00 lapointe i-xiifm - plural publishing

Contents

Foreword by Audrey L. Holland, PhD vii

Preface ix

PART I: BASICS; WHAT DO WE NEED TO KNOW ABOUT

GOOD BRAINS AND BAD BRAINS?

1 The Neurologic Basis of Speech and Language 1

2 Basic Anatomy and Physiology of the Speech Mechanism 39

3 Neurological Causes of Communication Disorders 67

PART II: ACQUIRED BRAIN-BASED COMMUNICATION DISORDERS:

WHAT DO THESE DISORDERS LOOK LIKE AND SOUND LIKE?

4 Aphasia 81

5 Nonfocal Brain Damage: Communication Disorders and a World 101of Other Problems

6 Right Hemisphere Syndrome 125

7 Acquired Aphasia in Childhood 151

8 Motor Speech Disorders in Adults: Dysarthrias and Apraxia of Speech 165

9 Motor Speech Disorders in Childhood 187

10 Acquired Neurologic Swallowing Disorders in Children and Adults 203

PART III: ASSESSMENT AND TREATMENT OF BRAIN-BASED

DISORDERS: WHAT CAN WE DO ABOUT IT?

11 Principles of Assessment of Child and Adult Neurologic 225Speech-Language Disorders

12 Principles of Treatment for Neurologic Communication Disorders 251

Index 267

[Note: Throughout the text all terminology introduced will be defined andexplained to ensure readability at a first year introductory level.]

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Preface

The world was a different place in 1861.The Civil War raged in the United Statesand brothers fought a horrific battle atBall’s Bluff in Virginia. The Canellasmeteorite struck the earth near Barce-lona, Spain. The telegraph left the PonyExpress obsolete and horses with mailpouches stopped racing across theAmerican West. Charles Darwin burston the scene with the publication of Ori-gin of the Species. Xian Feng, a ChineseEmperor, died and was succeeded byhis 6-year-old son. Explorers Burke andWills set out with camels and horsesand 18 men to cross Australia’s outbackfrom South to North. Both died on thereturn trip of exhaustion and hunger.San Francisco was rocked by a series of small tremors, followed by a majorearthquake on July 4.

In France, history was being madeas well. Tremors across the intellectualcommunities were created by PierrePaul Broca, who opened a dialogue onbrain and language by presenting thefirst of two landmark papers (Broca,1861a, 1861b). These papers have sinceserved as a clear demarcation and turn-ing point in the history of understandingbrain-based disorders of language andspeech. Broca is one of our heroes. Heencapsulates all that a good clinician,scholar, and neuroscientist should be.He cared for and about his patients.Broca understood the whirlpool ofdespair into which a shoemaker fromrural France could be plunged by an

unseen stroke in his brain. He guided,nurtured, and studied the small victo-ries of recovery from torn brains in hispractice. Clearly, 1861 was a big year. Soit came to pass that Carl Sagan (1979)rhapsodized in Broca’s Brain about theexquisite experience of standing in theMusée de l’Homme as he contemplatedand gazed upon the preserved brain ofPierre Paul Broca (June 28, 1824–July 9,1880) this scientific giant of the 19th cen-tury who contributed so much of whatwe know about the localization of artic-ulate speech in the brain of humans.Broca was a French physician, anthro-pologist, and eventually a senator whobelieved that by studying the brains ofcadavers and correlating the knownexperiences and behaviors of the formerpossessor of the organs, human behav-ior could be revealed, associated withbrain function, and better understood.For that purpose, he collected hundredsof human brains in jars of the preserva-tive formalin. Upon his death in 1880,with exquisite irony, his own brain waspreserved in formalin and added to thecollection in the museum, along withhundreds of skulls that Broca had usedin his comparative cephalometric stud-ies. When Sagan happened upon Broca’sbrain in the museum, along with that of Broca’s milestone patient “Tan” Le-borgne, he was awestruck by the ironyof it all. Here was Broca, for whom theregion of the frontal lobe of the cortexthat he had described was subsequently

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named, with his own Broca’s area dis-cernible. Sagan was mesmerized by theincongruity of all of this. In Broca’sBrain, he used that visit to the Museumof Man to launch philosophical ques-tions that challenge some core ideas ofhuman existence and consciousnesssuch as “How much of that man known asPaul Broca can still be found in this jar?”

These questions were ponderedagain as we looked upon the brains of Broca’s patients in the DupuytrenMuseum in Paris in July of 2009. Thisquestion and other brain puzzles arepondered in the essay, “Broca’s brain:Brother, wherefore art thou?” (LaPointe,2010). Indeed, we are indeed in the debtof this French scientist and scholar aswell as of his patients whose brains resteven today in these jars.

In 2010 the world is different andthe world is the same. Twitter, social

networking, texting, and 24-hour infor-mation access have created digital autismand consume us as we text our way offof the curbs into the traffic of perpetualconnectivity. Neural imaging that wouldhave appeared to be magic in 1861 is nowcommonplace. Diffusion tensor imaging(DTI) and magnetoencephalography(MEG) are guiding us to better visionsof broken brains and their consequences.Sophisticated ways of viewing brainactivity have led to speculations aboutthe study of different gamma oscillationpatterns for true versus false memoriesand even into the seeming brain sciencefiction of “mind gaming” or thoughtcontrolled activities. What was rudi-mentary in 1861 and speculative in 2010may be commonplace in days to come.But people with brain-based communi-cation disorders still will require atten-tion and intervention by clever and

x Brain-Based Communication Disorders

The brain of Broca’s patient LeBorgne (“Tan”) in formalin at the Duputryn

museum in Paris (LaPointe photo).

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educated experts. That is what this bookis all about.

Brain-Based Communication Disor-ders introduces the reader to the majorclinically recognized types of acquiredspeech/language, cognitive, and swal-lowing disorders encountered by clin-icians working with child and adultneurologic cases. The text provides con-temporary and state-of-the-art contenton these disorders in terms of their neuropathologic bases, clinical sympto-matology, and prognosis. Basic anatomyand physiology of human communica-tion and swallowing are introduced, as well as the neural mechanisms con-trolling speech, language, cognitive, andswallowing functions. In addition to thetraditional acquired speech/languagedisorders of the nervous system (aphasia;neuromotor speech disorders), contentincluding communication impairmentscaused by traumatic brain injury, multi-system blast injuries, and degenerativedisorders of the nervous system also isprovided. The reader also is introducedto the principles that govern the assess-ment and treatment for both pediatric andadult populations. We are indebted to

those who passed before, such as PierrePaul Broca who showed us the path. Weare indebted as well to all those whohave undergone the slings and arrowsof brain damage from whom we havelearned. We hope the future generationsof brain scientists and clinicians willgrow in their ability to understand andto help.

Broca, P. (1861a). Perte de la parole, ramol-lissement chronique et desstruction par-tielle du lob antérieur gauche de cerveau.Bulletins de la Société d’Antrhopologie, 62,235–238.

Broca, P. (1861b). Remarques sur le siége dela faculté du langage articulé, suiviesd’une observation d’aphemie (Perte de laParole). Bulletins et memoires de la SociétéAnatomique de Paris, 36, 330–357.

LaPointe, L. L. (2010). Voices: Collected essayson language, laughter, and life. Albany, NY:Cengage Delmar Publishing.

Sagan, C. (1979). Broca’s brain: Reflections onthe romance of science. New York, NY: Ran-dom House.

References

Preface xi

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Jason is sitting in a therapy room talking about his workout regimen. He is a youngman of 22, with a sleeveless shirt to show off his “guns.” He is enrolled part-time asa student at a local university where he also attends speech therapy. When he talks,the reason for speech therapy becomes clear. He is difficult to understand. In fact, lis-tening to him and understanding requires a good bit of concentration on the part ofthe listener. His speech rate is slow; he stops occasionally to adjust his palatal liftprosthesis, which sometimes rattles in his mouth. “It needs an adjustment,” Jasonsays. He also must work very hard to coordinate breathing and speech, getting a fewwords out then pausing to take another lengthy breath for a few more words. On hisneck is a telltale scar, indicating that, at one time, a machine had to do the breathingfor him.

Jason is the classic picture of a young person whose life was dramatically changedafter a motor vehicle accident. When asked to tell his story, Jason reflects . . .

Three years ago . . . I went to a party . . . and got really drunk . . . then decidedto drive home . . . 30 miles. I made it 29 . . . when I passed the officer . . . (makes acar steering motion) I went off . . . hit three trees . . . going 90 miles an hour (anotherbig breath). I was lucky he was there . . . it was the middle of the night . . . I neverwould have made it . . .

8

Motor Speech Disorders inAdults: Dysarthrias and

Apraxia of Speech

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Such is the story for many of the peoplewe work with. An accident, a disease, astroke, can change life in an instant. Somany of the things that were once takenfor granted—the ability to speak clearly,to breathe without effort—are now a con-stant challenge. Communication/speechis so integral to everything we do, andwhen it becomes difficult to produceclearly, what a dramatic change it makesto the overall quality of a person’s life.

In reading through these chapters andthe many individual stories about brain-based communication impairments, youhave learned more about the complexi-ties of communication. We hope thatyour interest as a future clinician hasbeen piqued by the fascinating array ofneurogenic disorders, even though yourheart aches for the suffering those indi-viduals experience (welcome to theworld of allied health). Throughout thisprocess, you probably began to developan appreciation for the differencesbetween speech and language. They areinextricably linked, yet can be differen-tially affected by damage to the brain.The previous chapters of this textbookwere devoted primarily to those disor-ders of language and cognition (apha-sia, disorders of a nonfocal nature, andright hemisphere dysfunction) that dealwith the organization, formulation, andsocial rules of communication. Whatyou will find in the following chaptersis a review of impairments that relatepurely to the motor execution of speech(i.e., muscle capability, motor plan). A motor speech impairment indicatesproblems with one or more aspects of

Introduction

the speech mechanism as reviewed inChapter 2. Just to remind you,, thosecomponent systems include respiration,phonation, resonance, and articulation.The speech difficulties experienced by aperson with a motor speech impairmentfall into one of two categories: sometype of disruption in (1) the speechmusculature or (2) the motor plan thatarrives from the brain, which directs themuscles how to move. These categorieseach carry a specific diagnosis:

Dysarthria: A group of neurologicspeech disorders resulting fromabnormalities in the strength, speed,range, steadiness, tone, or accuracyof movements required for control ofthe respiratory, phonatory, resonatory,articulatory, and prosodic aspects ofspeech production.

Apraxia: A neurologic speech dis-order reflecting an impaired capacityto plan or program sensorimotorcommands necessary for directingmovements that result in phoneticallyand prosodically normal speech.(Duffy, 2005, p. 5)

When you consider the followingexcerpt from the definition of dysarthria,“ . . . abnormalities in the strength, speed,range, steadiness, tone or accuracy ofmovements . . . ” you can derive that thisdefinition is really referring to the statusof the speech musculature, somethingabout the muscles of the speech mech-anism is causing a problem with thecoordination and execution of speech.On the other hand, the definition forapraxia makes no mention of how speechis produced, but how it is planned orprogrammed. Therefore, although bothare considered motor speech disor-ders, they are two distinctly differentproblems.

166 Brain-Based Communication Disorders

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In Chapter 3, we learned that 49 millionAmericans have a communication dis-order. That number reflects both devel-opmental (problems you are born with)and acquired (a problem that occurs afternormal development of speech/lan-guage has occurred) causes. An exten-sive study of acquired communicationdisorders in over 14,000 cases thatoccurred in the Department of Neurol-ogy Mayo Clinic from 1987 to 1990 and1993 to 2001 revealed that roughly 41%suffered from motor speech disorders(Dufy, 2005). Based on that number, it isprobably safe to say that you willencounter an individual with a motorspeech disorder at some point in yourpractice as a speech-language patholo-gist. It is just as likely that currently youmay know someone who has motorspeech impairment, perhaps a friend ofthe family with Parkinson disease, or aneighbor who was in a car accident, ora grandparent who suffered a stroke.

From the above definition of the dys-arthrias as a “group of disorders,” itbecomes obvious that there is more thanone type of dysarthria. In the late 1960s, agroup of master clinicians (Darley, Aron-son, & Brown, 1969a, 1969b) suggestedthat dysarthria, which up to that pointwas only differentiated from aphasiaand perhaps apraxia of speech, actuallyseemed to contain several subtypes. Theircareful analysis of over 200 patients withdysarthria led to six specific types (flaccid,spastic, ataxic, hyperkinetic, hypoki-

Definition

Scope of the Problemnetic, and mixed), classified by commonlesion sites as well as unique character-istics of motor (muscle) performance.

Flaccid Dysarthria

Flaccid dysarthria is named for thenature of the muscle in those who suf-fer from this diagnosis. Flaccidity meansa lack of muscle firmness or tone somuscles will appear to be somewhatfloppy or droopy. The general lack oftone in the muscles is also known ashypotone (hypo- meaning less thanoptimal) and it can be an indication ofmuscle weakness. A look at Figure 8–1reveals characteristics of flaccid paraly-sis. The individual in Figure 8–1 has acondition Bell’s palsy, which is a flaccidparalysis of the hemiface (half the face).Notice the droopiness or sagging of thestructures surrounding the eye, nose,and mouth on the right side of the indi-vidual’s face. Another example of thecondition (Bell’s palsy) is seen in Fig-ures 8–2A through 8–2E. Notice that, inthis case, the condition is less obviouswhen the facial structures are at rest.When the structures are functioning,however, you can see that movement iscompromised and the weakness becomesmore apparent.

In Chapter 1, you learned about thegeneral organization of the nervous sys-tem into the central nervous system(CNS) and the peripheral nervous sys-tem (PNS). As a reminder, the CNS con-tains the brain and spinal cord, and thePNS is composed of the cranial andspinal nerves that arise primarily fromthe brainstem and spinal cord. Flaccid

Dysarthria

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dysarthria is a result of damage to thePNS. More specifically, flaccid dysarthriais present following damage to the cra-nial nerves that are involved in speechand/or the spinal nerves that supplythe respiratory system. Table 8–1 containsa listing of the cranial nerves that con-tribute to speech production. In review-ing this list, you should recognize thatthese cranial nerves are responsible fora large portion of the sensory and motorfunction of speech execution.

In Chapter 2, the structures of thespeech mechanism were reviewed, in-cluding the respiratory, phonatory, andresonance systems and the articulators.Flaccid dysarthria can affect just one, a combination of, or even all of the sys-tems that contribute to speech. The systems that are affected are dependenton where the damage lies in the PNS.Seven of the twelve cranial nerves in thePNS contribute in some way to speechproduction. Functionally, these nervesprovide sensation and movement tothose structures responsible for phona-tion (larynx), resonance (soft palate orvelum), and the articulators (lips, teeth,hard palate, jaw, and tongue). It is easyto imagine, then, that damage to thesenerves would result in problems withspeech execution, making individualswho suffer from flaccid dysarthria diffi-cult to understand (unintelligible). Al-though there are many speech character-istics that can fall under the umbrella offlaccid dysarthria, those most frequentlynoted are hypernasality, imprecise artic-ulation, breathy voice quality, and short-ened utterances.

With your knowledge of the cranialnerves, let’s analyze these symptoms(Appendix 8-A). Hypernasality means“too much nasal resonance.” You havelearned from this text that resonance hasto do with the movement of the velumor soft palate. You also know that thevelum typically is elevated to seal offthe nasal passages so that, for mostspeech sounds, sound resonates and air-flow passes through the oral cavity, notthe nasal cavity. Thus, hypernasalitymust mean that the velum is not doingits job effectively and allowing too muchsound and airflow to pass through thenasal cavity. Simply put, the sound res-onating in the nasal passages when itshould not distorts the sound. In addi-


FIGURE 8–1. An illustration of Bell’s palsy,

paralysis of the facial nerve (cranial nerve

VII). From Wikimedia Commons. Patrick J.

Lynch; illustrator; C. Carl Jaffe; MD; cardiol-

ogist Yale University Center for Advanced

Instructional Media Medical Illustrations by

Patrick Lynch, generated for multimedia

teaching projects by the Yale University

School of Medicine, Center for Advanced

Instructional Media, 1987–2000. Patrick J.

Lynch (http://patricklynch.net), Creative Com-

mons Attribution 2.5 License 2006.

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tion, the airflow traveling through thenasal cavity detracts from the airflow thatis needed in the oral cavity to accuratelyarticulate many of the speech sounds.All this occurs when there is damage to

the motor portion of cranial nerve X orvagus, which supplies the velum.

Imprecise articulation indicates aproblem with the function of the articu-lators, specifically, those articulatory


A B

FIGURE 8–2. A–E. Signs of Bell’s palsy.

Notice that during rest (A), the face looks

fairly symmetric. However, during functional

tasks (B, C, D), the weakened side is pulled

toward the stronger more intact side. Finally,

when the cheeks are filled with air (E), the

lips on the weakened left side cannot main-

tain a functional seal to keep the air from

escaping.

C D

E

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structures that are dynamic or moveable(lips, jaw, and tongue). In order to pro-duce intelligible speech at a normal rate(around 140 words per minute), the artic-ulators must move rapidly and with agreat deal of precision. If they are notable to, the rate of speech productionwill slow and the precision or crispnessof speech will be affected. The cranialnerves that are implicated for the mov-able articulators include trigeminal, facial,glossopharyngeal, vagus, spinal acces-sory, and hypoglossal (see Table 8–1). I amsure that you notice another nerve thatis included in the table that is not listedhere. Although not directly involvedwith the innervation (nerve supply) tothe articulators, cranial nerve eight(vestibulocochlear) also is importantbecause it is the auditory nerve, andhearing speech does influence how it is produced.

Another of the primary features of flaccid dysarthria is a breathy vocalquality. The quality of the voice has to

do with phonation. A breathy vocalquality is an indication of excessive airleaking through the glottis (the spacebetween the folds). In the case of flacciddysarthria, excessive air goes throughthe glottis due to incomplete closureduring voicing, likely secondary to thehypotone and weakness in the laryn-geal musculature. In some individuals,there may be bilateral weakness of allthe muscles of phonation and in othersonly one side may be affected by weak-ness (paralysis).

A number of possible etiologies(causes) may lead to flaccid dysarthria.Traumatic injuries, which may be sec-ondary to everyday accidents involvingthe head and neck, inadvertent injuryduring surgeries to the neck, and motorvehicle accidents that place a great dealof stress on the brainstem area, all couldcontribute to damage to the PNS affect-ing speech (Freed, 2000). Flaccid dysarthriaalso may be present following a stroke.The type of stroke would have to be


Table 8–1. Cranial Nerves That Contribute to Speech Production

Motor/

Cranial Sensory

Nerve Name Mixed Primary Function for Speech

V Trigeminal Mixed Facial sensation (S)

Jaw movement (M)

VII Facial Mixed Oral cavity (S)

Facial expression (M)

VIII Auditory Sensory Hearing and balance

IX Glossopharyngeal Mixed Pharyngeal sensation (S)

Pharyngeal movement (M)

X Vagus Mixed Laryngeal sensation (S)

Phonation, Velar elevation (M)

XI Spinal-Accessory Motor Head and shoulder movement

XII Hypoglossal Motor Tongue movement

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very specific, however. In Chapter 3,you learned about strokes that occur inthe brain. In order to impact the PNS,the stroke would have to occur in thebrainstem. Remember that the majorityof cranial nerves originate along thebrainstem so a stroke (whether ischemicor hemorrhagic) in this location likelywould have a direct impact on the adja-cent cranial nerves (see Figure 1–16).

Disease is another potential cause offlaccid dysarthria. There are conditionsor diseases that directly impact the PNS.Several examples include Guillain-Barrésyndrome, myasthenia gravis, and mus-cular dystrophy. The common theme to all etiologies that result in flacciddysarthria is that they somehow impactthe PNS.

Spastic Dysarthria

Spastic dysarthria, like flaccid dysarthria,is named for the nature of the muscleimpairment present in this condition.Spasticity in muscle refers to hypertone,or excessive muscle tone. So, whereasthe muscles in flaccid dysarthria are lack-ing tone or floppy, muscles in an individ-ual with spasticity have increased tone.An understanding of spasticity is impor-tant here. People may think of increasedmuscle tone, or tight muscles, indicatestrength (aren’t tight muscles what wewould all like to have?). For the “buff”people working out at the gym, that maybe the case. In the situation of spasticity,however, increased tone should not beequated with strength. Instead, spastic-ity exists in muscle after there has beenbilateral damage to the motor pathwaysin the brain. Therefore, although spasticmuscles are tight, they are not strong. Infact, they more typically demonstrateweakness. The combination of increased

tone and weakness can make it difficultto move structures (Figure 8–3); in ex-treme cases, tight contractures causedby spasticity can lead to changes in thestructure. This phenomenon can anddoes occur in the speech musculature aswell. As a result, the most salient speechfeatures of spastic dysarthria are impre-cise articulation, reduced pitch andstress variation, and harsh vocal quality,implicating primarily the articulatory,phonatory, and respiratory systems.Although some degree of hypernasalitymay be present, resonance typically isnot one of the primary problems forindividuals with spastic dysarthria.

Spasticity, then, is a condition thatcould affect all subsystems of the speechmechanism although it is likely that


FIGURE 8–3. Spasticity in the lower limb.

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some aspects will demonstrate moreimpairment than others. Unlike flaccid-ity, however, the effects of spasticity willimpact the entire system. For example,if phonation is impaired by spasticity,then muscles in the entire system willdemonstrate the effects of increased orhypertone. In flaccid dysarthria, youmight see just one aspect of phonation(one vocal fold) demonstrate weaknessin a system that otherwise functions well.Because one of the primary features ofspastic dysarthria includes imprecisearticulation, it is clear that the increasedtone has a direct impact on the articula-tory system. Restricted movement ofthe articulators from the spasticity leadsto difficulty in making full articulatorycontacts and difficulty with the rapidmovements required to transition be-tween sounds. These restrictions trans-late directly to imprecision and a slowedrate of speech. The inaccuracy thatoccurs will affect all speech: consonantsas well as vowels.

Phonation is another speech sys-tem often affected by spastic dysarthria.In fact, the phonatory characteristicsmay differentiate spastic dysarthria fromother dysarthrias, as many of the dysar-thrias also include imprecise articulationand slowed rate. Spasticity affects theintrinsic laryngeal musculature exactlyin the manner you would expect. Theexcessive tightness of muscles leads totight adduction (hyperadduction) of thevocal folds. The result is the perceptionof a “strained” vocal quality. The tight-ness in the musculature also impactsthe muscles that are responsible forchanging vocal pitch. Thus, individualswith spastic dysarthria tend to have lit-tle pitch variation or intonation in theirspeech (monotone).

Now let’s consider the respiratorysystem. Remember that the respiratory

system never rests, breathing is neces-sary 24/7; thus, those muscles are con-tinuously working. Tight muscles of therespiratory system can limit the amountof movement for breathing, resulting inshallow breaths. Shallow breaths willcertainly impact speech (fewer wordsper breath, reduced stress patterns) butalso may compromise gas exchange(oxygenation of the blood and tissues).If this restricted movement occurs overa long period of time, it can actuallychange the shape of the rib cage, whichwill contribute even more to limitationsin movement. Because you understandthat respiration is akin to the powersource that drives speech production,then you know that with more shallowbreaths there is less air pressure to gen-erate voice and shape into speech. There-fore, when spasticity affects the respira-tory system, the result will be reducedbreath support for speech resulting inshort utterances, low volume, reducedstress patterns, and less air pressure forgenerating speech sounds.

Etiologies that lead to spastic dys-arthria include any condition or injurythat results in bilateral brain damage.Remember that, in order to demonstratespasticity, damage has to occur in themotor pathways in both left and righthemispheres. The usual culprits arestroke (most likely a second stroke as ithas to occur in both hemispheres), alack of oxygen to the brain (anoxia),traumatic brain injury, multiple sclero-sis, and the list goes on. Although thislist looks diverse in the type of injury,the common thread is the diffuse natureof brain injury that occurs. Widespreadinjury, such as what occurs with trau-matic brain injury or anoxia, most cer-tainly will include both hemispheres.Conditions like stroke or multiple scle-rosis, on the other hand, can impact


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smaller, more discrete areas, but if theyoccur in both hemispheres, spasticitycan result.

Ataxic Dysarthria

Another of the dysarthrias is calledataxic dysarthria. Ataxic dysarthria isnamed for the condition of ataxia, whichis defined as a general lack of coordina-tion in muscle movements. In Chapter 1,you learned about the cerebellum, astructure that is located at the back andbelow the cerebral hemispheres. Thecerebellum is “highly connected” tomotor pathways on several levels. First,there are connections to and from thecerebral hemispheres, there is proprio-ceptive feedback from the speech mech-anism, connections with the brainstem,and interaction with the basal ganglia.Functionally, the cerebellum helps tocoordinate and refine motor move-ments, an activity that actually soundsmuch simpler than it really is.

Let’s consider an example. On alate spring day, you come in from a hot,steamy walk around campus and makewhat of course would be your first stop,the refrigerator for a nice cold beverage.You approach the refrigerator and reachout for the handle. Instead of slammingyour hand into the door of the fridge,you slow your movements so that yougrasp the handle with just the rightamount of force. Then you open the doorand look inside. Once you spy the objectyou want, you once again reach forwardto grasp the can/bottle. Now, chances areyou won’t knock the can or bottle overin your attempt to pick it up. Instead,your hand slows to a stop just as youreach the object and you will grasp itwith just enough force to keep it con-tained in your hand as you pull it from

the fridge. This describes such an easytask, something we do every day with-out even considering how difficult it is.At each phase of movement, there is agreat deal of planning, refining, coordi-nating, and smoothing movement sothat the end result occurs without inci-dent. The cerebellum is the structure thatfacilitates and oversees this process inits entirety. More specifically, the cere-bellum assists with the timing, degree,and coordination of motor movement.Consequently, damage to the cerebellumwill result in movements that are halt-ing, jerky, and lacking in precision andtiming, with a general lack of coordina-tion that affects entire movements.

The movements just described areataxic in nature. Following cerebellardamage, ataxic characteristics will be seenacross all motor systems of the body,those responsible for walking (ambula-tion), standing, speech, or any motoractivity that you might attempt. Anotherexample of ataxia is in the speech ofindividuals who are inebriated. Excessalcohol is toxic to the cerebellum and itseffects, although transient (short-term)are presented as ataxia. The speech of individuals who have ataxic dysar-thria has been described as similar to“drunken” speech. The distinguishingfeatures of ataxic dysarthria then, relateto the irregular movements that canoccur within the speech mechanism. Inparticular, the articulatory system dem-onstrates the most salient features ofataxic dysarthria.

When disruptions in the articula-tory timing and force of movement arepresent, the production of consonants,vowels, and the transitions betweenthem are uncoordinated. Consequently,the precision we have discussed as nec-essary for intelligible speech is sorelylacking. Instead, the articulators tend to


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overshoot or undershoot their place-ment targets, sounds may be prolonged,distorted, or possibly even omitted alto-gether. Another important feature isthat the pattern of imprecision is notalways predictable. An example can beseen in one of the common assessmenttasks, diadochokinetics. In this task,speakers are asked to produce a syllable(usually /puh/, /tuh/, or /kuh/; seeChapter 11 for a full description of thistask) as accurately and rapidly as possi-ble. Performance on this task in a “nor-mal” system yields approximately 5 to7 repetitions per second (Tomblin, Mor-ris, & Spriestersback, 2000). An individ-ual with flaccid or spastic dysarthria wouldperform much slower but the produc-tions would be steady and rhythmic.However, an individual with ataxicdysarthria would have productions thatvary. They might produce two syllablesslowly followed by three rushed andone prolonged syllable. Because theunderlying problem of ataxia is sys-temic, the coordination of all the motorsystems for speech is a difficult task.Additionally, the demand for coordina-tion can change based on the speakingtask, context, even the emotional stateof the speaker. As such, articulatory dis-ruptions are irregular and perhapsunpredictable; for example, a word thatmay be produced perfectly in one sen-tence may be distorted in another.

The effects of ataxia also may dis-rupt movements of the respiratory sys-tem, more specifically, the coordinationbetween respiration and phonation.Phonation occurs on the exhalationcycle of breathing, and when the sys-tems are in sync, speech is an efficient,almost effortless product. When the twosystems are not well coordinated, theresult may be speech that is not so easy.As an illustration, try the following:Breathe in, and as you breathe out, begin

counting at a comfortable rate. How fardid you get? Counting to 10 should berelatively easy for an intact system.Now count to 10 again but breathe inand before you begin to count let abouthalf of the air escape before you begin tocount. How did that go? Counting to 10on less air is more difficult, isn’t it? Youprobably had to push harder at the endof the utterance to keep speech going.That concept of “pushing harder” meansthat you were engaging additional mus-cle systems (probably the abdominals)just to complete the utterance. This sim-ple comparison of using air efficientlyand not so efficiently shows how “out of sync” systems can impact speech.During that task you may also havenoticed that stress patterns were atypi-cal. Did you notice stressing each num-ber equally? Abnormal stress patternsthat overlie speech are another of thefeatures that differentiate ataxic dys-arthria from the other dysarthria types.Careful orchestration of all the systemsworking together is what makes speechso easy for most individuals. For indi-viduals with cerebellar damage, how-ever, imagine systems that are out ofsync and working less efficiently all thetime (Murdoch, Chenery, Stokes, &Hardcastle, 1991). Ataxia is a conditionthat makes that scenario a reality.Speech for individuals with ataxicdysarthria, then, is hard work!

The conditions that contribute tocerebellar damage resulting in ataxicdysarthria are similar to what you mightfind with the other dysarthrias with afew exceptions. First, the primary con-tributors are degenerative conditions.Examples include unspecified cerebel-lar degeneration, olivopontocerebellaratrophy, multiple systems atrophy, andShy-Drager syndrome to mention a few.Demyelinating diseases, such as multi-ple sclerosis, can also cause cerebellar


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damage. Stroke or CVA is another causethat is actually common across almostall dysarthria types. Of interest to note,however, is that if a stroke occurs in onecerebellar hemisphere, the prognosis forrapid recovery is favorable. Strokes thatoccur in the vermis (midline) or thataffect both hemispheres will have morelasting effects and disability. One causeof ataxic dysarthria that is unique relatesto toxic or metabolic disturbances. Alco-hol toxicity, alluded to earlier, is oneexample, but there are other substances/medications that can reach toxic levelsand result in ataxia. For the most part,the ataxia that comes from toxic ormetabolic influences can be reversed.However, if the toxicity continues or issevere, there may be permanent dam-age with irreversible effects.

Hypokinetic Dysarthria

The diagnosis “hypokinetic dysarthria”is similar to some of the other dysar-thrias in that the name itself describeswhat to expect in speech features. As areminder, “hypo-” means a lack of, or lessthan expected, and “kinetic” means move-ment. Right away, understanding themeaning of the diagnosis reveals thatindividuals who suffer from hypokineticdysarthria will demonstrate generallyless movement, as seen throughout thecomponents of the motor speech mech-anism. The general lack of movementstems from disruptions with the basalganglia control circuit as described inChapter 1. The basal ganglia and its con-nections really function to regulate mus-cle tone, support motor behaviors, makepostural adjustments during movement,respond to environmental changes, andassist with the initiation of motor move-ments and new motor learning. A list-ing of these functions illustrate that

damage to the basal ganglia circuit def-initely will impact motor control andmovement. In hypokinetic dysarthria,damage to the basal ganglia is second-ary to a depletion of the neurotransmit-ter dopamine, which is provided by thesubstantia nigra. The prototype exam-ple for this diagnosis is Parkinson dis-ease. Cardinal features of Parkinson dis-ease include resting tremor, rigidity,bradykinesia (also known as hypokine-sia or akinesia), and reduced or lack ofpostural reflexes. Considering these fea-tures, bradykinesia/hypokinesia is per-haps the condition that contributes themost to the clinical signs of hypokineticdysarthria.

Muscle rigidity in the speech mus-culature will restrict movements. Youmight see parallels between the musclerigidity as a feature of hypokinetic dys-arthria and the hypertone seen in spasticdysarthria. Indeed, the impact on speechsystems can be similar, but there is anunderlying difference in muscle rigidityand spasticity. Increased muscle tone orspasticity is a condition that results inmuscle tightness. However, spasticitycan be alleviated through deep massageor range of motion (ROM) activities.When a structure with spasticity ismoved, the initial resistance of spastic-ity will ease as the structure continuesthrough the movement. Although mus-cle rigidity also results in muscle tight-ness, it does not respond to massage orROM exercises. The tightness demon-strated by muscle rigidity will resist allthe way through a movement.

The speech characteristics that bestrepresent hypokinetic dysarthria reflectthe underlying primary features ofParkinson disease. The most commonspeech impairments include reducedpitch, loudness and stress variation,short rushes of speech, dysphonia, andthe perception of rapid speech. (It is


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worth noting that hypokinetic dysarthriais the only motor speech impairment inwhich speech rate is perceived as fastrather than slow.) Muscle rigidity isanother muscle condition that is sys-temic in nature. Thus, components ofspeech production may have decreasedfunctionality because of the “tightness”of the musculature. With regard to res-piration, the symptoms are similar towhat may be present in spastic dysar-thria. The restricted movements of therespiratory muscles result in a reducedlung capacity. Reduced capacity, andthus air support for speech, will resultin an overall reduced intensity (volume)as well as less variation of intensity(used for stress patterns). The phonatorysystem also demonstrates the effects ofmuscle rigidity in a general lack of pitchvariation. The muscles that manipulatelaryngeal structures to change vocalfold tension (thus pitch) are tight, notmaking the fine adjustments to the system for normal pitch contours, likethe rising pitch you typically hear at theend of an utterance when an individualasks a question. Muscle rigidity leadingto the lack of pitch variation is some-what expected in these individuals.However, another aspect of laryngealfunction in hypokinetic dysarthria hasbeen a bit perplexing. Dysphonia com-monly has been listed as a feature of thediagnosis. Dysphonia is a voice qualityalso known as hoarseness, which in-cludes some degree of breathiness. Anypresence of breathiness in a systemwith rigidity in the musculature iscounterintuitive. If the muscles ofphonation are rigid, then you mightexpect an excessive or hyperadductionof the vocal folds, which would lead tomore of a “strained” vocal quality.Instead, the vocal folds actually arehypoadducted, which results in that

hoarse, breathy voice quality. Theunderlying mechanism for this unex-pected clinical sign is unclear and keep-ing some researchers busy trying to findan explanation. Articulatory functionalso is affected by the nature of the mus-cles in hypokinetic dysarthria. Theeffects of Parkinson disease lead toarticulators that are restricted in theirrange of motion; thus, they tend toundershoot targets. The imprecision inmeeting articulatory contacts results inspeech that is difficult to understand.The strength of the articulators may be in the normal range (at least until the advanced stages of the disease) but muscle rigidity limits movements.The restricted movement also is notedin the muscles of facial expression. Thelips are an active articulator of the face,but the rest of the face also adds con-tent to what we express through speech.Individuals with hypokinetic dysarthriahave what is known as “masked facies”or a general lack of facial expressionduring speech or to express emotion.The face may have features that are still, like the immovable features on amask.

Degenerative conditions are by farthe primary cause of hypokinetic dysar-thria. Parkinson disease is the major con-tributor, but there are other conditionsthat share some of the characteristics ofParkinson disease that have additionalsymptoms as well. Those diseases areoften called Parkinson-plus syndromesand contain such diagnoses as multiplesystems atrophy, progressive supra-nuclear palsy (PSP), and corticobasaldegeneration. Involvement of the sub-stantia nigra and dopamine depletionare all common elements, although mostof these other diagnoses demonstratemore of a mixed dysarthria (hypokineticplus another dysarthria type).


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Hyperkinetic Dysarthria

As you have just learned, the diagnosishypokinetic dysarthria means too littleor reduced movement of the speechmusculature resulting in impairment.At the other end of the spectrum is“hyperkinetic dysarthria,” which is definedas excessive movement of the speechmusculature also resulting in disrupted

speech. A large number of movementdisorders result in excessive, involuntarymovements of the body. When thosemovements affect the components ofspeech, hyperkinetic dysarthria is theresult. Depending on the movement dis-order, a single speech component (as inthe jaw opening dystonia in Figure 8–4)may interfere with speech, or it is pos-sible that the entire system will be


FIGURE 8–4. An example of jaw opening dystonia, one type of

hyperkinetic dysarthria.

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affected by the involuntary movementsmaking speech difficult to produce.

The movement disorders that resultin hyperkinetic dysarthria range fromslow to fast movements, small tics of asingle body part to whole body move-ments. Each diagnosis demonstrates aunique pattern of movements. The widerange of disturbance makes it difficultto predict speech characteristics basedon simply “hyperkinetic dysarthria” asyou can with other dysarthria types(flaccid, spastic). However, there is oneunifying symptom that spans the diag-noses: involuntary movement.

The movement disorders that resultin hyperkinetic dysarthria are often asso-ciated with damage to the basal ganglia.Remember that hypokinetic dysarthriaalso is linked to the basal ganglia; how-ever, the mechanism for hypokineticdysarthria (i.e., depletion of the neuro-transmitter dopamine) is fairly wellunderstood and is isolated to basal gan-glia connections, specifically the substan-tia nigra. The mechanisms for the widerange of movement disorders linked tohyperkinetic dysarthria are not as wellunderstood. The importance of the basalganglia in regulating the movementsplanned by the motor cortex is not dis-puted, but the mechanism of injury/disease that results in such a wide vari-ety of impairments remains a questionand a source of ongoing inquiry.

Exactly how the speech mechanismis affected by movement disorders reallydepends on the type and extent of thecondition. As previously mentioned andillustrated in Figure 8–4, an individualmay have a fairly focal (isolated) dysto-nia that only interferes with one struc-ture. In the case of the jaw opening dystonia, an individual might be talk-ing and suddenly (often where there isan open mouth posture for a vowel) thejaw begins to open and perhaps stays

open on its own accord. Imagine howeven a relatively isolated impairmentsuch as this might disrupt speech. Justtry saying the days of the week, andwhen you get to Wednesday, open yourjaw slowly to an extreme open posture.Were you able to keep talking? If thejaw opening was not extreme, speechmight be possible. However, rememberthat these are involuntary movements soit is unlikely that you will have a choicein how wide the jaw opens. Now let’sconsider a more extreme movement dis-order that affects the entire body. Hunt-ington’s chorea is a genetic disordercharacterized by random movements of the head, neck, trunk, and even thelimbs. It is difficult to even simulatesuch a condition for the purposes ofillustration as you did just now with ajaw opening dystonia. Imagine, though,what a sudden hard rotation of yourentire trunk would do to the careful bal-ance of breathing, phonation, . . . speechproduction in general. If you have neverseen this condition, the impact can bequite dramatic. Some individuals haveso little control that their flailing limbscan even strike them in the face, send-ing glasses flying. In spite of the widerange of impairments, there are speechfeatures that seem to predominate inhyperkinetic dysarthria. Those featuresinclude imprecise consonants, variablespeaking rate, prolonged speech seg-ments and pauses, harsh vocal quality,distorted vowels, variable loudness, andvoice interruptions. To further reviewhow speech systems might be affectedby hyperkinesias, view Table 8–2.

Mixed Dysarthria

The dysarthrias are a group of disorders,each single diagnosis with a unique setof features that include muscle charac-


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teristics, nervous system lesions, andmotor behaviors. Although the list iswell described, there are some individ-uals who may not fit neatly into thecharacteristics of just one diagnosis. Infact, because damage to the brain is notalways specific to one system, manyindividuals show signs of more thanone dysarthria type. Typically, they suf-fer from widespread or diffuse nervoussystem damage. For these individualsthere is a “mixed dysarthria” category.For example, the disease amyotrophiclateral sclerosis (ALS or Lou Gehrig’sdisease) is a demyelinating conditionthat affects the CNS as well as the PNS.People who have been diagnosed withALS frequently show signs of both spas-tic dysarthria (often in phonation) andflaccid dysarthria (resonance and artic-ulation). To conclude our overview of

the dysarthrias, the mixed dysarthriacategory completes the group of dys-arthrias. When an individual suffersfrom nervous system injury that is dif-fuse or widespread, then many featuresof the diagnoses discussed above maybe seen in combinations, rather than fit-ting neatly into an isolated category.

We are going to move away from thefocus on dysarthria onto another motorspeech disorder, apraxia of speech. Thecommon thread of impairment thatspanned the dysarthrias was muscle ormotor impairment, which resulted inspeech disturbance. The manifestationof speech disruption in apraxia of

Apraxia of Speech


Table 8–2. Characteristics of the More Common Movement Disorders

Movement Disorder

Chorea

Dystonia

Myoclonus

Tics

Essential tremor

Spasmodic dysphonia

Movement Characteristics

Rapid, unpredictable, jerky

involuntary movements

Slower, more gradual

movements

Rhythmic, periodic muscle

contraction

Brief involuntary movements

(can also be sounds) during

normal activity

Periodic movements

occurring at around 4 to

7 Hz (cycles per second)

Involuntary muscle spasms/

contractions

Systems

This is a progressive disease

that will likely impact the

entire speech mechanism

May impact all systems;

however, resonance is not

typically implicated

Can affect multiple systems;

however, the resonance and

articulatory systems are

often implicated

May be isolated or inclusive

of all speech components

Phonation and articulatory

systems are often implicated

The phonatory system

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“‘Sorry, Jill . . . it’s a brain tumor.’ Two of the most feared words in the English lan-guage. She broke it to me as gently as she could. Brain tumor. Unwanted growth. Itwasn’t malignant and they said it probably wouldn’t grow back. But they had to dosurgery to take it out. I hope they got it all. They said it was pretty much confinedto the region of my frontal lobes right behind my eyes. What could make that stuffgrow in my brain? I need my brain. Dr. Firlik said the surgery was a success, thoughthey had to destroy some healthy brain tissue to get all of the “neoplasm,” their termfor the unwelcome, infiltrating little bitch that grew in my head and tried to ruin my33-year-old life. I don’t have any trouble walking or with my arms but I’m worriedabout whether I’ll be able to take care of my baby. I can’t seem to concentrate. Myattention wanders. I don’t know why I can’t finish the things I start. My speech getslost a little, too. Sometimes I get lost in the middle of telling them something. Eventhings I should know like what I did last summer at Lake Ellen during our trip toUpper Michigan. My brother and sisters were there. We made pasties, those littleCornish meat pies. I couldn’t even remember the steps. What comes first, the potatoesor the crust? Screwed up pasties. Screwed up following directions. Screwed up life.What’s going to happen? They said they could treat it. Maybe further surgery. Maybesome different medications. Maybe some speech therapy. Maybe I’ll need some coun-seling as well. This is not what I had in mind for my life. Maybe I’ll get better.Maybe all this treatment stuff will work. It better. I’ll need all the help I can get toraise precious little Adrienne with only part of a brain. Oh, well. Such is knife.”

12

Principles of Treatment forNeurologic Communication

Disorders

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“Treatment” can have many meanings.In apparel and fashion design, it refersto modifying fabrics or clothing. In film,treatment refers to turning prose into ascreenplay. In ecology, sewage treatmentrefers to processes of removing contam-

Introductioninants from wastewater. In health care,treatment is synonymous with therapy,the process of attempts to remediate med-ical or behavioral problems to a resultthat is desirable and beneficial. Treatmentof health issues and disorders of commu-nication can range widely from medical,surgical, pharmaceutical, and/or behav-ioral approaches (Figure 12–1).


FIGURE 12–1. Care of the sick. From Care of the Sick, Domenico di Bartolo, 1441–1442.

Public domain on Wikimedia Commons.

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In Jill’s case, in the scenario listedabove, treatment was multimodal andinvolved several different professions.After complaints to her family physi-cian, her brain tumor was diagnosed bya neurologist, a medical specialist inbrain diseases. She then was referred to a neurosurgeon who operated on herto remove the meningioma that hadgrown slowly in her brain behind hereyes. Her hospital stay necessitatedassociation with several others on thehealth care team. Nurses, rehabilitationprofessionals in occupational therapyand physical therapy, specialists insocial work who attended to her needsafter discharge, the hospital pharmacist,and the speech-language pathologist allentered the picture as part of her treat-ment team. The focus of Jill’s treatmentis rehabilitation and the skills she hadacquired but were lost or impaired bythe tumor.

What distinguishes habilitation from re-habilitation is that habilitation is intendedfor people with functional impairmentscaused by congenital injuries or disease,or to injury or disease acquired early inlife. Its objective is to help a person inevery way develop the best possiblefunctional ability. Rehabilitation involveshelping the functionally impaired per-son in every way regain the best possi-ble functional ability and physical andmental well-being after the reduction orloss of a function due to injury or dis-ease. Habilitation and rehabilitationboth aim to prevent and ameliorate thedifficulties that functional impairmentscan cause in daily life. The goal of both

Rehabilitation

is maximal function and best possiblequality of life. The goal of habilitationand rehabilitation is a noble one: thatpeople with functional impairmentsshould be able to live their lives as inde-pendently as possible with the samerights, opportunities, responsibilities, andobligations as the rest of society. Habil-itation and rehabilitation usually areused as comprehensive terms to coverall medical, psychological, social, edu-cational, and work-oriented measuresundertaken to help children and adultswho are suffering from a medical condi-tion or have been injured to develop, orregain, the best possible function andlay the foundations for a good life. Inbrain-based communication disordersall of the modes and venues of treat-ment may be necessary. We rely heavilyon behavioral treatment, that is, inter-ventions designed to change communi-cation behaviors, but along the waymany other professionals get involved.

Communication is a multidimensionaldynamic process that allows people whohave learned language to interact withtheir environment. Through the marvelof communication, we are able to expressour thoughts, needs, and emotions. It isso fundamental that it has been charac-terized as essential ingredients for the“Three Ls,” Living, Learning, and Lov-ing (LaPointe, 2005). Without it, we can-not carry out the mundane activities ofdaily living like ordering a cappuccinowith a cranberry bagel, listening to aStephen Lynch song about beautifulbabies, or the hundreds and hundreds

Treatment of CommunicationDisorders: Fundamentals

Principles of Treatment for Neurologic Communication Disorders 253

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of other interactions we engage in everyday that require us to write, talk, listen,or speak. We cannot read directions,assignments, medicine labels, or listento lectures. Most importantly of all, wecannot generate and nurture our inter-personal relationships; without discourseour contact with friends and familywould wither and fade away. Commu-nication is an intricate process thatinvolves cerebration, cognition, hearing,speech production, and motor coordi-nation. Evaluation and treatment of acommunication disorder includes con-sideration of all aspects of the normalcommunication process as brain-baseddisorders can interrupt, corrupt, anddisrupt any or all of these processes.

Language is the transformation of thoughts into meaningful symbols(sounds in the air or squiggles on paperor screen) communicated by speech,writing, or gestures. Thoughts are organ-ized by the brain, specifically the leftcerebral hemisphere, and encoded intoa sequence according to whatever thelearned grammatical and linguistic rulesof the culture and language might be.These rules govern the way sounds areorganized (phonology), the meaning of words (semantics), how words areformed (morphology), how words arecombined into phrases (syntax), and theuse of language in context (pragmatics)(Emedicine.medscape, 2010).

Speech involves the coordinatedmotor activity of muscles involved inrespiration, phonation, resonance, andarticulation. The entire system is modu-lated by both central and peripheralconnections of brain cell bodies andaxons to muscles and organs. Speech isgreatly dependent on a specialized net-work of cranial nerves V, VII, VIII, IX, X,XI, and XII, as well as the phrenic andintercostal nerves. The cranial nerves

are traditionally labeled with Romannumerals, but these paired nerves alsohave names. For speech, the primarycranial nerves are the trigeminal (V),facial (VII), vestibulocochlear (VIII),glossopharyngeal (IX), vagus (X), spinalaccessory (XI), and the hypoglossal (XII)(Emedicine.medscape, 2010).

For speech, the respiratory muscles,specifically the muscles associated withexpiration, must generate enough airpressure to provide adequate breathsupport to make speech loud enough tohear (Emedicine.medscape, 2010). Thediaphragm is the main muscle of expi-ration; however, the abdominal andintercostal (between the ribs) muscleshelp control the force and length ofexhalation for speech. A great dance of muscles is necessary to produce thevibrations of phonation and these mus-cles of the larynx generate vibratoryenergy during vocal fold approxima-tion so that sound is produced. Say“AHHHH.” It happens. Vocal pitch andintensity are modified by air pressurebelow the level of the vocal folds (sub-glottic), tension of the vocal folds, andposition of the larynx. We can screamand we can whisper. We can sing infalsetto like the Bee Gees of the goldenoldies or we can assume our habitualnatural pitch level. Articulatory muscleswithin the pharynx, mouth, and nosemodify and valve the tone of the soundand produce all of the little beads on thestring of speech that consists of phonemes(speech sounds) and their transitions.The intricate and coordinated action of these muscles produces speech. Byaltering the shape of the vocal tract, weare capable of producing a tremendousrange of sounds. Speech requires thebalanced coordination of over 100 mus-cles at speeds that are a blur. Speech isour most complex, balanced, coordinated


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human neuromuscular activity. It mustbe nearly perfectly innervated to createthese time-space movement coordinates.No wonder little things, such as strokes,head banging, golf-ball sized tumors, ornasty diseases that strip the nerves oftheir conductivity, can throw it off.

Sound waves are transformed by theauditory system into neural input forboth the speaker and the listener. Theouter ear detects sound pressure wavesin the air (or even under water, but notnearly as distinctly) and converts theminto mechanical vibrations in the middleand inner ear. The cochlea, that magicalsnail-like shell full of hair cells andfluid, then transforms these mechanicalvibrations into vibrations in fluid, whichact on the nerve endings of the vestibu-locochlear (XIII) cranial nerve. Thus, theprocess of communication begins andends in the brain (Figure 12–2). Com-munication is what makes us human.The brain lends itself to the creation ofa never ending list of metaphors. The

brain is a computer; the brain is a web;the brain is a river; the brain is an orches-tra; the brain is a cookbook; the brain isa snowflake; the brain is a dream fac-tory. No wonder we value it more than,say, our great toe or our appendix.

All of the disorders previously dis-cussed and feared may impair a person’sability to communicate. These disordersmay involve voice, speech, language,hearing, cognition, or even the basic taskof taking food and swallowing it. Rec-ognizing and addressing communica-tion disorders is important; failure to doso may result in isolation, depression,and loss of independence. Life withoutcommunication caused by brain dam-age has been described as a living deathby those who have recovered enough to comment on it. So we do our best tounderstand the clinical science of brain-based communication disorders inter-woven with the clinical science and artof rehabilitation and restoration of thismost human and complex function.


FIGURE 12–2. Brain.

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In a European Neurology Society Meet-ing on neurorehabilitation, Butterworthand Howard (1990) articulated sometheoretic suppositions that can serve as useful principles for rehabilitation ofbrain-based disorders. They listed sev-eral assumptions, some of which mayappear as a firm grasp of the obvious,but nevertheless form an elemental fir-mament for treatment. Because theirsuggestions did not include as muchemphasis on the acknowledgment ofthe effects of these impairments on lifeparticipation, we have modified themto reflect contemporary approaches torehabilitation. These basic assumptionsoblige reflection and realization.

■ We must identify the exact nature ofimpairments and determine theirimpact on acceptable life participa-tion and activities

■ We must match treatment to the iden-tified impairments and life participa-tion needs of each unique individual

■ We must be eclectic in our adoptionof treatment approaches. Treatmentmay encompass any or all of thestrategies of:■■ relearning information or proce-

dures that have been lost■■ facilitation of access to informa-

tion or skills that are intact butinaccessible

■■ reconstitution or compensation forlost functions, that is, finding newways to achieve goals

■■ accommodation, adjustment, andAristos (i.e., making the best of agiven situation) (LaPointe, 2005)

■ We must ensure that the person andfamilies with whom we are working

Rehabilitation Assumptionsand Principles

have the opportunity to communi-cate their treatment objectives andoutcomes and that these desires areincorporated overall treatment goals

■ We must incorporate the principlesof evidence-based practice and eval-uate the effectiveness of treatment(Dollaghan, 2007)

■ We must utilize principles of cross-disciplinary collaboration and cooper-ation by participating in professionalteams.

In their book Aphasia: A Clinical Approach(1989), Rosenbek, LaPointe, and Wertzdevoted a chapter to “Principles of Clin-ical Aphasiology.” These principles havebroader application than just to the disor-der of aphasia and may well be germaneto most of the brain-based communica-tion disorders. These authors stated:

We learned our principles from others—other professionals and the [menand women with aphasia] who haveagreed over the years to spend timewith us.

We have learned the same thingsover and over from some, and uniquethings from a few. Like a code for liv-ing, the principles governing our dailyactivities with [people with aphasia]have evolved, sometimes so subtlythat they escape our notice until we sitdown, as now, and take stock.

The clinical principles outlined byRosenbek, LaPointe, and Wertz (1989)included some that have evolved a bit,some that are relatively timeless, and allthat seemed to reflect the opinions ofdeeply committed clinical professionals

Other Principles Worthy ofConsideration


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who had a passion for their work withhundreds of people with communica-tion disorders. For example, they opined:

■ Clinical aphasiology requires clinicalaphasiologists—Part-time clinicians,if they are full-time clinical aphasiol-ogists, can treat people with aphasia.But simple caring is not enough.Intellect and a subscription to Brainand Language also are not enough.Nor is having earned one’s 10-yearpin or 10 ASHA-approved CEUs in a year. Training in neurolinguistics is not enough, nor is knowing how to run a successful private practicefrom a garage after working all dayin the public schools. [People withaphasia] deserve the care of a clinicalaphasiologist. Clinical aphasiologistscare about [people with aphasia];they spend time with them every day;they read, remember, and integratewhat they read; they go to workshopsto stay abreast; and they specialize in the understanding, diagnosis, andtreatment of aphasia and [peoplewith aphasia].

■ Treatment has three goals—The goalsof treatment are: (1) to assist peopleto regain as much communication astheir brain damage allows and theirneeds drive them to, (2) to help themlearn how to compensate for residualdeficits, and (3) to help them learn tolive in harmony with the differencesbetween the way they were and theway they are.

■ The most important goal usually is toprepare persons with aphasia for alifetime of aphasia—This is not truein all cases but certainly is true inmost of the chronic conditions withwhich we are confronted. Too manypeople (and health care profession-als) generalize the acute-care medical

model concept to the challenge ofdealing with chronic conditions. Thisproblem is reflected not only in themisguided or failed expectations ofworking with people with chronicconditions, but also gravely reflectedin the reimbursement and insuranceissues that permeate many health caresystems. Get ’em in; get ’em out is notan adequate model for dealing withchronic conditions and many brain-based disorders indeed are chronic.Until this philosophy of economic,bottom-line approaches to health careis radically changed, professionals andsufferers must prepare for the frus-trations of inadequately allocatedreimbursement for chronic condi-tions. That will indeed “ensure” (nopun intended) that our clients mustbe prepared for long-term chronicity.

■ Treatment should be influenced byan attitude about what a person withaphasia is—Persons with aphasia donot talk at all or nearly as well asbefore becoming ill, and all their othercommunicative acts are impaired invarying degrees as well. In addition,they are likely to be more irritable,scared, depressed, and distractible thanbefore they got sick. Despite thesechanges, they often are unchanged atthe core. If they were loving before,they will be again. If they were iras-cible, they will remain so. If theywere making their ways through life,they will continue to do so. If theywere dying, regardless of how subtly,the episode causing the disorder willnot be an antidote. Above all, if theywere doing the best they could before,they will set about doing the bestthey can to adjust to their disabilityand to the treatments that are likely toaccompany it. All of this is not fatal-ism or resignation. It is applause for


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the resiliency of people with brain-based disorders, and it is an appealfor professionals to avoid getting inthe way of each person’s recovery. Itis also the summary of an attitudethat profoundly influences what wethink. Clinicians should reinforce theclient’s personal strengths and sup-port their natural processes. Theyshould treat people with aphasia andnot aphasia. Knowing what to sup-port, what to change, what to accom-modate, and what to ignore are marksof clinical maturity. Many of thesethoughts and philosophies about treat-ment were generated and hatched bythe outstanding clinician Jay Rosen-bek, and the egg was then warmed ifnot scrambled by Wertz and LaPointe.These principles guided all three oftheir clinical lives.

The skills and knowledge involved inassessing and treating brain-based dis-orders of communication and swallow-ing require some general and some veryspecific competencies. These include:

■ assessment, appraisal, and diagnosisskills with emphasis on interview-ing proficiency, preparation and testadministration, interpretation of theresults with subsequent ability tointegrate and present what has beenlearned in both oral and written form

■ clear and concise report writing withemphasis on the goal of comprehen-sible documentation and explanation

■ therapy practices that incorporatetask analysis, behavioral objectives,and implementation (Figure 12–3),

Specific Skills andKnowledge

and integration of information fromothers on the professional team

■ documentation of treatment out-comes, progress, and accountabilitythat conform to the scope of practiceand ethical standards of the appro-priate discipline

■ implementation or referral for appro-priate client and family counseling.

Some of the material in this section hasbeen considered in a chapter on socialvalidation of treatment for aphasia thathas appeared in a Festschrift for ChrisCode in a book edited by Ball and Dam-ico (2006). As LaPointe and Lenius (2006)have reviewed, traditionally, clinicianshave used standardized tests such asthe Western Aphasia Battery (Kertesz,1982) to determine areas of impairment,select therapy goals, and possibly docu-ment change. This focus on impairmenthas been consistent with traditionalapproaches to disease characteristic ofthe medical model, but may not be themost efficient way to determine sociallyrelevant goals. The seemingly ever chang-ing terminology of the World HealthOrganization is being integrated intomodels of aphasia treatment (Rogers,Alarcon, & Olswang, 1999; Threats, 2006),and the concepts involved are impor-tant. Changes in social activities andparticipation are emerging as more rel-evant goals of treatment and are erod-ing the stone face of impairment-basedapproaches to intervention. The LifeParticipation Approach to Aphasia con-tinues to have an impact on approachesto aphasia intervention and is shapingthe very core of the aphasia treatmentmodel (LPAA Group, 2000). Most stan-

Social Models of Treatment


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dardized tests of aphasia are predomi-nantly impairment based. Recently, someefforts have been made to incorporatethe social model of aphasia into assess-ment procedures. The latest edition ofEisenson’s classic Examining for Aphasia(LaPointe & Eisenson, 2009) incorpo-rates principles of the social model ofaphasia into assessment in an effort toguide clinicians in the quest to developrelevant participation-based treatmentgoals. This approach does not suggestthat we discard the infant with thecleansing aqua, for impairments andcognitive-linguistic processes also mayneed to be targeted for treatment; butfor far too long it has been impairmentor nothing, with little emphasis on rein-tegration of the person into an active,participating milieu. This attitude and

set of values is epitomized by the recentwork of Audrey Holland on the impor-tance of counseling in communicationdisorders from a wellness perspective(Holland, 2008).

The traditional biographic standard-ized test interview needs to be supple-mented or indeed replaced with specificinformation gathering as to the goals,values, hobbies, likes, dislikes, hopes,fears, anticipations, and motivations ofeach unique individual for whom we areplanning treatment. This will assist theinformed clinician with planning, deliv-ering, and evaluating services (Pound,Parr, & Duchan, 2001). The LPAA Pro-ject Group (2002), Simmons-Mackie & Damico (2001), LaPointe (2002), andCruice et al. (2005) all provide socialmodel flesh and humanity to the bones


FIGURE 12–3. Example of therapy practice.

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of treatment planning in aphasia. Thisentire movement of course harkens backto the birth and upbringing of languagein context and person-centered conceptsof aphasia intervention nurtured andinfluenced so thoroughly by AudreyHolland (Holland, 1982),

Interview questions appropriate todetermining and creating socially rele-vant and valid treatment goals can begleaned, inferred, or directly createdfrom all of the above sources and fromthe assessment protocol of LaPointe andEisenson (2008). The interview allowsthe client and any others present toexpress what life was like before theonset of aphasia, how life is impactednow, and what areas of communicationbreakdown generate the most stress onrelationships.

In an effort to define socially validaphasia therapy goals, Ross and Wertz(2003) set out to determine the differ-ence in quality of life as rated by peoplewith and without aphasia. Two groups(people with aphasia for at least sixmonths and non-brain-damaged indi-viduals) completed quality of life mea-sures. The greatest difference betweenthe groups was evident in areas of activ-ities of daily living, opportunities toacquire new information and skills,social support, mobility, and sexualactivity. Of course, it is imperative tocustomize treatment planning and weavespecific treatment goals around the idio-syncrasies of each person, but this studyshows support for language therapyfocusing on enhancing communicationfor specific functional situations andexpanding participation in society. Recentwork by Ross and her colleagues (Ross,LaPointe, and Katz, 2008) has suggestedthat loneliness and sense of belongingalso are factors that impact people withbrain-based communication disorders

and should be a consideration in treat-ment planning and the attempt at imple-menting treatment outcomes.

Sometimes we tend to err on theside of overzealous treatment planningand realization. One of the authors ofthis book (LLL) remembers well an earlytreatment planning faux pas when a fullcourt press of intervention (twice perday; intensive reading comprehensionstrategies integrated into the treatmentschedule) was probably not in keepingwith the personal goals of the personwith aphasia. After two weeks of ratherintensive treatment, I remember hiswords well: “Doc, I thank you for allyou’re trying to do here, but, you know,I never have completely read through awhole book. I don’t really care if I everdo. I just want to go up on the St. JohnsRiver and live with my brother in thetrailer there, and maybe sit out on the dock and fish a little. I know you’retrying real hard Doc, and I appreciate it, but I really don’t care if I can’t readvery good.”

If the treatment goals of the personwith aphasia are not built into the treat-ment plan, misguided expenditures oftime, effort, and money can be the result.This clinical lesson made it abundantlyclear that precise activity and participa-tion therapy must be harmonious withthe expectations and needs of the personin therapy. Sometimes the people withwhom we work are content to fish, plantkumquats, or join the circus (Figure 12–4).

These principles set the ground forour belief system in interacting withpeople with brain-based disorders ofcommunication and swallowing. Weknow not what the future holds, it willsurely be trials and tribulations, but justas surely it will contain family holidays,fish curry, happy weddings with hennahands (Figure 12–5), faithful pets, art,


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261

FIGURE 12–4. Circus. From “Circus Amok Jugglers” by David Shankbone,

New York City, 2006. Taken from Wikimedia Commons under the Creative

Commons Attribution 2.5 License.

FIGURE 12–5. Henna.

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music, and sports peak moments, walkson the beach (Figure 12–6) and newdirections and accomplishments. Goodtreatment in both principle and imple-mentation can help restore or compen-sate for these joys of living to peoplewith brain-based disorders (Figure 12–7).As Small (2000) has implied, we can

expect not only advancement of ourunderstanding of how the brain oper-ates in order and disorder, but also anabundance of new mysteries that willpique our curiosity and motivate ourquestions. That is one of the many rea-sons we get up in the morning.


FIGURE 12–6. Sunset on the beach.

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Ball, M., & Damico, J. (Eds.). (2007). Clinicalaphasiology: Future directions. New York,NY: Taylor and Francis (Psychology Press).

Chapey, R., Duchan, J. F., Elman, R. J., Gar-cia, L. J., Kagan, A., Lyon, J. G., & Sim-mons-Mackie, N. (2001). Life participa-

Referencestion approach to aphasia: A statement ofvalues for the future. In R. Chapey (Ed.),Language intervention strategies in adultaphasia (4th ed., pp. 235–245). Baltimore,MD: Williams & Wilkins.

Code, C., & Herrmann, M. (2003). The rele-vance of emotional and psychosocial factors in aphasia to rehabilitation. Neu-ropsyhological Rehabilitation, 13, 109–132.


FIGURE 12–7. Fireworks celebrating the joy of life.

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