencies ofan incoming signal. Their shallow U-shaped stereo-cilia bundle lends itself to stimulation by the ow ofendolymph. The OHCs, on the other hand, contain anunusual structural characteristic usually associated with muscle cells and the chemical makeup to changeshape. Both factors enable the OHCs to be motile ,meaning they can shorten or lengthen in response tobeing stimulated or inhibited (Pickles, 1988). Dam-age to the hair cells results in a permanent sensoryhearing loss. The most likely cause of hair cell death isfrom excessive noise exposure. Because the cochlea is

unable to generate new hair cells, damage is irrevers-ible. It is interesting however that hair cell regenera-tion is possible in all vertebrates except mammals.

Experimental evidence demonstrated that Bekesy(1960) was correct in describing the mechanical char-acteristics of the BM and its passive contribution tothe tuning of the incoming acoustic signal. The BMacts like a mechanical resonator, varying in thickness, width, and stiffness. It is thinner, narrower, and stifferat the base making it more resonant to high-frequencyvibration. At the apex, the BM is thicker, wider, andmore accid, making it more resonant to lower fre-

quencies. The process of audition begins when theuid within the cochlea is disturbed by the vibrat-ing stapes in the oval window. As illustrated in Figure12-16, the vibration of the stapes creates a uid wavethat travels from the base to the apex. There is mini-mal displacement of the membrane until it reachesthe point where its physical characteristics are mostreceptive to the stimulus frequency. In other words,the area of maximum membrane displacement cor-responds to the frequency of the stimulus and to thetuning of the hair cells of the organ of Corti.

In addition to the passive mechanical contribution

of the BM, researchers beginning with Dallos (1992)described an active contribution the hair cells make inthe analysis of the incoming signal. He revealed thatthey too resonate best at select frequencies. The IHCsand OHCs play different roles in their contribution.The IHCs are necessary for frequency coding. TheIHCs are not embedded in the tectorial membraneand therefore must rely on the strong turbulence ofendolymph around their stereocilia for their displace-ment and subsequent excitement. The ow of endo-lymph alone is not strong enough to disturb the IHCs

Why You Need to Know Cotanche (1987) and others discovered in the mid-1980s that mature birds exposed to loud noise or oto-toxic drugs like antibiotics, in as little as 28 days wereable to regenerate and replace dead hair cells andreturn their hearing to near normal levels. Within the

avian cochlea at least, the secret seems to be in thesupporting cells reentering the cell cycle after injuryto regenerate into hair cells complete with stereo-cilia. Researchers Stone and Cotanche (2007) haveinduced cell division in the inner ear of mice, guineapigs, and rats using a variety of growth-promotingmolecules. They have also discovered one gene (butthere are probably more) that is responsible for “turn-ing off” the production. Researchers such as Staecher,Praetorius, Kim, and Douglas (2007) have been mostsuccessful in restoring hair cells for the vestibularportions of the inner ear. They know that it is morethan knowing how to manipulate the inhibitorygenes to control for the appropriate number of cellsin the inner ear but also how to keep the cells aliveand functional. It is exciting to think that someday(perhaps in the next 10 to 15 years) there may be atreatment for sensory hearing loss in humans.




until the intensity of the stimulus is above approxi-mately 40 dB SPL. The OHCs contribute to hearingsensitivity for less intense sounds. Remember, thedifference in the pivot points for the BM and the tec-torial membrane contributes to the shearing actionof the OHCs. A 40 dB sound is fairly quiet; however,it will still displace the BM so that the OHCs becomesheared. The shearing causes the OHCs to react,pulling on the tectorial membrane. The “tightening” ofthe tectorial membrane modies the tectorial–reticularlamina spatial relationship. The result is the constric-tion of the ow of endolymph causing the turbulentow necessary to stimulate the IHCs. Therefore, themotile activity of the OHCs adjusts the mechanicsof the organ of Corti so that the IHCs can react toless intense stimuli, providing the minute frequencycoding. The OHCs act as the “cochlear amplier”providing the necessary sensitivity for humans tohear soft level sounds (Zwislocki, 1990). At the reso-

nate frequency of the hair cell, threshold is easilycrossed generating a response. A hair cell can bestimulated at frequencies other than its resonantfrequency, but the threshold must be greater thanthe one required to stimulate the hair cell at its ownselect frequency.

Neural Pathways

All cochlear hair cells receive both afferent (i.e., sen-sory) and efferent (i.e., motor) innervation; however,the majority of bers are afferent. This section willprovide a discussion of the afferent and efferent audi-tory pathways as they relate to the process of hearing.The central processing of auditory information withinand between the two cerebral hemispheres was cov-

ered in Chapter 4.

Neurotransmission

The hair cells are innervated by no less than 30,000nerve bers. Before joining with the bers of theIHCs, the nerve bers that connect to the OHCscourse through the tunnel of Corti. Together they movethrough the habenula perforata. The nerve bers carryinformation along their peripheral processes to thespiral ganglia . The nerve bers are unmyelinated inthe region between their endings on the hair cells

Pressure waveScala vestibuli

Reissner’s membrane

Helicotrema

Scala media(endolymph)Basilar membraneScala tympani

(perilymph)

Round window

Stapes

Figure 12-16 The cochlea uncoiled to demonstrate the place of maximum displacement along the basilar membranefor a pure tone.

Why You Need to Know Otoacoustic emissions (OAEs) are acoustic sig-nals generated by normal functioning OHCs. The

OHCs spontaneously generate the emission as theyexpand and contract to incoming acoustic stimula-tion. These emissions can be detected by inserting atiny microphone into the ear canal. A mild hearingimpairment typically begins as a loss of the motileability of the OHCs. Consequently, evoked OAEsprovide audiologists with a useful clinical tool in

the evaluation of cochlear function.




and the habenula perforata but become myelinatedas they pass through the internal auditory canal (IAC).

For the OHCs, the neural information is a product ofthe shearing action of the tectorial membrane. For theIHCs, the neural information is a product of the turbu-lence created in the ow of the endolymph. Althoughthere are approximately three times as many OHCs asIHCs, the OHCs send only 5% of the afferent informa-tion along the cochlear nerve. The IHCs send 95% ofthe afferent information. Each IHC communicates with as many as 10 to 18 ganglion cells (see Figure12-17). The remaining 5% of peripheral nerve bersbranch with as many as 10 to 50 OHCs (this is a rela-tively small number of afferent nerve bers spread outover a relatively large number of OHCs) (Spoendlin,1974).

The process known as transduction , the changing(i.e., transforming) of mechanical vibrations from theBM into neural information, occurs at the level of thehair cells. Endolymph is rich with the positivelycharged ions potassium and calcium. Endolymph hasa resting potential (the voltage potential present withno stimulation) of 100 millivolts (mV) to 80 mV(Tasaki & Spiropoulis, 1959). Therefore, the scalamedia has a strong positive potential called the endo-

cochlear potential (EP) . Transduction is dependenton the intracellular resting potential of the hair cells,

which are about 40 mV for the IHCs and 70 mV forthe OHCs (Dallos, Santos-Sacchi, & Flock, 1982). Thepositive resting potential of endolymph and the nega-tive resting potential of the hair cells yield a very largevoltage potential difference of 120 to 150 mV depend-ing on the cell type. As described by Hudspeth (1989), when a stimulus is delivered a mechanical gate on thestereocilia is opened. As seen in Figure 12-18, the tiplinks reach up from the top of the shorter cilia to theside of the adjacent taller cilia. This arrangementallows them to be stretched much like a spring to opena gate (Pickles, Comis, & Osborne, 1984). With the gatenow open, a route is provided for the higher concen-tration of potassium (K ) in the endolymph to owtoward the lower concentration within the hair cells. As a result of the ow of potassium, the EP shifts nega-tively from its highly positive charge (the oppositepositive and negative charge differences want to bal-ance). The EP shifting of a positive charge is termeddepolarization . Depolarization activates channelopening along the lateral cell membrane. These chan-nels allow for the inux of calcium and the efuxof potassium from the hair cell. The inux of

C o n t r a l

a t e r a l

Outer hair cells

Innerhair cell

Ganglion cell

Cochlear nerve

Ganglion cells

Medial superiorolive(MSO)

Lateral superiorolive (LSO)

Superior olivarycomplex (SOC) Afferent

Efferent olivocochlear pathway

Figure 12-17 There are several differences in the inner and outer hair cells, from shape to innervation pattern. Theinner hair cells send 95% afferent information to the cochlear nerve. The outer hair cells receive 95% crossed efferentinformation from the olivocochlear bundle.




calcium triggers the release of the neurotransmitter glutamate into the nerve terminals in contact withthe hair cell base. The diffusion of the neurotransmit-ter across the terminal triggers an action potential tobe propagated down the nerve bers. For a splitmoment, the shifting of the ion concentrations withinthe hair cells causes the cell to be hyperpolarized . When a cell is in a state of hyperpolarization, it isunable to be stimulated. It is not until it regains itsresting potential that it is again ready to respond. Dur-ing the action of transduction, the ion balance withinthe endolymph is shifted dramatically. It is the func-

tion of the stria vascularis to return the endolymph toits resting (potassium, sodium, and calcium) balance(Pickles, 1988).

The act of transduction is triggered by the fre-quency of the sound that causes the point of maxi-mum displacement along the passive BM. Researchershave also examined the intensity level necessary tobring about depolarization (Dallos, 1992). The dis-placement of the membrane increases in magnitudeas the stimulus intensity increases. A tuning curve (see Figure 12-19) is a graph of the intensity levelnecessary to trigger (i.e., reach threshold) the hair

A

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Hair cells (–40 mV forIHCs and –70mV forOHCs)Perilymph

Scalatympani

Scalavestibuli

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+80 mV

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Figure 12-18 Depolarization of a hair cell. A . Tip links are stretched to open the potassium (K ) channels. B . Depolarization servesto open the calcium (Ca ) channels, releasing the neurotransmitter. C . Endocochlear potential: strong positive potential, negativeintracellular resting potential. (Reprinted with permission from Bear, M.F., Connors, B.W., Paradiso, M.A. (2006). Neuroscience exploring thebrain (3rd ed.). Baltimore: Lippincott Williams & Wilkins.)




cell response to an input stimulus. The greater theintensity level, the broader the range of frequen-cies whose thresholds are crossed (i.e., the broaderthe shape of the graph). The broadness of the BMresponse to high intensities decreases the frequency

selectivity. The increase number of hair cells that arestimulated creates a greater neural response from thecochlear nerve. In contrast, for less intense stimuli,a response is seen at a limited range of frequencies where threshold is crossed. The magnitude of BMdeection is limited. There is progressively less andless membrane deection as the intensity of a soundincreases.

Once threshold has been crossed and depolar-ization takes place, impulses (i.e., action potentials)travel down the peripheral processes of the nervebers to the spiral ganglion and continue along until

they enter the brainstem. As soon as the bers col-lect at the exit point from the cochlea’s modiolus theyform the cochlear branch of the vestibulocochlearnerve (cranial nerve VIII). Yost (2000) reviewed thetonotopic organization of the cochlear branch of cra-nial nerve VIII. He noted the bers originating fromthe apex of the cochlea form the core or center ofthe branch. The outer layer originates from the basalend of the cochlea and twists around the core, whichmeans that the high-frequency bers twist aroundthe low-frequency bers.

Afferent Auditory Pathway

The cochlear branch of the vestibulocochlear nervemerges with the vestibular branch that has bundledfrom the nerve bers of the ampullae, saccule, and utri-cle. The two branches maintain their separate identi-ties but combine to become cranial nerve VIII. Cranialnerve VIII meets cranial nerve VII (the facial nerve) totravel through the internal auditory canal (IAC). The

cochlear branch occupies a position beneath the facialnerve and to the side of the vestibular nerve.

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Figure 12-19 Tuning curve for a 3000 Hz tone. The 3000 Hztone seen along the basilar membrane at the point of maximumdisplacement.

Why You Need to Know Auditory neuropathy (AN), or to be more exact audi-tory dys-synchrony (AD), is an unusual hearing dis-order that is primarily a timing decit affecting thenormal synchronous activity of the IHCs or the audi-tory nerve (Zeng et al., 1999). The OHC function is

unaffected. The degree of hearing loss is not predict-able and may even uctuate from day to day. Theneural dys-synchrony causes speech understandingdifculties that are worse than can be predicted fromthe pattern of hearing loss. Amplication unfor-tunately has minimal benet in improving speechdiscrimination. Sign language may be necessary for language learning. Identication of auditorydys-sychrony is a diagnosis of exclusion. Otoacousticemissions are present; however, evoked potential[auditory brainstem response (ABR)] testing of theauditory pathway is abnormal as well as the middle

ear muscle reex. Radiologic evaluations are normalas there is no obvious lesion.

Why You Need to Know The IAC is a site for the growth of a benign Schwan-noma neuroma that tends to arise from the ves-tibular nerve but with time will encroach on thecochlear nerve. The neuroma is contained withinthe narrow meatus and therefore quickly com-presses on the nerve causing unilateral symptomssuch as balance disturbances, tinnitus, and hear-ing loss. Remembering the tonotopic organizationof the cochlear nerve, a lesion will initially resultin a high-frequency hearing loss. An undiagnosedneuroma may grow large enough to affect the midto low frequencies and compress on the facial nerve(cranial nerve VII) causing facial paresis.

Figure 12-20 illustrates the auditory pathway. Alesion along the auditory pathway (e.g., a Schwan-noma or acoustic neuroma ) creates a retrocochlearhearing loss. Audiometrically, a retrocochlear hear-




from the cochlear nucleus but bypassed the superiorolivary complex. The second- and third-order neu-rons may terminate at the lateral lemniscus or con-tinue to the inferior colliculus at the dorsal midbrain.The majority of neurons will synapse at the inferiorcolliculus. The inferior colliculus has a large bundleof nerve bers that cross to communicate with the

nucleus on the opposite side. A commissural tractallows the two inferior colliculi to communicate witheach other. Interaural time and intensity differencesoccur at this level, playing a role in auditory localiza-tion. Fourth-order neurons leave the inferior collicu-lus to terminate at the medial geniculate body of thethalamus. The third-order neurons that bypassed theinferior colliculus will terminate here. In other words,all ascending (i.e., afferent or sensory) neurons willhave a nal synapse at this subcortical level beforeproceeding to the auditory cortex. The nal destina-tion of afferent bers is Heschl’s gyrus (also referred toas the anterior and posterior transverse gyri), which isfound within the superior temporal gyrus along thetemporal lobe of the cerebrum (Brodmann areas 41and 42) in both hemispheres. The frequency organi-zation of the cochlea is preserved along the pathwayand in bands across the cortical surface of the supe-rior temporal gyrus. The orderly representation isknown as tonotopic organization . Researchers (e.g.,Troost & Waller, 1998) have demonstrated the tono-topic organization of the medial geniculate body in which low frequencies are represented laterally and

high frequencies are located medially in the principaldivision. The peripheral auditory mechanism is thesite for the detection of sound but it is the central cor-tical level that is the location for conscious processingof sound that we refer to as “hearing.”

Binaural representation is critical in the processingof acoustic information. It is used for localization as indetecting the origin of a sound. The interaural acous-tic information is processed for time, intensity, andfrequency characteristics. The differences are con-veyed throughout the pathway to the auditory cortex.Damage to the pathway, after the point of binaural

representation, usually has no effect on the detectionof sound, thanks to the redundancy of informationbeing sent to the brain. Hearing loss (a detection ofimpaired frequency and intensity of sound) is theoret-ically only caused by damage to the outer and middleear, cochlea, or cochlear nerve. Auditory processing isthe brain using the frequency, intensity, and patternof sounds (speech in particular) that our ears detect(the brain using what the ear hears). A lesion alongthe auditory cortex interferes with the processing ofspeech creating a central hearing loss. This is mostobvious when the speech signal is in competition withor imbedded in background noise. The individual hasan inability to lter out competing auditory signals. A central auditory processing disorder (CAPD) isthe result of a central hearing loss. For the most part,auditory processing works ne in simple face-to-faceconversation in a quiet environment. However, whenthe system is stressed, as when trying to conversein the presence of background noise or listening toinstruction while the teacher walks around a largereverberant classroom, a lesion in the system willbecome apparent and the auditory information will

be misunderstood or missed altogether. Many sitescan be at fault for a central hearing loss: a decit in theinterpretation of the signal; disruption in the redun-dant auditory pathway; or lack of communicationbetween the two auditory cortices. The prevalence ofCAPD in children is estimated to be between 2% and3% (Chermak & Musiek, 1997) with it being twice asprevalent in males than females. It often coexists withother disabilities. These include speech and languagedisorders or delays, learning disabilities or dyslexia,attention decit disorders with or without hyperac-tivity, and social and/or emotional problems. Testing

for CAPD is complicated and time-consuming. Dueto neuromaturation of the central auditory nervoussystem, assessment of children under age 7 is notrecommended due to the high degree of variabilityin their performance. After an extensive case historyand assessment is completed, specic suggestions formanagement will be shared. Keep in mind this is not aperipheral loss so traditional amplication is not thetreatment. CAPD management is usually in the formof an auditory training program and phonologicalawareness training, therapy for any existing language

Why You Need to Know Auditory brainstem response (ABR) audiometryrefers to the measurement of the electrical poten-tial of the auditory pathway as it passes throughthe different levels of the brainstem. The responsesare elicited by an auditory stimulus. Test admin-istration and interpretation are performed by anaudiologist. The signal travels along the auditorypathway from the cochlear nucleus to the inferiorcolliculus. The elicited response can be measuredby surface electrodes. The response normally occurswithin a 15-millisecond time period after a stimu-lus is presented. ABR audiometry is considered aneffective tool in the evaluation of hearing loss andsuspected retrocochlear pathology.




and/or behavior decits, and methods for improvingthe quality of the incoming signal. This can be accom-plished with the use of a personal auditory trainer toenhance the signal (e.g., the teacher’s voice) over therandom background (e.g., other sounds in the class-room), thereby improving the signal-to-noise ratio.

Efferent Auditory Pathway

All the information from the peripheral hearingmechanism is carried along the afferent pathway tothe cortex for processing. The efferent pathway is the way the brain communicates information down tothe peripheral structures. The olivocochlear pathway (refer back to Figure 12-17) carries efferent informa-tion from the olivocochlear bundle (OCB) in the supe-rior olivary complex in the brainstem to the hearingmechanism.

Guinan, Warr, and Norris (1983) described two mainolivocochlear pathways, one crossed and the otheruncrossed. The uncrossed pathway originates from thelateral superior olivary complex (LSOC) and consistsof unmyelinated bers that terminate on the affer-ent bers of the IHCs. The OHCs receive few of thesesame uncrossed bers. The crossed pathway originatesfrom the medial superior olivary complex (MSOC).These bers are myelinated and terminate directlyon the OHCs. The role of the efferent pathways (bothcrossed and uncrossed) is believed to be the produc-tion of inhibitory effects. Information along the efferentpathway seems to inhibit the OHCs’ ability to amplify

the BM motion. It is believed that this function furtherfacilitates the active tuning effect of the hair cells.

Middle Ear Muscle Reex Arc

The auditory pathway described above has beenrelatively simplied into the major afferent andefferent tracts. There are many lesser tracts thatreceive stimulation from the cochlear neurons thatenter the brainstem. The middle ear muscle reexarc deserves discussion as its presence or absenceis used clinically as an indicator for site of lesion .Borg (1973) described the middle ear muscle reex

as being dependent upon contraction of the stape-dius muscle in response to loud sounds. An intensesound (e.g., 70 to 110 dB HL) presented to either ear will illicit a contraction of the stapedius muscle in

both ears and therefore can be measured in eitheran uncrossed (i.e., ipsilateral) or a crossed (i.e., con-tralateral) condition. The sensory component of thereex arc is provided by afferents of the cochlearportion of the vestibulocochlear nerve (cranial nerve VIII). The motor component of the reex is providedby efferent nerve ber tracts of the facial nerve (cra-

nial nerve VII). The reex is initiated by a stimulusthat is carried to the brainstem by cranial nerve VIII.Once in the brainstem, the afferent bers travel tothe ventral cochlear nucleus, synapse, and then go tothe superior olivary nucleus on the ipsilateral side. A portion of the bers at the superior olivary com-plex will continue through and cross to the oppositesuperior olivary nucleus and synapse. Now both theipsilateral and contralateral superior olivary nucleihave received communication from the stimulusear. The arc continues from both the ipsilateral andcontralateral sides to send efferent information backdown to the motor nucleus of the facial nerve (cranialnerve VII). The synapses at the motor facial nucleus will then send an impulse out to elicit a contractionof the stapedius muscles. When measured in healthy,normal-hearing ears, the reex is roughly symmetri-cal so that when either ear is stimulated, the reex will appear on both sides.

Summary

The anatomical ear is easily divided into the two func-tional systems related to hearing and balance. Theanatomical structures of the two systems were identi-ed and the function or physiology of the structures was discussed. The next step in your education is tolearn how disease, injury, and genetics can disruptthis normal function to result in a hearing or balancedisorder. Proper identication of a disorder is criticalin determining what treatment options are available(e.g., surgical vs. medical). Clinicians who specializein the identication of hearing or balance disordershave a fond appreciation of the anatomy and physi-

ology of the hearing and balance system. In the nextchapter, you will learn how diseases and other dis-orders of the auditory system can negatively impacthearing and balance.



Knowledge Outcomes for ASHA Certication for Chapter 13• Demonstrate knowledge of the developmental and life span bases of the basic human commu-

nication processes (III-B)• Demonstrate knowledge of the etiologies of receptive and expressive language disorders (III-C)• Demonstrate knowledge of the etiologies of hearing disorders (III-C)

• Demonstrate knowledge of the characteristics of hearing disorders (III-C)• Demonstrate knowledge of the prevention of hearing disorders (III-D)

Learning Objectives• You will be able to list the ve cardinal signs of ear pathology and refer them back to the

client’s chief complaint.• You will be able to differentiate the clinical characteristics of common ear pathology.

• You will be able to discuss the communicative impact of ear pathology.• You will be able to identify genetic and environmental hearing disorders.• You will be able to recognize the clinical characteristics of congenital syndromic and nonsyn-

dromic hearing disorders.

CHAPTER 13

Pathologies Associated withthe Auditory/Vestibular System

327


dys- bad, difcult dys function

-gram a record or picture audio gram

-itis inammation ot itis media

-metry process of measuring audio metry

-oma tumor cholesteat oma

os-/osseo-/osteo- bone osseo us labyrinth

oto- relating to the ear oto scope

-otomy to cut into myring otomy

-plasty the surgical formation of tympano plasty

-sclerosis a hardening of oto sclerosis

-scopy to look into oto scopy



328 PART 6 ANATOMY, PHYSIOLOGY, AND PATHOLOGIES OF THE AUDITORY/VESTIBULAR SYSTEM

Introduction

Anatomy can best be learned when the physiology(i.e., function) of the mechanism is taught in parallel.Included in the anatomy section was a smattering ofpathology to demonstrate how pathogens, disease,trauma, and genetic aberrations affect the delicate,intricate function of the ear. This chapter will proceed toelaborate on common congenital anomalies and movethrough acquired pathologies of the outer, middle, andinner ear. There are complete texts on hearing disor-ders but at the conclusion of this chapter you will beable to demonstrate knowledge of the characteristicsand etiologies of some of the more common hearingdisorders. Hearing losses are caused by lesions , whichby denition are changes in either the structures and/or function of the auditory mechanism due to injury ordisease. The patient with a hearing loss seeks treatment

or assessment from an otologist (i.e., ear physician) orotolaryngologist , (i.e., ear, nose, and throat physician orENT). The hearing loss may be the chief complaint ormay, as in the case of a draining ear, be a secondarycomplaint. The clinician (physician or audiologist) willbegin the examination by taking a case history. Accord-ing to Jafek and Barcz (1996), the case history shouldinclude questions that are identied as the ve “cardi-nal signs” of ear pathology. The patient’s responses willhelp identify the presence of ear pathology:

1. Is there a presence of hearing loss?

2. Is there a presence of ear pain (i.e., otalgia )?3. Is there a presence of ear discharge (i.e., otor-

rhea )?4. Is there a presence of ringing, buzzing or hum-

ming in the ears (i.e., tinnitus )?5. Is there a presence of dizziness, subjective vertigo

(i.e., the patient feels as if he or she is spinning),or objective vertigo (i.e., the patient feels as if theroom is spinning)?

When a physician determines the pathology tobe idiopathic in nature, the specic underlying eti-

ology cannot be identied. Without a known cause,the physician is left to treat the symptoms of the dis-order. If the cause is hereditary or familial , it meansthe pathology is transmitted by the genetic code thatone inherits from one or both of their parents. Geneticdisorders are often congenital meaning they are pres-ent at birth or very shortly after. If the disorder shouldhave an impact on speech and language develop-ment as in the case of hearing loss, then timing is veryimportant. If the loss is prelingual , the timing is priorto the development of speech and language and it

will have a greater impact than a postlingual loss (i.e.,after speech and language patterns have been fairly well established). Disorders that occur after birth andare the result of disease or injury are acquired . Thepathology can have an effect on one ear (i.e., uni-lateral ) or both ears (i.e., bilateral ). The onset of thepathology can be sudden or gradual . Much pathology

is acute (i.e., having a short duration) but some canbe very debilitating because of their chronic or long-standing nature. Finally, the pathology can be eithertemporary or permanent , and can uctuate or beprogressive . Many disorders, especially syndromes,have a set of characteristics that set them apart. Thepathology will not only disrupt the anatomy, butthe function (i.e., physiology) as well. If you spend timelearning the structures involved in a particular disor-der, then you should be able to predict the effect of nothaving the structures work the way they should.

In order to assess the nature of ear pathology, theclinician (i.e., audiologist) starts by physically exam-ining the outer ear. This process begins with a grossinspection of the outer ear. First, the clinician willnote the position of the pinna. In referring back toFigure 12-3, it can be seen that the normal positionof the pinna is determined by noting the relationshipof the superior border of the helix of the pinna to theouter canthus (i.e., corner) of the eye. The two shouldbe in alignment on a horizontal plane. The clinician will look for the presence of malformations such aspits, tags, sinuses, or suture lines in front of or behind

the pinna. The clinician will also inspect for any obvi-ous drainage from the ear canal. If there is no drain-age, the clinician will perform an otoscopic exam.The presence of cerumen is expected but should notbe excessive. A buildup of excessive cerumen maymake it difcult to visualize the tympanic membrane.The clinician will note any deviations of the anatomi-cal structures that can be visualized through otos-copy. With a case history completed and otoscopyperformed the audiologist then compares the normalfunction of the mechanism to any abnormal ndingsobserved in the patient. This is accomplished by the

audiologist performing a battery of tests that deter-mine hearing acuity, middle ear function, speech rec-ognition, and in some cases, electrophysical measuresof the vestibular and auditory mechanism. These testsare collectively referred to as audiometry .

The degree of hearing loss affected by injury orpathology can range from slight to profound. The effectmay be limited to the high frequencies, low frequen-cies, or create a at conguration where a broad rangeof frequencies are affected. Thresholds are obtained foreach ear and each pathway. Air conduction scores are




during the rst trimester of pregnancy is devastating,causing cardiac defects, cataracts, mental retarda-tion, microcephaly , short stature, and hearing loss. Ifmaternal rubella is contracted during the second orthird trimester, hearing loss may be the only result.

Therefore, if one understands timetables relative toprenatal development of the various structures withina system and among the various systems, the suspi-cion of hearing loss and its subsequent identica-tion and assessment can be accomplished early sothat effective intervention can be provided as soon aspossible.

At 20 weeks gestation (full term is between 38and 40 weeks), the pinna reaches its adult-likeshape. The pinna is one of the few auditory structuresthat continues to grow in size after birth. It will con-tinue to grow for approximately 9 to 12 years untilits adult size is reached. A “normal” pinna can take a wide variety of shapes and forms as seen in Fig -ure 13-3.

Complete maturation of the entire cochlea is com-plete at approximately the 20th week (fth month)of gestation. The inner ear is the only sense organto reach full adult size by fetal midterm. Thus, thecochlea is susceptible to developmental deviations,malformation, and acquired agents.

Anomalies of the Outer Ear

CONGENITAL ANOMALIESOF THE OUTER EAR

Anotia and Microtia

At birth, the pinna will be either completelyformed, partially absent or completely absent. Ano-tia refers to complete absence of the pinna whilemicrotia refers to partial development of the pinna.Figure 13-4 illustrates several congenital anomaliesof the pinna. A genetic disturbance is the etiologyfor microtia of the pinna in 5% of the population, whereas microtia is present 50% of the time as partof a syndrome. The remaining 45% of cases of micro-tia are categorized as idiopathic or of unknown etiol-ogy (Mastroiacovo et al., 1995). Authors/physiciansStephen Park and David Chi (2005) in a recent dis-

cussion on microtia reported an overall incidence of1 in 5000 to 1 in 20,000 births. They further reportedthat the incidence of microtia ranges from 1 in 900to 1200 births in the Navajo population to 1 in 4000births in the Japanese population. The male-to-female ratio for microtia is 2.5:1 and is four timesmore likely to be unilateral than bilateral. The rightear is affected more frequently than the left ear (right-to-left ear ratio of 3:2). Microtia does not cause sub-stantial hearing loss but can cause major cosmeticproblems. The wearing of eyeglasses can be espe-cially problematic.

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Air-bone gap

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Figure 13-2 Audiograms illustrating how to interpret theair-bone gap. A . This audiogram shows a signicant gap betweenbone ( ) and air (X) conduction thresholds for the left ear. Thisis indicative of a conductive hearing loss because the patient hasnormal cochlear sensitivity (through the bone conduction path-way, which stimulates the cochlea directly) while having elevatedthresholds for the air conduction pathway (where sound mustpass through the outer and middle ears before stimulating thecochlea). B . This audiogram reveals no air-bone gap. Air and boneconduction thresholds are the same and both are outside therange that is considered “normal” (i.e., 0 to 20 dB). This is indica-tive of a sensorineural hearing loss because hearing thresholdsare beyond normal whether the test signals are stimulating thecochlea directly through the bone conduction pathway or arepassing through the outer and middle ears to stimulate thecochlea (i.e., the air conduction pathway).



CHAPTER 13 PATHOLOGIES ASSOCIATED WITH THE AUDITORY/VESTIBULAR SYSTEM 331

Tags, Pits, and Sinuses

Preauricular tags, pits, and sinuses are probably themost common minor ear malformations with a fre-quency of 5 to 6 per 1000 live births (Kugelman et al.,1997). Most often they are benign and occur unilat-erally but occasionally they will occur bilaterally. Inreferring to Figure 13-4, it can be seen that a preau-ricular tag is a mound of epithelial skin that arisesnear the front of the ear in the area of the tragus. Tagsalone do not pose any threat to the structure of the earand are merely a cosmetic deformity (Kankkunen &Thiringer, 1987). A pit or sinus results from an abnor-mal connection between the skin and the underlyingtissue. They are the result of incomplete closure froman invagination of the embryologic tissue. Ear tags areoften seen in isolation; however, pits can be associ-ated with renal anomalies, occurring with a frequencyof 5% to 40% (Wang, Earl, Ruder, & Graham, 2001).

The incidence of spontaneous formation of ear pits inpersons who do not exhibit some type of syndrome isless than 1%.

Atresia and Stenosis

Atresia occurs when the external auditory canal hasfailed to develop. Atresia of the ear canal often accom-panies microtia of the pinna (see Figure 13-4). If the earcanal is present but is abnormally narrow, the conditionis referred to as stenosis . Atresia of the external audi-tory canal may occur unilaterally or bilaterally, and is

almost always accompanied by ossicular abnormality.The nature and degree of hearing loss should be evalu-ated for both ears. Because of the differential timing ofthe development of the inner and outer ears, the innerear structures may not be affected, thereby limiting thehearing loss to being conductive in nature. The audio-metric results will determine the need for amplicationin one or both ears and the need for a traditional or abone conduction aid. If there is unilateral involvement with normal hearing in the uninvolved ear, then sur-gery is delayed until the child is at least 5 years old. Thesurgical risk in a young child is in injuring an abnor-mally situated facial nerve (cranial nerve VII).

A

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DFigure 13-3 Normal variations in size and shape of the pinna(auricle). A . Normal pinna. B . Prominent ears (normal whenoccurring bilaterally and having familial characteristics). C . Incom-plete structures such as an incomplete helix are often seen inpremature infants, but they typically become normal as the babymatures. D . Darwin’s tubercle is a normal variant frequentlyappearing as a nodule along the posterior segment of the helix.(B, C, and D. Reprinted with permission from Michael Hawke,MD. Hawke Library, hawkelibrary.com.)

Why You Need to Know The Baha ® system utilizes the body’s natural boneconduction pathway to conduct sound. For peoplewith hearing loss, this provides another pathway toperceive sound. Typical hearing aids rely on air con-duction and a functioning middle ear. In cases wherethe outer or middle ear function is damaged oroccluded, the Baha implant is an alternative device




ACQUIRED PATHOLOGIESOF THE OUTER EAR

Trauma

Cauliower ear is an acquired pathology of the pinnaresulting from trauma. Wrestlers and prizeghtersare at high risk of acquiring this lesion. It is a directresult of the cartilage of the pinna and its connectivetissue covering (i.e., perichondrium ) being sepa-

rated during the trauma. Blood collects in the space,called a hematoma , causing the pinna to lose its nor-mal shape, as seen in Figure 13-5. In the acute stage,the pinna will be tender and marked redness will bepresent. The pinna will not return to its normal shapeunless treated. The hematoma will need to be aspi-rated and direct pressure applied until the tissue canreattach itself to the cartilage. A successful outcomeis dependent on early treatment. Hearing loss is not

usually a factor unless the opening of the externalauditory meatus is occluded.

Neoplasms

Squamous cell carcinoma is a malignant tumor thatis commonly seen on the pinna because of its obviousexposure to the sun. Squamous cell carcinoma is char-acterized by persistent thickening of the skin with redscaling, development of a painless pale outgrowth,and formation of open sores with a raised edge (see

A B

C D

Figure 13-4 Anomalies of the pinna.A . Microtia with atresia and preauricular tag.B . Preauricular pits (arrows). C . Microtia withatresia. D . Atresia.

as it bypasses these structures altogether. Instead,sound is sent around the damaged or problematicarea, naturally stimulating the cochlea through boneconduction. Once the cochlea receives these soundvibrations, the organ “hears” in the same manner asthrough air conduction; the sound is converted intoneural signals and is transferred to the brain, allow-ing a Baha recipient to perceive sound.




Figure 13-6). The tumor can increase in size to a largemass and metastasize if not treated early. Basal cellcarcinoma is a slow growing malignant skin cancerthat also is prevalent on the pinna and also is a result

of repeated sun exposure. It presents as a at, pain-less lesion with the edges becoming slightly raised.

The lesion develops a rolled edge with a penetratingcentral ulcer that bleeds easily. It typically remainslocalized but there is a small possibility for metasta-sis. Although hearing may not be adversely affected,these cancers can be life threatening and should bereported to a physician immediately.

Obstructions

Obstructions of the ear canal are common. The vastmajority of objects found in the ears are placed there,usually by children, and are a common reason foremergency room visits. Objects are limited only by thediameter of the ear canal, and might include earringbacks, articial ngernails, beans, beads, or insects.The vast majority of the objects are harmless. Some,however, can be extremely uncomfortable and requirean anesthetic to be removed. If medical treatment isdelayed, the object can quickly produce an infection.

Excessive cerumen is the most likely natural causeof ear canal obstruction (see Figure 13-7). Ceru-men is created when the migrating skin of the canalmixes with the cilia and secretions from the ceru-minous glands located in the outer one-third of thecanal. Cerumen buildup occurs when the cilia thatprotect the entrance to the ear canal become mat-ted with the migrating dead skin cells, impeding thenatural sloughing process. Impaction is more com-mon in males due to the presence of thicker, coursercilia. Cerumen also tends to become drier with age.

Cotton swabs, earplugs, and hearing aids all can impactcerumen. Impaction can cause a temporary mild con-ductive hearing loss and in some cases discomfort.Removal of excessive cerumen is accomplished bycurette , suction, or irrigation. However, before clean-

Figure 13-5 Cauliower ear is the result of trauma to thepinna. Blood collects between the layers of tissue causing the de-formity. The ear will not return to its normal shape unless treated.

Basal cell carcinoma

Squamous cell carcinoma

Figure 13-6 Basal cell and squamous cell carcinoma are typesof skin cancers commonly seen on the pinna as a result of over-exposure to the sun. (Reprinted with permission from AnatomicalChart Company.)

Figure 13-7 Otoscopic view of complete cerumen obstruction.(Reprinted with permission from Weber, J., Kelley, J. (2003).Health assessment in nursing (2nd ed.). Philadelphia: LippincottWilliams & Wilkins.)




ing the ear canal by irrigation, the tympanic membraneshould be examined for the presence of a perforationor pressure equalization (PE) tube, so that cleaningagents are not forced into the middle ear cavity duringthe removal process.

Another common obstruction occurring in the earcanal is an osteoma . These are smooth, benign bony

tumors that reside in the ear canal, most commonly atthe isthmus where bone and cartilage meet. They aretypically a result from swimming, surng, or diving incold water. Upon otoscopic examination, they appearas singular or multiple masses. They are usually notpainful unless touched. Osteomas can continue togrow and interfere with the normal process of migra-tion of skin to the outer ear. If large enough, they mayblock the canal and cause a conductive hearing loss.Osteomas can be surgically removed if necessary.

Inammation

Figure 13-8 illustrates external otitis (i.e., otitisexterna ), which is an inammatory condition of theear canal. The organism that causes the inammationis either fungi or bacteria that invade breaks in the epi-thelial lining of the ear canal. The organism resides in water and becomes trapped in the tortuous ear canal when it is repeatedly exposed to the water. Swimmersare prone to external otitis, hence its common name“swimmer’s ear.” The normally oily lining of the canalbecomes inamed, swollen, and itchy, creating a whitedischarge. The pinna can be painful to the touch, par-ticularly in the area of the tragus. External otitis caneither be acute or chronic. The individual prone tochronic inammation prevents reoccurrence by pro-tecting the ears from water. This can be accomplished with the use of custom earplugs worn during hair washing or swimming. Hearing aid users must be par-ticularly careful to dry their ears before inserting their

aids. The ear mold or shell can trap moisture in the earcanal exposing the skin to bacteria or fungi.

Anomalies of the Middle Ear

Although anomalies of the middle ear can be congeni-tal in nature, especially if they are part of a genetic syn-drome, they tend to be relatively rare. The most commonproblems associated with the middle ear are acquired.Two acquired anomalies of the middle ear deserve athorough discussion because of their prevalence in chil-dren and adults: otitis media (OM) and otosclerosis.

ACQUIRED PATHOLOGIESOF THE MIDDLE EAR

Otitis Media

OM is an inammation of the lining of the middle ear.It is the most common of childhood infections andone of the most frequent reasons parents take theirchildren to the physician. According to Schappert(1992) from the National Center for Health Statistics,visits to the physician for OM in 1975 totaled 10 mil-lion. By 1990, the number had increased to 25 mil-lion. As a population, children younger than 2 yearsof age have the highest rate of ofce visits for OM. Ithas been hypothesized that the high rate of OM inchildren is because they are together in large groupssuch as daycares and preschools, where exposure to

the viruses and bacteria that cause the inammationis more likely. Grundfast and Carney (1987) offeredsome additional statistics related to OM. In the UnitedStates, 85% to 90% of all children before the age of 6 years will have had at least one ear infection. Half ofthe children who have one ear infection before theage of one will have six or more episodes in the fol-lowing 2 years. Therefore, the younger they start hav-ing infections, the more likely they are to continue.Nearly 20% of children who suffer ear infections willat some point require surgery to correct the problem.In addition, 25% to 40% of all upper respiratory infec-

tions (URIs) are associated with OM.Howie, Ploussard, and Sloyer (1975) reported that

gender and family history play a role in the incidenceof OM. In terms of gender, males have a higher inci-dence of OM than females. In terms of family history,if a parent or parents had many ear infections whenthey were children, their own children will most likelyhave several infections. There is no OM gene per se ,but facial features are inherited. For example, poorfunction of the structures of the nasopharynx suchas the Eustachian tube (ET) can be inherited and canlead to bouts of OM.

Figure 13-8 Acute external otitis (otitis externa) is an inam-mation of the skin lining the ear canal. It is typically very painfuland is caused from repeated exposure to water. (Reprinted withpermission from Bickley, L.S., Szilagyi, P. (2003). Bates’ guide to physi-cal examination and history taking (8th ed.). Philadelphia:Lippincott Williams & Wilkins.)




There are several contributing factors that place achild at risk for OM. One is the exposure to second-hand cigarette smoke (Ey et al., 1995). The products incigarette smoke can irritate the nasopharynx and leadto the onset of OM. A child of low socioeconomic sta-tus who lives where there are poor sanitary conditionsor overcrowding and repeated exposed to chemicals,

viruses, and bacteria that cause URI will place thechild at greater risk for OM. Climate in and of itselfis not a direct contributor to OM, but children whospend most of their time indoors because of poor out-door weather conditions may be in close contact withmany people and therefore may pass around virusesand bacteria that lead to URIs.

OM is nearly always the result of the Eustachian tube(ET) not opening to ventilate the middle ear. It maybecome blocked by inammation of surrounding tis-sue. In particular, adenoid tissue may swell in responseto irritants, viruses or bacteria. The inamed adenoidsblock the nasopharyngeal opening of the ET. As wasdiscussed in Chapter 12, the ET must be able to open toventilate the middle ear cavity and thereby equalize airpressure between the middle ear and the atmosphere.In its acute form, OM commonly develops in associa-tion with an URI. Children and adults who have a syn-drome or disorder whose sequelae include structuralor functional abnormalities of the pharyngeal musclesare signicantly at risk for middle ear disease.

There are basically three stages of OM: acute OM ,OM with effusion and OM with tympanic membrane

perforation . Acute OM commonly presents with asudden onset of otalgia in association with symptomsof URI such as rhinorrhea , nasal congestion, coughand fever; however, these symptoms are not alwayspresent. Similarly, not all cases of otalgia are causedby OM.

Otoscopy performed on an individual who pres-ents with acute OM reveals a red or yellow tympanicmembrane depending on the degree of inamma-tion and the amount of purulent material in themiddle ear cavity. There may be bulging of the parsaccida or the entire eardrum. The movement of the

tympanic membrane may be diminished. If the tym-panic membrane is ruptured, ear pain will dimin-ish but cloudy or purulent drainage in the ear canal will be visible. Antibiotic therapy is used to treat theinfection and anti-inammatory medication is usedto treat the pain.

OM with effusion is the stage where uid occu-pies the normally air-lled middle ear cavity. Theuid may be a remnant from the acute stage or maydevelop silently without the presence of a bacterialinfection. OM with effusion creates a mild conduc-tive hearing loss. On average there is a 27 dB hearing

loss based on pure tone air conduction thresholds(see Figure 13-9). The majority of the loss is in thelower frequencies. Long standing, untreated OMcan lead to much more complicated and severe eardisease processes, not to mention the concomitanthearing loss causing a delay in speech developmentof children who are in the critical years for speechand language acquisition.

When the ET does not function properly, it doesnot allow for ventilation of the middle ear cavity.The air that is normally in the cavity becomes stag-

nant and is absorbed by the membranous lining ofthe walls of the cavity. As a result, air pressure withinthe cavity will decrease (i.e., become negative) relativeto atmospheric air pressure outside the cavity. Thenegative pressure causes the eardrum to be drawninward or retracted from its normal position. Thearea of the pars accida is more susceptible to thisnegative pressure. Retraction of the eardrum is whatcauses the ear pain. Also as a result of the negativeair pressure, serous uid is secreted by the mucousmembrane that lines the middle ear cavity. This uidis thin and watery in consistency. If the ET continues

to remain closed or inamed, the consistency of themiddle ear uid will become thick and mucous-like.Bacteria can cause inammation at any stage andcreate a pus-lled space. The term mucoid OM wouldeventually be applied with continued thickening ofthe effusion leading to adhesive OM or “glue ear.” Asthe middle ear uid gets thicker in consistency, hear-ing loss gets progressively worse. At the point whereadhesive OM is present, there may be as much as a40- to 50-dB conductive hearing loss. The hearing lossfrom serous OM may be the only sign of ear pathol-ogy. Middle ear uid may not be obvious on otoscopic

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Figure 13-9 Typical audiometric pattern and hearing levels fora right ear with otitis media.




examination, so detection is aided by the audiologistperforming tympanometry to measure the immit-tance (i.e., mobility) of the eardrum. Middle ear uidis indicated by a lack of movement, which revealsitself as an abnormal (i.e., at-type B) tympanogram (see Figure 13-10).

There are several surgical options for treatmentof OM. When OM has been attributed to blockage ofthe ET by hypertrophic (i.e., enlarged) adenoids, an

adenoidectomy will be recommended. If uid haslled the middle ear cavity, a myringotomy may beperformed. A myringotomy is an incision that is madein the tympanic membrane, with suctioning of theuid from the middle ear cavity being done throughthe incision. The incision in the eardrum will heal ina matter of days. There is a chance that uid will form

again if whatever is causing the inammation of theET is not treated. A pressure equalization (PE) tube , made of silastic

material, is placed through a myringotomy incisioninto the eardrum (see Figure 13-11). The tube acts toventilate the middle ear cavity by allowing outsideatmospheric air to enter through the eardrum, therebycircumventing the function of the ET. The result isthat the middle ear space is ventilated, with hearingreturning to normal. Insertion of PE tubes buys timefor the ET to begin working on its own or the child tooutgrow whatever caused the ET to dysfunction in therst place. A PE tube will stay in place for months, untilthe eardrum heals and the tube is expelled into theear canal. The normal migration of the ear canal epi-thelium will carry the tube along until it reaches theentrance of the canal where it will simply be sloughedoff or can be reached by the physician’s curette. Whentubes are in place, there is concern about keeping water out of the ears. Conceivably, bacteria carried in water could enter the middle ear through the patentPE tube and cause an infection. Custom earplugs canbe t for hair washing, bathing, and swimming.

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Figure 13-10 Tympanograms: Type A tympanogram result fora normal ventilated middle ear; Type B pattern indicates effusion

(lack of ventilation) in the middle ear space.

PE tube

Myringotomy (Radial incision)

Pressure equalization (PE) tube insertion

Front view

Side view

Figure 13-11 Myringotomy and placement of a pressure equalization (PE) tube into the tympanic membrane. (Reprintedwith permission from Anatomical Chart Company.)




Complications of OM

Some complications of OM can be very signicantand some can be minor. The most common compli-cation is tympanosclerosis or scar tissue on the ear-drum. It is the result of tissue changes that form onthe TM as a result of recurrent ear infections. Tym-panosclerosis is often seen as a white calcium plaqueor scar tissue on the pars tensa. Fortunately, it haslittle effect on hearing.

Perforations of the eardrum can be caused bychronic ear infections where the TM ruptures andfails to heal, but can also be caused by trauma suchas a puncture or forceful slap to the ear by a cuppedhand or loud explosion. A perforation is described byits location on the eardrum: central, attic or marginal. A central perforation is shown in Figure 13-12. Smallperforations will usually heal spontaneously. However,larger perforations generally require a surgical repaircalled a myringoplasty or Type I tympanoplasty. Thesurgeon uses the patient’s own tissue (usually takenfrom the back of the ear) to create a graft that will beinserted underneath the eardrum remnant to closethe perforation.

Remember that the middle ear cavity has the abilityto communicate with the mastoid air cells; thus, bacte-rial secretory mucous (i.e., acute OM) can spread intothe mastoid cavity, resulting in mastoiditis , a poten-tially life-threatening infection . Infected debris in themastoid is trapped and can only be removed by sur-gical cleaning of this space. The surgeon removes the

infected debris by drilling out the individual air cellsleaving one large cavity (referred to as a mastoidec-tomy ). The healthy cavity must then be mechanicallycleaned periodically to prevent further disease. Anothercomplication of OM is the formation of a cholestea-toma , a cyst made of layers of epithelial debris from the

tympanic membrane. The cyst contains considerableamounts of keratin, a protein found in cells. Forma-tion of a cholesteatoma is usually associated with poorET function and chronic OM where the TM has beenin a long-standing retracted state. A pocket is formedin the area of the pars accida by the continual retrac-tion from negative middle ear pressure. As illustratedin Figure 13-13, the pocket retains sloughed debris.

Inammation causes the pocket to swell and expand.It can eventually invade the epitympanic recess or atticof the middle ear cavity. The expanding cholesteatomadestructively encroaches upon the middle ear cavityand structures. As it continues to grow, it has the poten-tial to erode away portions of the ossicles and invadeother structures such as the mastoid air cells, the hori-zontal semicircular canal, and even the bones of thecranium. Its aggressive capability makes it potentiallylife threatening. It is also a major cause of a conduc-tive hearing loss. A cholesteatoma should be surgicallyremoved and monitored because of its ability to reform.

Otosclerosis

Otosclerosis is a middle ear disease in which nor-mal bone is progressively reabsorbed and replacedby spongy bone growth. This condition most oftentakes place around the footplate of the stapes andthe oval window. The new growth of bone interferes with the normal vibration of the stapes footplate. It isnot painful and the patient does not even know whatis happening except for the progression of a hearing

Lateralprocess

of malleus

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AnnulusPosteriorcanal wall

Central TMperforation

Figure 13-12 Central left tympanic membrane perforationtypically caused by chronic ear infections.

Figure 13-13 A cholesteatoma is a complication from poorEustachian tube function and otitis media. Debris forms in a retrac-

tion pocket in the pars accida region of the tympanic membrane.(Reprinted with permission from Anatomical Chart Company.)

Cholesteatoma

Tympanic membrane

Ear canal




loss. There are often head noises, typically a roaringor seashell-like sound. The progression of the diseaseis slow and takes place over several years. Otosclerosisis usually bilateral, rst seen in one ear and then pro-gressing to the other ear. However, the disease tendsto progress at different rates for each ear. The ears areotoscopically normal with the possible exception ofSchwartze’s sign , a reddish or pinkish glow visual-ized through the tympanic membrane produced byincreased vascularity on the promontory.

Otosclerosis impedes the vibration of the footplate

of the stapes resulting in a conductive hearing loss.The hearing loss worsens in degree as the disease pro-gresses. Audiometry and immittance measures areperformed to aid in the identication of this disease.

As charted in Figure 13-14, the conductive portion ofthe loss is usually moderate (no greater than a 60-dBloss) depending on the disease progression. Bone con-duction thresholds are often elevated at 2000 Hz. Thisclassic pattern is called Carhart’s notch and is typicallyonly seen with otosclerosis. The notch in the bone con-duction threshold for 2000 Hz is thought to be a result

of the diminished resonance of the ossicular chain.There are varying estimates of the prevalence ofhearing loss as a result of otosclerosis. Pearson (1974)reported the prevalence as high as 10% of the generalpopulation. Declau et al. (2001) also studied preva-lence and compared it to what was seen clinically.Their estimate of 0.3% (3 per 1000) was much moreconservative than Pearson’s estimate. Many clinicians would agree that the prevalence reported by Declauet al. (2001) is a more realistic estimate. The cause ofotosclerosis is not fully understood. It may begin atany age but there seems to be a relationship betweenotosclerosis and the timing of hormonal changes typ-ically seen in puberty, pregnancy, or menopause. Oto-sclerosis tends to be more prevalent in families andmore so in Caucasian women.

Otosclerosis cannot be treated medically but sur-gery is an option. The goal of surgery is to restorethe air conduction hearing levels for the patient. Amplication is also an option when surgery is notelected. A good candidate for surgery should exhibita substantial air-bone gap (greater than 20 dB) withnormal or near-normal bone conduction thresh-

olds and good word recognition scores. The surgery,called a stapedectomy , involves removal of the sta-pes superstructure and footplate (see Figure 13-15).Upon removal of the stapes, the oval window is sealed

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Figure 13-14 Typical audiometric pattern and bone conduc-tion Carhart’s notch for a left ear with otosclerosis.

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C DFigure 13-15 Stapedectomy for otosclerosis. A . Arrow points to spongy bone growth on the stapes footplate. B . Stapes removed.C . Footplate is removed. D . Prosthesis placed into position. (Reprinted with permission from Smeltzer, S.C., Bare, B.G. (2000). Textbook ofmedical-surgical nursing (9th ed.). Philadelphia: Lippincott Williams & Wilkins.)




with connective fascia tissue. The stapes is thenreplaced with a prosthetic device made of Teon andtitanium. The head of the prosthesis is crimped to thelenticular process of the incus, thereby reestablishingthe ossicular chain. The other end of the prosthesis isarticulated with the oval window. The intact chain canonce again transmit vibrations to the cochlea. When

otosclerosis is bilateral, surgery is performed on oneear at a time; the ear with the larger air-bone gap isusually operated on rst. The second ear surgery isdelayed a minimum of 6 months to ensure that theinitial result is successful. Surgery is considered suc-cessful when the preoperative air-bone gap is closed.

Anomalies of the Inner Ear

GENETICS OF HEARING LOSS

Smith, Green, and Van Camp (1999) authored an excel-lent review of genetics and hearing loss. They reportedthat genetics account for approximately 50% of thecases of hearing loss. The remaining 50% are acquired(i.e., nongenetic) from environmental causes. Thereis however, within the acquired environmental group25% that are idiopathic in nature, meaning that thereis no known cause.

Hereditary hearing loss through genetic trans-mission may be syndromic or nonsyndromic. A syn-drome is a consistent pattern of abnormalities and/or symptoms that results from the same underlying

cause. The term nonsyndromic refers to a disorderthat occurs in isolation of any other genetic features.Seventy percent of genetic hearing losses are nonsyn-dromic and 30% are syndromic.

The mode of inheritance typically takes one of threeforms: autosomal dominant, autosomal recessive , or X-linked recessive . For autosomal dominant, one par-ent carries the dominant gene on at least one chromo-some and he or she is affected by the trait (in this case,hearing loss). The genetic transmission from one parentis sufcient to produce the disorder. Therefore, eachtime there is a pregnancy, there is a 50% chance the baby will receive the dominant gene trait (see Table 13-1).

Autosomal recessive trait is illustrated in Table13-2. The parent carries the gene but does not exhibitthe trait (i.e., hearing loss). The parent most likely would not even be aware that they carry the gene.The genetic trait from only one parent is not enoughto produce the disorder in the offspring. With auto-somal recessive transmission, both carrier parents areneeded for the trait to be expressed (i.e., a deaf or hardof hearing offspring). Each time there is a pregnancy,the baby will have a 25% chance of the recessive trait

being expressed, 50% chance of receiving the reces-sive gene and being a carrier like the parents, and 25%chance of losing the recessive gene altogether.

A genetic (but nonsyndromic) hearing loss is sus-pected when a child is either born with a hearing lossor acquired it very early in their life. During the period1996–1997, researchers such as Kumar and Gilula (1996)identied the gene responsible for the majority of reces-sive inherited sensorineural deafness. The offspring oftwo (hearing) carrier parents inherits the mutated gene(GJB2) located on the 13th chromosome. The geneGJB2 encodes for the gap junction channel proteinconnexin 26 . Gap junctions are clusters of intercellu-

lar channels that allow communication between cells. Without proper cellular communication, the chemicalbalance of the endolymph and the perilymph withinthe organ of Corti cannot be maintained.

TABLE 13-1

AUTOSOMAL DOMINANT MODE OFINHERITANCE

N/n Normal hearing N n parent*H/h Hearing loss*Dominant gene trait

50% chance forhearing loss50% chance for

normal hearing

*H *HN *Hn (Hearing loss) (Hearing loss)

h Nh hn

TABLE 13-2

AUTOSOMAL RECESSIVE MODE OFINHERITANCE

N/*n Normal hearing N

*n but a carrier*Recessive gene trait50% chance of

carrying the gene25% chance for

hearing loss25% chance to lose

the trait

N NN N*n (Carrier)

*n N*n *n*n (Carrier) (Hearing loss)




X-linked recessive trait accounts for only about2% of the cases of congenital hearing loss. Transmis-sion is always from mother to son as males get eithertheir dominant X or recessive x chromosome fromtheir mother. The mother does not have the hearing

loss and she most likely is unaware that she is a car-rier. When the gene trait is expressed, the son inher-its his mother’s recessive x for hearing loss. Whenthat son has children, his daughters will inherit therecessive gene trait making them carriers; his sons will be ne because they will inherit either their X orx from their mother. X-linked recessive trait is illus-trated in Table 13-3.

CONGENITAL DISORDERSOF THE INNER EAR

Anomalies of the inner ear may be associated withgenetic syndromes or may occur alone. The mostextreme and rare form of an inner ear anomaly iscalled Michel dysplasia . The term dysplasia means amalformation of the bone that may occur in any partof the body. Michel dysplasia results when cochleardevelopment is arrested early during the embryonicperiod. With extreme dysplasia, there are no denitivecochlear or vestibular structures (Kavanagh & Magill,1989). A common cavity may occur and in some casesthe entire auditory nerve may also be absent. Micheldysplasia may affect only the cochlea and the vesti-

bule, with the semicircular canals being essentiallynormal. Michel dysplasia is seen in 1% of individuals with profound hearing loss.

Mondini dysplasia involves the normal develop-ment of the rst 1½ turns of the cochlea. The remain-ing turn will be either absent or markedly malformedin that there is no separation between the osseous andmembranous labyrinth. The vestibule and semicircu-lar canals may or may not be normally developed.Mondini dysplasia may be present at birth or developlater in adult life. Since the basal end of the cochlea

is essentially missing, the loss in the high frequencies will be profound.

Scheibe dysplasia is the most common form ofcongenital malformation of the inner ear. The bonylabyrinth is typically complete and intact. However,

the membranous labyrinth is intact for the semicir-cular canals and utricle but the saccule and cochlearduct (scala media) are poorly dened with atrophyof the organ of Corti. The degree of hearing loss is ofcourse profound.

Alexander aplasia is typically limited to the absenceof the basal turn of the cochlear duct, organ of Corti,and ganglion cells. Absence of the basal portion ofthe cochlea will result in high-frequency hearing loss while low-frequency hearing remains relatively intact.

Associated AnomaliesSyndromes present themselves from a genetic origin30% of the time. Hearing loss is but one of the associ-ated anomalies. The other anomalies that are frequentlyseen in syndromes with hearing loss are classied as:

• integumentary (pertaining to the skin)• skeletal• ocular (visual impairment)• other (commonly, renal or cardiac). When an error in the genetic message interrupts the

embryologic developmental process in one area (suchas skin), another area (such as skeletal formation)may also be disrupted. Integumentary anomaliespertain to pigmentation changes of the skin. Integ-umentary anomalies and congenital sensorineuralhearing loss are the chief sequelae of many syn-dromes. Both skin and portions of the cochlea havethe same embryological origin. The genetic messagethat results in the abnormal patterns of pigmenta-tion such as albinism (i.e., a lack of pigmentation)or piebaldism (i.e., strips of too much or too little

TABLE 13-3

X-LINKED RECESSIVE MODE OF INHERITANCE

X/Y Dad X Y X/*x Mom (Carrier)*Recessive gene trait50% chance a son will have hearing loss50% chance a daughter will be a carrier

X XX daughter XY son

*x X*x daughter *xY son (Carrier) (Hearing loss)




pigmentation) may also result in a severe congenitalsensorineural hearing loss. Waardenburg syndrome is an example of a syndrome with multiple associ-ated anomalies.

A syndrome characterized by a skeletal defect isKlippel-Feil syndrome . Persons with this syndromeexhibit a shortened neck, curvature of the spine, and within the middle ear a poorly shaped stapes. The ori-gin of skeletal and ossicular malformations can oftenbe traced back to the same embryologic beginnings.Poor fusion of the cranial structures is sometimesassociated with atresia of the ear canal.

Ocular anomalies are commonly associated withhearing loss. A variety of ocular anomalies are seen withCrouzon syndrome . These anomalies can range from

complete absence of the eyes, to widely separated eyes,to bulging of the eyes. Usher’s syndrome is associated with a slow progressive loss of vision resulting fromretinitis pigmentosa (i.e., atrophy of the retina) and agradual loss of hearing. Visual impairment is one of thethree most common disorders associated with hearingloss. Table 13-4 presents a brief chart of genetic syn-dromes associated with hearing loss. Note the associ-ated anomalies that often accompany the hearing loss.

ACQUIRED ETIOLOGY OF CONGENITALHEARING LOSS

The TORCH Complex

Twenty-ve percent of the cases of congenital hear-ing loss are acquired from various etiologies. Fromthe third to ninth week of gestation, the developingembryo is extremely susceptible to teratogenic agents.It is during this period that the fetal organs are formedfrom the primitive germ cell layers ; therefore, it is thetiming of fetal exposure that determines the severity ofthe problem. When present in the fetal environment, ateratogenic agent may cause disorders that affect the

baby’s development and/or learning. Maternal infec-tions are of primary concern; in particular, the majorteratogenic agents that cross the pregnant mother’splacenta to infect the fetus are referred to by the acro-nym TORCH : Toxoplasmosis, Other (including syphi-lis), Rubella, C ytomegalovirus, and Herpes. Someof the TORCH infections, such as toxoplasmosis andsyphilis, can be effectively treated with antibiotics ifthe mother is diagnosed early in her pregnancy. Manyof the viral TORCH infections have no effective treat-ment, but some, notably Rubella, can be preventedby vaccinating the mother prior to pregnancy. If themother has active herpes simplex, delivery by Cae-sarean section can prevent the newborn from contactand consequent infection with this virus.

Toxoplasmosis is a parasitic infection contractedby consumption of contaminated raw meats and eggsas well as from improper handling of cat feces. Theparasite called Toxoplasma gondii multiplies in theintestine of cats and is shed in cat feces, mainly into lit-ter boxes and garden soil. Healthy mothers usually donot suffer ill effects from toxoplasmosis; at most theymay feel like they have the u. The disease is trans-mitted to the developing fetus through the placenta.Infected babies may not develop the disease or theymay become very ill. The exposed newborn often haslow birth weight, jaundice, an enlarged liver, inam-

mation of the retina, and hearing loss which may bemoderate to severe and progressive. Toxoplasmosis ispreventable by avoiding exposure to the agents thatcarry the parasite. If you have been infected previ-ously (at least 6 to 9 months before your pregnancy) with toxoplasma, you will develop immunity to it. Theinfection will not be active when you become preg-nant, and so there is rarely a risk to the baby.

Congenital syphilis is a sexually transmitted bac-terial infection ( Treponema pallidum ) that is passedfrom the mother to her fetus. The infection affects

TABLE 13-4

GENETIC SYNDROMES AND SEQUELAE TO IDENTIFY ASSOCIATED ANOMALIES

Syndrome Associated Sequelae

Alport Kidney problemsBrachio-Oto-Renal (BOR) Neck cysts and kidney problemsJervell and Lange-Nielsen Cardiac problemsPendred Thyroid enlargement or low thyroid functionStickler Unusual facial features, cleft palate, eye problems (e.g., nearsightedness,

cataracts, or retinal detachment), arthritis, cardiac problemsUsher Progressive blindness Waardenburg White patch of hair or light-colored skin patches; eyes of two different colors, or

bright blue eyes, or widely spaced eyes




many of the baby’s systems and early signs includeskin lesions, meningitis, mental retardation, seizures,and hearing loss to list just a few. The disease wasdubbed the “great imitator” because so many of itssigns and symptoms are indistinguishable from thoseof other diseases. The sensorineural hearing loss istypically delayed in onset, developing at any time

during childhood or adulthood. The loss may have asudden onset or may progress slowly, and may be uni-lateral or bilateral. Early identication and prompttreatment with high doses of antibiotics improves thepotential for reversibility.

Congenital rubella is a viral infection passed fromthe mother to her baby through the placenta. Infec-tion spreads through direct contact with dischargefrom the nose or throat of an affected individual. Ifthe infection is contracted within the rst trimester ofpregnancy, it poses the greatest risk to the developingfetus. Rubella syndrome in the newborn results in aconsistent pattern of physical abnormalities charac-terized by rash, low birth weight, small head size (i.e.,microcephaly), cardiac abnormalities, hearing loss,visual problems, and bulging fontanelle. Since it is aviral infection, there is no cure; only treatment of thesymptoms is possible. An epidemic of rubella occurredin the 1960s; however, the development of a vaccine in1968 has greatly reduced the incidence of this disease.

Cytomegalovirus (CMV) , a virus of the herpesgroup, can be transmitted sexually or by close contact with infected secretions. It is a virus most humans are

exposed to at some time in their life, but typically onlyindividuals with a weakened immune system becomeill from CMV infection. By 40 years of age, between50% and 80% of adults in the United States have beeninfected with CMV. Adults acquire CMV through sex-ual contact with an infected partner who is sheddingthe virus in blood, semen or vaginal uids. Adults andchildren can acquire it from contact with infectedchildren shedding the virus in blood, saliva, and urineas might be the case in a daycare environment. Aninfected mother may even transmit the virus to herinfant through contact with breast milk. Pass, Hutto,

Reynolds, and Polhill (1984) tested a cohort of chil-dren less than 12 months of age at a typical daycarecenter. Less than 10% of the children were sheddingthe virus at the time they enrolled in the daycare but 6to 12 months later 78% were shedding the virus. Oncean individual is infected with the virus, it remains forlife. Eventually, the virus goes dormant and the indi-vidual’s immune system develops antibodies to ghtit. Therefore, for the majority of people, it is “silent”and not a serious problem. However, a primary (orrst) CMV infection in a pregnant woman can causeserious harm to the developing fetus. About 1% to

4% of pregnant women experience a primary CMVinfection. Thirty-three percent of these women passthe virus to their unborn babies. High levels of stresscan also reactivate the dormant virus in a pregnant woman but this happens less than 1% of the time.

A baby infected in utero (i.e., congenital CMV)may be symptomatic or asymptomatic at birth. Five

percent of infected newborns are symptomatic andpresent with symptoms ranging from mild to severe.The mild symptoms may include being small for ges-tation age (SGA), having an enlarged spleen or liver,exhibiting jaundice, and having a distinctive purplishrash. Up to 10% of symptomatic infants die shortlyafter birth; of the survivors, many suffer from seriousimpairments such as mental retardation, hearing loss,and visual impairment. Sensorineural hearing loss ispresent in approximately 40% of these symptomaticinfants. Infants with the more severe effects from pri-mary CMV are born to women who contracted theinfection in the rst trimester of pregnancy.

Approximately 95% of babies who are infected withthe virus in utero are asymptomatic at birth (Oshiro,1999). There is approximately a 5% chance of thesebabies developing a complication. Hearing loss is themost common complication (in 7% to 15% of cases)and very often is delayed in its onset, with 4 years ofage being the average age of onset. Researchers suchas Foulon et al. (2008) have seen the onset of hear-ing loss attributed to congenital CMV up to the age of15. Once the hearing loss presents itself, it is always

progressive and usually severe to profound in degree.To summarize the incidence of congenital CMV, onechild out of 150 births is infected. Approximatelyone child out of 750 born with the infection developspermanent disabilities; this equates to 6000 childreneach year. Congenital CMV is as common a cause ofserious disability as Down syndrome and fetal alcoholsyndrome. Being a common cause of hearing loss inchildhood, regular audiometric evaluations should beconducted in children with known congenital CMV.

Neonatal herpes is a sexually transmitted viral dis-ease that can be passed from the infected mother to her

fetus either during pregnancy or during delivery if thedisease is active. One of every 3000 newborns deliveredis infected with neonatal herpes. Over 70% of infantsinfected with the herpes simplex virus are from moth-ers with a primary infection who have asymptomaticviral shedding during labor. Infected infants even withimmediate treatment may have central nervous sys-tem involvement and sensorineural hearing loss.

Bacterial Meningitis

Bacterial meningitis is an acquired pathology that is

spread by direct contact with nasal secretions, saliva




or sputum from an infected individual. It can also bea major complication from an untreated ear or sinusinfection. It is seen almost exclusively in children lessthan 5 years of age. Contracting the infection places theindividual at signicant risk for hearing loss. The bacte-ria enter the blood stream and spread to the meningescovering the brain and the spinal cord (in particular the

subarachnoid space). The extent the infection spreadsexplains the symptoms including high fever, vomiting,a stiff neck, and malaise. Several bacterial strains canbe responsible for meningitis but 70% of the infectionsare from the haemophilus inuenzae Type b (Hib) . Although Hib is the most common bacteria to causemeningitis, fortunately it is the least likely to result inhearing loss (in only 3% to 16% of cases). Other causesof bacterial meningitis include the pneumococcal and meningococcal strains. These have a much lower inci-dence of causing meningitis but a higher incidence ofcausing hearing loss (24% to 36% of cases). Treatmentfor meningitis is with antibiotics delivered intravenously.Successful treatment depends on prompt diagnosis. A lumbar puncture is often necessary to check for thepresence of the bacteria in the cerebrospinal uid. Thehaemophilus inuenzae Type b bacteria can be safelyand effectively prevented from causing meningitis withthe use of the Hib vaccine that was introduced in 1990.

Severe to profound sensorineural hearing loss occurs when the cochlea is invaded by the bacterial infection. Any episode of meningitis warrants a hearing evalu-ation even before the patient is discharged from the

hospital. It is recommended that any nding of hear-ing loss be followed with monthly reevaluation untilthe hearing loss stabilizes. The major complication ofan infection invading the cochlea is the ossication ofthe bony labyrinth. The ossication process begins toappear within 3 months of the onset of meningitis andmay be complete by 1 year. The ossication is oftenbilateral. If the hearing loss is profound and a cochlearimplant (CI) is considered (see Figure 13-16), the pres-ence of ossication within the cochlea can create prob-lems with placement of the electrode array (refer to the Why You Need to Know box on the CI); therefore, the

typical waiting period is waived to expedite the sur-gery before ossication can become too advanced andreduce the likelihood of successful implantation.

Other Risk Factors

There are several other birth complications that placean infant at risk for an acquired hearing loss. Prior tothe advent of universal newborn hearing screening,the presence of “risk factors” were used to aid in earlyidentication efforts. It is now accepted that screen-ing children based on risk factors alone is not enough.

Recall that 25% of cases of hearing loss are idiopathic

in origin. Additionally, there might not be an obviousfamily history of hearing loss. As previously discussed,70% of the cases of nonsyndromic hearing loss aredue to autosomal recessive gene transmission wherethe individual is unaware of the genetic link. Withthat said, the 2007 Joint Committee on Infant Hear-ing (JCIH) established a position statement outliningprinciples and guidelines for Early Hearing Detectionand Intervention (EHDI) programs.

The JCIH endorses early detection of and interven-tion for infants with hearing loss. The goal of EHDIis to maximize linguistic competence and literacy

Microphone

Transmittingcoil

Electrodes

Transmittingcoil

Microphone and processorfor ear-level device

Speech processorfor body worndevice

CI in place

CI components

Figure 13-16 A typical cochlear implant (CI) system. Soundsare picked up by the small directional microphone located in theheadset at the ear. A thin cord carries the sound from the mi-crophone to the speech processor which, in turn, lters, analyzes,and digitizes the sound into coded signals that are sent from theprocessor to the transmitting coil. The transmitting coil sends thecoded signals (RF signals) to the CI located under the person’sskin. The implant delivers the appropriate electrical signals toan array of electrodes that have been inserted into the cochlea.The electrodes within the cochlea stimulate the remaining bersof the cochlear portion of the vestibulocochlear nerve (cranialnerve VIII). These bers then send the sound information to theauditory cortex for interpretation. (Reprinted with permissionfrom Nettina, S. M. (2001). The Lippincott manual of nursing practice (7th ed.). Philadelphia: Lippincott Williams & Wilkins.)




development for children who are deaf or hard ofhearing. Without appropriate opportunities to learnlanguage, these children will fall behind their hear-ing peers in communication, cognition, reading, andsocial–emotional development. Such delays mayresult in lower educational and employment levels inadulthood. To maximize the outcome for infants who

are deaf or hard of hearing, the hearing of all infantsshould be screened at no later than 1 month of age.Those who do not pass screening should have a com-prehensive audiological evaluation at no later than 3months of age. Infants with conrmed hearing lossshould receive appropriate intervention at no laterthan 6 months of age from health care and educa-tion professionals with expertise in hearing loss anddeafness in infants and young children. Regardless ofprevious hearing–screening outcomes, all infants withor without risk factors should receive ongoing surveil-lance of communicative development beginning at 2months of age during well-child visits in the medicalhome [boldface added]. EHDI systems should guar-antee seamless transitions for infants and their fami-lies through this process (Joint Committee on InfantHearing, 2007, p. 898).

The position statement does establish several cri-teria for identifying children at risk for congenital,delayed-onset, permanent, or progressive hearing lossduring childhood (several of these criteria have beendiscussed in this chapter). These criteria include:

• caregiver concern regarding hearing, speech,language, or developmental delay

• a family history of permanent childhood hearingloss

• a stay in the neonatal intensive care unit (NICU)of more than 5 days

• in utero infections, such as CMV, herpes, rubella,syphilis and toxoplasmosis

• syndromes known to be associated with hearingloss or progressive or late-onset hearing loss

• physical ndings that are associated with a syn-

drome known to include a sensorineural or per-manent conductive hearing loss• the presence of craniofacial anomalies, including

those that involve the pinna, ear canal, ear tags,ear pits, and temporal bone anomalies

• culture positive postnatal infections associated with sensorineural hearing loss including con-rmed bacterial meningitis

• neurodegenerative disorders or sensory motorneuropathies

• head trauma, especially basal skull/temporalbone fractures that require hospitalization

• chemotherapy.The position statement recommends that the hos-

pital-based EHDI screening program provides theparents with information about hearing, speech, andlanguage milestones. The screening results will besent to the medical home for management and anyneed for referral and follow-up. The primary care pro-vider will refer to an audiologist any patient for whomthere are concerns or ndings consistent with hearingloss. Therefore, for infants with a risk factor which maybe considered low risk, at least one audiology assess-ment by 24 to 30 months is the recommendation. Incontrast, for an infant with risk factors known to beassociated with late onset or progressive hearing loss(such as CMV or family history), early and more fre-quent assessment is appropriate. Early and more fre-

quent can be interpreted as every 6 months or more,depending on the clinical ndings and concerns.

Why You Need to Know The cochlear implant (CI) is a management tool fordeafness, not a treatment for deafness. In fact, the CIrelies on the functioning structures of the auditorymechanism. The implant provides electrical stimu-lation to the cochlear nerve bers by bypassing themissing or damaged hair cells. In most cases of deaf-ness, the cochlear nerve remains functional. Sounds

are picked up by the implant’s external microphoneand sent to a processor. The processor converts theacoustic signal into a digital signal. The transmitter,held in place by a magnet, sends the signal via radiowaves to the implanted receiver to be delivered by theelectrode array hugging the modiolus. The receiveris surgically placed in a well drilled into the mastoidprocess. The electrode array is inserted through ahole drilled into the promontory (basal turn of thecochlea). The processor takes advantage of the tono-topic organization of the cochlea, delivering high- frequency information to electrodes hugging the basalend of the cochlea and low-frequency information toelectrodes hugging the apex. The main indication forCI candidacy (adults and children) is limited speechrecognition with amplication. Also paramount is foradults who are prelingually deafened and parents ofchildren with severe-to-profound hearing loss to havea strong desire for oral communication. The FederalDrug Administration has approved CIs for childrenat age 12 months with enrollment in an educationalenvironment that stresses oral communication.




ACQUIRED DISORDERS OF LATER ONSET

Ménière’s Disease

Ménière’s disease was rst described in 1861 by theFrench physician, Prosper Ménière. Classic Ménière’ssyndrome is characterized by vertigo, uctuatinghearing loss, ear noise, and a pressure sensation in

the ear. Episodic vertigo is often accompanied bynausea and vomiting. The hearing loss is sensorineu-ral in nature. In the initial stages, the typical con-guration involves low-frequency hearing loss, butas the disease progresses the higher frequencies willdecline as well, attening out the audiometric pat-tern. The hearing loss often uctuates, worsening just prior to an attack and usually improving as theother symptoms subside. The individual may experi-ence an unusual intolerance to loud sounds known asrecruitment . The involved ear will likely be afictedby low-pitch seashell or roaring tinnitus. The tinnitususually gets more intense just prior to an attack. A full,plugged or pressure sensation may be experienced inthe involved ear. This may be a constant symptom orone that is only present just prior to an attack. Manysufferers experience an aura or premonition of animpending attack. The disease usually affects one earbut there may be bilateral involvement. Males underthe age of 50 are more prone to the disease.

The symptoms of Ménière’s are associated withdisturbances that affect the entire inner ear. The dis-ease, therefore, involves the structures related to both

the vestibular and auditory systems. Recall the onestructure that is common to both is the membranouslabyrinth. The disease causes a change in the endo-lymphatic uid volume within the labyrinth. It is notclear if the cause is related to excessive production ofendolymph or the inefcient reabsorption of exces-sive endolymph.

Many experts believe that endolymphatic uidvolume builds within the labyrinth to the point thatReissner’s membrane will bulge and eventually rup-ture. Recall, Reissner’s membrane separates endo-lymph in the scala media from perilymph in the scalavestibuli. When Reissner’s membrane ruptures thereis a mixing of the two uids. The abrupt chemical dis-ruption accounts for the sudden severe attack of ver-tigo with nausea and vomiting. After the acute attackof vertigo subsides, hearing will improve and the earnoise will alleviate. Attacks vary in their frequencybut the patient experiences vertigo for several hoursand may experience unsteadiness for days. This pro-cess may repeat itself in as little as several days ormay not occur again for several months. Hence, theepisodic nature of the disease is very unpredictable.

Ménière’s disease has been attributed to many dif-ferent causes: allergic reaction, trauma, viral infection,syphilis, and genetic origin. However, the primaryetiology of Ménière’s disease is idiopathic, meaningthe underlying cause is unknown. There is no curefor Ménière’s disease, but medical intervention isoften helpful in managing the symptoms. Treatment

involves controlling the dizziness with medicationthat suppresses the central nervous system’s reac-tion to the unequal information from the vestibularstructures. Treatment also focuses on prevention offuture attacks by diet and lifestyle changes. It is rec-ommended that the sufferer avoid factors known toexacerbate the symptoms such as alcohol, caffeine,tobacco, foods high in sodium, and to the extent pos-sible, stress. Diuretics may be prescribed to controlsymptoms by reducing uid retention and antihista-mines may be used to control allergies.

Ménière’s syndrome is diagnosed by an extensivecase history and audiometric evaluation to docu-ment the hearing loss by conguration and degree.Serial audiometric evaluations are performed todocument the uctuation of hearing levels. Theintegrity of the vestibular system may be measuredand monitored with electronystagmography (ENG) .The physician will use nuclear imaging techniquesto rule out the presence of a tumor on the vestibulo-cochlear nerve.

Surgical procedures are usually attempted only when medical treatment has been exhausted and

the patient is incapacitated by the disease. Theleast invasive procedure involves the placement ofa shunt to reestablish the function of the endolym-phatic sac. In theory, the shunt should decompressthe excessive uid in the sac and allow the inner earto reequilibrate, taking pressure off the nerve end-ings of hearing and balance. The uctuating hearinglevels should stabilize. When there is residual hear-ing worth preserving a vestibular neurectomy is theprocedure of choice (Mattox, 2000). The vestibularbranch of the vestibulocochlear nerve is sectioned.Control of vertigo is successful in 90% of patients as

it insures that the diseased vestibular system can nolonger send signals to the brain. In individuals whohave very little functional hearing and very poordiscrimination, where preservation is not the goal,a labyrinthectomy can be performed. This is a pro-cedure where the entire diseased inner ear is surgi-cally removed or chemically poisoned with ototoxicdrugs (i.e., drugs that are toxic only to the hearingmechanism).

Following surgery, there is usually a period of severevertigo. This can be controlled with medication and




should be temporary as the opposite (i.e., healthy) eartakes over the command of the entire balance func-tion and assumes full control. If one vestibular sys-tem is sending damaged signs to the brain, the brainhas trouble adapting since it is intermittently getting wrong signals mixed with correct ones. However, ifthe inner ear balance nerve is completely shut off on

one side and the damaged system removed, the brain will adapt to this new situation since it now receivesonly correct signals from the one remaining healthysystem which will control the entire balance function.Sadly, about 20% of people with Meniere’s disease willalso develop the illness in their opposite ear later intheir lifetime.

Autoimmune Inner Ear Disease

The immune system is very complex and is the rstline of defense against infectious organisms and for-eign substances that invade our body and cause dis-ease. The immune system is made up of a networkof cells and proteins that work together to ght theinvaders. For the most part the immune system func-tions without a problem. However, when dysfunctionoccurs, the result can be relatively minor or can resultin major disease. Certain lifestyle issues (i.e., poordiet, cigarette smoking) and even some prescriptionmedications can trigger an improper response fromthe immune system. Some diseases, such as rheuma-toid arthritis, are believed to be caused by an overac-

tive immune system. How the immune system worksis not completely understood. A healthy immune sys-tem recognizes “invaders” such as viruses, bacteria oranything foreign that is not a normal part of the bodyand destroys it. Inammation is a major function of theimmune system, yet sometimes this works against us. Autoimmune inner ear disease (AIED) is the result ofan improper response from the immune system thataffects the auditory and balance system. This is a syn-drome characterized by progressive hearing loss and/or dizziness which is caused by antibodies that attackand cause damage to the inner ear. The classic set of

symptoms (and hence the term syndrome) are: bilat-eral progressive hearing loss accompanied with tin-nitus (i.e., ringing, buzzing or humming in the ears),spells of dizziness, and abnormal blood tests for gen-eral autoimmune diseases. The diagnosis is based onhistory, physical examination, blood tests, and hear-ing and balance tests. AIED may resemble other innerear disorders such as those seen in Meniere’s disease,auditory neuropathy, and even syphilis. In general,autoimmune disorders occur more frequently in women than men and less frequently in children and

the elderly. There are several theories as to what causes AIED. One theory is bystander damage . In this theory,damage to the inner ear causes cytokines (involved inthe regulation of various inammatory responses) tobe released which provoke, after a delay, additionalimmune reactions. This theory might explain theoccasional cyclical nature of the disease.

Why You Need to Know Cytokines are a class of proteins that are secreted bycells into the circulation or directly into the tissue.The cytokine proteins locate the target immunecells and act by binding with them. The result isinammation. A certain amount of inammationis necessary for healing; however, overproductionor inappropriate production of certain cytokines bythe body can result in disease. For example, in manytypes of arthritis, the body’s inammatory response

is misdirected.

Another theory is cross-reaction . Antibodies cre-ated to ght a virus or bacteria that are attackingthe body can mistakenly attack the inner ear too asthey can share common antigens (Boulassel, Tornasi,Deggoui, & Gersdorff, 2001). It is also common forantigens to be released following surgery, so the bodymay wrongly mount an attack on the “foreign” anti-gen residing in the inner ear.

An early diagnosis is important in the treatment of AIED. With proper treatment, the hearing loss may bereversed or at least the progression arrested. The stan-dard treatment for an autoimmune reaction is oftenthe same antirejection medications used for trans-plant patients. Chemotherapy is an option sometimesdelivered as long-term therapy. Unfortunately, theside effects of these medications can be numerous ordramatic and can affect the entire body.

Presbycusis

An acquired hearing disorder that is the result ofaging is referred to as presbycusis . This term has beenused to describe the “deafness of aging.” Not surpris-ingly, the prevalence of presbycusis increases as ageincreases. The incidence of hearing loss is approxi-mately 30% to 40% for all individuals over 65 yearsof age, increasing to 40% to 66% for individuals olderthan 75 years, and more than 80% for individuals olderthan 85 years (American Speech-Language-Hearing Association, 2008). As an overall health concern forthe elderly, hearing loss is the third most prevalent




chronic health concern ranking just behind arthritisand hypertension.

Presbycusis is difcult to study as an isolated hear-ing disorder. By the time an individual’s life extendsinto the 70s through 90s, their auditory mechanismhas been exposed to many agents (e.g., medications,noise, and trauma) that could contribute to a loss of

hearing sensitivity. The loss of sensitivity is gradualand the affected person notices that they have increas-ing difculty understanding conversation.

There are many peripheral changes that occur tothe outer and middle ear structures with advanc-ing age. The tissue of the pinna loses elasticity andthe skin becomes scaly and dry, appearing translu-cent with pigmentation spots. Males experience anincrease in hair growth within the folds of the pinna.The changes in the appearance of the pinna do notdirectly affect hearing sensitivity. The epithelial liningof the ear canal becomes thin and dry. The skin hasdifculty migrating to the external meatus, which canresult in obstruction or impaction that can then resultin a temporary conductive hearing loss.

Changes that occur in the middle ear affect the con-duction of sound into the inner ear. The middle earmuscles and tendons atrophy with advanced age. Theremay be a loss of elasticity in the ossicular joints, rigidityof the ossicular chain, and a loss of elasticity of the tym-panic membrane. These structural changes may add aslight conductive component to the hearing loss.

The majority of the changes related to advanced age

occur within the structures of the cochlea or cochlearnerve. Degeneration of the hair cells and basilar mem-brane will take place initially at the basal end of thecochlea. The cochlear branch of the vestibulocochlearnerve (cranial nerve VIII) may partially atrophy as wellas the spiral ganglion. Degeneration of the stria vascu-laris causes a disruption in the ion balance necessaryfor cellular function for the entire cochlea.

Schuknecht (1974) described specic audiometriccongurations that are predictable from the struc-tural changes. The type of hearing loss is sensorineu-ral in nature but as seen in Figure 13-17, the patterns

vary. The changes within the cochlea and cochlearnerve exhibit a sloping high-frequency loss due to thechanges along the basal end of the basilar membrane. Audiometrically, the stria vascularis changes will alsoproduce a sensorineural hearing loss but exhibit a moreat conguration since the stria vascularis degenera-tion affects the physiology of the entire cochlea.

Peripheral structures may deteriorate, but thereis also apparent involvement in the central auditorysystem. Recall this system allows for interpretation orprocessing of what the peripheral system detects. As a

person ages, the ascending auditory pathway from thecochlea through the various levels of the brainstem will typically experience a reduction in the numberof functioning neurons, especially at the level of thesuperior olivary complex. The outcome of this centralstructural change is a disproportionate difculty inunderstanding speech, greater than one would expectfrom audiometric results. This condition is termedphonemic regression .

Many structural changes do not occur in isola-

tion. Depending on the degree of outer or middleear involvement, a conductive component yielding aslight air-bone gap may also be seen. Speech discrim-ination may be fair to poor depending on the degreeof central involvement.

The longevity of the auditory mechanism variesgreatly from person to person. The high-frequencyinformation affected by the aging process makes it dif-cult for the individual to hear conversations clearly.The aging listener will complain that most speak-ers sound as if they are mumbling. Appropriately tamplication will help the individual be more aware

of conversational speech but may not aid in clarifyingspeech if the person is experiencing central process-ing changes.

Noise-Induced Hearing Loss

Noise-induced hearing loss (NIHL) is the most com-mon form of acquired hearing disorder. It is completelypreventable and yet 10 million Americans suffer itseffects. The National Institute for Occupational Safetyand Health (1998) has designated NIHL as one of the

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Typical audiometric configuration Strial presbycusis Sensory presbycusis Neural presbycusis

Figure 13-17 Typical audiometric congurations for speciccauses of presbycusis.




ten leading occupational diseases and injuries. Elevatedrecreational noise will also permanently damage thecochlea. It is not the source of the noise that is damag-ing but rather the level of the noise and time of exposurethat causes the damage.

There are two types of noise-induced damage: (1)acoustic trauma resulting in permanent damage from

a single exposure to very high noise levels and (2)continuous exposure to repeated moderately intenselevels resulting in a gradual hearing loss. Continuousexposure initially affects thresholds for high frequen-cies (3000 to 6000 Hz) with a typical “notch” at 4000 Hz(Clark & Bohne, 1999). As exposure continues, the midto lower frequencies become affected. Both forms ofNIHL can be prevented by the regular use of hearingprotection such as earplugs or earmuffs.

Tinnitus (e.g., ringing, buzzing or humming in theears) or difculty understanding conversation is oftenthe rst symptom of an NIHL. Hearing loss and tinnitusmay be experienced in one or both ears, and tinnitusmay be constant or just occasional after noise exposure.

Sound intensity is measured on a logarithmic scaleknown as the decibel (dB) scale. Noise exposure mea-surements are often expressed as dB (A). The A scaleis weighted toward the higher frequency sounds to which the human ear is most sensitive. Unprotectedexposure to impulse or continuous noise levels inexcess of 90 dB (A) for an 8-hour period will cause ashift in an individual’s hearing thresholds. This shift inthreshold is referred to as a temporary threshold shift

(TTS) . In most instances, the TTS largely subsides 16to 48 hours after exposure (Clark, Bohne, & Boettcher,1987). However, with repeated exposure and repeatedTTS, damage occurs, and hence the insidious natureof noise. As the decibel level of a sound increases,the exposure time before there is permanent damagedecreases. Decibel values are based on a logarithmicscale, so what seems like a slight increase in decibels—say from 80 dB IL to 90 dB IL—is actually a ten-foldincrease in intensity. OSHA’s table of permissiblenoise exposure outlines a worker’s duration per dayin hours against the decibel level. Basically, for every

5 dB increase in noise level, the exposure time is cutin half. Therefore, a 4-hour exposure to noise at 95 dB(A) is considered to provide the same noise “dose” as8 hours of exposure to noise at 90 dB (A). Think aboutthis: a single gunshot of approximately 140 dB (A) hasthe same sound energy as 40 hours of 90 dB (A) noise!Gradual NIHL typically affects both ears equally creat-ing a symmetric audiometric pattern. By comparison,noise from such sources as tractors or rearms exposeone ear more than the other producing an asymmetrichearing loss.

In today’s noisy world, young adults are exposedto many sources of loud noise that place them at riskfor hearing loss. Most high school industrial arts pro-grams must include education on hearing conserva-tion. The simplest solution is to simply turn downthe volume or, if possible, wear appropriate hearingprotection. The following signs are an indication that

the noise level around you is too loud and could causedamage if exposure is continued:• You have to shout to be heard above the noise.• You cannot understand someone who is speak-

ing to you from less than 2 feet away.• A person standing near you can hear the sound

from your stereo headset while it is on your head.Noise causes permanent changes to the cochlea

resulting in a sensorineural hearing loss. The physi-cal structures of the cochlea literally get beat to deathby the insidious pounding of acoustic pressure waves.The stereocilia of the cochlea’s hair cells are damaged,bent or broken. When stereocilia are damaged, thecorresponding hair cell body dies and the neuronsthat synapse with the hair cell degenerate.

Why You Need to Know Loud rock concerts have contributed to hearing lossin the baby boomer generation but iPod and similarplayers are much worse for the present generation.The problem begins with the headphones restingdirectly in the ear canal (concha bowl). This allowsthe user to easily overcome any background noisesuch as the noise of the school lunch room or lawnmower. As a result, they easily desensitize the user todangerously high sound levels. Portable CD playersdo too, but iPods pose an additional danger becausethey hold thousands of songs and can play for hourswithout recharging so users tend to listen continu-ously for hours at a time. The user does not have tostop to change a CD or a tape. Damage to hearingcaused by high volume is determined by its duration;continuous listening even at a seemingly reasonable

level can damage the hair cells in the inner ear result-ing in permanent hearing loss. Denying the dangerof noise-induced hearing loss would not be so easy ifloud music made the ears bleed, but the early symp-toms tend to come on gradually. It typically startswith ringing in the ears. The problem often timesbecomes advanced before people realize they are hav-ing serious difculty hearing. Adapted from a CBSNews interview August 25, 2005, by Lloyd de Vries,MP3s May Threaten Hearing Loss: Experts DiscussRisk to Hearing from Listening to Music Devices.




Avoiding noise exposure or using appropriatehearing protection stops further progression of thedamage. In the future, the use of chemoprotectiveagents such as antioxidants as well as identicationof possible risk factors for susceptibility to NIHL mayenhance prevention and treatment efforts. Risk fac-tors include but are not limited to cigarette smok-

ing, excessive caffeine consumption, and concurrentexposure to ototoxic substances such as solvents andheavy metals (Morata et al., 1993).

The characteristic audiometric pattern indicatingNIHL is a notch in the high frequencies. Figure 13-18illustrates the classic research by Taylor, Pearson,Mair, and Burns (1965) which demonstrates the effectof long-term exposure to noise on hearing levels. Thegure demonstrates the hearing threshold levels of workers comprised over many years of exposure. Thehearing loss continues to get more severe as the yearsof exposure continue. The purpose of the study was todemonstrate the detrimental effect of chronic noiseexposure on hearing.

Noise Exposure Regulations

An employer must provide for his workers a place ofemployment that is free from recognized hazards. TheOccupational Safety and Health Administration (2002)requires employers to provide hearing conservationprograms for employees where an 8-hour exposureexceeds an 85-dB weighted average. An occupationalhearing conservation program includes:

• engineering and administrative controls to reducenoise exposures

• monitoring of noise levels• annual audiometric testing for the purpose

of monitoring for signicant threshold shifts(dened as a shift of 10 dB or more in the worsethreshold of 2000, 3000 or 4000 Hz)

• use of hearing protectors (i.e., the employer mustprovide a reasonable choice of adequate hearingprotectors free to all employees)

• employee training on the use of hearing protec-tion

• adequate record keeping.Claims for occupational hearing loss are typically

handled through state Labor and Industry Workman’sCompensation. A mathematical formula is used toconvert the worker’s degree of hearing loss into apercentage of impairment. Only certain frequenciesare considered compensable and a minimum amountof hearing loss must be present. The American Medi-cal Association (1979) uses the average thresholds of500, 1000, 2000, and 3000 Hz to determine the amountof hearing loss. A 25 dB threshold fence is then sub-tracted and that gure is multiplied by a constant (1.5)to obtain the percentage of monaural hearing loss.

Noise exposure, whether occupational or recre-ational, is the leading cause of a preventable acquiredhearing disorder. Occupational hearing loss is mini-mized by well tting hearing protection and workercompliance. Recreational NIHL can be reduced bypublic education of the harmful effect of noise on the

delicate auditory mechanism.

Summary

A good clinician will begin patient evaluation by tak-ing a thorough case history. The case history willinclude questions that are identied as the ve “cardi-nal signs” of ear pathology. The patient’s responses willhelp identify the presence of ear pathology. A clinicianoften times feels like a detective, asking several spe-

cic questions to get more and more detail. Is the lossin one ear or both? Is there any pain or pressure pres-ent, and if so, when did it start? As a student you willlearn to recognize the classic signs and symptoms fora particular pathology. For example, a patient sufferingfrom Ménière’s disease will experience low-pitch tin-nitus and a low-frequency hearing loss. On the otherhand, a person suffering from an NIHL will suffer fromhigh-pitch tinnitus and a high-frequency hearing loss.Genetics and environmental agents are equally respon-sible for the cause of most hearing disorders and the

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Exposure 1–2 years 5–9 years 15–19 years 25–29 years 35–39 years

Figure 13-18 Audiometric conguration illustrates the long-term effect of noise on hearing levels compromised over manyyears of exposure.




patient is simply at their mercy. What is unfortunate is when a hearing loss is preventable as is often the case with hearing loss from exposure to excessive levels ofnoise. Part of our job as a speech or hearing specialistis to inform the public about the dangers of exposureto high levels of noise in one’s daily life.

Clinical Teaser—Follow-UpAt the beginning of this part, you were asked to noteany terms and concepts in the case study that were un-familiar to you. As you read Chapter 12, you were topay particular attention to the anatomy and physiologypertinent to this case. Now we return to the case forfurther discussion. We can interpret this case regarding etiology and pathol-ogy. The gentleman did not report a head injury or trauma

or a family history of ear disease or hearing loss. The etiol-ogy of the disease is unknown (i.e ., idiopathic). The gentle-man suffered from both auditory and vestibular symptoms,

thereby leading us to conclude that the entire inner ear mustbe involved. The perilymph and endolymph uids are com-mon to both the auditory and vestibular systems. There areseveral diseases that can have this effect on the entire innerear. The results of a battery of audiometric and vestibular

tests lead us to the conclusion that this patient evidencesMénière’s disease in his right ear. What pertinent informa-

tion from the case history assisted you in drawing this con-clusion? What pertinent (though limited) information from

the audiometric evaluation assisted you in drawing this con-clusion? Lastly, using the information about Ménière’s in thischapter, explain a treatment option for this patient payingparticular attention to the anatomy that would be affectedby the disease.



PART 6 SUMMARYThe ear, organ of hearing and balance, is mostly invisible with the pinnae being the onlyvisible structures. We recognize that they are similar in shape among individuals, but when we closely examine each one, there are many differences. Even the right and leftpinna within the same person can be very different. The remaining structures of the outer,middle, and inner ear have some uniqueness as well but must not deviate far from theintended design. Injury, disease, and genetics can produce an acquired or congenital hear-ing or balance disorder. Timing is the key to the overall effect on the structures involved.

The mechanical role of the outer ear may not be as dramatic as that of the electro-chemical role of the inner ear but is still very necessary. The ear canal resonance boostsan incoming signal by a signicant amount at a very specic and useful frequencyrange (20 dB in the range from 1500 to 7000 Hz). The curvature of the ear canal servesto protect the ne structures of the tympanic membrane and middle ear. The tym-panic membrane and ossicular chain obey the laws of physics. The transformer actionof the structures boosts the signal by approximately 27 dB to overcome the impedancemismatch of the air-lled middle ear to the uid-lled inner ear.

The inner ear vestibular system is the primary organ for allowing independent and

precise head and eye control in the execution of many complex motor activities suchas running. Vestibular input is critical for balance when there is misleading informa-tion from the other senses (e.g., visual and somatosensory).

The inner ear auditory system is remarkable. The structure and function of thecochlea is so intricate that we have yet to completely understand how it all works. Theouter hair cells embedded in the tectorial membrane mechanically amplify the softsounds so that the inner hair cells may respond. The endolymph ow displaces thestereocilia of the hair cells. The tip links attached to the stereocilia act as mechani-cal gates opening channels for ion (i.e., potassium and calcium) exchange. The ionexchange depolarizes the hair cell stimulating the release of a neurotransmitter.The stria vascularis then recycles the cochlear uids so that the process can then berepeated over and over again at a mind-boggling rate.

Once the cochlear nerve enters the brainstem, we begin the discussion of the audi-tory pathway. The reex arc of the middle ear muscles relies on the auditory pathway.The processing of the acoustic information along the pathway facilitates the local-ization of a sound source. The redundancy of the auditory pathway as it travels toHeschl’s gyrus preserves and protects the acoustic information that was sensed by theperipheral structure.

The moment an acoustic pressure wave is directed by the pinna down the ear canal,the reaction of the ear structures is set in motion. Many inuences, natural or otherwise, disrupt the function of the aural anatomy and cause a hearing disorder. The hear-ing impairment that accompanies the hearing disorder may cause a communicationproblem. Timing is everything. The earlier in life and the more severe the impairment,

the more detrimental the effect will likely be on both aural (i.e., listening) and oral (i.e.,speaking) communication.

PART 6 REVIEW QUESTIONS 1. Describe how the anatomical structures of the outer, middle, and inner ear each

contributes to the physiology of the auditory and/or vestibular systems. 2. Discuss the similarities and differences between the sensory receptors of the

semicircular canals (crista ampullaris) and the vestibule (macula). Draw asimple illustration of each identifying the landmarks.

351




3. Discuss the differences and similarities between the inner and outer hair cellsand draw a simple illustration of each identifying the landmarks.

4. Choose and describe one of the three ways the conductive mechanism over-comes the impedance mismatch between the air-lled middle ear and the uid-lled inner ear.

5. Choose an ear pathology; identify a chief complaint for that pathology. Answerthe “ve cardinal signs of pathology” as if you were the patient suffering fromthe pathology you chose.

6. Choose a syndromic hearing disorder of genetic origin. Identify the systems thatare affected in addition to the auditory system and identify the syndrome’s modeof inheritance. List the possible transmission probabilities (i.e., percentages) if you marry someone without any trace of the disorder. List the possible transmis-sion percentages if you marry someone with the exact same syndrome.

7. Choose an ear pathology that is typically seen within each of the following agegroups: 0 to 18, 18 to 50, 50 to 64, and 65 . Discuss the etiology of each pathology.



353

TABLE A-1

TERMS AND PREFIXES USED TO DESCRIBE MOVEMENT

Term Denition

Abduction Movement away from the median plane; separation of two structures (e.g., the vocal folds) Adduction Movement toward the median plane; bringing together of two structures (e.g., the vocal folds)Circumduction Movement in a circular direction (e.g., rotating the eyeballs)Deglutition The process of swallowing Depressor The process of lowering a structure (e.g., depressor anguli oris—a muscle that lowers the corner of

the mouth)Eversion Turning outward (e.g., turning the sole of the foot laterally)Extension Stretching out (e.g., straightening the arm by extending it outward)Flexion Bending (e.g., bending the forearm toward the shoulder by contracting the biceps)Hyper- Excessive (e.g., hyperkinesis—excessive, uncontrollable movements)Hypo- Diminished or decient (e.g., hypokinesis—diminished or slow movement)

Inversion Turning inward (e.g., turning the sole of the foot medially)Levator The process of raising a structure (e.g., levator veli palatini—a muscle that raises the soft palate)Mastication The process of chewing Opposition Moving a structure toward another structure (e.g., contacting the thumb and index nger)Tachy- Rapid movement (e.g., tachycardia—an unusually fast heart rate)Tensor The process of tensing a structure (e.g., tensor veli palatini—a muscle that tenses the soft palate)

APPENDIX

Terms and Affixes to AssistYou in Learning the Meanings of Anatomical andPhysiological Words

TABLE A-2

TERMS AND AFFIXES USED TO DENOTE ANATOMICAL STRUCTURES OR THEIR PARTS

Term Denition Example

Ary- Pertaining to the arytenoid cartilage

Ary epiglottic fold—the fold of tissue that runs from the lateral aspect of the epiglottis to the arytenoid cartilages

Clavius Pertaining to the clavicle Sub clavius —a muscle found immediately below, and running parallel to, the clavicle

Cleido- Sterno cleido mastoid—a muscle that has three attachments, to the sternum, clavicle, and mastoid process

Costal Pertaining to the ribs Costal pleura—a layer of connective tissue that adheres to the inner rib cageCostalis Lateral ilio costalis —a muscle that runs from the ilium to the lower ribs,

assisting in depressing themCostarum Levator costarum brevis—short muscles just lateral to the spinal

column along the rib cage that assist in elevating the ribs

Continued on following page



354 APPENDIX

TABLE A-2

TERMS AND AFFIXES USED TO DENOTE ANATOMICAL STRUCTURES OR THEIR PARTS (Continued)


Crico- Pertaining to the cricoid cartilage

Crico arytenoid—the joint formed by the articulation of the cricoid cartilage with each of the arytenoid cartilages

-dontia Pertaining to the teeth Ano dontia —any number of missing teethGenio- Pertaining to the chin Genio glossus—a muscle that runs from the inside of the chin to the

tongueGlosso- Pertaining to the tongue Glosso pharyngeal—cranial nerve IX that provides motor bers to parts

of the tongue and pharynx -glossus Genio glossus —a muscle that runs from the inside of the chin to the

tongue-gnathia Pertaining to the jaw Micro gnathia —an unusually small mandibleHyo- Pertaining to the hyoid

boneHyo thyroid—a membrane that lls the space between the hyoid bone and the thyroid cartilage

Iliac Pertaining to the ilium Iliac crest—the prominent ridge of the ilium, more commonly referred to as the hip bone

Ilio- Lateral ilio costalis—a muscle that runs from the ilium to the lower ribs, assisting in depressing them

Labio- Pertaining to the lips Labio version—any number of anterior teeth that are tilted toward the lipsLaryngo- Pertaining to the larynx Laryngo pharynx—the lowermost part of the pharynx in the general region of the larynx, immediately above the esophagus

Lingua- Pertaining to the tongue Lingua nigra—a tongue disease caused by excessive use of antibiotics; also known as “black hairy tongue”

Linguo- Linguo version—any number of teeth that are tilted toward the tongueLingual Lingual frenulum—a fold of mucous membrane extending from the

oor of the mouth to the undersurface of the anterior tongueLumbo- Pertaining to the lumbar

vertebrae or the lowerback

Lumbo costal ligament—connective tissue that binds the twelfth rib to the rst two lumbar vertebrae

Lumborum Quadratus lumborum —a rectangular-shaped muscle deep within the abdomen in the region of the lower back

Mandibular Pertaining to the mandible (jaw)

Temporo mandibular joint—the joint formed by the condyle of the mandible and the mandibular fossa of the temporal bone of

the skullMental Pertaining to the

protruding part of thechin (mentum)

Mental foramen—a small opening in the mandible in the region of the chin

Mylo- Pertaining to the lower jaw, more specically

the molar teeth

Mylo hyoid—a muscle that runs from the mylohyoid line (a prominent ridge along the inner aspect of the lower jaw) to the hyoid bone

Naso- Pertaining to the nasal cavity

Naso pharynx—the uppermost region of the pharynx in the general region of the posterior nasal cavity

Oculo- Pertaining to the eyes Oculo motor—cranial nerve III, responsible for movements of the eyeballOmo- Pertaining to the

shoulder regionOmo hyoid—a two-bellied muscle that runs from the hyoid bone to the scapula (shoulder blade)

Oro- Pertaining to the oral cavity

Oro pharynx—the middle region of the pharynx in the general region of the back of the oral cavity

Palatine Pertaining to the palate, either hard or soft

Palatine processes—the bony shelves of the maxilla that help form the hard palate

Palatini Pertaining to the palate, more often the soft palate

Tensor veli palatini —a muscle that makes up the bulk of the body of the soft palate; its function is to tense the soft palate

Palato- Palato glossus—a muscle that runs from the sides of the soft palate, around the sides of the posterior oral cavity, and into the sides of the

posterior tongue



TERMS AND AFFIXES TO ASSIST YOU IN LEARNING THE MEANINGS OF ANATOMICAL AND PHYSIOLOGICAL WORDS 355

TABLE A-2

TERMS AND AFFIXES USED TO DENOTE ANATOMICAL STRUCTURES OR THEIR PARTS (Continued)


Pharyngeal Pertaining to the pharynx

Pharyngeal aponeurosis—the broad, at, funnel-shaped tube of connective tissue that forms the skeleton of the pharynx

Pharyngo- Pharyngo palatine—a muscle that runs from the pharynx to the soft palatePterygo- Pertaining to the

pterygoid process of thesphenoid bone of the skull

Pterygo mandibular ligament—a ligament that connects the mandible to the pterygoid process

Sacro- Pertaining to the sacrum Sacro spinalis—muscle that runs from the sacrum to the lower spinal column

Spheno- Pertaining to the sphenoid bone of the

skull

Spheno -occipital—pertaining to the sphenoid bone and the basilar process of the occipital bone

Sternal Pertaining to thesternum (breastbone)

Sternal notch—the indentation along the superior border of the manubrium of the sternum

Sterni Manubrium sterni —the upper part of the sternumSterno- Sterno thyroid—a muscle that runs from the sternum to the thyroid

cartilageStylo- Pertaining to the

styloid processStylo hyoid—a muscle that runs from the styloid process (on the inferior surface of the temporal bone of the skull) to the hyoid bone

Thyro- Pertaining to the thyroid cartilage

Thyro epiglottic ligament—a ligament that attaches the petiolus of the epiglottis to the thyroid cartilage

Tracheo- Pertaining to the trachea (windpipe)

Tracheo -esophageal puncture—a surgical procedure where an airway is established between the trachea and esophagus, so that a person who

has undergone a laryngectomy can produce voicing Tracheal Crico tracheal ligament—the ligament that anchors the cricoid cartilage

onto the superior border of the trachea Veli Pertaining to the

velum (soft palate)Levator veli palatini—a muscle whose purpose is to raise the soft palate

Velo- Velo pharyngeal port—the variable-sized opening between the soft palate and the posterior pharyngeal wall

Vertebro- Pertaining to the spinal column Vertebro sternal—the articulation between the true ribs and the sternum;in this case, vertebro- comes from the fact that all the ribs have a posteriorattachment to the vertebral column

TABLE A-3

TERMS AND PREFIXES USED TO DESCRIBE COLOR, FORM, GENERAL LOCATION, RELATIVE SIZE, OR SHAPE


Abdominus Pertaining to the abdomen (belly)

Transversus abdominus —a muscle of the abdominal wall whose bers run from side to side

Alba White Linea alba —“white line”; a white line of connective tissue running vertically down the midline of the belly Apical Toward the apex or tip Apical foramen—an opening at the tip of the roots of the teeth where

blood vessels and nerve bers pass into the interior of the toothBid Separated or split Bid uvula—a uvula that is split into two partsBrevis Muscle bers of relatively

short lengthLevator costarum brevis —short muscles just lateral to the spinal column along the rib cage that assist in elevating the ribs

Buccal Pertaining to the cheeks Buccal cavity—the space between the inside of the cheeks and the premolar and molar teeth

Cyan- Blue Cyan osis—the condition of turning blue because of a lack of oxygenDi- Two Di gastricus—a muscle having two bellies




356 APPENDIX

TABLE A-3

TERMS AND PREFIXES USED TO DESCRIBE COLOR, FORM, GENERAL LOCATION, RELATIVE SIZE, ORSHAPE (Continued)


-gastricus Pertaining to the belly or stomach

Digastricus —a muscle having two bellies

Jaun- Yellow Jaun dice—a yellow pigmentation of the skin and eyeballs due to the

presence of bileLatissimus Pertaining to a lateral

directionLatissimus dorsi—a muscle whose bers swing laterally from the lower spinal region and sacrum to the humerus of the arm

Leuko- White Leuko cyte—a white blood cellLinea A line Linea alba—the line of connective tissue running longitudinally down

the midline of the belly, separating the abdominal muscles into pairs,left and right

Longissimus Pertaining to a longitudinal direction

Longissimus dorsi—a back muscle whose bers run longitudinally from the sacrum to the uppermost ribs, traversing the entire length of the

rib cageLongus Muscle bers of relatively

greater lengthLevator costarum longus —muscles conned to the lower ribs, just lateral to the spinal column and approximately twice the length of

the levator costarum brevis musclesMacro- Large, long Macro dontia—any number of disproportionately large teethMajor Of relatively larger size Pectoralis major —a muscle of the lateral upper chest, larger in size than

the pectoralis minorMicro- Small, short Micro dontia—any number of proportionately small teethMinor Of relatively smaller size Psoas minor —a muscle deep within the abdomen in the region of the

pelvic girdle, smaller in size to the psoas majorNigra Black Substantia nigra —darkly pigmented nerve cell bodies in the

midbrainOblonga Having an oblong,

somewhat ovalappearance

Fovea oblonga —an oblong depression along the anterolateral base of the arytenoid cartilages

Petrous Dense, hard (like a rock) Petrous portion of the temporal bone—the denser portion of the

temporal bone where the hearing mechanism is housedQuadrate Somewhat square or rectangular shaped

Posterior quadrate lamina—the somewhat square-shaped posterior wall of the cricoid cartilage

Quadratus Quadratus lumborum—a somewhat rectangular-shaped muscle in the deep abdomen in the region of the pelvic girdle

Rubro- Red Rubro spinal tract—a part of the extrapyramidal motor system that originates in the red nucleus and proceeds down the spinal cord

along with the corticospinal tractSerratus Jagged or sawtooth

shapedSerratus anterior—a muscle of the anterolateral rib cage that inserts into the ribs from a somewhat oblique direction, giving the muscle a

jagged appearanceThoracis Pertaining to the thorax

(chest)Transversus thoracis —a muscle of the inner rib cage that extends transversely from the sternum to the ribs

Torus A rounded bulge or ridge Torus palatinus—a rounded bulge on the midline of the hard palate in some people

Trapezius Having a somewhat trapezoidal shape

Trapezius —a muscle that is shaped somewhat like a trapezoid, running from the spinal column of the neck and thorax to the clavicle (collar

bone) and scapula (shoulder blade)




TABLE A-4

TERMS AND AFFIXES USED IN REFERENCE TO BONES, CARTILAGES, CAVITIES, MEMBRANES, OR SPACES


Aditus An inlet or opening Aditus laryngis—the opening into the interior of the larynx Alveolus A small cavity or socket Dental alveolus —a tooth socket Arcuate Arched or bow shaped Arcuate ridge—a bow-shaped ridge on the anterolateral surface of

the arytenoid cartilageCecum A cul-de-sac Foramen cecum —a small cul-de-sac depression at the sulcus

terminalis of the tongueCerato- Pertaining to a horn Cerato glossus—the posterior portion of the hyoglossus muscle

whose origin is the greater horn of the hyoid boneChondro- Pertaining to cartilage Chondro blasts—cells that allow for growth of cartilageConcha A structure that is somewhat

shell shapedNasal concha —a turbinate bone within the lateral wall of the nasal cavity that is somewhat shell shaped

Condyle A rounded articular surface at the end of a bone or bony

process

Mandibular condyle —the rounded surface at the superior marginof the ramus of the mandible that articulates with the temporalbone of the skull

Corpus Body Corpus of the hyoid—the body of the hyoid boneCrest A bony ridge Palatine crest —a bony ridge on the inferior surface of the

horizontal plate of the palatine boneCribriform A plate of bone containing many perforations

Cribriform plate—the horizontally directed plate of the ethmoid bone of the skull containing many perforations through which

nerve bers from the olfactory nerve pass as they enter the nasalcavity

Crus A structure that is somewhat shaped like a leg

Crus cerebri—the mass of nerve bers resembling a leg that passes through the ventral surface of the midbrain

Fossa A longitudinally directed depression in bone

Glenoid fossa —the depression in the head of the scapula that receives the head of the humerus

Fovea A somewhat shallowdepression or pit

Fovea oblonga—a shallow depression along the base of the anterolateral surface of the arytenoid cartilage

Fronto- Pertaining to the frontal boneof the skull

Fronto parietal—the joint between the frontal and parietal bones of the skull

Glottic Pertaining to the glottis Sub glottic space—the space immediately below the level of the glottis

Lamina A thin plate or at layer (usually in reference to bone

or cartilage)

Posterior quadrate lamina —the somewhat at, square-shaped posterior portion of the cricoid cartilage

Meatus A channel or passageway External auditory meatus —the channel that runs from the pinnaon the outer surface of the head to the eardrum within thetemporal bone

Musculo- Pertaining to muscles Musculo skeletal—the attachments of muscles to the skeletonMyo- Myo fascial pain dysfunction syndrome—a condition where

the muscles of mastication spasm, causing great pain to the sufferer

Nuchal Pertaining to the back of the

neck

Superior nuchal line—a small ridge running horizontally across

the occipital bone of the skull where some posterior neckmuscles attach

Occipito- Pertaining to the occipital bone of the skull

Occipito mastoid—the region of the mastoid process of theoccipital bone

Orbital Pertaining to the eye sockets Infra orbital foramen—a small opening just below the orbit ofthe eye

-osseo- Pertaining to bone Chondro- osseo us union—a junction between cartilage and boneOsteo- Osteo blasts—bone-forming cellsParieto- Pertaining to the parietal

bones of the skullParieto- occipital—the joint between the parietal and occipital bones of the skull




358 APPENDIX

TABLE A-4

TERMS AND AFFIXES USED IN REFERENCE TO BONES, CARTILAGES, CAVITIES, MEMBRANES, OR SPACES (Continued)


Pars A part or portion Pars oblique—a bundle of diagonally directed bers of the cricothyroid muscle

Pectoral Pertaining to the chest Pectoral girdle—the bones, ligaments, and muscles that formthe shoulder region

Pectoralis Pectoralis major—a large fan-shaped muscle of the upperlateral chest

Pelvic Pertaining to the lower region of the abdomen and the hips

Pelvic girdle—the bones, ligaments, and muscles that make upthe lower abdominal and hip region

Process A projection or outgrowth on bone or cartilage

Vocal process —the projection at the base of the arytenoidcartilage where the medial and anterolateral surfaces meetthat serves as the posterior point of attachment of thevocal fold

Salpingo- Referring to a tube Salpingo pharyngeus—a muscle that makes up the medial wall of the cartilaginous portion of the Eustachian tube

Spine A short thorn-like process of a bone

Spine of the scapula—the sharp process of the scapula where the trapezius muscle attaches

Symphysis The union of two structures Pubic symphysis —the brocartilaginous joint between the two pubic bones

Temporo- Pertaining to the temporalbone of the skull

Temporo mandibular joint—the joint formed between the mandibular fossa of the temporal bone and the condyle of the

mandible Ventricular Pertaining to the ventricular

(false) foldsVentricular ligament—the skeleton of connective tissue on which a ventricular fold attaches

Vocal Pertaining to the vocal folds Vocal ligament—the skeleton of connective tissue on which a vocal fold attaches

TABLE A-5

TERMS AND AFFIXES USED IN REFERENCE TO THE NERVOUS SYSTEM


Afferent Inowing or toward the center Afferent nerves—nerves that send impulses toward the central nervous system, that is, sensory nerves

Amygdaloid Almond shaped Amygdaloid nucleus—an almond-shaped collection of nerve cell bodies in the temporal lobe of the cerebrum, immediately

anterior to the inferior horn of the lateral ventricle Arachnoid Resembling a spider’s web Arachnoid —the intermediate (middle) layer of the meninges Arbor vitae Literally, “tree of life” Arbor vitae —the white matter of the cerebellum; upon sagittal

sectioning, its appearance is similar to a tree with branchesBulbar Pertaining to the brainstem Bulbar palsy—progressive muscular paralysis that results from

degeneration of the cell bodies of the cranial nerves in thebrainstem

Callosum Huge, massive Corpus callosum —a massive bundle of myelinated bers connecting the two cerebral hemispheres

Cauda equina Literally, “horse tail” Cauda equina —the roots of all of the spinal nerves below the rst lumbar spinal nerves, somewhat resembling a horse’s tail due to

their arrangementCaudate Pertaining to a tail Caudate nucleus—a mass of nerve cell bodies that consists of a

head with a long curved tail




TABLE A-5

TERMS AND AFFIXES USED IN REFERENCE TO THE NERVOUS SYSTEM (Continued)


Cerebellar Pertaining to the cerebellum Cerebellar gait—a wide-based gait with unsteadiness evident upon lateral movement

Cerebelli Tentorium cerebelli —a strong fold of the dura mater that separates the cerebellum from the occipital region of the cerebrum

Cerebello- Cerebello pontine angle—a recessed area where the cerebellum, pons, and medulla converge

Cerebral Pertaining to the cerebrum Cerebral palsy—a neurological condition affecting motor ability and coordination due to damage to the primary and/or

secondary motor pathwaysCerebri Crus cerebri —the tightly compacted nerve bers passing through

the ventral midbrainCerebro- Cerebro vascular accident—a stroke, caused by damage to the

vascular system of the cerebrumCingulate To surround Cingulate gyrus—a long curved convolution of the medial cerebral

hemisphere immediately above the corpus callosum and surrounding it to a certain degree

Colliculus A small mound or elevation Inferior colliculus —one of two paired swellings in the dorsal midbrain that are part of the auditory pathway

Corona A crown Corona radiata—widely radiating bers of the internal capsulethat somewhat resemble a crown

Corpora A body Corpora quadrigemina—four oval masses (superior and inferior colliculi) found in the dorsal midbrain that are part of the visual

and auditory pathwaysCortical Pertaining to the cerebral

cortex Cortical blindness—a loss of vision as a result of damage to the visual areas of the cerebral cortex

Cortico- Cortico spinal tract—the primary motor pathway that originates in the precentral gyrus of the cerebral cortex and provides input to

the spinal nervesCranial Pertaining to the cranium or

headCranial nerves—the nerves originating in the brainstem that primarily supply the muscles and viscera of the head and neck

Dural Pertaining to the dura mater Sub dural hematoma—a hemorrhage into the space immediately below the dura mater

Efferent Outowing or away from the center

Efferent nerves—nerves that send impulses away from the central nervous system, that is, motor nerves

Encephalon Pertaining to the brain Mes encephalon —the midbrainFasciculus A bundle, usually in reference

to nerve bers Arcuate fasciculus —a bowed bundle of nerve bers in the cerebrum connecting Broca’s area with Wernicke’s area

Fissure A deep furrow or cleft Longitudinal ssure —the deep cleft that separates the two cerebral hemispheres

Flocculo- Pertaining to the occulus(a part of the cerebellum)

Flocculo nodular lobe—a small lobe of the cerebellum that is part of the vestibular system

Geniculate Bent sharply, like a knee Medial geniculate body—one of a pair of bodies on the posterior

and inferior surface of the thalamus that are part of the auditorypathway Lemniscus Ribbon-like Lateral lemniscus —a thin tract of bers in the brainstem that sends

auditory information to the inferior colliculus in the midbrainLenticular Bi-convex or lentil shaped Lenticular nucleus—a bi-convex lens-shaped nucleus consisting of

the putamen and globus pallidusMeningeal Pertaining to the meninges

covering the brain andspinal cord

Meningeal vessel grooves—a series of depressions on the inner surface of the bones of the cranium where the blood vessels

covering the brain reside-neurium Pertaining to nerve tissue or

nervesEpineurium —the outermost layer of connective tissue surrounding peripheral nerve trunks




360 APPENDIX

TABLE A-6

TERMS AND PREFIXES USED IN REFERENCE TO THE AUDITORY / VESTIBULAR SYSTEM


Audio- Pertaining to hearing Audio meter—an electronic instrument for the measurement of hearing thresholds

Auricular Pertaining to the ear Auricular cartilage—the cartilage that makes up the skeleton of the auricle or pinna

Cochlear Pertaining to the cochlea Cochlear nerve—the portion of cranial nerve VIII that sends sensory information regarding hearing to the brain, originating in the cochlea

Incudis Pertaining to the incus Fossa incudis —a hollow within the middle ear cavity where the short process of the incus resides

Incudal Incudal ligament—a singular ligament that suspends the incus in placeIncudo- Incudo stapedial joint—the point of articulation between the incus and

stapesMalleo- Pertaining to the malleus

Malleo incudal joint—the point of articulation between the malleus and incus

Malleolar Malleolar ligaments—a series of three ligaments that suspend the malleus in place

TABLE A-5

TERMS AND AFFIXES USED IN REFERENCE TO THE NERVOUS SYSTEM (Continued)


Neuro- Pertaining to the nervous system or nerves

Neuro muscular junction—the point where nerve bers innervate muscle bers to create a contraction

Nodular Pertaining to the nodulus (a part of the vermis of the

cerebellum)

Flocculo nodular lobe—a small lobe of the cerebellum that is part of the vestibular system

Olivo- Pertaining to the olivary nucleus

Olivo cerebellar—nerve bers that pass from the olivary nucleus in the medulla to the opposite hemisphere of the cerebellum

Pontine Pertaining to the pons Cerebello pontine angle—a recessed area where the cerebellum, pons, and medulla converge

Pyramidal Pertaining to the pyramids on the anterior surface of

the medulla

Pyramidal motor tract—the primary motor pathway that originates in the precentral gyrus of the cerebral cortex and eventually

decussates at the pyramids before traveling down the spinalcord

Quadrigemina Fourfold Corpora quadrigemina —four oval masses (superior and inferior colliculi) found in the posterior midbrain that are part of the

visual and auditory pathwaysSpinal Pertaining to the spinal

columnCortico spinal tract—the primary motor pathway that originates in the precentral gyrus of the cerebral cortex and provides input to

the spinal nervesStriatum Striped Corpus striatum —a subcortical mass of gray matter just anterior

to the thalamus, consisting of the caudate and putamenSulcus A slight groove or depression,

not quite as deep as a ssureCentral sulcus —an obliquely directed groove in each cerebral hemisphere that separates the frontal from parietal lobes

Thalamic Pertaining to the thalamus Sub thalamic nucleus—a subcortical mass of nerve cell bodies within proximity to the substantia nigra

Thalamo- Thalamo cortical tract—an efferent nerve tract running from the thalamus to the cerebral cortex

Uncinate Hook shaped Uncinate fasciculus—nerve bers that hook around the lateral sulcus to connect the orbital cortex with the anterior temporal cortex




TABLE A-7

MISCELLANEOUS TERMS AND AFFIXES USED IN ANATOMY, PHYSIOLOGY, AND PATHOLOGY


TABLE A-6

TERMS AND PREFIXES USED IN REFERENCE TO THE AUDITORY / VESTIBULAR SYSTEM (Continued)


Ot- Pertaining to the ear Ot itis media—inammation of the middle earOtic Otic capsule—the hollow area of the inner ear in which the cochlea,

vestibule, and semicircular canals resideOto- Oto sclerosis—a condition in which spongy bone forms around the

stapes, preventing it from functioning properly Scala A cavity or chamber Scala tympani—the lower chamber within the cochlea below the

spiral laminaSpiral Coiled (usually in reference to

structures within the cochlea)Spiral ligament—the connective tissue within the cochlea that forms the outer wall of the scala media and anchors it to the spiral lamina

Stapedial Pertaining to the stapes

Incudo stapedial joint—the point of articulation between the incusand stapes

Stapedius Stapedius muscle—a tiny muscle in the middle ear that tenses the stapes so that the stapes does not excessively drive the oval window

Tympani Pertaining to the eardrum Tensor tympani —a tiny muscle in the middle ear that tenses theeardrum and malleus to dampen vibration of the ossicular chain

Tympanic Tympanic membrane—the eardrum, which forms the lateral wall of the middle ear cavity

Vestibular Pertaining to the balanceportion of the inner ear

Vestibular nerve—the portion of cranial nerve VIII that sends sensory information regarding head position and movement to the brain,

originating in the vestibule and semicircular canals Vestibulo- Vestibulo cochlear nerve—cranial nerve VIII that sends sensory

information (hearing and balance) from the inner ear to the brain


A- Without, absence of, inability A phonia—absence or loss of voice An- An oxia—without oxygen Amelo- Enamel Amelo genesis imperfecta—poorly formed enamel on the teeth-arthria Articulation (speech) Dys arthria —a disturbance in the ability to speak -blast A germ or cell (usually in an

immature form)Chondro blast —a cell that assists in the growth of cartilage

Cemento- Cementum Cemento enamel junction—the point where the cementum and enamel of a tooth meet

-clast A germ or cell that breaks down tissue

Osteo clast s—cells that break down bone tissue so that it can be absorbed

-cyte A cell Leuko cyte —a white blood cellDeci- One-tenth Deci bel—unit of measure for expressing the relative loudness of

a sound on a logarithmic scale; literally one-tenth of a bel

Deciduous Nonpermanent Deciduous teeth—the primary set of teeth that are shed during childhood and replaced by permanent teeth

Dentino- Dentin Dentino genesis imperfecta—poorly formed dentin, the substance comprising the bulk of a tooth

Dys- Difculty, distress, or abnormal Dys pnea—difculty breathing -ectomy Removal of an anatomical part Laryng ectomy —surgical removal of the larynx Edema An accumulation of uid in the

cells, tissues, or cavitiesReinke’s edema —swelling of the vocal folds due to an accumulation of uid within them

Eu- Well, good, or normal Eu pnea—normal breathing -graphia Writing A graphia —impaired ability to write



362 PART 2 THE NERVOUS SYSTEM

TABLE A-7

MISCELLANEOUS TERMS AND AFFIXES USED IN ANATOMY, PHYSIOLOGY, AND PATHOLOGY (Continued)


Hema- Pertaining to the blood Hema toma—a localized mass of blood that collects within tissue, organs, or in cavities or spaces

Hemi- One-half Hemi anopsia—loss of half of the visual eldIncisive Pertaining to the incisors Incisive foramen—a small opening in the alveolar ridge

immediately posterior to the central incisors-itis Inammation Otitis media—inammation of the middle ear-kinesia Pertaining to motion or

movementDys kinesia —difculty in performing voluntary movements

-lexia Reading Dys lexia —Difculty in the ability to readMalacia A softening or loss of consistency

of tissues or organsChondro malacia —cartilage that is too soft

-oma A tumor Carcin oma —a malignant tumor-opia Pertaining to vision Presby opia —diminished sight as a result of aging -opsia Hemian opsia —loss of half of the visual eld-osis A process, condition, or state Cyan osis —the condition of turning blue because of a lack of

oxygen

-otomy An operation involving cutting Trache otomy —an operation in which a small opening is cutinto the anterior trachea to assist the patient in breathing -phagia Eating (usually in reference to

swallowing)Dys phagia —disruption of the ability to swallow properly

-phonia Pertaining to the voice A phonia —absence (loss) of voice-plasia Growth Dys plasia —abnormal development or growth of cells, tissues, or

organs-plasty A surgical procedure to mold or

shape a structureRhino plasty —plastic surgery to repair a defect of the nose

-pnea Pertaining to respiration (breathing)

A pnea —cessation of breathing

Pneumo- Presence of air or gas; the lungs; breathing

Pneumo thorax—the presence of air or gas in the pleural cavity

Presby- Pertaining to the aging processor old age

Presby cusis—a gradual loss of hearing that tends to occur as a person gets older

-sclerosis The hardening of a structure Oto sclerosis —a condition in which spongy bone forms around the stapes, hardening and preventing it from functioning properly

-scopy Viewing (usually by means ofsome type of instrument)

Oto scopy —visual inspection of the ear through the use of a special instrument called an otoscope

-tonia Pertaining to muscle tone Dys tonia —a state of abnormal muscle tone Vaso- Pertaining to blood vessels Vaso constriction—narrowing of a blood vessel’s interior due to

smooth muscle contraction



363

GLOSSARY

abducens: cranial nerve VI, involved with lateral eyemovement.

abduction: movement of the vocal folds away fromthe median position, thereby opening the glottis.

absolute refractory period: the time immediately fol-lowing an action potential when a neuron cannotre.

acetabulum: the crater-shaped depression on thelateral aspect of the ischium where the head of thefemur articulates.

acoustic: pertaining to sound and its perception.acoustic neuroma: see Schwannoma neuroma .

acoustic reex: middle ear muscle (i.e., stapediusand tensor tympani) contraction in response tothe direction of loud sound; muscle contractionserves to stiffen the ossicular chain for the pre-sumed purpose of protecting the inner ear fromloud noises.

acquired: obtained after birth.acrocephalosyndactyly: also known as Apert syn-

drome; a craniofacial anomaly affecting primarilythe head, face, hands, and feet.

acromion: the process of the scapula where the clav-icle articulates.

acute: of immediate concern; medically the stage where a patient presents with severe symptoms andshort duration of immediate illness.

acute otitis media: quick onset of middle ear inam-mation, lasting fewer than 21 days.

adduct: to close (adduction); movement of the vocalfolds toward midline.

adduction: movement of the vocal folds toward mid-line, thereby bringing them together and closingthe glottis.

adenoidectomy: surgical removal of the adenoid tis-sue in the nasopharynx.

adenoids: the mass of lymphoid tissue at the back ofthe pharynx, above the soft palate.

adhesive otitis media: prolonged inammation ofthe middle ear with a retracted opaque, immobiletympanic membrane.

adipose: loose connective tissue with a high numberof fat storing cells.

aditus: opening that connects the epitympanic recessof the middle ear cavity to the mastoid antrum.

aditus laryngis: the entrance to the larynx, formed bythe superior border of the epiglottis anteriorly, thearyepiglottic folds laterally, and the arytenoid carti-lages posteriorly.

afferent: the conduction of nerve impulses towardthe central nervous system (i.e., sensory).

agnosia: a perceptual impairment related to theinability to recognize stimuli despite an intact sen-sory system; it can occur in any sensory modality—vision, audition, touch, etc.

agrammatism: a term meaning without grammar; acharacteristic of nonuent aphasia manifested by

the omission of function words (e.g., articles, conjunctions, prepositions) in verbal expression.air-bone gap: the difference between bone conduc-

tion thresholds and air conduction thresholds,reported in decibels for each ear at each frequency;used to determine type of hearing loss.

air conduction: in reference to audiometric testing,a method that is typically used to evaluate hear-ing threshold levels for a wide range of frequencies;the stimuli (pure tones) are delivered through a setof earphones in an attempt to evaluate the entireauditory system so that what is measured is what is“heard” through the air as opposed to what is heardthrough vibrations of the bones of the skull; thetransmission of sound to the inner ear through thestructures of the ear canal and middle ear cavity.

alar plate: dorsal region of the spinal cord duringneurodevelopment that develops into nervoustissue serving sensory purposes.

albinism: condition of a person who is congenitallydecient in pigment. The individual typically hasmilky or translucent skin, white or colorless hair, andeyes with a pink or blue iris and a deep-red pupil.

Alexander aplasia: incomplete or faulty developmentof the membranous labyrinth of the cochlea; theorgan of Corti and the spiral ganglion at the basalturn are most affected, resulting in a high-frequencyhearing loss, while low-frequency hearing is rela-tively preserved.

alveoli pulmoni: tiny pouches along the alveolar sacs,alveolar ducts, and terminal bronchioles wherethe exchange of oxygen and carbon dioxide takesplace.



364 GLOSSARY

Alzheimer’s disease: the most common type ofdementing disease resulting in progressive cogni-tive decline.

amphiarthrodial: pertaining to joints that yield.ampulla: bulbous portion of the semicircular canal

that communicates with the utricle and containsthe receptor end organ, the crista ampullaris; plu-

ral: ampullae.amygdala: almond-shaped subcortical nuclei deep tothe uncus in the anterior temporal lobe, part of thelimbic system and involved in emotion.

amyotrophic lateral sclerosis (ALS): a degenerativedisorder of the upper and lower motor neurons;commonly referred to as “Lou Gehrig’s disease.”

anastomoses: the communication between two arter-ies.

anatomical position: the general position of a cadaverused as a reference point in describing position andspatial orientation of various parts of the body; thecadaver is upright facing the observer with armsextended to the sides, and head, eyes, and palms ofthe hands facing forward.

anatomy: the scientic study of the structure andorganization of living organisms.

aneurysm: the bulging out of weak blood vessel walls,a precursor to hemorrhage.

annular ligament: the ligament that holds a mem-brane in place within a cartilaginous ring or sul-cus, for example, the tympanic membrane in thetympanic sulcus and the footplate of the stapes in

the oval window.annular sulcus: the ringlike structure in which thetympanic membrane resides, held in place by theannular ligament; also referred to as the tympanicsulcus.

anosognosia: denial of illness; associated with righthemisphere syndrome.

anotia: a congenital absence of the pinna.anterior arch: the narrower, anterior portion of the

cricoid cartilage.anterior cranial fossa: two forward-most depressions

in the base of the interior cranium where the frontal

lobes of the brain reside.anterior cricoarytenoid ligament: connective tissue

anchoring the anterior base of the arytenoid carti-lage to the posterior quadrate lamina of the cricoidcartilage, thereby restricting the posterior rockingmovement of the arytenoid.

anterior crus: anatomical structure resembling a leg;this crus and the posterior crus of the stapes con-nect to the footplate.

antigens: substances that trigger the immune systemto produce antibodies.

antitragus: a cartilaginous prominence on the infe-rior concha ridge of the pinna opposite the tragus.

aperiodic sounds: complex sounds whose waveformshave no discernible repetitive pattern.

aphasia: a central nervous system disorder in whichthere is partial or complete impairment of languagecomprehension and/or production typically affect-

ing several modalities (e.g., gesturing, listening,reading, speaking, writing).aphonia: absence of phonation; a lack of sound pro-

duced by vocal fold vibration; no voice.apical foramen: a small opening at the tip of the root

of a tooth where nerve bers and blood vesselsenter the interior of the tooth.

apneustic area: the respiratory area in the pons thatpromotes inspiration.

aponeuroses: broad, tendinous sheets of connectivetissue.

apraxia of speech (AOS): a sensorimotor disorder ofarticulation originating in the central nervous sys-tem characterized by impaired ability to volitionallyprogram the position and sequencing of musclesinvolved in speech.

aprosodia: decreased use of the prosodic features oflanguage including pitch, intensity, and timing tosignal intonation; associated with right hemispheresyndrome.

arachnoid granulations: projections of arachnoidmater into dural sinuses for cerebrospinal uid dif-fusion into the venous blood supply.

arachnoid mater: the middle meningeal layer thatenvelopes the central nervous system.arcuate fasciculus: an association tract connecting

the frontal lobe speech and language centers with thetemporal lobe language centers; also known as thesuperior longitudinal fasciculus.

arcuate ridge: the horizontally directed ridge along theanterolateral surface of the arytenoid cartilage thatseparates the triangular fovea from the fovea oblonga.

area advantage: the large area of the tympanic mem-brane (TM) being focused down to the smaller areaof the oval window serving to increase the pressure

placed upon the uids of the inner ear.areolar: loose connective tissue that forms the bed for

skin.arteriosclerosis: the accumulation of plaque (e.g., fats

and cholesterol) in blood vessels resulting in a nar-rowing of the arterial lumen.

arteriovenous malformation (AVM): congenitalabnormality of capillary beds in brain tissue.

arthro-ophthalmopathy: also known as Stickler syn-drome; a craniofacial anomaly affecting primarilythe joints and eyes.



GLOSSARY 365

articulation: the process of forming and producingthe speech sounds of a language; the process ofspeech production produced by movements of thestructures of the vocal tract.

articulation disorder: an impairment in the abilityto produce the speech sounds that make up a lan-guage.

aryepiglottic folds: folds of tissue that begin at thelateral-superior borders of the epiglottis and pro-ceed posteriorly to the arytenoid cartilages alongthe inner surface of the thyroid cartilage; thesefolds form the superior border of the quadrangularmembrane.

arytenoid articular facets: small projections on thesloping borders of the posterior quadrate lamina ofthe cricoid cartilage where the arytenoid cartilagesarticulate with the cricoid.

arytenoids: two somewhat pyramid-shaped cartilagesthat rest upon the sloping borders of the posteriorquadrate lamina of the cricoid cartilage; the pos-terior attachment of the vocal folds is on the vocalprocesses at the base of these cartilages.

aspiration: the penetration of liquid or food belowthe true vocal folds into the lower airway.

association areas: cortical regions of the cerebralhemispheres involved in elaboration of respectiveprimary areas (unimodal) or involved in higher cor-tical functions (multimodal).

association ber tracts: bundles of axons that runin the cerebral hemispheres; these can be short or

long.asthma: a disease characterized by muscularspasms of the bronchial tubes and subsequentmucous membrane edema resulting in wheezing,difculty breathing, and cough; often triggered byallergens.

astigmatism: irregular curvature of the cornea of theeye resulting in blurred vision.

astrocytes: a type of glial cell that supports neuronsand contributes to the blood–brain barrier.

astrocytomas: benign tumors of the central nervoussystem; a type of glioma.

ataxic: a type of cerebral palsy or dysarthria charac-terized by poor coordination of motor movement.

atherosclerosis: the buildup of fatty deposits (i.e.,plaque) within arterial walls.

athetoid: a type of cerebral palsy characterized byslow, writhing, involuntary movements of thehands, feet, and other body parts.

atmospheric pressure: the force that air exerts uponobjects within the external environment.

atresia: absent formation of the external auditorymeatus (ear canal).

atrophy: the withering away of a body part due to lackof use.

attack phase: that part of vocal fold vibration fromthe point where the vocal folds have adducted tothe rst cycles of vibration.

attic: upper portion of the middle ear cavity where theheads of the ossicles reside; also referred to as the

epitympanic recess.audibility: state of being audible.audible: capable of being heard.audiogram: the output of audiometry; a graph that

shows hearing thresholds through air and boneconduction for each ear at various frequencies.

audiologist: as stated in the American Academy of Audiology (AAA) Scope of Practice, an audiologist isa professional who diagnoses, treats, and managesindividuals with hearing loss or balance problems. Audiologists have received a master’s or doctoraldegree from an accredited university graduateprogram. Their academic and clinical training pro-vides the foundation for patient management frombirth through adulthood. Audiologists determineappropriate patient treatment of hearing and bal-ance problems by combining a complete history with a variety of specialized auditory and vestibularassessments. Based upon the diagnosis, the audi-ologist presents a variety of treatment options topatients with hearing impairment or balance prob-lems. Audiologists dispense and t hearing aidsas part of a comprehensive habilitative program.

Audiologists may be found working in medical cen-ters and hospitals, private practice settings, schools,government health facilities and agencies, and col-leges and universities. As a primary hearing healthprovider, audiologists refer patients to physicians when the hearing or balance problem requiresmedical or surgical evaluation or treatment.

audiometry: hearing measures such as pure tonethresholds and speech discrimination performed with an audiometer.

auditory radiations: the nal component of the audi-tory pathway carrying auditory information from

the medial geniculate nucleus to the primary audi-tory cortex.

auditory tube: structure connecting the middle earcavity to the nasopharynx; responsible for theequalization of air in the middle ear space withthat of atmospheric pressure; also referred to as theEustachian tube (ET).

augmentative and alternative communication (AAC):a specialty of speech–language pathology and otherdisciplines (such as medicine, occupational therapy,physical therapy) that has an emphasis in providing



366 GLOSSARY

systems of communication for persons who have nospeech ability or whose speech is not sufcient tomeet their daily communication needs.

auricle: the visible portion of the outer ear used for thecollection of sound; also referred to as the pinna.

auricular cartilage: cartilaginous framework of thepinna.

autoimmune inner ear disease (AIED): a syndromecharacterized by progressive hearing loss, tinnitus,and/or dizziness which is caused by immune cellsthat attack and cause damage to the inner ear.

autonomic nervous system (ANS): also referred toas the visceral nervous system; the division of thenervous system that innervates smooth muscles,glands, cardiovascular function, and internal organs;the parasympathetic and sympathetic branches arefurther divisions of the ANS.

autophonia: abnormal resonance of one’s own voiceheard inside their head.

autosomal dominant: a pattern of genetic transmis-sion from one parent to offspring where only onegene of a pair is necessary to express the trait; notrelated to the sex chromosomes.

autosomal recessive: a pattern of genetic transmis-sion from both parents to offspring where two cop-ies of a gene are necessary to express the trait; notrelated to the sex chromosomes.

axon: the part of the neuron specialized to transmitimpulses away from the cell body and toward theterminal.

axon hillock: the enlarged junction of the axon withthe cell body; it has a lower threshold for the initia-tion of an action potential than the rest of the cell.

bacterial meningitis: a bacterial inammation of themeninges of the brain, labyrinth, or lining of cranialnerve VIII (the vestibulocochlear nerve).

Baha ®: a commercially available system that utilizesa surgically implanted bone-conduction device.The receiver is implanted and is designed tocommunicate with an external amplier bypass-ing air-conducted delivery. This allows the bone totransfer sound to a functioning cochlea, thereby

bypassing the outer and middle ear. Once thecochlea receives these sound vibrations, the soundis converted into neural signals and is transferredto the brain, allowing a Baha recipient to perceivesound.

basal cell carcinoma: slow-growing malignant skincancer with a raised or rolled border and a centralulcer; usually a result of chronic sun exposure.

basal ganglia: a collection of subcortical nucleiincluding the telencephalic caudate nucleus, glo-bus pallidus, putamen, and subthalamic nucleus;

functionally, the mesencephalic substantia nigra isalso included.

basal plate: ventral region of the spinal cord duringneurodevelopment that develops into nervous tis-sue serving motor purposes.

basilar artery: a major supply of blood to the brain;begins at the foramen magnum where the vertebral

arteries converge on it and feed into the circle of Willis.basilar membrane (BM): along with the spiral lam-

ina, it forms the oor of the scala media runningthe length of the cochlea and supporting the organof Corti.

benign paroxysmal positional vertigo (BPPV): briefepisodes of vertigo that occur with changes in headposition with respect to gravity; results from looseotoconia from the utricle oating into the posteriorsemicircular canal and adhering to its cupula.

Bernoulli effect: an increase in the velocity of a uid(e.g., air) results in a decrease in its pressure.

bilateral: both sides; both ears.binaural representation: reception of information

from both ears to one location.biology: the scientic study of life and living organ-

isms.blood–brain barrier: specialized barrier to the trans-

port of noxious substances to the extracellular uidof the brain due to the unique anatomical congu-ration of brain capillaries.

bolus: a small, soft, cohesive mass of food formed

through mastication prior to a swallow.bone conduction: in reference to audiometric testing,the transmission of test signals to the cochlea byvibrations of the skull; the transmission of sound tothe inner ear through forced vibrations of the bonesof the skull.

Boyle’s law: the principle that states: with temperaturebeing constant, volume and pressure are inverselyrelated to each other.

bradykinesia: slow movement; difculty initiatingand regulating movement once begun; associated with Parkinson’s disease.

brainstem: area of the brain located between thespinal cord and diencephalon; composed of themidbrain (i.e., mesencephalon), pons (i.e., partof the metencephalon), and medulla (i.e., myel-encephalon).

breath groups: verbal utterances spoken on a singlebreath.

breathy attack: vocal fold vibration characterized byexpired air escaping through the glottis before thevocal folds have fully adducted, thereby creating abreathy vocal quality.



GLOSSARY 367

Broca’s area: frontal lobe premotor region involved inexpressive speech and language function.

Brodmann areas: numbered regions of the cerebralcortex reecting its cytoarchitecture.

buccae: the cheeks.cadaver: from the Latin phrase “caro data vermibus,”

meaning “esh given to worms”; a deceased human

body donated for the advancement of science.calcarine sulcus: the furrow that divides the medialaspect of the occipital lobe.

callosal sulcus: the furrow that surrounds the supe-rior border of the corpus callosum.

calvaria: the skullcap which is formed by the vaultedfrontal, parietal, and occipital bones.

canthus: either of the angles formed by the meetingof the eye’s upper and lower eyelids.

capsular ligaments: a general term used to denotethe ceratocricoid ligaments collectively.

cardiac impression: the indentation along the medial wall of the left lung where the heart resides.

Carhart’s notch: audiometric pattern of bone con-duction thresholds typically at 2,000 Hz; associated with otosclerosis.

carina: the keel-shaped landmark formed by thebifurcation of the last tracheal ring into the twomain stem bronchi.

cartilaginous joint: the anatomical classication of joints that yield but do not freely move.

cataracts: clouding of the lens of the eye, resulting inopacity and visual impairment.

cauda equina: the collection of spinal nerves cau-dal to lumbar vertebra number one (L1); literally,horse’s tail.

caudate nucleus: one of the telencephalic basal gan-glia; involved with higher order motor functions.

cauliower ear: caused by trauma to the pinna; sepa-ration of skin from underlying connective tissue withswelling, thickening, and malformation; related totrauma from the sport of wrestling or boxing.

cementoenamel junction: the part of the outer surfaceof a tooth where the cementum ends and the enamelbegins, located approximately at the gum line.

cementum: the calcied covering of the root of a tooth.central auditory processing disorder (CAPD): a dis-

order resulting from lesions along the higher lev-els of the auditory pathway or auditory cortex; thelesion interferes with the processing of auditoryinformation fed to the brain by the peripheral ear.

central canal: narrow lumen within and running the len-gth of the spinal cord; part of the ventricular system.

central chemoreceptors: sensory receptors respond-ing to alterations in carbon dioxide in cerebral spi-nal uid; located at the medulla.

central sulcus: furrow separating the frontal lobefrom the parietal lobe.

central tendon: the three-lobed connective tissuecore on which the bers of the diaphragm insert.

centriole: an organelle that assists with nuclear andcell division.

ceratocricoid ligaments: a series of three ligaments

(anterior, posterior, and lateral) that hold in placethe articulation between the inferior cornua (horns)of the thyroid and the cricoid.

cerebellar peduncles: three major pairs of tracts—thesuperior, middle, and inferior—running from thebrainstem to the cerebellum.

cerebellopontine (CP) angle: the anatomical anglecreated by the junction of the pons with the cere-bellum where the facial (VII) and vestibulocochlear(VIII) nerves enter the brainstem.

cerebral aqueduct: the canal that joins the third andfourth ventricles.

cerebral peduncles: major motor tracts running inthe ventral midbrain.

cerebrospinal uid: a thin, watery substance pro-duced by the choroid plexus that circulates through-out the ventricles and the subarachnoid space tocushion and provide nourishment to the centralnervous system.

cerebrovascular accident (CVA): see stroke .cerumen: substance created by a mixture of sloughed

skin cells and secretions from the sebaceous glandslocated in the ear canal; also referred to as ear wax.

cervical segment: the most superior of the ve parts ofthe spinal cord corresponding to the neck region.checking mechanism: the action of the external inter-

costal muscles upon the rib cage during expiration;these muscles relax gradually during expiration toprevent the rib cage from recoiling too quickly.

choanae: the posterior openings of the nasal cavityinto the region of the nasopharynx.

cholesteatoma: a pearl-like epithelial mass invadingthe middle ear space, usually secondary to prolongedretraction of the pars accida of the tympanic mem-brane from chronic Eustachian tube dysfunction.

chondro-osseous juncture: any juncture betweencartilage and bone, for example, the juncture wherethe bony ribs terminate at cartilages that articulate with the sternum.

chorda tympani: a branch of the facial (VII) nerve thatpasses through the middle ear space; conveys tastesensation from the anterior two-thirds of the tongue.

choroid plexus: the delicate tissue composed of piamater, capillaries, and ependymal cells that pro-duces cerebrospinal uid (CSF); found in the wallsof the ventricles.



368 GLOSSARY

chronic: a longstanding condition.chronic bronchitis: a longstanding and persistent

inammation of the mucous membranes of thebronchi.

chronic obstructive pulmonary disease (COPD):various diseases of the lower airways; often refer-ring to emphysema and chronic bronchitis.

cilia: short, hairlike structures protruding from someepithelial tissue types.cingulate sulcus: the furrow surrounding the superior

border of the cingulate gyrus.cisterna magna: a large subarachnoid space also

referred to as the cerebellomedullary cistern for itslocation; contains cerebrospinal uid (CSF).

Claudius’ cells: lateral support cells for the organ ofCorti, in particular the outer hair cells.

clavicle: commonly referred to as the collarbone, itruns in a horizontal plane from the sternum (breast-bone) to the scapula (shoulder blade).

coarticulation: the simultaneous or overlappingarticulation of two phonemes; for example, in the word “sweet,” the lips round for the /w/ sound evenas the /s/ sound is being produced (which by itselfdoes not require lip rounding).

coccygeal segment: the most inferior of the ve partsof the spinal cord; corresponding to the tailbone.

cochlea: contains the sensory organ of hearing (theorgan of Corti); found within the inner ear labyrinth, within the petrous portion of the temporal bone.

cochlear aqueduct (CA): the canal or passage leading

away from the cochlea to terminate within the sub-arachnoid space of the brain; it contains perilymphbecause it originates at the scala tympani.

cochlear duct: the membranous labyrinth of thecochlea where the organ of Corti resides; lled withendolymph, it is bordered by the basilar membrane,spiral lamina, spiral ligament, and Reissner’s mem-brane; also referred to as the scala media.

cochlear implant (CI): surgically implanted receiverthat when coupled with its external processor offersdirect electrical stimulation of the cochlear nervebers for the purpose of hearing.

cochlear nuclei: the rst large collection of nerve cells within the brainstem along the auditory pathway,at the level of the caudal pons.

cochlear partition: the anatomical structure madeup of the osseous spiral lamina, basilar membrane,and the spiral ligament that separates the scalamedia from the scala tympani.

cochleariform process: bony process projecting intothe middle ear space from the anterior wall; thetendon of the tensor tympani angles over the pro-cess to attach to the manubrium of the malleus.

cognate pair: two speech sounds that have the sameplace and manner of articulation, but differ onlyin the fact that vocal fold vibration occurs for onesound but not the other.

cognitive–communicative disorder: a communica-tion impairment that results from underlying cog-nitive decits.

commissural ber tracts: bundles of axons that runfrom one cerebral hemisphere to the other; the cor-pus callosum is the largest of these.

common carotid arteries: large arteries ascendingthe neck to supply blood to the head; they haveexternal and internal branches.

common crus: the point where the legs of the posteriorand superior semicircular canals meet and merge.

complex tone: any sound composed of two or moreindividual (pure) tones blended together; mostsounds in the environment are complex tones,including the human voice.

concha bowl: deep bowl-like portion of the pinna justabove the lobule that leads to the external auditorymeatus.

conductive: in reference to diminished hearing acu-ity, a reversible hearing loss due to pathology of theouter and/or middle ear; treating the pathologyusually results in a reversal of the loss.

conductive hearing loss: a correctible hearing lossoriginating in the outer or middle ear, caused by abreakdown in the eardrum’s and/or ossicular chain’sability to transform acoustic energy into mechani-

cal energy, or to transmit mechanical energy to theinner ear.condylar process: the posterior rounded process on

the ramus of the mandible that articulates with thetemporal bone of the skull, forming the temporo-mandibular joint (TMJ).

cone of light: the reection of otoscopic light thatappears on the surface of the tympanic membrane(TM) as a bright streak of light when the TM is rest-ing at its normal 55-degree angle.

cones: one type of photoreceptor found in the retina;they code color and shape for visual acuity.

congenital: present at the time of birth.congenital rubella: rubella (German measles) pres-

ent in the pregnant mother that may cause devel-opmental anomalies in the fetus.

congestive heart failure (CHF): inadequate pumpingof blood by the heart, resulting in poor circulation.

connective tissue: tissue that combines body struc-tures, supports the body, and aids in body mainte-nance.

connective tissue cell: any cell involved with connect-ing, anchoring, and supporting body structures;



GLOSSARY 369

specialized for the formation of various types ofextracellular connecting and supporting elements.

connexin 26: transmembrane proteins that facilitaterapid transport of ions or small molecules betweencells.

constructional impairments: marked by decreasedability to draw or put together objects using visu-

ospatial skills; associated with right hemispheresyndrome.contralateral: pertaining to the opposite side of the

body.contrecoup: focal area of lesion opposite the initial

site of impact in a closed head injury.conus elasticus: the lower portion of the elastic mem-

brane that extends from the anterior arch of thecricoid cartilage inferiorly to the vocal ligamentssuperiorly.

conus medullaris: the inferior, terminal point of thespinal cord.

corium: a dense, feltlike network of connective tissuelying beneath the mucous membrane of the tongue,in essence forming the skeleton for the tongue.

corniculate tubercles: the medial bumps or swellingsin the posterior aryepiglottic folds created by thecorniculate cartilages lying within.

corniculates: two tiny cone-shaped cartilages thatrest upon the apices of the arytenoid cartilages andare embedded within the aryepiglottic folds.

coronal suture: the seam running transverselyacross the anterior part of the skull that serves as

the joint between the frontal bone and two pari-etal bones.coronoid process: the at, anterior process on the

ramus of the mandible that serves as the insertionfor the temporalis and masseter muscles.

corpora quadrigemina: the collection of four nuclei—two superior and two inferior colliculi—found inthe dorsal midbrain.

corpus callosum: the large commissural tract con-necting the right and left cerebral hemispheres.

corticobulbar tract: bundles of axons carrying motorinformation from the cortex to the brainstem; part

of the pyramidal tracts.corticospinal tract: bundles of axons carrying motor

information from the cortex to the spinal cord; partof the pyramidal tracts.

cortilymph: uid within the tunnel of Corti that issimilar in composition to perilymph.

costal pleura: the connective tissue membrane thatlines the interior of the rib cage; also known as theparietal pleura.

coup: focal area of lesion at the site of impact in aclosed head injury.

cranial nerves: bundles of axons carrying a combina-tion of motor, sensory, and autonomic nervous sys-tem (ANS) information in the peripheral nervoussystem; there are 12 pairs of cranial nerves.

craniofacial anomaly: a disorder or syndrome affect-ing the structures of the skull and/or face.

craniofacial dysostosis: also known as Crouzon syn-

drome; a craniofacial anomaly that is similar to Apert syndrome but less severe, affecting the bonesof the face and skull.

cranium: the rounded part of the skull posterior tothe face that houses the brain.

cribriform plate: the perforated central part of theethmoid bone through which bers of the olfactorynerve (I) pass from the nasal cavity to the olfactorybulbs.

cricoarytenoid joint: the articulation between eacharytenoid cartilage and the posterior quadrate lam-ina of the cricoid cartilage.

cricoid: the ring-shaped cartilage forming the base ofthe larynx; it articulates with the thyroid cartilageand the arytenoid cartilages.

cricoid articular facets: two small projections on thesuperior sloping border of the posterior quadratelamina of the cricoid cartilage that serve as thepoint of articulation for the arytenoid cartilages.

cricothyroid joint: the articulation between the cri-coid and thyroid cartilages; there are two of these joints, each formed by an inferior cornu of thethyroid and the lateral surface of the cricoid in the

region where the anterior arch ends and the poste-rior quadrate lamina begins.cricothyroid ligaments: the inferior portions of the

conus elasticus that bind the cricoid and thyroidcartilages.

cricotracheal ligament: connective tissue that bindsthe cricoid cartilage to the trachea at the rst tra-cheal ring.

crista ampullaris: receptor end organ for balance(specically angular acceleration) found in theampulla of the semicircular canals; plural: cristaeampullares.

crista galli: literally “cock’s comb”; the vertically ori-ented process of the ethmoid bone on which a por-tion of the dura mater of the brain anchors.

Crouzon syndrome: congenital autosomal dominantdisorder with manifestations related to prematurefusion of the cranial sutures including atresia; con-ductive or mixed hearing loss may be a component.

crura: plural of crus.crus: anatomical structure resembling a leg; the ante-

rior and posterior crura of the stapes connect to thefootplate.



370 GLOSSARY

cul-de-sac resonance: an aberration of oral–nasalresonance in which the vocal tone resonates exces-sively within the pharynx and/or nasal cavityinstead of within the oral cavity.

cuneiform: two tiny wedge-shaped cartilages that areembedded within the aryepiglottic folds somewhatlateral and anterior to the corniculate cartilages.

cuneiform tubercles: the lateral bumps or swellingsin the posterior aryepiglottic folds created by thecuneiform cartilages lying within.

cupid’s bow: the superior border of the upper lip thatresembles an archer’s bow due to the impressionof the philtrum upon the medial part of the upperlip.

cupula: gelatinous membrane covering the stereociliaof the crista within the ampullae of the semicircularcanals.

curette: a surgical instrument that has a scoop, wireloop, or ring at its tip and is used to clean the earcanal of debris.

curved membrane buckling: the eardrum vibratesin segments rather than as a whole unit serving toincrease the pressure propagated to the ossicles.

cytoarchitecture: the structure and arrangementof cell bodies in different regions of the cerebralcortex.

cytokines: proteins secreted by cells especially of theimmune system that are involved in the regulationof inammatory responses.

cytomegalovirus (CMV): a herpes virus; a prenatal

intrauterine infection which can cause central ner-vous system disorders, brain damage, hearing loss,vision loss, and seizures in the infant.

cytoplasm: the uid interior of the cell outside of thenucleus.

Darwin’s tubercle: anatomical feature of the pinnathat is present in approximately 10.4% of the popu-lation; it presents as a thickening on the helix at the junction of the upper and middle thirds; the genefor Darwin’s tubercle is inherited in an autosomaldominant pattern, but has incomplete penetrance,meaning not all who possess the gene will neces-

sarily possess the ear tubercle; it is thought to be asign of wisdom.

decibels (dB): one-tenth of a bel; the unit of soundintensity based on the logarithmic relationship ofan observed intensity or pressure to a referenceintensity or pressure.

declarative memory: explicit and conscious recall offacts.

deglutition: referring to the process of swallowing.Deiter’s cells: supporting cell group for the outer hair

cells, resting on the basilar membrane residing in

the organ of Corti; cradles the bases of the outerhair cells.

dementia: a progressive brain disease resulting incognitive decline over time.

dendrites: multiple branches off the cell body of aneuron that transmit neural information towardthe cell body.

dens: a toothlike, vertically oriented projection onthe axis (C2) upon which the atlas (C1) rotates; alsoreferred to as the odontoid process.

dentate nucleus: the most laterally located of thedeep cerebellar nuclei.

dentin: the body of a tooth overlying the pulp cavityand covered by the enamel and cementum of thetooth.

depolarization: positive change in neuronal mem-brane potential moving it from resting membranepotential (i.e., − 70 mV) to a less negative value(e.g., − 15 mV); this allows for membrane channelsto open so that calcium may infuse the cell causingthe release of a neurotransmitter.

desaturation: decreased levels of oxygen in the arte-rial blood.

developmental articulation disorder: a term used todenote an articulation disorder that occurs duringchildhood, usually functional in nature.

diarthrodial: freely moving joints.diencephalon: centrally located region of the brain

that develops from the prosencephalon; includesthe thalamus, hypothalamus, and epithalamus.

differentiation: one of the stages of neurodevelop-ment during which neurons become further spe-cialized making their functional connections.

diphthongs: vowel sounds that have two articulatorypositions during production, resulting in a shiftingacoustic spectrum.

diplophonia: the simultaneous perception of twopitches during phonation; a phenomenon fre-quently associated with dysphonia.

diplopia: double vision (one object seen as two) due todisrupted innervation to the muscles of the eyes.

distoversion: malposition of a tooth away from the

midline of the dental arch.dorsal cochlear nucleus: the dorsal portion of the

cochlear nucleus; the rst central synapse for thecochlear nerve as it travels the pathway to the audi-tory cortex.

dorsal fasciculus: the dorsal or posterior region ofspinal cord white matter where ascending bundlesof nerve bers are found.

dorsal root ganglion: a cluster of neuronal cell bodiesfor sensory functions found in the dorsal root of thespinal cord.



GLOSSARY 371

dowagers hump: colloquial term for hyperkyphosisdescribing excessive posterior curvature of the tho-racic vertebrae; usually seen in elderly women.

ductus reunions: a small tube of the membranouslabyrinth where the cochlea and the saccule meet;it carries endolymph between the auditory and ves-tibular systems.

dura mater: the most supercial and toughest layerof the meninges; cranial dura is double layered(periosteal outer layer and meningeal inner layer),spinal dura is single layered.

dysarthria: a motor speech disorder due to muscleparesis, paralysis, incoordination, or altered toneaffecting speech processes of respiration, phona-tion, articulation, resonance, and prosody.

dysphagia: any difculty, discomfort, or pain associ-ated with swallowing; a swallowing disorder.

dysphonia: disordered phonation; phonation thatbrings negative attention to the speaker; oftendescribed by such terms as hoarse, breathy, tense,harsh, weak, strident or thin, among others.

dyspnea: general term for difcult or labored breath-ing.

ear canal: the tubular portion of the outer ear lead-ing from the pinna to the tympanic membrane; alsoreferred to as the external auditory meatus (EAM);part of the canal is bone and part of it is cartilage.

eardrum: also referred to as the tympanic membrane(TM), the thin membrane that forms the borderbetween the outer and middle ear; the TM vibrates

in response to acoustic pressure waves and trans-mits the resulting mechanical vibrations to thestructures of the middle ear (i.e., ossicles).

earlobe: see lobule .ectrodactyly–ectodermal dysplasia-clefting syn-

drome: also known as EEC syndrome; a craniofa-cial anomaly affecting the hands, feet, skin, nails,hair, and oral structures.

edema: swelling of tissues.edematous: swollen with an accumulation of uid.efferent: the conduction of nerve impulses away from

the central nervous system (i.e., motor).

elastic cartilage: specialized connective tissue thatprovides some structural support and is extremelyexible.

elastic membrane: a thin, broad sheet of connectivetissue that binds the laryngeal cartilages togetherfrom within; it is composed of the quadrangularmembrane superiorly and the conus elasticus infe-riorly.

electronystagmography (ENG ): electrical measure-ment of involuntary eye movements (i.e., nystagmus)to assess the integrity of the vestibular mechanism.

eleidin: a gel-like, translucent substance in the sec-ond layer of the skin of the lips that exposes theunderlying vascular tissue, giving the lips a darkerhue than the rest of the skin of the face.

embolic: a type of stroke due to an embolus—a travel-ing clot or plug that occludes an artery.

emboliform nucleus: medially located deep cerebel-

lar nuclei.emphysema: chronic and irreversible lung diseasecharacterized by enlargement of the alveoli due tobreakdown of their walls and loss of elasticity; oftenassociated with smoking.

enamel: the calcied covering of the crown of atooth.

encephalitis: inammation of the brain.endocochlear potential (EP): the differentiated

potential between voltages of the endolymph within the scala media and the perilymph of thescala tympani.

endolymph: uid of the membranous labyrinth; itscomposition has a high concentration of potassiumand calcium and a low concentration of sodium.

endolymphatic sac: saclike portion of the membra-nous labyrinth connected to the endolymphaticduct, believed to play a role in absorption of endo-lymph.

endomysium: the connective tissue covering a mus-cle ber.

endoneurium: the connective tissue covering a nervecell ber.

endoplasmic reticulum: an organelle that synthe-sizes, stores, and releases various substances withinthe cell.

endothelial tissue: a type of epithelial tissue thatmakes up the vessel linings for the circulatory andlymph systems.

endotracheal: within or passing through the trachea.enlarged vestibular aqueduct syndrome (EVAS): a

collection of symptoms that results from an alreadyenlarged vestibular aqueduct becoming trauma-tized such as in the case of a head injury or sud-den change in barometric pressure; the collection

of symptoms typically comes on suddenly—a ator sloping hearing loss and vertigo or symptoms ofdisequilibrium. The hearing loss is not present atbirth and can uctuate with each traumatic inci-dent to the ear.

ependymal cells: a type of glial cell that lines the ven-tricular cavities and is part of the choroid plexus.

epiglottis: the leaf- or shoehorn-shaped cartilagelying immediately behind the hyoid bone and thy-roid cartilage. It moves backward and downward tocover the opening of the larynx during swallow.



GLOSSARY 373

accid paralysis: a loss of voluntary movement asso-ciated with a reduction in muscle tone.

exibility: in speech, the perception of frequencyand intensity variation; the complexity of pitch andloudness for linguistic effectiveness and appropri-ate cultural affect.

occulonodular lobe: the oldest part of the cerebel-

lum on its inferior surface.uctuate: to alternately increase and decrease inseverity.

uent aphasias: a classication of language disor-ders due to brain lesion characterized by relativelyeffortless speech production and average utterancelength of more than three words.

footplate: the base of the stapes bone to which thecrura are attached; the portion of the stapes that tsinto the oval window.

foramen cecum: a small depression in the middle ofthe sulcus terminalis at the root of the tongue.

foramen magnum: the large opening at the base ofthe occipital bone through which the spinal cordpasses on its way down the spinal column.

formants: peaks of resonance in the vocal tract, thatis, bands of frequencies with relatively high energyor amplitude.

Fourier analysis: a process by which a complex tonecan be analyzed into its individual pure tone com-ponents.

fourth ventricle: part of the ventricular system; thespace located at the dorsal surface of the brainstem

between the pons and medulla (anterior) and thecerebellum (posterior).fovea: the retinal depression in the eye where light

rays are focused for the best acuity.fovea oblonga: a depression along the base of the

anterolateral surface of the arytenoid cartilage where the bulk of the posterior vocal fold attaches.

frequency: a physical measure of the number of timesan object vibrates per second; frequency is per-ceived by humans as the pitch of a sound; the unitof measure for frequency is Hertz (Hz).

frons: the forehead.

frontal paranasal sinuses: a pair of cavities within thefrontal bone that open into the nasal cavity.

frontotemporal dementias: subtypes of dementiathat have primary degeneration of nervous tissuein the frontal and temporal lobes; includes Pick’sdisease and primary progressive aphasia.

functional disorder: an impairment that exists in theabsence of a known or observable etiology.

functional residual capacity (FRC): the amount ofair that remains in the lungs after a normal tidal

expiration; it includes expiratory reserve volumeand residual volume.

fundamental frequency: the lowest individual fre-quency (i.e., pure tone) in a complex tone.

fungiform: approximately 100 mushroom-shapedpapillae on each side of the anterior tongue, eachone housing approximately two to four taste buds.

gap junction channel: intercellular passages thatopen to allow certain chemicals to pass.genetic: related to the inheritance from one’s imme-

diate family.genetic mutation: a permanent change in one spe-

cic gene; associated with single-gene hereditarydisorders such as Huntington’s disease.

genetic variants: changes in a gene that act as geneticrisk factors.

germ cell layers: primal embryologic source of organs.gingivae: the gums; the mucous membrane that sur-

rounds the teeth.GJB2: the gene on chromosome 13 that codes for the

development of connexin 26, a gap junction protein.glabella: the portion of the frontal bone between the

eyebrows and immediately superior to the nasalbones.

glenoid fossa: the crater-shaped depression on thescapula where the head of the humerus articulates.

glial cell: support cells of the nervous system.gliomas: tumors of the central nervous system of glial

cell origin.globose nucleus: medially located deep cerebellar

nuclei.globus pallidus: a telencephalic nucleus of the basalganglia involved in higher order motor control.

glossectomy: surgical removal of the tongue, either inpart or totally.

glossoepiglottic folds: slips of mucous membranethat extend from the posterior base of the tongue tothe lingual (anterior) surface of the epiglottis.

glossopharyngeal: cranial nerve IX; innervates somepharyngeal and lingual muscles, transmits tasteand sensation from the throat.

glottal attack: vocal fold vibration characterized

by complete adduction of the vocal folds beforeexpired air reaches the larynx; the result is often aninitiation of phonation that is explosive in nature.

glottal chink: any opening of the vocal folds whilethey are adducted in the median position; a poste-rior glottal chink is typically seen during whisper.

glottal fry: phonation of excessively low frequencydue to maximum mass and minimum tension ofthe vocal folds; vocal fold vibration composed ofthe lowest frequencies in the vocal range—the voice



376 GLOSSARY

inner pillar cells: supporting cells for the organ ofCorti that stabilize the inner hair cells; they formthe tunnel of Corti.

inspiratory capacity (IC): an individual’s maximumcapacity to inspire air; it includes tidal volume andinspiratory reserve volume.

inspiratory reserve volume (IRV): the volume of air

that can be further inhaled after a normal tidalinhalation.insula: region of the cerebral cortex deep to the lateral

ssure involved with speech functions, the limbicsystem, and visceral function.

intensity: a physical measure of the amount of pres-sure that is generated within a medium by a vibrat-ing object; intensity is perceived by humans as theloudness of a sound; the unit of measure for inten-sity is the decibel (dB).

interarytenoid muscles: a term used to denote thetransverse and oblique arytenoid muscles collec-tively.

interaural: between the two ears.intermaxillary suture: the seam or joint between the

two maxillae.intermediate tendon: a short inscription of tendon

that connects two bellies of the same muscle; theomohyoid and digastricus muscles each have twobodies that are bound together by an intermediatetendon.

internal auditory canal (IAC): the bony pathway inthe petrous portion of the temporal bone in which

the vestibulocochlear (VIII) and facial (VII) nervespass; blood vessels that supply the inner ear alsopass through this canal.

internal auditory meatus: see internal auditory canal(IAC) .

internal capsule: large projection pathway connectinghigher (e.g., telencephalon) with lower (e.g., dien-cephalon) central nervous system regions.

internal carotid artery: a pair of arteries ascending onthe superior anterior lateral neck that runs throughthe carotid foramen of the petrous portion of thetemporal bone to join the circle of Willis at the base

of the brain.interthalamic adhesion: loose brous tissue con-

necting the two halves of the thalamus; also calledthe massa intermedia.

interventricular foramen: the paired set of canals joining the lateral ventricle to the third ventricle;a passageway for cerebrospinal uid (CSF); some-times referred to as the foramen of Monro.

intervertebral discs: cartilaginous discs betweenadjacent vertebrae in the spinal column.

intonation: a feature of spoken language in whichpitch and stress are varied for phonemic and affec-tive purposes; the rising and falling modulation ofvocal pitch during speech production.

intracellular: originating or occurring within a cell.intraoral air pressure: air pressure that is generated in

the oral cavity for the production of speech sounds;

the pressure is generated by the obstruction (e.g.,plosives) or constriction (e.g., fricatives) of expiredair by the articulation of various oral structuressuch as the lips, teeth, tongue, palate, etc.

intratracheal membrane: a connective tissue mem-brane that lines the interior of the trachea; musclebers and mucous membrane are superimposedupon it.

intrinsic: a membrane or muscle whose origin andinsertion reside within an anatomical structuresuch as the larynx or tongue.

ipsilateral: on the same side.ischemia: decreased oxygen to the brain.ischium: the middle of the three bones that comprise

the pelvis (the other two being the ilium and pubis).isthmus: anatomical part or passage where bone and

cartilage meet. jargon: a series of uently spoken neologisms and

inappropriately used real words that make little orno sense to the listener.

jugular bulb: bulbous protrusion of the oor of themiddle ear to accommodate the jugular vein.

kinesthetic: pertaining to the unconscious sense that

detects position, weight, or movement of the mus-cles, tendons, and joints; also referred to as prop-rioception.

kinocilium: the tallest cilium of a bundle projectingfrom a cell body in the receptor end organs for bal-ance.

Klippel–Feil syndrome: a craniofacial disorder withcleft palate and skeletal anomalies characterized bya short neck, scoliosis (abnormal curvature of thespine), kidney problems, and malformed stapes.

kyphoscoliosis: referring to scoliosis.kyphosis: an abnormal anterior curvature of the

spine; also known as “swayback.”labioversion: malposition of an anterior tooth (inci-

sor or cuspid) so that it is tilted toward the lips.labyrinth: the name for the mazelike structures of the

inner ear; includes the cochlea, vestibule, and thesemicircular canals.

labyrinthectomy: surgical destruction of the innerear.

labyrinthine arteries: paired arteries arising from thebasilar artery to supply blood to the inner ear.



GLOSSARY 377

labyrinthine wall: the most medial wall of the middleear space.

lambdoidal suture: the seam or joint between theoccipital bone and the two parietal and temporalbones.

lamina papyracea: the thin plate forming the lateralsurface of the labyrinths of the ethmoid and form-

ing a large part of the medial wall of the orbit of theeye.laryngectomee: a person who has had his or her larynx

surgically removed because of cancer or trauma.laryngopharynx: a division of the pharynx that

extends from the level of the hyoid bone to theesophagus, found immediately posterior to the larynx; also referred to as the hypopharynx.

larynx: a singular, musculocartilaginous structure within the neck that serves two purposes: (a) a pro-tective device for the lower respiratory passageway;(b) the source of phonation for vocal activity.

lateral fasciculus: lateral region of spinal cord whitematter where ascending and descending bundles ofnerve bers are found.

lateral geniculate nucleus (LGN): a point of synapsein the thalamus for primary visual system bers;also referred to as the lateral geniculate body.

lateral glossoepiglottic folds: two folds of connectivetissue that extend from the lingual (anterior) sur-face of the epiglottis to the base of the tongue; theyare separated from each other by the median glos-soepiglottic fold and valleculae.

lateral hyothyroid ligaments: somewhat thickerportions of the hyothyroid membrane that bindthe superior cornua of the thyroid cartilage to thegreater cornua of the hyoid bone; in many individ-uals, tiny cartilages (triticial cartilages) are embed-ded within these ligaments.

lateral lemniscus: the auditory tract or nerve bundlelocated on the lateral edge of the pons between thesuperior olivary nucleus and the inferior colliculus.

lateral semicircular canal: one of the three canals ofthe vestibular system; contains the sensory recep-tors for angular acceleration; also referred to as the

horizontal semicircular canal.lateral sulcus: the dividing ssure between the frontal

and temporal lobes of the cerebrum, also referredto as the Sylvian ssure.

lateral ventricles: telencephalic brain cavities thatproduce cerebrospinal uid.

left hemispatial neglect: the failure to report, respond,or orient to novel or meaningful stimuli to the lefthemispace following damage to the right cerebralhemisphere.

lenticular process: small bony knob at the end of thelong process of the incus that articulates with thehead of the stapes.

lenticulostriate arteries: small arterial branches fromthe middle cerebral arteries that supply blood toportions of the basal ganglia and internal capsule.

leptomeninges: the collective name for the pia mater

and arachnoid meningeal layers.lesion(s): pathological changes to tissue structure orfunction due to injury or disease.

levator veli palatini: along with the tensor tympani,one of the two muscles responsible for opening theEustachian tube; this muscle also elevates the softpalate during swallowing.

lever action: the ossicles work together as a lever toincrease the pressure placed on the uids of theinner ear.

lexical memory: a type of declarative memory specicto word meaning, spelling, and pronunciation.

ligament: dense connective tissue found at joints thatattaches bone to bone, bone to cartilage, or carti-lage to cartilage.

limbic areas: cortical regions (e.g., cingulate gyrus) andsubcortical nuclei (e.g., hippocampi) involved in thelimbic system functions of emotion and memory.

linea alba: a tight band of connective tissue extend-ing from the xiphoid process to the pubis, formedby the aponeuroses of the external oblique, internaloblique, and transversus abdominus muscles; thisvertical line separates the abdominal muscles into

left and right mirror-image pairs.lingual frenulum: a fold of mucous membrane thatextends from the gingivae of the mandible and oorof the mouth to the anterior undersurface of thetongue.

Lissauer’s tract: dorsolateral white matter region ofthe spinal cord involved with transmitting pain andtemperature sensations.

literal (phonemic) paraphasias: unintentional errorsof word retrieval in aphasia where wrong soundsare substituted for the correct sounds.

lobule: literally means small lobe, the anatomical

structure hanging at the base of the pinna; the lob-ule is devoid of cartilage but is composed of adi-pose (i.e., fatty) connective tissue; also known asthe earlobe.

loft register: the range of vocal pitches that is associ-ated with falsetto, that is, the highest pitches of thevocal range.

logorrhea: excessive language output with little or noself-monitoring; can be seen with uent aphasia;also known as press of speech.



378 GLOSSARY

long process: the prominent bony structure of theincus that terminates at the lenticular process which articulates with the head of the stapes.

longitudinal ssure: large furrow that divides theright cerebral hemisphere from the left.

longitudinal median sulcus: a depression on themidline superior surface of the tongue that runs

along its length.longitudinal tension: the force that is created bylengthening and shortening of the vocal folds; when the vocal folds are lengthened, longitudi-nal tension increases and when the vocal foldsare shortened, longitudinal tension decreases; thelaryngeal adjustment that regulates frequency ofthe vocal tone.

longitudinal wave: a wave that propagates (i.e.,spreads out) in the same direction as the move-ment of the air molecules being displaced; that is, when an object vibrates, the air molecules are dis-placed by to-and-fro movements and the wave thatis generated by the displacement also spreads outin the same direction (i.e., along the same plane asthe molecules). Contrast this to a transverse wave which is seen when a rock is thrown into a pond.The water molecules move up and down but the wave spreads out horizontally from the point wherethe rock entered the water, creating a ripple effect. With a transverse wave, propagation is perpendicu-lar to the movement of the molecules.

long-term memories: see retrospective memories .

lordosis: an abnormal posterior curvature of thespine; also known as “roundback.”loudness: the perceptual correlate of sound intensity.lower motor neuron (LMN): a nerve cell whose body

is located in the spinal cord or in the brainstem and whose axon passes by way of a peripheral nerve toinnervate skeletal muscle.

lumbar cistern: enlarged subarachnoid space sur-rounding the inferior end of the spinal cord; con-tains cerebrospinal uid (CSF).

lumbar segment: one of the ve segments of the spi-nal cord corresponding to the lower back region.

lysosome: an organelle that is responsible for thedigestion of bacterial and cellular debris.

macula: receptor end organ of the utricle and sac-cule housed in the vestibule; sensitive to linear andgravitational stimulation; plural: maculae.

macula ava anterior: the region immediately belowthe thyroid notch, somewhat yellowish in color, where the two vocal folds converge anteriorly.

main sensory nucleus: brainstem nucleus found inthe pons that receives sensory information fromthe trigeminal (V) nerve regarding touch.

malleoincudal joint: articulated joint between themalleus and incus.

malleolar fold: a ridge along the tympanic membraneformed by ligament attachments to the anteriorprocess of the malleus.

malleus: the largest and most lateral bone in theossicular chain; articulates with the tympanic

membrane and the incus.mandible: the jaw bone.mandibular fossa: also known as the glenoid fossa;

a depression in the temporal bone immediatelyanterior to the external auditory meatus where thecondylar process of the mandible articulates withthe skull, thereby forming the temporomandibular joint (TMJ).

manubrium: the long process of the malleus thatarticulates with the tympanic membrane (TM) oreardrum.

masked facies: an expressionless face typically seenin Parkinson’s disease.

mass effect: the resulting compression of surround-ing nervous tissue by a lesion such as a hemorrhageor tumor.

mass lesions: foreign masses on the vocal folds thataffect their ability to phonate properly, such as nod-ules, papillomae, or polyps.

mastication: the process of chewing food throughmandibular and tongue movements to form abolus.

mastoid air cells: the labyrinth of variable-sized cavi-

ties within the mastoid bone.mastoid process: the rounded, posterior part of thetemporal bone immediately behind the externalauditory meatus and lateral to the styloid process;it serves as an attachment for several muscles.

mastoidectomy: the surgical removal of the bony par-tition of the mastoid air cells for mechanical clean-ing of infection within the mastoid process of thetemporal bone.

mastoiditis: inammation of the mastoid air cells within the mastoid bone.

matrix: extracellular material that is part of connec-

tive tissue.maxillary paranasal sinuses: spaces within the max-

illae that open into the nasal cavity.maximum minute volume: the amount of air that

can be forcibly and maximally inspired and expiredover the course of one minute.

mechanoreceptors: sensory receptors that respondto mechanical deformation of tissue such as com-pressing, stretching, etc.; for the respiratory system,these are found in the pulmonary apparatus andchest wall.



GLOSSARY 379

medial compression: the force of vocal fold adduc-tion; as medial compression increases, the vocalfolds become more resistant to subglottic air pres-sure; the laryngeal adjustment that regulates vocalintensity.

medial cranial fossa: two middle depressions at thebase of the interior cranium where the temporal

lobes of the brain reside.medial geniculate body: the auditory nucleus withinthe thalamus that receives primary ascending bersfrom the inferior colliculus and then relays them tothe auditory cortex.

medial geniculate nucleus (MGN): see medial genic-ulate body .

medial lemniscus: a sensory tract traveling from thenuclei gracilis and nuclei cuneatus (dorsal columnnuclei) in the medulla to the thalamus.

medial longitudinal fasciculus: ascending brainstemtract carrying information from the vestibular nucleito the motor nuclei that control eye movement.

median glossoepiglottic fold: a single midline foldof connective tissue that courses from the lingual(anterior) surface of the epiglottis to the base of thetongue.

mediastinum: the cavity between the pleurae of thelungs containing the heart and thoracic viscera.

medical home: an approach to providing compre-hensive primary medical care that facilitates apartnership between an individual patient andtheir personal physician; a medical home allows

better access to health care and increased satisfac-tion with care by insuring the patient’s continuityof care; also known as Patient-Centered MedicalHome (PCMH).

medulla: see medulla oblongata .medulla oblongata: referred to as the medulla, it is

the most caudal component of the brainstem andis continuous with the spinal cord.

medullaris: the lower, tapering part of the spinal cordat the level of the rst lumbar segment (L1); alsoknown as the conus medullaris.

medullary centers: large volume of white matter

bers found in the cerebral hemispheres; the threetypes of bers comprising the medullary centers areassociation, projection, and commissural bers.

medullary rhythmicity center: the part of the medullaoblongata that controls the rate, depth, and rhythmof breathing.

Ménière’s disease: a disease of idiopathic etiology thatresults from the excessive accumulation of endo-lymph within the membranous labyrinth; syndromesinclude episodic vertigo, uctuating sensory hearingloss, and a sensation of fullness in the affected ear.

meninges: connective tissue coverings of the centralnervous system (CNS); there are three meningealcoverings: the dura mater, the arachnoid, and thepia mater.

meningiomas: central nervous system tumors arisingfrom meningeal connective tissue.

meningitis: an inammation of the meninges from

bacterial or viral causes.meningococcal: referring to an organism that is onecause of bacterial cerebrospinal meningitis.

mental symphysis: the brocartilaginous juncture atmidline of the two halves of the mandible that ossi-es during the rst year of life; the chin.

mesencephalic nucleus: a brainstem sensory nucleusreceiving information regarding proprioceptionfrom the trigeminal (V) nerve.

mesencephalon: the midbrain, found caudal to thediencephalon.

mesioversion: malposition of a tooth toward the mid-line of the dental arch.

mesothelial tissue: a type of epithelial tissue that linesthe internal body cavities.

metamemory: a higher level cognitive function denot-ing the ability to know and predict recall; memoryabout memory.

metencephalon: developed from the rhombenceph-alon; consists of the pons and cerebellum.

metopic suture: the seam that divides the two halvesof the frontal bone in infants and children that usu-ally disappears by the age of 6 so that the frontal

bone is a singular unit.Michel dysplasia: a malformation of the inner earcharacterized by its failure to develop, resulting incomplete unilateral or bilateral deafness.

microcephaly: abnormal smallness of the head.microlament: an organelle that assists with cell

movement and transport of substances within thecell.

microglia: a type of glial cell with many small, neprocesses; involved in phagocytosis following neu-ronal death.

micropascals (µPa): unit of measurement of pressure

representing one-millionth of a pascal.microtia: malformation of the pinna.microtubule: an organelle that assists with cell

movement and transport of substances withinthe cell.

middle ear: portion of the hearing mechanism medialto the tympanic membrane and lateral to the vesti-bule of the inner ear.

middle ear cavity: air-lled space in the temporalbone where the contents of the middle ear reside;also referred to as the middle ear space.



380 GLOSSARY

midline raphe: the midline seam where the twomylohyoid muscles (left and right) meet as theirbers course to insert onto the hyoid bone.

migration: one of the stages of neurodevelopmentduring which neurons move to their destined loca-tions.

millivolts (mV): one-thousandth of a volt; a unit of

measure for electrical current.minute volume: the amount of air that is exchangedduring quiet, tidal breathing over the course of oneminute.

mitochondria: an organelle that provides the energysource for the cell.

mixed: in reference to diminished hearing acuity,a hearing loss that has both conductive and sen-sorineural components; the conductive componentcan be treated but the sensorineural component ispermanent.

modal register: the range of frequencies associated with the vocal midrange; it is associated with habit-ual pitch.

modiolus: the bony central core of the cochlea thathouses the nerve ber ganglia of cranial nerve VIIIas well as blood vessels.

Mondini dysplasia: a specic malformation of thecochlea where only the basal turn is developed,thereby restricting the bony cochlea to 1.5 turns.

monophthongs: vowel sounds that have only onearticulatory position throughout their production;also known as pure vowels.

motile: capable of movement.motor homunculus: the topographical map of theprecentral gyrus indicating body representationregarding motor function.

motor speech disorder: a disorder in which the plan-ning, initiation, timing, coordination, or strengthof voluntary muscle movements for speech isadversely affected; includes apraxia of speech (AOS)and dysarthria.

mucoperiosteum: the lining of the interior parana-sal sinuses (as well as other parts of the body suchas the auditory structure) formed by the intimate

union of the periosteum and a mucous mem-brane.

mucosal wave: the repetitive, undulating vibration ofthe mucous membrane covering of the vocal foldsduring phonation; aberrations of the mucosal wavemay indicate vocal fold pathology.

multiple sclerosis: an acquired, degenerative, demy-elinating disease of the central nervous system.

muscle cell: synonymous with muscle ber; special-ized for the production of mechanical force.

muscular dystrophy: a genetic disease characterizedby progressive muscle deterioration and weak-ness.

muscular process: the rounded projection at the baseof each arytenoid cartilage where the posterior andanterolateral surfaces meet; the muscular processesare the insertion point for the lateral and posterior

cricoarytenoid muscles.musculocartilaginous: referring to an anatomicalstructure that is composed primarily of cartilagesand muscles; the larynx is a musculocartilaginousstructure.

myelencephalon: develops from the rhombencepha-lon; consists of the medulla.

myelin: axonal covering necessary for rapid impulseconduction; oligodendroglia make up myelin in thecentral nervous system (CNS) and Schwann cellsmake up myelin in the peripheral nervous system(PNS).

mylohyoid line: a ridge running transversely alongthe interior surface of the corpus of the mandible;it is the point of origin for the mylohyoid and othermuscles.

Myoelastic Aerodynamic Theory: a theory thatdescribes how the vocal folds vibrate according toprinciples of aerodynamics (e.g., airow, Bernoullieffect, pressure); the explanation of the phonatoryprocess that accounts for the vibratory capacityof the vocal folds based on their mass and elastic-ity (myoelastic) and the movement of air (aerody-

namic) through the glottis.myopia: nearsightedness.myringoplasty: a surgical procedure to close a tym-

panic membrane perforation.myringotomy: surgical incision of the tympanic

membrane to remove effusion of the middle ear.nasal cannulae: tubes inserted into the nasal open-

ings to deliver oxygen.nasal murmur: an additional resonance below 500

Hz for the nasal consonants.nasal septum: the midline division between the two

halves of the nasal cavity which is formed by bone

(the perpendicular plate of the ethmoid and thevomer) posteriorly and cartilage (septal cartilage)anteriorly.

nasopharynx: a division of the pharynx whichextends from the base of skull to the level of thevelum; the pharyngeal region posterior to thenasal cavity.

natural resonant frequency: the frequency at whicha system vibrates with greatest amplitude whendriven by an external force.



GLOSSARY 381

nebulizer: a mechanical device used to administermedication to individuals with respiratory diseasevia a liquid mist to the airways.

neocortex: the newest cortex from an evolutionaryperspective; it is six-layered and makes up the cere-bral cortex.

neologisms: made-up words that are not found in the

patient’s language.neonatal herpes: herpes infection in the newbornbaby.

neoplasm(s): tumors, whether benign or malignant.nerve cell: synonymous with neuron; specialized for

the initiation and conduction of impulses.neural arch: the bony arch on the dorsal side of a ver-

tebra formed by the pedicles and laminae extend-ing from the corpus.

neural crest: neuroectodermal tissue that separatesfrom the neural tube and develops into structuresof the peripheral nervous system.

neural pathway: the nerve cells and pathways of theauditory and vestibular systems.

neural plate: early stage of neurodevelopment fol-lowing induction; neuroectoderm thickening thatdevelops into the neural tube.

neural tube: neuroectodermal tissue that folds inupon itself to form a tube and later develops intothe central nervous system.

neuralgia: pain associated with a nerve.neurectomy: the surgical excision of part of a nerve.neurogenic dysphagia: a swallowing disorder with a

neurological etiology.neurological disorder: any disorder whose etiology canbe traced to the central or peripheral nervous system.

neuromas: tumors of the nervous system, whetherbenign or malignant.

neuromuscular junction: the point of synapsebetween a neuron and the muscle bers it inner-vates; also referred to as the myoneural junction.

neuropathy: a disease or abnormality of the nervoussystem.

neurotransmitter(s): chemical agents at synaptic junctions that allow neural impulses to propagate.

nodes of Ranvier: intervening spaces between myelinsegments on an axon where the axon communi-cates directly with the extracellular space.

noise-induced hearing loss (NIHL): hearing loss dueto exposure to excessive noise levels; the loss is sen-sorineural and permanent in nature.

nonuent aphasias: a classication of language dis-orders due to a brain lesion characterized by effort-ful speech production and average utterance lengthof less than three words.

nucleus: the control center of a cell which housesgenetic material.

oblique line: a somewhat ill-dened ridge runningdiagonally along each thyroid lamina.

occipital condyles: two processes on either side of theforamen magnum that serve as the point of artic-ulation between the base of the skull and the rst

cervical vertebra (C1 or the atlas).occipitomastoid suture: the seam or joint betweenthe occipital bone and the mastoid process of thetemporal bone which is continuous with the lamb-doidal suture.

occiput: the back of the cranium.octave: in speech science, a doubling of frequency

usually in reference to the fundamental frequency;for example, if the fundamental frequency is 150Hz, the rst octave is 300 Hz.

oculomotor: cranial nerve III, innervates multiplemuscles for eye movement.

odontoid process: a toothlike, vertically oriented projection on the axis (C2) upon which the atlas (C1)rotates; also referred to as the dens.

ohms: unit of measure of resistance for electrical orother forms of energy.

olfactory: cranial nerve I, projects from the nasal cav-ity to the olfactory bulb transmitting sensory infor-mation regarding smell.

oligodendroglia: a type of glial cell responsible forproducing myelin in the central nervous system.

olivocochlear pathway: efferent pathway projecting

from the medial and lateral superior olivary com-plex and coursing down to the inner and outer haircells for the purpose of inhibition.

operculum: area of the cerebral cortex that overliesthe insula; includes the frontal opercula, temporalopercula, and parietal opercula.

optic: cranial nerve II, transmits visual informationfrom the retina exiting the optic disc and travelingcaudally on the ventral surface of the frontal lobes.

optic canals: two short openings in the lesser wingsof the sphenoid bone where the optic nerves (cra-nial nerve II) and ophthalmic arteries pass from the

orbits of the eye into the cranial cavity.optic chiasm: partial crossing point of the optic nerve

and part of the primary visual pathway.optic radiations: part of the primary visual pathway

carrying bers from the lateral geniculate nucleusof the thalamus to the primary visual cortex in theoccipital lobe.

optic tract: part of the primary visual pathway carry-ing bers from the optic chiasm to synapse at thelateral geniculate nucleus of the thalamus.



382 GLOSSARY

optimal pitch: natural pitch; the voice fundamentalachieved at maximum phonatory efciency in themodal register.

oral preparatory stage: the rst stage of swallow,including removing food from a cup or utensil andchewing (i.e., mastication) to form the bolus.

oral stage: the second stage of the swallow where the

bolus is propelled toward the pharynx to initiate aswallow reex.oral transit time (OTT): the amount of time it takes

to move the bolus toward the pharynx and initiatea swallow.

orbit: the large opening in the facial part of the skull where an eyeball resides.

organ of Corti: organ within the scala media of thecochlea where the receptor hair cells and support-ing cells reside resting on the basilar membrane.

organelles: structures inside a cell that perform vitalfunctions for the life of the cell.

organic: relating to the structure, function, or healthof living things; see also organic disorder.

organic disorder: an impairment that can be tracedback to an observable structural or physiologicaletiology.

oropharynx: a division of the pharynx that extends fromthe level of the velum to the level of the hyoid bone;the pharyngeal region posterior to the oral cavity.

ossicles: the bones of the middle ear: malleus, incus,and stapes.

ossicular chain: the collection of the articulated bones

of the middle ear: malleus, incus, and stapes.osteoblasts: specialized cells that are responsible forforming or reforming bone.

osteoclasts: specialized cells that are responsible forthe resorption of bone.

osteoma: benign slow growing bony mass in the earcanal usually located at the junction of the carti-laginous portion and the bony portion; exposure tocold water is thought to stimulate their growth.

osteoporosis: signicant loss of bone density.otalgia: ear pain.otitis externa: an inammation of the skin lining of

the external auditory meatus or ear canal.otitis media (OM ): inammation of the middle ear

resulting primarily from poor Eustachian tubefunction.

otitis media with effusion: inammation of the mid-dle ear with the development of uid in the middleear space.

otitis media with tympanic membrane perforation:inammation of the middle ear with a secondaryperforation of the tympanic membrane (TM) oreardrum.

otoconia: calcium crystals that add mass to the struc-ture of the maculae of the utricle and saccule; they arelocated on the gelatinous (i.e., otolithic) membrane in which the stereocilia of the hair cells are embedded.

otolaryngologist: a physician who specializes in thediagnosis, management, and treatment of ear, nose,and throat conditions; also known as an ENT.

otolithic membrane: the gelatinous membrane thatthe otoconia rest upon that provides for the stimu-lation of the embedded stereocilia hair cells of themaculae.

otologist: a physician who specializes in the diagno-sis, management, and treatment of ear disease.

otorrhea: drainage from the ear.otosclerosis: formation of new spongy bone growth

around the stapes footplate and oval window result-ing in stapes xation and a concomitant conductivehearing loss.

otoscopy: inspection of the external auditory meatusand tympanic membrane through use of an oto-scope.

outer ear: the outermost portion of the hearing mech-anism, beginning with the pinna, that functions togather and conduct sound waves down to the levelof the tympanic membrane.

outer hair cells (OHC): motile cells within the organof Corti that seem to be responsible for enhancingtectorial membrane movement at low intensity lev-els to facilitate stimulation of the inner hair cells.

outer pillar cells: supporting cells for the organ of

Corti that stabilize the outer hair cells; they formthe tunnel of Corti.oval window: the opening on the medial wall of the

middle ear leading into the scala vestibuli of the innerear; the footplate of the stapes ts in this window.

palatal aponeurosis: a broad, at sheet of connectivetissue that serves as the skeleton for the velum (softpalate).

palatine processes: the horizontally directed pro-cesses of the maxillae that form the anterior por-tion of the hard palate.

palatoglossal arches: also known as the anterior fau-

cial pillars; two folds on either side of the posteriororal cavity that are formed by the palatoglossusmuscles.

palilalia: a pathological condition in which words arerapidly and involuntarily repeated.

palliative care: care that is focused on the comfort ofthe individual through the prevention and relief ofsuffering to improve quality of life.

palsy: partial or complete paralysis of muscles, oftenaccompanied by loss of sensation and uncontrol-lable body movements such as tremors.



GLOSSARY 383

papilloma: also known as juvenile papillomatosis;benign tumors of the larynx in children.

paradoxical vocal fold movement (PVFM): adductoryrather than normal abductory vocal fold movementduring inspiration resulting in constriction or com-plete occlusion of the airway.

paragrammatism: language errors in the use of gram-

matical markings seen in persons exhibiting uentaphasia.parahippocampal gyrus: cortical region inferior to

the cingulate gyrus at the medial surface of thetemporal lobe.

paramedian position: the somewhat halfwayabducted position that the vocal folds take at rest;the vocal folds can either adduct from this positionor more fully abduct.

parasympathetic division: a division of the auto-nomic nervous system; serves to conserve bodyenergy and maintain the internal balance of bodysystems.

parenchyma: organ tissue.parenchymal: deep to the cerebral cortex; also

referred to as intracerebral.parietal pleura: see costal pleura .parietal–temporal–occipital (P-T-O) region: the

multimodal association cortex at the convergenceof the parietal, temporal, and occipital lobes.

Parkinson’s disease: a degenerative disease of themesencephalic basal ganglia, specically the sub-stantia nigra.

pars accida: the superior region of the tympanicmembrane (TM) having less support from the cen-tral brous layers.

pars oblique: a bundle of bers from the cricothyroidmuscle that course in a somewhat diagonal direc-tion; the lateral bundles of the cricothyroid muscles.

pars recta: a bundle of bers from the cricothyroidmuscle that course in a somewhat vertical direction;the medial bundles of the cricothyroid muscles.

pars tensa: make up the body of the tympanic mem-brane (TM); consisting of three sturdy brouslayers.

Passavant’s pad: a bulging of the posterior wall of thenasopharynx created by contraction of the musclesthat comprise the superior pharyngeal constric-tors.

pathology: the scientic study of the nature of dis-eases and of the structural and functional changesthat occur to the living organism due to diseaseprocesses.

patulous: abnormally open.pericardial cavity: internal body cavity that houses

the heart.

pericardium: the membranous sac that contains theheart.

perichondrium: brous membrane surrounding theouter surface of cartilage.

perilymph: cochlear uid found in the scala vestibuliand scala tympani; it is high in concentrations ofsodium and calcium and low in concentration of

potassium.perimysium: connective tissue covering each musclefasciculus.

perineurium: connective tissue covering each nervefascicle.

periodic sounds: sounds whose waveforms repeatthemselves at equal intervals over time.

periodontal ligament: the connective tissue thatholds a tooth within its alveolus, thereby forming a joint called a gomphosis.

periosteum: brous membrane surrounding theouter surface of bone.

peripheral chemoreceptors: sensory receptorsresponding to changes in oxygen levels in the blood;located at the bifurcation of the common carotidarteries.

peristalsis: the unidirectional wavelike muscular con-tractions in the pharynx and esophagus that forcefood and drink down toward the stomach.

peristaltic: referring to a wavelike action.peritoneal cavity: internal body cavity that houses

the abdominal viscera.permanent: continuing indenitely without funda-

mental change.perpendicular plate of the ethmoid: a vertically ori-ented lamina of the ethmoid bone that extends belowand perpendicular to the cribriform plate, formingthe superior part of the bony nasal septum.

petiolus: the narrow stalk at the inferior end of theepiglottis that is bound to the thyroid cartilage justbehind the thyroid notch by way of the thyroepi-glottic ligament.

phagocytic cells: cells that capture and absorb wastematerial, harmful microorganisms, and other for-eign bodies.

phagocytosis: the process of ingesting cellular debris.pharyngeal aponeurosis: a broad, at sheet of con-

nective tissue that serves as the skeleton for thepharynx.

pharyngeal fricative: an unvoiced sound occur-ring naturally in some languages (but not English)that is produced by creating turbulence within thepharynx; in speakers for whom the sound doesn’toccur naturally, this sound is sometimes used as acompensatory strategy when intraoral air pressureis insufcient to produce the oral fricatives.



384 GLOSSARY

pharyngeal stage: third stage of the swallow that isinitiated with the swallow reex and ends with thebolus entering the esophagus.

pharyngeal transit time (PTT): the time it takes forthe bolus to pass through the pharynx and into theesophagus.

pharyngeal tubercle: the region immediately ante-

rior to the foramen magnum on the basilar partof the occipital bone where the pharyngeal rapheattaches (the pharyngeal raphe, in turn, serves asthe point of origin and insertion for the pharyngealconstrictor muscles).

pharynx: the upper end of the alimentary canal thatextends from the oral and nasal cavities to theesophagus; also known as the throat.

philtrum: the vertically oriented groove or depressionlocated midline between the nose and the upper lipbordered on either side by the columellae nasi.

phonation: the physiological process by which vocalfold vibration results in a vocal tone; the process ofproducing a voice by way of vocal fold vibration.

phonation breaks: phonatory discontinuity; phona-tion is interrupted with brief periods of aphonia.

phonemic paraphasias: see literal (phonemic) para-phasias .

phonemic regression: age-related reduction in theability to recognize words greater than expectedfrom the amount of documented hearing loss.

phonological disorder: a speech disorder character-ized by speech sound errors that are cognitively or

linguistically based, as opposed to simple errors inmotor production.photoreceptors: sensory receptors for vision; these

include the rods and cones of the retina.phrenic nerve: the nerve created by combined

branches of spinal nerves C3, C4, and C5 that inner-vates the diaphragm.

phrenology: the correlation of the structure of thehead with personality and intellect proposed byFranz Joseph Gall in 1809.

physiology: the scientic study of the function of theliving organism and its parts.

pia mater: the innermost of the three meningeal lay-ers; very delicate and transparent.

piebaldism: an autosomal dominant genetic disor-der of pigmentation characterized by congenitalpatches of white skin and hair.

pinna: visible portion of the outer ear for the collec-tion of sound; also referred to as the auricle.

pitch: the perceptual correlate of sound frequency.pitch breaks: a sudden, noticeable, often unexpected

shift from one pitch to another during phonation;commonly an upward shift of an octave or more

from the modal register to the loft register (fal-setto).

plane of reference: the vertical, horizontal, or otherdirection in which an anatomical structure is beingviewed by the observer; these include the coronal,sagittal, and transverse planes.

plasma membrane: double-layered outer membrane

of a cell.plethysmograph: a device that allows one to studymovements of the chest and abdomen by observingchanges in thoracic and abdominal volumes.

pleurae: the serous membrane that surrounds thelungs and interior of the thorax consisting of twolayers: the costal pleura and the visceral pleura.

pleural cavities: internal body cavities that house thelungs.

pleural linkage: the binding of the lungs to the inte-rior of the rib cage by way of the airtight adhesion ofthe visceral pleura of the lungs to the costal pleuraof the rib cage, and of the lungs to the superior sur-face of the diaphragm by way of the visceral pleurathey both share.

pneumococcal: referring to an organism that is onecause of bacterial cerebrospinal meningitis.

pneumonia: lung inammation that is secondary toinfection or other causes such as aspiration.

pneumotachometer: a device that allows one to studychanges in air pressure and air ow.

pneumotaxic area: the respiratory area in the ponsthat inhibits inspiration to prevent overination of

the lungs.pneumothorax: the presence of gas in the pleuralcavity which results in a collapsed lung.

polyps: nonmalignant growths or tumors protrudingfrom the mucous membrane of a structure such asthe nasal cavity or vocal folds.

pons: a broad mass of chiey transverse nerve bersin the brainstem lying ventral to the cerebellumat the anterior end of the medulla oblongata; thebridge between the brainstem and the structures ofthe midbrain.

pons-medullary junction: the junction on the ventral

aspect of the brainstem that demarcates the ponsfrom the medulla oblongata; cranial nerve VIIIemerges here.

pontine cisterns: enlarged subarachnoid spaces thatare ventral to the pons; contains cerebrospinal uid(CSF).

posterior cranial fossa: the two rear-most depres-sions in the base of the interior cranium where thetwo lobes of the cerebellum of the brain reside.

posterior cricoarytenoid ligament: connective tis-sue anchoring the posterior base of the arytenoid



GLOSSARY 385

cartilage to the posterior quadrate lamina of thecricoid cartilage, thereby restricting the anteriorrocking movement of the arytenoid.

posterior crus: anatomical structure resembling a leg;this crus along with the anterior crus of the stapesconnect to its footplate.

posterior faucial pillars: bands of tissue running

from the soft palate to the pharynx, overlying thepalatopharyngeus muscles.posterior quadrate lamina: the broader posterior

portion of the cricoid cartilage that projects superi-orly to occupy some of the open space in the poste-rior inner region of the thyroid cartilage.

postlingual: after speech and language skills havebeen developed.

precentral gyrus: convoluted gray matter anteriorto the central sulcus; involved in volitional move-ment.

prefrontal cortex: the multimodal association area ofthe most rostral region of the frontal lobes.

prelingual: prior to the development of speech andlanguage skills.

premaxilla: the triangular part of the anterior hardpalate that is formed by two tiny sutures originatingbilaterally between the lateral incisors and cuspidsand coursing back to terminate at the incisive fora-men; this region is typically fused in humans.

prephonation phase: that part of the vibratory cycle where the vocal folds move from the paramedianposition to the median position by means of adduc-

tion.presbycusis: age-related progressive hearing lossmost often sensorineural and bilateral in nature.

presbylaryngis: progressive voice degenerationattributed to the aging process.

press of speech: see logorrhea .pressure = force/area: a law of physics that states that

pressure change occurs as a force is displaced overa change in area; with force being constant, pres-sure increases as area decreases and vice versa.

pressure consonants: consonant sounds that requirea degree of intraoral air pressure to be produced;

includes the plosives and affricates primarily butcan include the fricatives.

pressure equalization (PE) tube: a silastic tube orgrommet surgically placed in the tympanic mem-brane to provide passive ventilation of the middleear space.

primary areas: regions of the cerebral cortex thathave single functions.

primary auditory cortex: receives projections fromthe auditory pathway, also called Heschl’s gyrus;Brodmann areas 41 and 42.

primary motor cortex: the precentral gyrus in thefrontal lobe; gives off projections for volitionalmotor movement; Brodmann area 4.

primary progressive aphasia (PPA): a subtype ofdementia with the primary symptom of progressivedeterioration of language abilities.

primary somatosensory cortex: the postcentral gyrus

in the parietal lobe that receives sensory projec-tions; Brodmann areas 3, 1, 2.primary visual cortex: the cuneus and lingual occipi-

tal gyri regions surrounding the calcarine ssure where the sense of sight is interpreted; Broadmannarea 17.

primary visual pathway: the axonal bers and nucleiinvolved in transmitting visual neural informationfrom the retina to the primary visual cortex in theoccipital lobe.

progressive: advancing in degree or severity.progressive neurological disorder: a pathological

condition arising from the central and/or periph-eral nervous system that gets progressively worseover time and is often fatal.

projection ber tracts: bundles of axons that transmitneural information from higher to lower (and viceversa) centers of the central nervous system (CNS).

proliferation: one of the stages of neurodevelopmentduring which neurons multiply.

promontory: the bony prominence in the medial wallof the middle ear cavity created by the basal turn ofthe cochlea.

propagation: the transmitting of an action potentialdown an axon toward the terminal.proprioceptive: pertaining to the sense of body posi-

tion, posture, and movement.prosencephalon: a term signifying the rostral vesicle

of the neural tube early in neurodevelopment; fur-ther differentiates to form the telencephalon anddiencephalon.

prosody: the intonation and stress that overlies theproduction of speech sounds during conversationalspeech, signaled by modications in vocal pitch,intensity, and duration.

prosopagnosia: an inability to recognize familiarfaces; a type of perceptual impairment.

prospective memory: memory for future events andinformation; remembering to remember.

protoplasm: the basic living substance of cells.pseudobulbar palsy: a condition resulting in dysar-

thria as a result of lesions occurring above the levelof the brainstem.

psychogenic: of psychological origin; from the mind;often used to mean functional or in the absence ofan organic etiology.



386 GLOSSARY

ptosis: droopy eyelid(s) secondary to oculomotor (III)nerve involvement.

puberphonia: also known as mutational falsetto; useof a high pitch, often falsetto, usually in postpubes-cent and young adult males such that age and gen-der identity may be lost and/or negative attentionresults.

pubic symphysis: the joint formed by the union of themedial aspects of the two pubic bones.pubis: the inferiormost of the three bones that com-

prise the pelvis (the other two being the ilium andischium).

pulmonary edema: abnormal buildup of uid in thelungs.

pulmonary pressure: the force that air exerts uponthe alveoli pulmoni within the lungs; also referredto as alveolar pressure.

pulmonologist: a medical doctor who specializes indiseases of the lungs and respiratory tract.

pulp cavity: the central cavity of a tooth that containssoft tissue pulp.

pulse oximeter: a medical device used to measuredheart rate or pulse as well as to estimate blood oxy-gen levels.

pulse register: the range of vocal pitches that is asso-ciated with glottal fry, that is, the lowest pitches ofthe vocal range.

pure tone: an individual, discrete sound frequency;tones produced by audiometers and tuning forksare pure tones.

putamen: one of the nuclei of the basal ganglia foundin the telencephalon lateral to the globus pallidus;involved in higher-order motor control.

pyramidal eminence: pyramid-shaped bony projec-tion lying on the posterior wall of the middle earcavity that houses the stapedius muscle.

pyramids: bulges on the ventral aspect of the rostralmedulla; corticospinal and remaining corticobul-bar tracts underlie the pyramids.

quadrangular membrane: the superior portion ofthe elastic membrane that extends from the adi-tus laryngis superiorly to the ventricular ligaments

inferiorly.recruitment: an abnormal sensitivity to loud stimuli

associated with sensorineural hearing loss.recurrent laryngeal nerve: a peripheral branch of

the vagus nerve (cranial nerve X) that innervatesall intrinsic muscles of the larynx except for the cri-cothyroid muscles; it is given the name “recurrent”because it takes an indirect route to the larynx byrst descending into the upper thorax.

Reissner’s membrane: membrane within the cochlearduct separating the scala vestibuli and the scala

media; projects obliquely from the osseous spi-ral lamina and the outer wall of the cochlea; alsoreferred to as the vestibular membrane.

relative refractory period: brief period of time fol-lowing the ring of an action potential when theneuron will only re if more depolarization thannormally required is generated.

residual volume (RV): the volume of air that remainsin the lungs and cannot be forcibly expelled; itspurpose is to prevent the lungs from collapsingcompletely.

resonance: selective amplication of certain soundfrequencies due to the natural resonant character-istics of a cavity; the enhancement of certain tones within the vocal tone as it passes through the vocaltract; those tones that are tuned to the shape andconguration of the vocal tract will resonate.

resonant: pertaining to the rate at which a mass willvibrate most effectively when set into free motion.

resonator: any object or entity that is set into vibra-tion by the action of an outside force.

respiration: the exchange of oxygen for carbon diox-ide at the level of the alveoli in the lungs.

resting membrane potential (RMP): the voltagecharge maintained across a neuronal membrane when no action potential is being generated; RMPsare approximately − 70 mV.

resting volume: the volume of air that is in thelungs when they are at their resting state betweenbreaths.

reticular lamina: the netlike structure forming theupper surface of the organ of Corti; formed fromthe phalangeal processes of the supporting cells.

retinitis pigmentosa: a disease caused by overactiv-ity of the pigmented retinal epithelial cells; leads todamage and occlusion of the photoreceptors result-ing in blindness.

retrocochlear: the structures of the auditory systembeyond the level of the cochlea, especially cranialnerve VIII and the brainstem.

retrospective memories: memories for past eventsand information; also known as long-term memo-

ries.reverse breathing: a respiratory anomaly seen in

some cases of athetoid cerebral palsy that is charac-terized by depression of the sternum during inspi-ration instead of elevation.

rhinorrhea: excessive secretion of mucous from thenose; also referred to as a runny nose.

rhombencephalon: term signifying the caudal vesicleof the neural tube early in neurodevelopment; fur-ther differentiates to form the metencephalon andmyelencephalon.



GLOSSARY 387

rima glottis: the technical name for the glottis, thevariable-sized opening between the vocal folds when they are in varying degrees of abduction.

rima oris: the mouth; the entrance into the oralcavity.

rods: one type of photoreceptor found in the retinaspecialized for sensing light.

round window: the membrane-covered window lead-ing to the scala tympani, located within the medial wall of the middle ear space.

saccule: the structure housed in the vestibule of theinner ear closest to the cochlea that contains theend organ (macula) sensitive to linear accelerationand gravity.

sacral foramina: a series of four paired holes or open-ings within the sacrum where nerves and bloodvessels pass from the lower abdomen to the lowerextremities.

sacral segment: one of the ve segments of the spinalcord corresponding to the hip region.

sagittal suture: the seam running longitudinallydown the center of the skull that serves as the jointbetween the two parietal bones.

saltatory conduction: the high-speed impulse con-duction of myelinated axons; propagation occursbetween nodes of Ranvier.

sarcoidosis: an autoimmune disease in which granu-lomatous substances are deposited into the tissuesof organs, including the nervous system.

scala media: see cochlear duct .

scala tympani : the lower chamber of the cochlea,lled with perilymph uid; it terminates at theround window and the helicotrema.

scala vestibuli: the upper chamber of the cochlea,lled with perilymph uid; it terminates at the oval window and the helicotrema.

scapula: known more commonly as the shoulderblade, the somewhat triangularly shaped bonethat is attached to the axial skeleton by way of theclavicle; it serves as the point of articulation for thehumerus.

Scarpa’s ganglion: a ganglion of the vestibular nerve

leading into the internal auditory canal within thevestibular branch of cranial nerve VIII; two gangliaconsisting of the bodies of the primary vestibularneurons which separate into a superior and an infe-rior group.

Scheibe dysplasia: the most common form of con-genital dysplasia of the inner ear; the bony laby-rinth and membranous utricle and semicircularcanals are fully formed, but the saccule and scalamedia are poorly differentiated; resulting from anautosomal recessive inheritance.

Schwann cell: a type of glial cell that produces myelinto insulate the axons in the peripheral nervous sys-tem (PNS).

Schwannoma neuroma: a benign neoplasm com-posed of Schwann cells arising from the vestibularportion of cranial nerve VIII; also referred to as anacoustic neuroma.

Schwartze’s sign: a reddish glow seen on the prom-ontory produced by increased vascularity; it can bevisualized through the tympanic membrane duringotoscopy; considered an early sign of otosclerosis.

scoliosis: a lateral spinal curvature or “sideways”bending of the spine.

selective permeability: the ability of a neuron to letcertain ions in to the cell and keep other ions out ofthe cell given certain conditions.

sella turcica: a saddle-shaped depression in thesphenoid bone at the base of the skull that containsthe hypophyseal fossa which in turn holds thepituitary gland.

semantic memory: a type of declarative memory spe-cic to conceptual or world knowledge.

semantic paraphasias: see verbal (semantic) para-phasias .

semicircular canals: a part of the vestibular systemof the inner ear, consists of three looped canals ofbony labyrinth oriented to anatomical directions:anterior, lateral, and posterior; contain sensoryreceptor end organs that are sensitive to angularacceleration.

sensorineural: in reference to diminished hearingacuity, an irreversible hearing loss due to pathologyof the inner ear; damage to the inner ear (e.g., thehair cells within the cochlea) cannot be alleviated.

sensory disorder: an impairment of any of the sensessuch as feeling, hearing, seeing, smelling, or tast-ing.

sensory homunculus: the topographical map of thepostcentral gyrus indicating body representationregarding sensation.

septal cartilage: the anterior, cartilaginous part of thenasal septum.

septum pellucidum: the thin, membranous coveringof the medial aspect of the lateral ventricles.

short process: the process of the incus that arisesfrom the bulky body portion of the ossicles.

silent aspiration: penetration of the airway by saliva,food, or drink that does not produce a coughreex.

simple: minute papillae found along the sides ofthe tongue approximately two-thirds of the waybetween the tip and root forming parallel grooves,each groove housing several hundred taste buds.



388 GLOSSARY

simultaneous attack: vocal fold vibration in whichexpired air reaches the vocal folds at the same timethey reach adduction; the result is relatively effort-less and smooth phonation.

site of lesion: the source or location of pathologicalchange in the structure of an organ due to injury ordisease.

SOAP notes: a method of documentation employedby health care providers to write out notes in apatient’s medical chart; SOAP is an acronym forsubjective, objective, assessment, and plan.

sodium–potassium pump (SPP): an ion pump in theplasma membrane of the neuron that exchangesintracellular sodium (Na ) for extracellular potas-sium (K ) to assist in restoring and maintaining theresting membrane potential.

somatic nervous system: a division of the peripheralnervous system; provides motor and sensory inner-vation to the joints, skin, and skeletal muscles.

spasmodic dysphonia: a voice disorder characterizedby spasmodic functioning of the larynx that resultsin extreme phonatory tension; the vocal folds canspasm shut resulting in the more common adduc-tor type or can spasm open resulting in abductorspasmodic dysphonia.

spastic: a type of cerebral palsy or dysarthria charac-terized by involuntary jerky muscular contractionsresembling spasms.

spatial summation: the addition of multiple postsyn-aptic potentials occurring at more than one syn-

apse site on the same cell.spectrum: a graphic depiction of the frequencies ofa complex tone (represented along the horizontalaxis of the graph) along with their amplitudes (rep-resented along the vertical axis).

speech–language pathologist (SLP): health careprofessional who is credentialed in the practiceof speech–language pathology to provide a com-prehensive array of services related to prevention,evaluation, and rehabilitation of speech, language,and swallowing disorders.

sphenoid paranasal sinuses: a pair of cavities

within the sphenoid bone that open into the nasalcavity.

spinal accessory: cranial nerve XI, having a cranialand spinal branch; the cranial branch assists theglossopharyngeal and vagus nerves in innervatingmuscles of the velum and pharynx while the spinalbranch innervates some muscles of the neck andshoulder.

spinal nerves: mixed (i.e., sensory and motor) nervesfrom the spinal cord that innervate the body (e.g.,muscles, glands, mucous membranes, joints).

spinal trigeminal nucleus: a brainstem sensorynucleus receiving information regarding pain andtemperature from the trigeminal (V) nerve.

spinous process: the posteriorly directed spine on avertebra; in some vertebrae, this process is hori-zontally oriented, and in others, it is more obliquelyoriented.

spiral ganglia: see spiral ganglion .spiral ganglion: the location of the cell bodies for theauditory nerve bers of the cochlea located in themodiolus; plural: spiral ganglia.

spiral lamina: two thin shelves of bone arising fromthe modiolar side of the cochlea between whichcourses the afferent and efferent nerve bers fromthe inner and outer hair cells.

spiral ligament: a band of connective tissue thatanchors the basilar membrane to the outer bony wall of the cochlear labyrinth.

spiral limbus: a mound of connective tissue in thescala media that provides the medial attachmentfor the tectorial membrane.

spirometer: a device that measures the amount of airthat enters and leaves the lungs; it is typically usedclinically to measure vital capacity.

squamous cell carcinoma: a form of skin cancer, themost common malignant tumor of the pinna, seenas a slow growing scaly patch of skin with a thicken-ing outgrowth; a result of chronic sun exposure.

stapedectomy: a surgical procedure to remove thestapes footplate after it has been xed in the oval

window due to otosclerosis; a prosthesis is usedin place of the stapes to restore the integrity of theossicular chain.

stapedial branch: a branch of cranial nerve VII (facialnerve) that innervates the stapedius muscle.

stapedius muscle: striated muscle of the middle earthat attaches to the neck of the stapes and contractsin response to loud incoming sounds; innervatedby the cranial nerve VII (facial nerve).

stapedius tendon: a tendon of the stapedius musclethat projects from the pyramidal eminence of themiddle ear to insert onto the head of the stapes

bone.stapes: the most medial bone in the ossicular chain;

the head of the stapes articulates with the lenticularprocess of the incus and the footplate resides in theoval window.

stenosis: a narrowing of a tube or passageway.stereocilia: hairlike projections from the cell body of

a hair cell; actin laments provide support for thecilia; disturbance of the stereocilia opens the chan-nels that allow for depolarization which results in aneural impulse.



GLOSSARY 389

sternum: also referred to as the breastbone, the elon-gated bone situated at midline of the ventral thoraxthat serves as a point of articulation for most of theribs as well as the clavicle.

stoma: a surgical opening into the body from the out-side.

strabismus: the misalignment of one eyeball with the

other; sometimes referred to as “lazy eye.”stria vascularis: a highly vascularized collectionof cells located on the lateral surface of the scalamedia; responsible for the recycling of endolym-phatic uids.

striatum: term indicating both the caudate nucleusand the putamen nucleus of the basal ganglia.

stroke: a sudden interruption of the blood supplyto the brain; also referred to as a cerebrovascularaccident.

structural disorder: an impairment whose etiologyinvolves anatomical deviation.

stylohyoid ligament: brous connective tissue thatoriginates at the styloid process of the temporalbone of the skull and terminates at the hyoid bone;the hyoid bone is suspended in place by two ofthese ligaments, one coming from each side.

styloid process: a pencil tip–shaped projection at thebase of the temporal bone that serves as a point ofattachment for the stylohyoid and stylopharyngeusmuscles.

subarachnoid space: the area immediately below thearachnoid layer of the meninges; blood vessels and

cerebrospinal uid (CSF) are found in this space.subclavian arteries: major arterial blood supply aris-ing superiorly off the aortic arch.

subglottic pressure: the force that expired air exertsupon the inferior surfaces of the vocal folds whenthey adduct and occlude the breath stream; thispressure is necessary to initiate and maintain pho-nation.

subglottic space: the region immediately below thelevel of the vocal folds, that is, the inner cricoid car-tilage and uppermost part of the trachea.

subthalamus: the nuclei that are inferior to the thala-

mus; part of the basal ganglia system.sudden: acute with rapid onset.sulci: grooves or furrows in the cerebral cortex run-

ning between adjacent gyri; singular: sulcus.sulcus limitans: the separation point in spinal cord

neurodevelopment of the alar plate from the basalplate; cells that develop into autonomic nervous sys-tem functions are located near the sulcus limitans.

sulcus terminalis: the transversely oriented groovealong the posterior dorsum of the tongue, shapedlike a chevron or inverted letter “V.”

superior colliculi: paired nuclei in the dorsal mid-brain where secondary bers from the visual pathway synapse; involved in visual reexes.

superior cornua: two long, narrow legs of carti-lage extending superiorly from the posteriormostregions of the thyroid laminae; they articulate with the greater cornua of the hyoid bone on each

side.superior laryngeal nerve: a branch of the vagus nerve(cranial nerve X) that innervates the cricothyroidmuscles; these nerves take a more direct path to thelarynx than the recurrent laryngeal nerves.

superior olivary complex: the auditory nucleuslocated in the hindbrain that relays informationfrom the cochlear nucleus to the lateral lemniscus.

superior olivary nucleus: a nucleus in the caudalpons and a point of synapse for the auditory pathway transmitting neural signals from the cochlearnuclei on to the inferior colliculi.

superior orbital ssures: clefts between the greaterand lesser wings of the sphenoid bone through which all or part of four cranial nerves (III, IV, V, and VI) as well as blood vessels pass from the cranialcavity into the orbits of the eyes.

superior sagittal sinus: a space found between thedural layers of the falx cerebri; venous blood drainshere and cerebrospinal uid (CSF) diffuses into thissinus.

suprahyoid: a term used to denote any muscle thathas an origin on a structure that is above the hyoid

bone, and then descends to insert onto the superiorsurface of the hyoid.suprasegmental: a feature that overlays the actual

production of speech sounds during conversa-tional speech such as intonation, stress, or junc-ture.

supratonsillar fossa: the part of the tonsillar fossaimmediately above the palatine tonsil.

supraversion: malposition of a tooth so that it extendsbeyond the line of occlusion, that is, the tooth is“higher” than adjacent teeth.

sympathetic division: a division of the autonomic

nervous system; serves to prepare the body for“ght or ight” situations.

symptoms: deviations from normal function.synarthrodial: referring to immovable joints.synchondrosis: a cartilaginous or amphiarthrodial

joint involving hyaline cartilage.syndrome: a collection of symptoms.synovial: pertaining to the secretion of uid associ-

ated with diarthrodial joints.synovial joint: anatomical classication of joints that

are freely movable.



390 GLOSSARY

syphilis: an acquired or congenital venereal disease which may result in secondary auditory or vestibu-lar disturbances of the membranous labyrinth.

tactile: pertaining to the conscious sense of touch orcontact.

tectorial membrane: the gelatinous membrane of theorgan of Corti projecting radially and overlying the

reticular lamina in which the cilia of the outer haircells are embedded.tegmen tympani: the roof of the middle ear cavity

that is created by the very thin anterior surface ofthe petrous portion of the temporal bone.

tegmental wall: the superior wall or roof of the mid-dle ear cavity.

telencephalon: anteriormost area of the brain thatincludes the cerebral hemispheres; developed fromthe prosencephalon.

telodendria: the projections extending from an axon’sterminal.

temporae: the temples.temporal summation: the addition of multiple post-

synaptic potentials occurring in rapid succession atone synapse site on a postsynaptic cell.

temporary: of short duration and eventually return-ing to a baseline.

temporary threshold shift (TTS): a temporary revers-ible hearing loss as a result of exposure to elevatednoise levels; can result in permanent loss withrepeated incidences of exposure.

temporomandibular joint (TMJ): the joint formed

by the articulation of the condylar process of themandible and the mandibular fossa of the temporalbone; although there are actually two joints, theyact as a single unit.

tendon: dense connective tissue that connects mus-cle to bone, cartilage, or another muscle.

tensor tympani: the striated middle ear muscleattached to the manubrium of the malleus that con-tracts in response to a loud stimulus; innervated bythe trigeminal nerve (V).

tensor veli palatini: a muscle found in the nasopharynx that serves to tense the soft palate upon eleva-

tion and facilitates opening of the Eustachian tube.tentorium cerebelli: the tentlike fold of dura mater

that separates the occipital lobes from the cerebel-lum.

teratogenic: an agent that negatively inuencesembryologic development resulting in an anomalyor malformation.

terminal boutons: end points of axon terminals thatmake synaptic contact with other cells.

thalamus: diencephalic structure composed of sepa-rate nuclei associated with sensory, motor, and

cognitive functions having multiple reciprocal con-nections with the neocortex.

third ventricle: a diencephalic cavity located in thecenter of the thalamus that provides a conduit forcerebrospinal uid (CSF).

thoracic segment: one of the ve segments of thespinal cord corresponding to the thoracic (i.e., rib

cage) region.threshold(s): (1) the lowest levels of sound intensitythat will yield a response 50% of the time; (2) thelowest millivolt depolarization that causes an actionpotential to occur.

thrombotic: a type of stroke due to a thrombus; agradual accumulation of material (i.e., plaque) within arterial walls to the point of occlusion.

thyroepiglottic ligament: a band of connective tissuethat binds the petiolus of the epiglottis to the inneraspect of the thyroid cartilage immediately belowthe thyroid notch.

thyroid: the largest of the laryngeal cartilages, itarticulates with and is immediately superior to thecricoid cartilage.

thyroid angle: the angle formed by the nearly completeunion of the two lamina of the thyroid cartilage; inadult males, this angle is approximately 90 degreesand in adult females, it is approximately 120 degrees.

thyroid laminae: the two prominent walls of the thy-roid cartilage that meet anteriorly at midline andfuse almost completely except superiorly where thethyroid notch is formed.

thyroid notch: a prominent indentation in the ante-rior midline of the thyroid cartilage, formed by theincomplete fusion of the two thyroid laminae.

thyroid prominence: a prominent protrusion of thethyroid cartilage anteriorly, immediately below thethyroid notch; also known as the Adam’s apple.

tidal volume (TV): the volume of air that is typi-cally exchanged during a cycle of quiet, vegetativebreathing.

tinnitus: a sensation of noise within the ears (per-ceived typically as a ringing, buzzing, or hummingsound) without an external cause.

tip links: extracellular linking proteins that runbetween the tips of the stereocilia; their function isto open the cell membrane channels for the processof transduction.

tonotopic organization: peripheral and central audi-tory nervous system maintenance of the frequencyorganization that originated along the basilar mem-brane within the cochlea.

tonsillar fossa: the cavity or space between the palato-glossal and palatopharyngeal arches (i.e., anteriorand posterior faucial pillars).



GLOSSARY 391

TORCH: an acronym for a small group of viral agents(toxoplasmosis, rubella, cytomegalovirus, herpessimplex, and “other” agents) that can cross the pla-cental barrier and cause similar symptoms in new-borns—one of which is hearing loss.

torsiversion: malposition of a tooth so that it istwisted upon its own vertical axis; for example, in

180-degree torsiversion, the back of the tooth is fac-ing the front and vice versa.torus tubarius: a comma-shaped ridge in the region

of the nasopharynx that is formed by the salpin-gopalatine and salpingopharyngeus muscles; theopening of the Eustachian tube is located beneaththe curved part of this structure.

total lung capacity (TLC): the sum of all lung vol-umes, including inspiratory reserve volume, tidalvolume, expiratory reserve volume, and residualvolume.

toxoplasmosis: an infection caused by a single cellparasite ( toxoplasma gondii ) that invades the tis-sues and may seriously damage the central nervoussystem, especially in infants.

tragus: the cartilaginous part of the pinna that projectsoutward from the face toward the external auditorymeatus; pressing down on it will effectively close offthe meatus to block incoming sound.

transduction: the conversion of mechanical energyto chemical to electrical energy; carried out in theinner ear by the sensory receptor cells.

transformer action: function of the structures of the

middle ear to overcome the impedance mismatchof the air-lled middle ear cavity to the uid-lledcavity of the inner ear.

transient ischemic attack (TIA): a brief interruptionof blood supply to the brain without lasting effects;a warning sign for stroke.

transverse foramina: the small holes or openingstypically found in the region of the transverse pro-cesses of the cervical vertebrae where nerves andblood vessels pass along the length of the neck.

transverse processes: the two projections of boneextending laterally from a vertebra at the juncture

of its corpus and neural arch.trapezoid body: ber tract of the auditory pathway

leading from the cochlear nucleus to the superiorolivary complex.

traumatic brain injury (TBI): brain damage dueto external forces; can be due to penetrating (i.e.,open) head injury or nonpenetrating (i.e., closed)head injury.

triangular fovea: a small depression toward the apexof the arytenoid cartilage on its anterolateral sur-face, immediately superior to the arcuate ridge.

trigeminal: cranial nerve V, innervates muscles ofmastication and carries sensory information fromthe head (including the dura mater) and mouth.

trisomy-21: a chromosomal disorder in which thereare three instead of two 21st chromosomes; theresult is Down syndrome.

trochlear: cranial nerve IV, innervates eye muscles for

movement.tuberculosis: a bacterial infectious disease character-ized by ulcerations and the formation of cavities inthe lungs; accompanied by cough and fever.

tuning curve: a plot showing the lowest intensity at which a nerve ber will respond as a function of fre-quency.

tunnel of Corti: within the organ of Corti, the triangu-lar space created by the inner and outer pillar cells.

turbinates: also known as conchae; three long, thinscrolls of bone that extend into the nasal cavityfrom its lateral walls.

tympanic antrum: a cavity within the petrous portionof the temporal bone that communicates posteri-orly with the mastoid air cells and anteriorly withthe epitympanic recess of the middle ear cavity.

tympanic membrane (TM): see eardrum .tympanic sulcus: see annular sulcus .tympanogram: a graph of tympanic membrane admit-

tance across a positive to negative pressure gradient,for the purpose of assessing the function of the Eusta-chian tube and the contents of the middle ear cavity.

tympanometry: the procedure used to determine

function of the middle ear; the output of this proce-dure is called a tympanogram.tympanoplasty: the surgical repair of the tympanic

membrane and contents of the middle ear; classi-ed by types (Type I, II) according to the magnitudeof repair.

tympanosclerosis: the formation of a whitish plaqueon the tympanic membrane usually as a result ofchronic otitis media.

umbo: the center of the tympanic membrane where thetip of the manubrium of the malleus is attached.

uncinate fasciculus: an association tract connecting

the rostral temporal lobe with the orbital gyri of thefrontal lobe.

uncus: gyrus found at the anterior end of the parahip-pocampal gyrus of the medial temporal lobe; theamygdala nucleus underlies the uncus.

unilateral: pertaining to one side only.universal newborn hearing screening: screening

for hearing loss in the newborn population, priorto the age of one month, typically hospital based,using otoacoustic emissions or automated auditorybrainstem response measures.



392 GLOSSARY

unvoiced: a term used to describe some consonantsounds that are produced without vocal fold vibra-tion.

upper esophageal sphincter (UES): the most supe-rior aspect of the esophagus which includes the cri-copharyngeus muscle; the valve that prevents acidfrom reuxing into the esophagus from the stomach.

upper motor neuron (UMN): a nerve cell whose bodyis located in the motor area of the cerebral cortexand whose processes connect with motor nuclei inthe brainstem or in the anterior horn of the spinalcord prior to exiting the central nervous systemtoward the periphery.

Usher’s syndrome: an inherited condition character-ized by congenital sensorineural hearing loss andprogressive loss of vision due to retinitis pigmen-tosa.

utricle: the structure housed in the vestibule of theinner ear closest to the semicircular canals thatcontains the end organ (macula) sensitive to linearacceleration and gravity.

uvula: the small, midline terminal of the velum cre-ated by the mucous membrane–covered musculusuvulae muscle.

vagus: cranial nerve X, which has multiple branchesinvolved in autonomic functions as well as skeletalmovement and sensation; it is involved with inner-vating the intrinsic muscles of the larynx and somemuscles of the velum and pharynx in addition totransmitting sensation.

vallate: also referred to as circumvallate papillae; largebutton-shaped papillae arranged in a row resem-bling an inverted letter “V” immediately anteriorto the sulcus terminalis, housing several hundredtaste buds.

valleculae: small furrows or pits at the base of thetongue immediately anterior to the lingual surfaceof the epiglottis and found between the median andlateral glossoepiglottic folds.

Valsalva maneuver: a procedure that manually forcesthe opening of the Eustachian tube to ventilatethe middle ear space, performed by blowing while

holding the nostrils and mouth closed; it also gen-erates greater subglottic pressure.

velocardiofacial syndrome: a craniofacial anomalyaffecting the velum, heart, and face.

velopharyngeal incompetence (VPI): a condition,either functional or organic in etiology, in which thesoft palate does not make a sufcient seal with theposterior pharyngeal wall, resulting in improperbalance between oral and nasal resonance.

velopharyngeal mechanism: the mechanism cre-ated by the soft palate and posterior pharyngeal

wall that mediates oral–nasal resonance; when thesoft palate meets the posterior pharyngeal wall,nasal resonance is diminished; when the soft palateis lowered, some of the vocal tone passes into thenasal cavity to resonate there.

velum: the soft palate. ventilation: the movement of air in and out of the

lungs. ventilator: a device that mechanically assists thepatient in exchanging oxygen and carbon dioxide;also referred to as an articial respirator.

ventral cochlear nucleus: portion of the cochlearnucleus for the rst central synapse for the cochlearnerve as it travels through the levels of the brain-stem to the auditory cortex.

ventral fasciculus: the ventral or anterior region ofspinal cord white matter where descending bundlesof nerve bers are found.

ventral posterior medial (VPM) nucleus: the medialpart of the ventral posterior nucleus receiving sen-sory input from the face and tongue.

ventricle: the space between the ventricular (or false)folds and the vocal folds, running horizontally alongthe length of the two sets of folds.

ventricular folds: the technical name for the falsevocal folds, found immediately superior to the truevocal folds and separated from them by the ven-tricle.

ventricular ligaments: bands of connective tissueforming the inferior border of the quadrangular

membrane and serving as the skeleton for the ven-tricular folds. verbal (semantic) paraphasias: unintentional errors

of word retrieval in aphasia where wrong words aresubstituted for the correct words.

vermilion zone: the part of the upper and lower lipsthat is darker in hue due to the visualization of vas-cular tissue below the translucent eleidin.

vermis: the central gray matter of the cerebellum. vertebral: a term used to describe R11 and R12, which

only have an articulation with the vertebral column;these ribs are more commonly referred to as “oat-

ing” ribs. vertebral arteries: supply blood to the brain; arise

from the subclavian artery and ascend via thetransverse foramen of the cervical vertebrae enter-ing through the foramen magnum to converge onthe basilar artery.

vertebral canal: the central space formed by the verti-cal orientation of the vertebrae; houses the spinalcord.

vertebrochondral: a term used to describe R8, R9,and R10 because the cartilages for these three ribs



GLOSSARY 393

merge to form a single piece that articulates with thesternum; these ribs are more commonly referred toas “false” ribs.

vertebrosternal: a term used to describe R1 throughR7 because each of these ribs has its own cartilagethat directly articulates with the sternum; theseribs are more commonly referred to as “true” ribs.

vertex: the uppermost part of the skull. vestibular aqueduct (VA): a narrow bony canal thatcourses from the vestibule of the inner ear to thecranial cavity; thought to regulate endolymphaticpressure within the inner ear.

vestibule: (1) the egg-shaped central portion of theinner ear that houses the balance receptors sensi-tive to linear acceleration and gravity—the utricleand saccule are housed within; (2) the wide space within the cavity of the larynx immediately supe-rior to the ventricular folds and inferior to the adi-tus laryngis.

vestibulocochlear (nerve): cranial nerve XIII, involvedin hearing and balance; the vestibular nerve andcochlear nerve branches combined.

vestibulo-ocular reex (VOR): a reexive eye move-ment that stabilizes vision during head movement(eye movement is in the opposite direction of thehead movement); the semicircular canals detectrotation of the head and send a signal to the oculo-motor nuclei of the brainstem, which in turn inner-vate the eye muscles.

vestibulospinal tracts: tracts originating from the

vestibular nuclei in the medulla to the spinal cord;involved in motor reexes and balance. videostroboscopy: an imaging technique that com-

bines exible endoscopy with a strobe light; theendoscope is used to view the vocal folds and thestrobe light is used to make the vocal folds appearas if they’re vibrating slowly so that one can viewtheir vibratory pattern.

visceral nervous system: a division of the peripheralnervous system; innervates glands, internal organs(i.e., viscera), and blood vessels; also called theautonomic nervous system.

visceral pleura: the connective tissue membrane thatcovers the surface of each lung as well as the supe-rior surface of the diaphragm.

vital capacity (VC): the amount of air that can be forc-ibly expelled from the lungs after a maximal inspi-ration; it includes inspiratory reserve volume, tidalvolume, and expiratory reserve volume.

vocal fry: see glottal fry . vocal ligaments: the thickened, free superior bor-

der of the conus elasticus extending from the

macula ava anterior to the vocal processes ofthe arytenoids, forming the point of attachmentof the thyroarytenoid muscles (i.e., the true vocalfolds).

vocal nodules: benign callous-like bumps on the edgesof the vocal folds, usually bilateral at the junctureof the middle and anterior third of the vocal folds.

vocal process: a projection at the base of the arytenoidcartilage where the anterolateral and medial sur-faces meet that serves as the posterior attachmentof the vocal ligament.

vocal registers: modes of vocal fold vibration thathave distinct physical, acoustic, and perceptualcharacteristics; see also loft register , modal register ,pulse register .

voice disorders: pathological conditions where thevoice is different enough in pitch, loudness, quality,and/or exibility that it calls negative attention tothe speaker and/or interferes with communication;also referred to as dysphonia.

voice fundamental: the basic laryngeal tone; the low-est vibratory frequency produced by the vocal foldsduring phonation; also referred to as the funda-mental frequency.

voiced: a term that is used to describe vocal foldvibration during the production of speech sounds;all vowels and most consonants are voiced.

Waardenburg syndrome: a dominantly inheritedsyndrome characterized by widely spaced eyes,broad nose, multicolored irises, white forelock, and

a sensorineural hearing loss. Waldeyer’s ring: a circle of lymphoid tissue formedby the adenoids superiorly, lingual tonsil inferiorly,and palatine tonsils laterally.

watershed area: the region of overlapping blood sup-ply from the anterior, middle, and posterior cere-bral artery distributions.

Wernicke’s area: the superior temporal lobe regioninvolved in language comprehension.

working memory: a short-term memory process where sensory input is compared to long-termmemory stores for decision making; a component

of executive functioning. X-linked recessive: a pattern of inheritance on the

X chromosome; the trait is linked from motherto son; 50% chance of son inheriting trait; 50%chance of a daughter being a carrier; an affectedfather will pass the carrier status to 100% of hisdaughters.

zygomatic arch: the cheekbone, which is formed bycontributions of the frontal, maxillary, temporal,and zygomatic bones.



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401

INDEX

ADbsolute refractory period, 63, 63f Academy of Neurologic Communicative Disorders and

Sciences (ANCDS), 153 Acoustic lter, 263 Acoustic neuromas, 86 Acoustics, basic principles of, 262–263 Acoustic signal, 164, 218, 257, 263, 310, 316 Acrocephalosyndactyly. See Apert syndrome Adam’s apple, 165, 166 Adenoidectomy, 336 Adenoids, 248, 309 Adipose, 23 Afferent auditory pathway, 323–326, 324f Affricate, 266, 271 Air-bone gap, 329 Alar plate, 41 Albinism, 340 Alexander aplasia, 340 Alveolar consonants, 265 Alveolar ridge, 239

role in speech production, 259 Alveolar sounds, 259

Alveoli pulmoni, 120, 133 Alzheimer’s disease (AD), 92, 92f risk factors for, 92–93

Amyotrophic lateral sclerosis (ALS), 84, 85f, 153–154,287, 287f

Anatomical position, 10, 10f Anatomy, 9 Aneurysm, 88

of middle cerebral artery, 90f Anomic aphasia, 95–96 Anosognosia, 97 Anotia, 330 Apert syndrome, 276, 276f Aphasia, 93, 286

agrammatism, 94classication scheme, 94uent aphasias, 94, 96t

anomic aphasia, 95–96conduction aphasia, 95transcortical sensory aphasia, 95 Wernicke’s aphasia, 95

nonuent aphasias, 94, 96tBroca’s aphasia, 95global aphasia, 95

transcortical motor aphasia, 95paragrammatism, 94types of, 94, 94t

Apneustic area, 150 Aponeuroses, 23 Apraxia of speech (AOS), 101–102, 285–286

denition of, 101 Aprosodia, 97 Areolar, 23 Arteriovenous malformations, 88 Articulation disorder and

phonological disorder,distinction between, 273

Articulatory groping, 102 Articulatory/resonance system, 30f, 218–219

afx and part-word related to, 217–218anatomy of, 219–257pathologies associated with, 269–291

afx and part-word related to, 269–270articulation disorder, 273articulatory phonetics and, 270–273classication of disorders, 273–274neurological disorder, 279–289

phonological disorders, 273sensory disorder, 289–291structural disorders, 274–279

physiology of, 257–267 ( See also Source-FilterTheory)

speech production, mechanics of, 257–262swallowing, process of, 266–267transformation of vocal tone into speech,

262–266skull, human, 220–222, 221f

cranial bones, 226–235facial bones, 222–226

vocal tract, 219, 270 ( See also Nasal cavity; Oral cavity;Pharyngeal cavity)

neural innervation, 256, 257toral, nasal, and pharyngeal

cavities, 219, 219f Aryepiglottic folds, 170, 170f Arytenoid cartilages, 168, 170, 170f Asthma, 120, 145–146 Astrocytomas, 86 Atherosclerosis, 87 Atmospheric pressure, 135 Atresia, 331, 332f

Note: Page locators followed by f and t indicates gure and table respectively.



402 INDEX

Attack phase, phonation, 193breathy attack, 193glottal attack, 193simultaneous attack, 193

Attention, 98 Audiograms, 329 Audiometry, 328 Auditory brainstem response (ABR) audiometry,

325 Auditory neuropathy (AN), 323 Auditory radiations, 73 Auditory/vestibular system, 71–74

afx and part-word related to, 297–298anatomical divisions of ear, 300–301, 300f anatomy and physiology of, 300–326, 300f auditory component, 72–73, 73f auditory pathway, 73f conductive auditory system, 301–311

Eustachian tube, 309middle ear, 302–305

middle ear cavity, 305–309outer ear, 300–301TM and ossicular chain,

transformer action of, 310–311cranial nerve VIII, 71–72incidence and prevalence of

hearing loss, 299inner ear, structure of, 311–326

auditory sensory-neural system, 316–326bony labyrinth and membranous labyrinth, 312,

312f ductus reuniens, 312endolymph, 312endolymphatic sac, 312perilymph, 312systems and sections of, 311, 311f vestibular system, 312–315

pathologies associated with, 327–349 ( See also Earpathology)

range of human hearing, 299–300vestibular component, 73–74, 74f

Augmentative and alternativecommunication (AAC)system, 278

Auricular cartilage, 301 Autoimmune inner ear disease (AIED), 346 Autonomic nervous system (ANS), 43

neurons of, 43parasympathetic division, 43sympathetic division, 43

BBacterial meningitis, 343Baha® system, 331–332Basal cell carcinoma, 333, 333f Basal plate, 41

Bell’s palsy, 281–282, 281f Benign paroxysmal positional vertigo (BPPV), 315Benign Schwannoma neuroma, 323Bernoulli effect, 189–190Better Hearing Institute (BHI), 299Bilabials, 258–259, 265Binge drinking, 150Biology, 9Bipolar neurons, 27, 60, 61f Blood–brain barrier, 60Body cavities, 22, 23f Body systems for speech production, 29tBolus, 80, 267Bone, 24Bone conduction pathway, 329Boyle’s law, 134, 134f Bradykinesia, 86Brain

anatomy of, 43brainstem, 50, 51f

diencephalon, 47–48metencephalon, 48–50telencephalon, 43–47

blood supply to, 56arteries from vertebral basilar system, 57, 57f cerebral arteries, 57origin of, 56–57venous system, 58, 58f

imaging techniques, 59Brainstem, 50, 51f

cerebral aqueduct, 50cerebral peduncles, 50corpora quadrigemina, 50fourth ventricle, 50medulla oblongata, 50pons, 50pyramids, 50

Brain tumors, 60Breath group, 146Breathing, 144. See also Respiratory pathologiesBroca’s aphasia, 95, 96tBroca’s area, 67Brodmann’s cytoarchitectural map, 65, 66f

CCanalith repositioning treatment (CRT), 315Capsular ligaments, 167Cardiac muscle, 26Carhart’s notch, 338Cartilage, 23–24Cartilaginous joints, 24Cauliower ear, 332, 333f Cells, 20–22

characteristics of, 20parts of, 21tstructure of, 20, 21f



INDEX 403

Central auditory processing disorder (CAPD), 325Central canal, 52Central chemoreceptors, 150Centrioles, 20, 21f, 21tCerebellar peduncles, 48Cerebral arteries, 57Cerebral function

association areas, 67Brodmann areas, 65, 66f limbic areas, 67primary areas, 65–67

Cerebral palsy (CP), 289Cerebrospinal uid (CSF), 52, 55, 56f Cerebrovascular accident. See StrokeCerumen, 302

obstruction, 333–334, 333f Checking mechanism, 140Cheeks, 236Cholesteatoma, 337, 337f Chondro-osseous juncture, 123

Choroid plexus, 55Chronic bronchitis, 146smoking and, 147

Chronic middle ear disease, 304Chronic obstructive pulmonary

disease (COPD), 146–147Chronic patulous Eustachian tubes, 309Cilia, 22Circle of Willis, 57, 57f Clavicle, 117–118, 118f Cleft lip and palate, 274–275, 274f Cleft palate, 222Closed head injuries (CHIs), 91Cochlea, 316–318, 317f Cochlear implant (CI), 343–345, 343f Cognitive-communicative disorders, 96–101Collagen, 23Colliculi, 50Complex tones, 188Computerized Speech Lab (CSL), 210Computerized tomography (CT), 91Concussion, 91Conduction aphasia, 95, 96tConductive auditory system

Eustachian tube, 309middle ear, 302

ossicular chain, 304–305, 304f stapedius and tensor tympani muscles, 305tympanic membrane (TM), 302–303, 303f

middle ear cavity, 305–309, 306–307f aditus, 305cochleariform process, 308epitympanic recess, 305ET orice, 308facial nerve branches, 308inferior wall, 308medial wall, 308

oval window, 308promontory, 308round window, 308superior wall, 308

outer ear, 301external auditory meatus (EAM), 302pinna (auricle), 301–302, 301f, 302f

Conductive hearing loss, 275Cone of light, 303Cones, 70Congenital rubella, 342Congestive heart failure (CHF), 147Connective tissue, 23–26

classication of, 22t, 23Connective tissue cells, 21Consonants, classication of, 265, 270Constructional impairments, 97Continuous phonation, 139–141

muscle activity during, 140f Contrecoup, 91, 91f

Contusion, 91areas for, 91, 91f Conversational speech, 141–142Corium, 242Corniculate cartilage, 170Coronal plane of reference, 10Corticobulbar tract, 75–76Corticospinal tract, 75Coup, 91, 91f Cover–Body Model, 190–191Cranial bones

ethmoid, 230–231, 233f frontal, 226, 230f occipital, 227–228, 232f parietals, 226–227, 231f sphenoid, 231, 234–235, 234f temporals, 228–230, 233f

Cranial nerves, 42, 68, 68tfor eye movements, 70in speech processes and swallow stages, 80t

Cricoarytenoid joints, 168Cricoid cartilage, 168Cricopharyngeus muscle, 255Cricothyroid joints, 168Cricothyroid muscles, 175–177, 177f Cricotracheal ligament, 168Crouzon syndrome, 276, 277f, 341Cul-de-sac resonance, 291Cuneiform cartilage, 170Cytokines, 346Cytomegalovirus (CMV), 342Cytoplasm, 20

DDarwin’s tubercle, 301, 331f Declarative memory, 99



INDEX 405

Epithelial tissue, 22, 23f Epithelial tissue proper, 22Ethmoid bone, 230–231, 233f Ethmoid paranasal sinuses, 231Excitatory postsynaptic potentials (EPSPs),

65Exocytosis, 64Expiration, 139. See also Muscles of expirationExpiratory reserve volume (ERV), 136External oblique muscle, 128, 129f Extrinsic laryngeal muscles, 11, 177–180

infrahyoid muscles, 11, 180, 180tomohyoid muscles, 180, 181f sternohyoid muscles, 180, 181f thyrohyoid muscles, 180, 181f

innervation of, 184miscellaneous extrinsic muscles, 180, 182suprahyoid muscles, 11, 177–180

digastricus, 177, 178f genioglossus muscle, 180

geniohyoid muscle, 178, 179f, 180mylohyoid muscle, 178, 178f origins, insertions, and actions of, 177tstylohyoid muscle, 178, 178f

Eyeball, structure of, 69, 69f cones, 70cornea, 69fovea, 69optic nerve, 70photoreceptors, 69retina, 69rods, 69–70sclera, 69

FFacial bones

infer ior nasal conchae, 226, 229f lacrimal, 224, 228f mandible, 224, 225f maxillae, 222–224, 223f nasal, 224, 226f palatine, 224, 227f vomer, 226, 229f zygomatic, 224, 228f

Facial expression, muscles of, 250, 250f, 251tFacial nerve, 77–78, 256Falsetto, 193, 196, 205Familial syndrome, 275Fascia, 23Fascicles, 27, 61Fasciculus, 26–27Faucial pillars, 247–248Fibrous cartilage, 23–24, 24f Fibrous joints, 24Fluid mechanics, 135Formants, 263

Fourier analysis, 188Freidreich’s ataxia (FA), 151–152Frequency, 187Fricative consonants, 265–266Frontal bones, 226, 230f Frontal paranasal sinuses, 226Functional residual capacity (FRC), 136Fundamental frequency, 188

GGenetic syndromes, associated with hearing

loss, 341Genioglossus, 244Glabella, 226Glaucoma, 69Glenoid fossa, 118Glial cells, 27, 59–60

astrocytes, 60, 60f microglia, 60, 60f oligodendroglia, 60, 60f

Gliomas, 86Global aphasia, 95, 96tGlobal Deterioration Scale, 100, 100tGlossary, 369–399Glossectomy, 278–279Glossopharyngeal nerve, 78Glottal chink, 197Glottal consonant, 265Glottal stop, 275Golgi apparatus, 20, 21f, 21tGomphosis, 237Graded potentials, 64

HHabitual pitch, 193, 205Haemophilus inuenzae Type b (Hib), 343Hamulus, 235Hard palate, 239

role in speech production, 259Harmonics, 188Hearing impairment, 289–291Hearing loss, incidence and

prevalence of, 299Hematoma, 332Hematomas, 91Hemorrhages, 87–88

sites of, 89f Hereditary hearing loss, 339–340

autosomal dominant inheritance, 339tautosomal recessive inheritance, 339t X-linked recessive, 340t

Hertz (Hz), 188, 299Hippocampus, 46, 47, 67, 92Human organism, organization of. See Organization of

human organism



406 INDEX

Human skullanterior view, 221f bones in, 220bony nasal septum, 220calvaria, 220cheekbone, 220external auditory meatus, 220facial bones, 222–226foramen magnum, 220inferior view, 222f lateral view, 221f mastoid process, 220nasal conchae, 220orbits of eye, 220styloid process, 220sutures, 222f temporae, 220

Huntington’s disease, 93Hyaline cartilage, 23, 24f Hydrocephalus, 87

communicating, 87infantile, 87noncommunicating, 87

Hyoid bone, 165, 165f Hyothyroid membrane, 167Hypernasality, 260, 275Hypoglossal nerve, 27, 61, 80Hypoxemia, 156–157Hypoxia, 91

IIA muscles, 175

Imaging techniques, to measure blood ow, 59Immittance meter, 305Infantile hydrocephalus, 87

shunt placement for, 88f Infarct, 87Inferior nasal conchae bones, 226, 229f Inferior pharyngeal constrictor muscles, 180, 182Inhalatory stridor, 145Inhibitory postsynaptic potentials (IPSPs), 65Inner hair cells (IHCs), 318, 319Inspiration, 137–138. See also Muscles of inspirationInspiratory capacity (IC), 136Inspiratory reserve volume (IRV), 136Intensity, 187Intercostal muscles, 123, 132Internal auditory canal, 57Internal intercostals, 130Internal oblique muscle, 129, 129f International Phonetic Alphabet (IPA), 258,

258tIntracellular movement, 20Intracerebral tumor, 86, 86f Intra-oral air pressure, 260Intrapleural pressure, 138

Intrinsic laryngeal muscles, 174cricothyroid muscles, 175–177, 177f innervation of, 184lateral cricoarytenoid muscles, 175oblique arytenoid muscle, 175origins, insertions, and actions of, 173tposterior cricoarytenoid muscles, 175, 176f thyroarytenoid muscles, 174–175, 174f transverse arytenoid muscles, 175

Ischemia, 87Ischemic brain damage, 91

JJargon, 95Joint Committee on Infant Hearing (JCIH), 344Joints, 24–26

K Klippel-Feil syndrome, 341Kyphosis, 148

LLabiodental consonants, 265Labiodental sounds, 259Labyrinthectomy, 345Labyrinthine arteries, 57Lacrimal bones, 224, 228f Laryngeal cavity, 185–186, 185f

aditus laryngis, 185f, 186glottic region, 187

glottis, 186paramedian position, 186subglottic region, 187subglottic space, 185f, 186supraglottic region, 186ventricle, 185f, 186vestibule, 185f, 186

Laryngeal feedback system, 182Laryngeal joints, 170

cricoarytenoid joints, 170cricothyroid joints, 170

Laryngeal membranes, 170–171extrinsic membranes, 171

cricotracheal membrane, 171hyoepiglottic membrane, 171hyothyroid membrane, 171

intrinsic membranes, 171–173, 171f, 172f conus elasticus, 172elastic membrane, 171–173, 171f quadrangular membrane, 172

Larynx, 165–166, 165f, 166f arytenoid cartilages, 168, 170f cartilages of, 166f cricoid cartilage, 166f, 167f, 168



INDEX 407

cuneiform and corniculate cartilages, 169f,170

epiglottis, 166f, 167f, 168laryngeal joints, 170membranes of ( See laryngeal membranes)mid-sagittal and superior views of, 169f thyroid cartilage, 166–168, 167f views of, 167f

Lateral cricoarytenoid (LCA) muscles, 175Lateral fasciculus, 52Lateral hyothyroid ligaments, 167Lateral iliocostalis, 125, 125f, 130Lateral lemniscus, 73Latissimus dorsi, 125, 125f, 130Lazy eye, 71Lee Silverman Voice Treatment (LSVT), 153Lenticulostriate arteries, 57Leptomeninges, 86Lesions, 328Levator costarum muscles, 125–126, 126f

Levator veli palatini (LVP), 240, 240f, 249, 267Lexical memory, 99Ligaments, 23Linea alba, 127Lips, 235–236, 235f

Cupid’s bow, 236layers of tissue in, 235–236orbicularis oris muscle, 236philtrum, 236role in speech production, 258–259vermilion zone, 236

Literal paraphasia, 95Living organism, 9Longitudinal tension, 189Lordosis, 148Loudness of voice, 206–207Lou Gehrig’s disease. See Amyotrophic lateral

sclerosis (ALS)Lower motor neuron (LMN), 75, 84, 281Lung capacities, 136Lung congestion, 147Lungs, 132–134, 133f

alveoli pulmoni, 133cardiac impression, 133costal pleura, 134mediastinum, 132, 133f pleurae, 134pleural linkage, 134

Lysosomes, 20, 21f, 21t

MMagnetic resonance imaging (MRI), 91Malleoincudal joint, 26, 26f Mandible, 245–247

mandibular depressor muscles, 246–247,246t

mandibular elevator muscles, 246, 246tmovement of, 246–247role in speech production, 261temporomandibular joint, 245

Mandible bones, 224, 225f Mandibular fossa, 230Manubrium, 304Mass effect, 88Masseter muscle, 246, 247f Mass lesions of vocal folds, 204f Mastication, 281Mastoid air cells, 230Mastoiditis, 337Mastoid process, 126Matrix, 23Maxillae, 222–224, 223f Maxillary alveolar ridge, 239Maxillary paranasal sinuses, 224Maximum minute volume, 137Mechanical ventilation, 156–157, 156f

Medial compression, 189Medial lemniscus pathway, 77Medial longitudinal fasciculus (MLF), 74, 74f Medullary rhythmicity center, 150Memory, 99–100Ménière’s disease, 345–346Meninges, 52

arachnoid granulations, 53, 54f layers, 53f

arachnoid mater, 53–54dura mater, 52–53pia mater, 54

subarachnoid space, 54Meningiomas, 86Meningitis, 86Mesencephalic nucleus, 77Mesencephalon, 41Mesothelial tissue, 22Metamemory, 100Metencephalon, 41, 48–50, 48f

anterior lobe, 48cerebellar peduncles, 48dentate nucleus, 48, 50f fastigial nucleus, 48, 50f occulonodular lobe, 48interposed nuclei, 48posterior lobe, 48right and left hemispheres, 48vermis, 48

Michel dysplasia, 340Microlaments, 20, 21f, 21tMicrotia, 330Microtubules, 20, 21f, 21tMidbrain. See BrainstemMiddle cerebral artery (MCA), 57, 58f, 93Middle ear muscle reex arc, 326Minute volume, 137



408 INDEX

Mitochondria, 20, 21f, 21tMixed dentition stage, 237Mondini dysplasia, 340Monophthongs, 260–261Motion sickness, 315Motor homunculus, 76, 76f Motor speech disorders, 101–103

apraxia of speech, 101–102denition of, 101dysarthria, 102–103

Motor speech system, 74–75corticospinal and corticobulbar tracts, 75–76, 76f facial nerve, 77–78glossopharyngeal nerve, 78hypoglossal, 80spinal accessory nerve, 79trigeminal nerve, 76–77vagus nerve, 78–79

Mouth, functions of, 235Mucoperiosteum, 235

Mucosal wave, 206Multiple sclerosis (MS), 84–85, 85f, 145, 152–153,287–288, 287f

Multipolar neurons, 27, 60, 61f Muscle

action of, 120cells, 21tissue, 26–27

types of, 26, 26f Muscles of expiration, 127

origins, insertions, and actions of, 128tprimary muscles, 127–130secondary muscles, 130

Muscles of facial expression, 250, 250f Muscles of inspiration, 120

origins, insertions, and actions of, 121tprimary muscles, 120–123

diaphragm, 122, 122f external intercostals, 123, 123f internal intercostals, 123, 123f

secondary muscles, 123dorsal thorax, 125–126, 125f neck muscle, 126–127, 127f ventral thorax, 123–125, 124f

Muscular dystrophy (MD), 145, 147–148, 288Muscular process, 170Musculus uvulae, 240, 240f Myelencephalon, 41Mylohyoid line, 224Myoelastic Aerodynamic Theory of phonation,

189–190Myringotomy, 336, 337

NNasal bones, 224, 226f Nasal cannulae, 146

Nasal cavity, 250, 252–253landmarks of, 252, 252f muscles of nose, 252–253, 252f, 253tnasal cartilages, 252, 252f nasopharynx, 250nose, 250

Nasal murmur, 259Nasal septum, 23, 24f National Institute on Deafness and Other

Communication Disorders, 299National Scoliosis Foundation, 148Natural resonant frequency, 262Nebulizer, 146Negative pressure breathers, 135Neglect, 97Neocortex, 65Neologisms, 95Neonatal herpes, 342–343Neoplasms, 86Nerve cells, 21–22

Nerve bers, 60Type A, 60Type B, 60Type C, 60

Nervous system, 38, 113anatomical orientation, 39–41

anatomical views and sections of brain,40f

anatomy of brain, 43–50CNS, 43–52neurons and glial cells, 59–61spinal cord, 50–52

brain, 38central nervous system, 38neurodevelopment, 41–43

of central nervous system, 41, 41f of spinal cord, 41, 42f

organization of, 41–43, 42f brain, 42–43CNS, 42–43PNS, 43spinal cord, 43

pathologies of afx and part-word related to, 83–84communication disorders, 93–103neuropathologies, 84–93swallowing disorders, 103–105

physiology of, 61auditory and vestibular systems, 71–74cerebral function, 65–67cranial nerves, 68, 68telectrochemical communication, 61–65motor speech system, 74–80neural systems, 68–81swallow function, 80–81visual system, 69–71



INDEX 409

stages in growth of, 41differentiation, 41induction, 41migration, 41proliferation, 41

supporting systems to, 52–58blood supply, 56–58meninges, 52–54, 53f, 54f ventricular system, 55, 55f, 56f

terminology related to, 38–39, 39tNervous tissue, 27Neural crest, 41Neural plate, 41Neural tube, 41Neurectomy, 345Neuroectoderm, 41Neurogenic dysphagia, 104Neurological disorders, of articulatory/resonance

system, 279–289cranial nerve damage, 279–281, 280t

facial nerve, damage to, 281–282glossopharyngeal nerve, damage to, 282hypoglossal nerve, damage to, 282–284trigeminal nerve, damage to, 281vagus and spinal accessory nerves, damage to,

282–284motor speech disorders, 284–286

apraxia of speech (AOS), 285–286dysarthria, 286

other neurological disorders, 286–289nonprogressive neurological disorders,

289progressive neurological

disorders, 287–288Neurologic communication disorders

aphasia, 93–96cognitive-communicative

disorders, 96–101motor speech disorders, 101–103

Neuromuscular junction, 27, 60–61Neurons, 27, 29f

anatomy of, 59, 59f axon, 59, 59f axon hillock, 59, 59f cell body, 59, 59f dendrites, 59, 59f nodes of Ranvier, 59telodendria, 59

classication of, 60, 61f and glial cells, 60

Neuropathologies, 84cerebral hemispheres, 90–93disruption of supporting systems,

86–89nerve cells and glial cells, 84–86

amyotrophic lateral sclerosis, 84, 85f multiple sclerosis, 84–85, 85f

neoplasms, 86Parkinson’s disease, 85–86, 85f

Neurotransmitter, 64, 64tsteps involved in release of, 64

Newton’s Third Law of Motion, 135Noise-induced hearing loss (NIHL), 347–349Nondeclarative memory, 99–100Nucleus, 20, 21f, 21t

OObstructions of ear canal, 333–334, 333f Occipital bones, 227–228, 232f Occipital condyles, 228Oculomotor cranial nerve, 70–71, 71f Odontoid process, 115Olfactory nerve, 81Olivocochlear pathways, 326Optic canals, 234Optic chiasm, 70Optic radiations, 70Optic tract, 70Oral cavity, 235–250

alveolar ridge, 239cheeks, 236function of, 235hard palate, 239lips, 235–236mandible, 245–247muscles of facial expression, 250, 250f teeth, 236–239tongue, 241–245tonsils, 248

velopharyngeal (V-P) mechanism, 248–249velum (soft palate), 239–241

Oral transit time, 80Orbicularis oris muscles, 258Organelles, 20, 21f Organic disorder and functional disorder, distinction

between, 273Organization of human organism

cells, 20–22medical terminology related to, 19–20organs, 27–29and speech processes, 30–31systems, 29–30tissues, 22–27

Organs, 27, 29Orientation to human body

anatomical position, 10, 10f planes of reference, 10–11, 11f terminology with spatial position and orientation, 11,

12–13t, 13, 14f Osteoclasts, 237Osteoma, 334Osteoporosis, 148Otitis externa, 334, 334f



410 INDEX

Otitis media (OM), 86, 275, 334–337acute OM, 335adhesive OM, 335in children, 334complications of, 337contributing factors, 335gender and family history, role of, 334myringotomy, 336OM with effusion, 335PE tube placement, 336, 336f serous OM, 335stages of, 335surgical treatment of, 336

Otoacoustic emissions (OAEs), 320Otolaryngologist, 328Otologist, 328Otosclerosis, 308, 337–339

stapedectomy for, 338f Otoscopy, 302, 303Outer hair cells (OHCs), 318, 319

PPalatal consonants, 265Palatine bones, 224, 227f Palatoglossus muscle, 240, 240f, 243, 244Palatopharyngeus muscle, 240, 240f, 255Papilloma, 204, 204f Paradoxical vocal fold movement (PVFM), 145–146.

See also AsthmaParietal bones, 226–227, 231f Parietal–temporal–occipital (P-T-O) region, 67Parkinson’s disease (PD), 85–86, 85f, 153, 153f, 288, 288f

Passive forces, 135Pathology, 10Pectoral girdle, 117–118, 118f Pectoralis major muscle, 124, 124f Pectoralis minor muscle, 124, 124f Pelvic girdle, 118, 118f

acetabulum, 118coxal bones, 118inguinal ligaments, 118pubic symphysis, 118

Pericardial cavity, 22Perichondrium, 26Perimysium, 27Periodic sounds and aperiodic

sounds, distinction between, 263Periosteum, 24Peripheral chemoreceptors, 150Peripheral nervous system (PNS), 42, 43

somatic nervous system, 43visceral nervous system, 43

Peristalsis, 266Peristaltic movement, 81Perisylvian language zone, 93, 93f Peritoneal cavity, 22

Phagocytosis, 60Pharyngeal aponeurosis, 254Pharyngeal cavity, 254–256

mucous membrane, 256pharyngeal aponeurosis, 254pharyngeal muscles, 254–256, 254f, 255tregions of, 256

Pharyngeal fricative, 275Pharyngeal transit time (PTT), 81Pharyngeal tubercle, 228Pharynx, 182, 261

role in speech production, 261–262Phonation, 113, 200

Cover–Body Model, 190–191mechanics of, 192–193

attack phase, 193prephonation phase, 193process, 192–193

Myoelastic Aerodynamic Theory, 189–190Phonation breaks, 209

Phonatory system, 30f, 164, 165f,218afx and part-word related to, 163anatomy of, 164–187framework of, 164

hyoid bone, 165, 165f laryngeal membranes, 170–173larynx, 165–170

laryngeal cavity, 185–187mucous membrane, 182muscles of, 173–182

extrinsic laryngeal muscles, 177–182intrinsic laryngeal muscles, 173t, 174–177neural innervation of, 182–184

pathologies associated with, 199–211and afx and part-word, 199parameters of voice, 205–209voice perspective, 201–205voice production, 200–201

physiology of, 187–197basic concepts, 187–189falsetto, 196phonation process, 189–193vocal tone frequency and intensity, modication of,

193–197 whisper, 196–197

Phonemic regression, 347Phrenic nerve pacer, 151, 152f Phrenic nerves, 131–132Phrenology, 65Physiology, 9–10Pick’s disease, 93Piebaldism, 340Pierre Robin sequence, 277, 277f Pitch, 188, 205–206Pitch breaks, 209Planes of reference, 10–11, 11f



INDEX 411

coronal plane, 10, 11f, 12tsagittal plane, 10–11, 11f, 13ttransverse plane, 11, 11f, 13t

Plasma membrane, 20, 21f, 21tPlethysmograph, 136Pleural cavities, 22Plosives (stops), 265Pneumotachometer, 136Pneumotaxic area, 150Pneumothorax, 144Positive pressure breathers, 135Posterior cricoarytenoid (PCA) muscles, 175, 176f Postsynaptic cells, 63, 63f Pragmatics, 98Prefrontal cortex, 67Presbycusis, 346–347Pressure equalization (PE) tube, 303, 310Presynaptic cells, 63–64Primary motor cortex, 66Primary progressive aphasia (PPA), 101

Primary somatosensory cortex, 66Primary visual pathway, 70, 70f Priming, 100Procedural memory, 99–100Propagation, 62Prosencephalon, 41Prosopagnosia, 97Prospective memory, 100Protoplasm, 20Pseudobulbar palsy, 103Ptosis, 70Puberphonia, 205Pulmonary pressure, 135Pulp cavity, 237Pulse oximeter, 147Pure tones, 187Pyramidal tracts, 75

QQuadratus lumborum muscle, 130, 131f

RRancho Los Amigos Levels of Cognitive Functioning

Scale , 98, 99tRecruitment, 345Rectus abdominus muscle, 129, 129f Recurrent laryngeal nerve, 184Recurrent laryngeal nerve paralysis, 208Reissner’s membrane, 318, 345Relative refractory period, 63, 63f Residual volume (RV), 136Resonance, concept of, 262, 270Resonator, 262Respiratory anatomy, 113–134

framework, 113–114

pectoral girdle, 117–118pelvic girdle, 118rib cage and sternum, 115–117trachea and bronchial tree, 118–120vertebral column, 114–115

lungs and pleurae, 132–134muscles of respiration, 120–130

expiration, muscles of, 127–130inspiration, muscles of, 120–127neural innervation of, 130–132, 132t

Respiratory pathologies, 144–145, 144tafx and part-word related to, 143airway obstruction, 145–147, 146f musculoskeletal conditions, 147–148neurological pathologies, 149–154tracheotomy and mechanical

ventilation, 154–157Respiratory physiology, 134

breathing and exchange of air, 137lung volumes and capacities, 135–137

passive forces, 135vegetative breathing, process of, 137–139expiration, 139inspiration, 137–138respiratory cycle, 139

vocal activity and, 139–142continuous phonation, 139–141conversational speech, 141–142respiratory cycle, 142

volume, pressure, and airow, 134–135Respiratory system, 30f, 113, 164

anatomy of ( See Respiratory anatomy)pathologies associated with ( See Respiratory

pathologies)physiology of ( See Respiratory physiology)and speech production mechanism, 113, 113f

Resting lung volume, 139Resting membrane potential (RMP), 61Resting volume, 135Retinitis pigmentosa, 341Retrospective memories, 99Rhombencephalon, 41Rib cage, 115–117, 116f

arthrodial joints, 116rib, 115

articulation with thoracicvertebrae, 115–116, 116t

landmarks of, 115, 116f sternum, 116–117vertebral ribs, 117vertebrochondral ribs, 117vertebrosternal ribs, 117

Right hemisphere syndrome (RHS), 96–98affect and prosody, 97higher cognitive functions, 97–98visuospatial decits, 97

Rods, 69–70



412 INDEX

SSacral foramina, 115Saddle joint, 26, 26f Sagittal plane, 10–11Saltatory conduction, 62Scalenus muscles, 126, 127f Scapula, 117–118, 118f Scheibe dysplasia, 340Schwann cells, 60Schwartze’s sign, 338Scoliosis, 148Sella turcica, 234Semantic memory, 99Semicircular canals, 73, 74Semivowels, 266

glides, 266liquids, 266

Sensory disorders, of articulatory/resonance system,289–291

Sensory-neural system, 316

cochlea, 316–318, 317f neural pathwaysafferent auditory pathway, 323–326efferent auditory pathway, 326middle ear muscle reex arc, 326neurotransmission, 320–323

organ of Corti, 318–320Septal cartilage, 252Septum pellucidum, 55Serratus anterior muscle, 124f, 125Serratus posterior inferior muscle, 130Serratus posterior superior muscle, 126, 126f Silent aspiration, 104Sinusitis, 235Skeletal muscle, 26–27, 28f Smooth muscle, 26Sodium–potassium pump (SPP), 62Somatic nervous system, 43Source-Filter Theory, 263–264, 264f

consonant, production of, 265–266source function, 264transfer function, 264vowels, production of, 264–265

Spasmodic dysphonia, 204, 208Spatial summation, 65Speaking valve, 155, 156, 156f Spectrogram, 263, 263f Speech–language pathologists (SLPs), 145Speech perception and production, 5–6

systems involved in, 4, 4t ( See also Specicsystems)

Speech processes, 30articulation /resonation, 30–31phonation, 30respiration, 30

Speech production, mechanics of, 257–262alveolar ridge, 259

English vowels and consonants and IPA characters,258t

hard palate, 259integration of oral structures, 262lips, 258–259mandible, 261pharynx, 261–262teeth, 259tongue, 260–261velum, 259–260

Sphenoid bone, 231, 234–235, 234f Sphenoid paranasal sinuses, 235Spinal accessory nerve, 79Spinal cord

anatomy of, 50–52gray and white matter, 52, 53f longitudinal axis, 52segmental axis, 50–52, 52f

Spinal cord injury (SCI)case examples, 151

cause of, 150cervical, 150f complete, 151incomplete, 151

Spinal nerves, 42, 51Spinal trigeminal nucleus, 77Spirometer, 136Sporadic syndrome, 275Squamous cell carcinoma, 332–333, 333f Stapedectomy, 338, 338f Stapedius muscle, 305Stenosis, 87, 331Sternocleidomastoid muscle, 126, 127f Sternothyroid muscle, 180, 182Sternum, 116–117, 117f Stickler syndrome, 277–278Stoma, 154Strabismus, 71Stria vascularis, 318Stroke, 56, 87

hemorrhagic, 87–88ischemic, 87risk factors for, 88

Structural disorders, of articulatory/resonance system,273, 274

Apert syndrome, 276, 276f cleft lip and palate, 274–275, 274f Crouzon syndrome, 276, 277f ectrodactyly-ectodermal dysplasia-clefting syndrome,

276–277glossectomy, 278–279Pierre Robin sequence, 277, 277f Stickler syndrome, 277–278velocardiofacial syndrome, 278velopharyngeal incompetence, 278

Styloglossus, 244Stylohyoid ligaments, 165



INDEX 413

Styloid process, 230Stylopharyngeus muscle, 255–256Subclavius muscle, 124–125, 124f Subcostal muscles, 130Subglottic pressure, 140, 146, 188–189Substantia nigra, 85Sulcus limitans, 41Superior laryngeal nerve, 184Superior olivary nucleus, 73Superior thyroarytenoid muscle, 175Swallowing, 80–81, 266–267

esophageal stage, 81, 267neural circuitry for, 80–81oral preparatory stage, 80, 266–267oral stage, 80, 267pharyngeal stage, 80–81, 267

Swallowing disorders, 103–105treatment for, 267

Swimmer’s ear, 334Symptom, dened, 84

Synapse, 27, 61, 61f, 63–65, 63f chemically gated channels, 64EPSP, 65graded potentials, 64IPSP, 65neurotransmitters, 64, 64tpostsynaptic cells, 63, 63f presynaptic cells, 63–64, 63f

Synarthrodial joints, 24Synchondrosis joint, 25, 25f Syndrome, denition of, 104Synovial joint, 25–26Syphilis, 344System, 3, 29–30, 29t

denition of, 29for speech production, 29, 29t

TTeeth, 236–239

deciduous set, 236, 237, 238f development of teeth, 237–239

and development of speech, 238–239per manent teeth, 236, 237, 238f role in speech production, 259structure of tooth, 236–237, 236f types of, 236

Tegmen tympanum, 230Telencephalon, 43, 44f

amygdala, 46association ber tracts, 47basal ganglia, 46–47, 47f calcarine sulcus, 45callosal sulcus, 45central sulcus, 44cingulate sulcus, 45corpus callosum, 44

gyri and sulci, 43–44, 44f, 45thippocampus, 46inferior frontal gyrus, 45insula, 46internal capsule, 47lateral sulcus, 44limbic lobe, 46lobes in, 43longitudinal ssure, 44medullary centers, 47operculum, 46parahippocampal gyrus, 46parietal lobe, 45precentral gyrus, 45temporal lobe, 45–46

Temporae, 220Temporal bones, 228–230, 233f Temporalis muscle, 246, 247f Temporal summation, 65Temporary threshold shift (TTS), 348

Temporomandibular joint (TMJ), 224, 245, 261Tendons, 23Tensor tympani muscle, 77, 305Tensor veli palatini ( TVP) muscle, 77, 240, 240f,

249Terminal boutons, 59Terminology associated with

anatomy and physiology, 11–17anatomical structures/parts, 15, 359–361tauditory/vestibular system, 16, 366–367tbones, cartilages, cavities, membranes, or spaces, 15,

364tcolor, form, location, relative size, or shape, 15,

361–363tmiscellaneous terms and afxes, 16, 367–368tmovement, 15, 359tnervous system, 364–366tplanes of reference and spatial relationships,

12–13tThrombosis, 87, 89f Thyroarytenoid muscles, 174–175, 174f Thyroid cartilage, 166–168Thyroid notch, 166Tidal volume (TV), 136Tissues

connective tissue, 23–26epithelial tissue, 22–23, 23f muscle tissue, 26–27nervous tissue, 27types and subclassications, 22t

TMJ dysfunction syndrome, 245Tongue, 29, 241–245, 270–272

anatomy of, 241–242, 242f foramen cecum, 241glossoepiglottic fold, 242lingual frenulum, 242longitudinal median sulcus, 241



INDEX 415

stereocilia, 313utricle, 312

Vestibulo-ocular reex (VOR), 315 Vestibulospinal tracts, 74 Videostroboscopy, 190 Visceral nervous system, 43 Visual system, 69–71

cranial nerves involved in eye movements,70–71, 71f

primary visual pathway, 70, 70f retina, role of, 69–70rods and cones, 70secondary visual pathways, 70, 70f structure of eyeball, 69–70, 69f

Vital capacity (VC), 136 Vocal fold length, 175 Vocal fold paralysis, 207f Vocal folds, mass lesions of, 204f Vocal fold symmetry, 207f Vocal fold vibration, 190–191, 191f

Vocal intensity (loudness), 195–196and vocal tone frequency, relationshipbetween, 196

Vocal ligaments, 172 Vocal nodules, 201, 208 Vocal pitch, modications of, 193

higher pitch, regulation of, 193–194lower pitch, regulation of, 194vocal registers, 194–195

Vocal process, 170 Vocal registers, 194–195, 206

loft register, 195, 206modal register, 195, 206pulse register, 194–195, 206

Vocal tone, 188, 218, 262, 263 Voiced and unvoiced speech sounds, distinction

between, 263 Voice disorders, 202–203t

201

clinical perspectives on, 209communication, 211documentation, 210emphasis, 211listening, 210medical clearance, 210

duration, 204life span, 205organic, 201prevalence, 201, 204psychogenic, 201

Voice production, 200–201, 200f Voice, psychological parameters of, 205

exibility, 209loudness, 206–207pitch, 205–206quality, 207–208secondary characteristics, 208–209

Voice quality, 207–208 Voltage-gated channels, 62

Vomer bone, 226, 229f Vowel quadrilateral, 260, 260f

W Waardenburg syndrome, 341 W aldeyer’s ring, 248 Watershed area, 57, 58f Wernicke’s area, 46, 67 Whisper, 196–197 Working memory, 100

Y Yawn, 137

ZZygomatic arch, 220

anatomia eng

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