Ilrl I)lorrk'rs

nd Their Diagnoses

,'tl.tt't l)(i, A4ttnltlt Illi l)ifferental pallerns of , lutt tttutttl lttr trrttl in\rurment in dysarthrc tl,, t: l,llt,rut!: \rrtft t:lrr\e head injtrry. In Robin l,',1\ttrt hIl, ll,'tk,'lnun DR, e.librs: Disotders oJ t't \ltt t t lt !\i'\!,r/r',r/, lrcoltilcllt, and clinicaL chartt tttttlt llttlttiltt)tr, 199(, PouL H Bookes ,t,1,t,t I ( ) ll,lunh h llli: LaryttgeaL dysfuncrion in
t tr r

162 163

Wesmer G et a[ Acoustic and nlellgbility chqracteF istics oJ sentence producton in neurogenic speech dsorder.\, Folia Phoniatr Logop 53:1, 2001 Efrct of speakinB rote manipulations on ucouslic and perceptual a,spects of the dysarthria in Weismer C et

()

a
(E C]

ol:

dmyolrophic Lateral sclerosis, Fola PhoniaLr Logop

52:201 , 2000

Apraxia of Speech

lt t

r,

t,',tkr' t t ll

tl

Ir

g seve re closed-lvad iniur',

164

h6/, lt)t),l tnl,ttt I )( i tt rrl I lvtrnataltv in dyvrthric speakI,ttlruutt ttwtr'tloel head injury: q perceplual tt
ltt ,\
I nt\tt ttnt tttttl

Weisner G et al: Formant trajectory chIroclerslics of males wilh amyotrophic lateral scleosis, J Acoust Soc

An 9l:1085,

165

Bntitt Inj 7:59, 1993 'ttttlysis, ,',1,,t,,t I t( i. Nlttnh h IlE, Stokes PD: Variabitty in lt tt t ttttttl tutl llt'sioktic feLlures of dysarthra , '[ rt \ rr',? , lvt! lrcud njtrry: an enmindtfun of
t tt\t
"r

166

\ lltttttt luj

t) 67

I,

1995

,',1,\tt\ t ,t ; ,\hn4ttn'l N, Murdoch BE: Molor speech ,,unt,ttt l,tllt',itt\ Irot.nlatk: brtin injury i.n ch[d'

c linical feqtures are mosl useJul deJinile multipLe ststem atrophy from Parknson's disease? J Neurol Neurostrrg Psychiatry 68:434, 2000 Wewng GK et al: Nutural hstor1, awl sunivaL of 14 patients with corlicobasql degeneratott conrme al postmorlem examnatotl, J Nearol Neurosurg Psychia-

1992 Wenning G K et al: What

to distinguish

try 64:184, 1998

"This morning I was appalled (rt m) terrible reading aloud a new passage. I had dfficuLty enunciatinB most every word. ParticuLarLy troublesom.e were the words manipulote' on' monipulated.' I couldn't seem to ge I past 'manifested.' Later I tried again and wa,s only barely pronouncing the wonls correctly. . . . Al,ro, I was fuLl of slurring the sountls of.ryllables."
'

',1 ,t 'ttttntlttryttl utrl percaptual anaLysis of one , l",lt,tt li,lutltil ) 107, 1998 ,t,ttt\ Il lttlirrk l: I'ttkinxnismplusdironlers In

167 Williams DB, Wndebank AJ: Motor neuron dsease

(amlolrophc lateraL scleross), ll4ayo CLin Proc 6 54,
1991

(From lhc ||rtten diotl of a 72 yeur old wonnn with a pngess^'e apraxia of speech and mild aphasfu)

rlitrt Ncurtilogicaltherapeutcs: prit l,t ,tt,l luttttttt rl I, New York, 2003, Martin
, y,' 11 I I l,,
,1,

168

Windebank AJ: Motor neuron liseases In Noseworlhy therdPeuLcs: principles arul prqctice, vol 2, New Y,rk, 2003, Martn Dunitz.

JH, editor: Neurological

u l lhn' O

SLtttt'nteL[ timng in amyotophc

Res

169

t,l :, l' ,,:ts, L\ttLr h Lung Hur

43:683,2000

,lt u A l nt ttt t ( i,\ \per trul Properlies of Jricalives tilr\t,tttl'lut liltttl rlensis, .l Speech Lanp Hear ilt lit,\ ltr)/ ,1, rt h ll'ttlruq l, ('lnrdueristics of dadochokne' trt rrnltt,1, r, lt'tti nnrl Parkinson's disease, FoLitt uutttt I t,\t,l) \i J I l, 2O0.1 (u1(l dlsdrlhr.1 4s ',tl't:ltt l t t ttl lh'ttot ol totl,gue ,'1, nnutlt \ttttnil t)l Wil,\o1't disease, Clin Nettrol t't)\, lr)90 ttttttttt! t)

ilt' ll I t t ttl /\iltvto|hc luleraL sclerosis mimc ,lt',uttt tt tttttlrttion-bosed study, Arch NeuroL ut lll t't ttl: (-linictl feutures of anyotroplric t,tl t, ltntt ,tr r onlinq kt the EI EscoriaL ond ArLie rt, 'lt'ttttrxltr t:ul(rLt: u Pq)uLaliul based stud,, tt N'tt,,t / llTl 2000b tt' t t i\ l ttlrtt K, Wcsner G: Tlrc inlluence of tt ttt: t tttt ,tt Lrrn'l tputc und speech inlelliyblily ut,ltt,lt,tlt tttl (rntyotrophi. Itteral sclerosis, J ,,lt ll,,tt litt lti:1001,1995 t' I I t I rrl /llk'iltilinl: Dlolotr tole as an ndex of , h rt,tt tlivtnlt t in tfttumalc brain injury, CLin :rt\t l'lutt I / l, )(I)J t, t (,\ ll/t tvtt' (i: (.-lnutcLeristics ol spetking rute lt, ,lt,utltltt tr\tt\ial! with amlolrophic lateral r,,ttt t .\1r,t r lt llttr Ilet 36: I 158, l99l

Yorkston KM, Strarul EA, Hume J: The relationship beween motor funclon dnd speech f.mction n amyotrophic loreral sclerosk In Cannito MP, Yorkstn KM, Beukelman DR, editors: Neuromotor speech disordert: naLure, astessttent, and managemenL Bdltimorc 1998, Paul H Brookes 170 Yorkston KM, Strand EA, M iller RM: Progression of res' piralory symploms in g,nyolrophi( loteral tleroit: implicatonsfor speethfiLnction ln Robin DA, Yorktton KM, Beukelman DR, eclitors: Dtnlers of motor speech: assessmet, lreotnreu, nnd cLnicaL charac terzqtion, Baltimore, 1996, Btookes Prblishng
17

CHAPTER OUTLINE I. Anatomy nd basic functirurs of the motor speech pr0grammer A Functions of the motor speech programmer

172

Company. Yorkston KM et tl.: Characteristics of multple sclerosis as a Iunctot1 oJ the severly of speech disorders, J Med Speech-Lang Pathol I I :71, 2003 Yorkston KM el al: Mana,qentent oJ motor speec;h disor ders in children antl aduLts, ed 2, Attstin, Tex, 1999, Pro Ed.

The motor speecb programmer ne[work

II. Nonspeech, nonoromotor, and nonlinguistic characteristics of patients with apraxia of speech

III. Etiologies
IV. Speech pathology
A. Terminology and theory B Distribution of etiologies, lesions, and associa[ed delicits in clinical practice C. Patient perceptions and complairts

173 Yorkston KM et qL: SpeeclLdeteroration n (myotto' phic lateral sclerosis: implcations for the tmng of intervention, J Med Speech-kng Pathol l:35, 1993
174
Yorkston KM et al: The relato,xshp belween sPeech an stvauowittg disorders in heatl injured patiettts, I Head Trauma Rehubil 4:1. 1989

D Clinical ndings E Acoustic and physiologic

V. Cases

findings

175, Young IvlC: Communication disorders

in

systemic

VI. Summary

lupus erythemutosLn, J Metl Speech-Lsn+ Pathol 4:141, I 966

We now tum our attention to a category of motor speech disorders (MSDs) rhat dilfers from the dysarthrias. Its designation, apraxia of speech (AOS), distinguishes it from the movement disorders represented by the dysarthrias, as well as fiom linguistically based speech eors associated with aphasia. The clinical manifestations of AOS ae believed to reflect a disturbance in the planning or prograrnming of movements for speech.

muscles for nonspeech tasks. Unlike aphasia, in which lhere are nearly always multimodality impairments of language, AOS can eKist independent of problems with verbal comprehensioo, readlng comprehension, and writing, as well as independent of verbal e(ors that are uffelated to articulation and prosody Although AOS often coexists with dysarthria and aphasia, the distinctiveness of its clinical characteristics, its apparent nature as a motor planning or programming disturbance, and its occasional emergenc-e as the only disturbance of communication justify its identification as a unique type o[ speech disorder. Its disrinction from other MSDs is additionally wananted becuse of its [ocalizing value; it is almost always the result of pathology in the left cerebral hemisphere. To repeat the simple definition provided in Chapter l, AOS is a neurologic speech disorder that reflects an impaired capaciy lo plan or program s?nsorimotor commands necessary

clinically apparent impairments in the

Unlikc the dysarthrias,,' AOS can exist withour

speech

for di.recttg movenlents that resuLt in phonetically and prosotlically normal speech. It
can occur in the absence of physi.ologic disturbances a.\.tocialed with the tlysttrthrias and in the absence o.f disturbance in any component of languoge.
*With the possible exception ofspeech-induced movement disorders, such as certain dystonia based hyperkinetc dysutlrias

]o7

308

The Disorders and Their Diagnoses

Chapter

Apraxia of Speech

309

AOS is encountered as the primary speech disorder in a large medical practice at a rate comparable to that of several of the major single dysarthria types. Based on dara tbr primary communication disorder diagnoses in the Mayo Clinic Speech Pathology practice. it accounts for I 6Va of all MSDs (see Figure l-3). It also occurs frequently as a secondary diagnosis in people with left (dominant) hemisphere lesions whose primary communication disorder is aphasia, and it can be a secondary diagnosis in pcople whose primary diagnosis is dysarthria or

lo lhem, there has in recent years been some honing ol the clinical boundaries of the disorder Rather than dwell too much on historic debate and controversy, an attempt is made here to focus on what at least
somc clinicians and researchers now propose may be the essential characteristics of AOS and how they

production oi temporally ordered sounds, syllables,

words, and phrases at particular |ates and pattems of stress and rhythm. The left hemispbere firnctions of the MSP seem to be more strongly tied to rhe linguistic attributes of speech (phonologic, semantic, syntactic, morphologic, plus linguistic components of prosody) than to its emotional or affective attributes, the latter components perhaps being rnore strongly influenced by contributions from the limbic system and right hemi-

8"r2r All of this permjts rapicl speech rates and greater allocation of resources to lhe mole conscious

tion

tbrmulation and monitoring of the cognitive and

linguistic goals o[communication This rapid, direct route for phonetic encoding may occur primarily for frequently used syllables, words, or phrases For novel syllables or movement pattems (e.g , infrequently or never-beforc-used multisyllabic or nonsense words), speaking under adverse conditions, or attempting to be particularly precise, it is likely that phonetic encoding is less direct (i.e , less automatic) because the motor patterns need to be freshly computed.i80 It has been suggested that at least some o1' the speech characteristics of people with AOS could reflect problems with the access to or use of preprogrammed subroutines and the subseqrLent need to

fit with notions

somc other neurologic communication disorder. Thus AOS is present in far more lha7 6Vo o[people
who have comnunication disorders associated with

leit hemisphere pathology

The cUnical features of AOS convey lhe impression that the appropriate message has been formulatcd but that what should be automatic "decisions" ahout its physical expression have been inefliciently or poorly organized or controlled, although not because of problems with basic motor abilities. Caretul study of AOS can illustrate some of the distinctions between motor speech planning/programming and the neuromuscular execution of speech, and between motor speech planning/programming and the formulation and organizaLion of the linguistic units that are spoken. Such study also hightights the dilficulty often encountered in attempts to make such distinctions, both theoretically and clinically The concept of AOS has had somewhat of a stormy history since Darleytu" introduced it in the 1960s and tied it to problems with the programming of rlovements for speech There bave been considerable and important debates about its very existence or its underlying nature * A fundamental problem has been uncertainty about its defining clinical attributes, with subsequent uncertainty about whether clinicians and researchers who claim to have studied the problem have actually been dealing with the same entity. This has introduced considerable "noise" into ef'tbrts to better understand the disorder's cognitive, motor, and anatomic bases. However, with renements in models of language and speech motor control and efTorts to fit careful clinical observations

about speech motor planning/ programming Wbat is presented here seems to make sense at this time Its staying power depends on future clinical and research efforts. In this chapter, the location and functions of the motor speech planning/programming network are summarized in broad, general terms. Some of the theoretical and clinical debate about the nature of AOS is reviewed but not dwelled upon Emphasis is placed on the clinical milieu in which AOS is encountered, its auditory and visible perceptual attributes, relevant acoustic and physiologic data, and sone clinical case studies. The distinctions between AOS and dysarthria and aphasia are addressed in some detail in Chapter 15, which
focuses on ililTerential diagnosis.

sphere. The linguistic input to the MSP comes largely from the left hemisphere's perisylvian area, which includes the temporoparietal cortex, posterior portions of the frontal lobe, the insula, and, in less definitive ways, the basal ganglia and lhalamus The anatomic proximity or overlap ol these language areas with those of the MSP makes it lkely that damage to the perisylvian language zone often results in a cooccunence of language-related deficits (aphasia) and AOS In clinical reality, this indeed is oiten the case.
When speech is the goal, it can be presumed that, once the phonologic representation of a message has been established, the MSP must be activated to organize and activate a plan for its motor execution. This seens to involve a tran.sformation of the ub.rtract phonemes to a neuraL code thal is compatibLe with the operatons of the notctr syslem-This neuromotor code presumably specifies lhe parameters of movement fbr specific muscles or muscle groups, although

construct programs anew

uttered (Ziegler, 2002;.to ttt 't"

for each syllable to

be

The Motor Speech [trogrannrner h{etworl<

The MSP seems to rely heavily on left hemisphere prefiontal, premotor areas- of which Broca's areu and the supplement(rtj motor area may be most important. BLoca's aLea is a candidate area for making important contlibutions to the specification of simultaneous and sequential speech movements based on input lrom sensory modalities and areas involved in linguistic formulation, Recal] also tht premotor areas are linked to the basal ganglia and

ffi

ANATOMY AND BAsC FI'NCTIONS OF T&{E MOTOR SPEECFI PROGRAMMER

Motor speech control involves the interactive, parallel, and sequential participation of all components of the motor speech system, as well as higher level activities related to conceptualization, language, and motor planning/programming. The motor planning/ programming component ol these activities is referred
to here as the motor speech programmer (MSP) The MSP is a network of interacting structurcs and pathways rather than a single anatomic structure.

McNeil, Robin, and Schmidts'? point out that '1he

exact parameters of movement rhat are programmed and that represent the contro variables for the motor programmer are not agreed upon." They suggest, howeve that specifications for movemen( duration and displacement (amplitude), acceleration, deceleration, lime to peak velocity, muscle stift'ness, and relative timing of speech events are examples o[ some of the kinematic parameters of movement that might be programmedBecause much of normal, mature speech is produced quickly and without conscious effort, it is reasonable lo assume thal the MSP commonly selects, sequences, activates, and controls preprogrammed

cerebellar control circuits that have reciprocal connections with the primary motor cortex lhat puts into effect the motor speech act Broca's area is often
identified as a lesion site in people wth AOS The supplementary motor area is also involved in the activities of the MSP, although it seems lurther removed than Broca's area from the actual specification of speech movements It has connections with the primary motor cortex and Broca's are, the basl ganglia. and the limbic system. It seems tied to cognitive and emotional processes that drive or motivate action and may play an important role in the initiation of propositional speech, as well as in its control. In general, however, it is not a common site of lesions associated with AOS The parietal Lobe somatosensotj cortex and fhe supramarginal gyrus are also implicated in the activities of the MSP, probably before initiation ol

It is influenced by sensory feedback, the basal

ganglia and cerebellar control circuits, thc reticular formation and thalamus, and the limbic system and righr hemisphere From this perspective, motor speech programming involves widespread areas of the central nervous system (CNS). Howeve( for the

*This history s raced with varying degrees of detail in a number of papers, chapters, and booksrts2s Comprehensive, citical (eviews that capture cu[ent thinking about the nature, clinical chactestics, and management of AOS can be found in McNeil, Robin, and Schmidt,? McNeil, Doyle, ud Wambaugh,so a 2001 Forum rn Aphasiology with a lead paper by Vrley and Whitesider2a and commentilies from several investigators, and numerous papers in a recent issue of Sminars in Speech and Language edired by McNeil '5

purpose of understanding the highest levels of speech programming-pathways and structures that specify the pattems and sequences ofmovements lor speech-the Lefi cerebral hemisphere, particularly parietal-frontal and related subcortical circuits, can be thought of as the headquarters of the MSP and the
locus of lesions that lead to AOS

movenlent sequencs+ that, through learning and

practice, can be activated automatically. It is thought that motor plans/programs are established before movement begins, but that they can be modified by

Functions of the Motor Speech Programmer The MSP has a leading role in establishing

peripheral feedback either belore the program is readicd for movement or during movement execu*Other tems that might apply include generalized motor programs; verbal motor memories; engrams; movement gestalts;
well-estblished subroutines; or "nacros-" to borow computer

'Cogent, comprehensive discussions of

planning/programming

motor

speech

the plans and programs for achieving the cognitive and linguistic goals of spoken messages. It organizes the the motor commands that ultimately result

in

teminology

and its relationship lo AOS can be founcl in several souces (McNeil, Robin, and Schmidt, 199?228088 r22 L2r fplus following comentily by several authors]: Ziegler, 2OO2),t\'1o

)rr0rlr'rr ,rltl Iltt'ir l)ratrrost's

Chapter

'l

Apraxia of Speech

nrovcnrcnt bul. oltviously, also duling series of rlovcrlrenls 'flrcse arcas may be particularly importirll in inlcgrating sensory infbrmation necessary for skrllcd rnotor ctivity and for transforming sensory rnlorllution rnd inlernal goals into plans and targets lor rction Hr Thc inszl" (Figure 2-16) also may have a specialized role in motor planning/programming lor specch, perhaps particularty during speech exeeLrtron " It reccntly has been identied as a shared sitc ol clarnage in people with AOSrr and sometimes the onlv site ol'damage,eo although AOS can occur u,ithout lesions in the insula.so Finally. Lhe basal ganglia, consistent with their l<nou,n rolc n motor control. seem active in the leti\ities oi the MSP Lesions of the left basal -unglir hrve been associated with AOS,erb although

Many patients have varying degrees of righr sided weakness and spasticity, and some have associated sensory deficits. A Babinski sign and
hyperactive stretch reRexes on the right side are also common A hyperactive gag reflex and pathologic oral reflexes (e.g., suck, snout, jaw jerk) are not commonly present unless there are bilateral upper motor neuron (UMN) lesions, a condition not required for the presence of AOS Patients with AOS sometimes, but by no means invariably, have limb ttpraxia (LA), a disorder also associated with left hemisphere pathology and characterized by deficits in the performance of purposive limb movements that cannot be explained by impairments of strength, mobility, sensation, or coordination LA usually aff'ects movements in both the right and left limbs. although it is ofien masked on the

ETIOTOGIES

thc disease.r'a' Nonverbal oral aDraxia (NVOAt also occus fre<uently in CBD,,snd its cooccur_ rence with AOS has been quite high
reports.a5

in

somc

Stroke is ilxe most conlmon cause ofAOS.Therc is nothing unique abour thc nature of rhe vascular

ilr lxln invar-iably ln gcneral, conclusions about the presumed

lnttonlv aud lunctions

of the MSP are supported by

clinical findrngs Thrt is, lesions that produce AOS arc usually located in the left posterior frontal lobe
pur ietui lobe, or in the insula or basal ganglia The srceeh characteristics of people said to have AOS are clistinguishable from those associated with the rir sarthris, and AOS can be evident in people whose speech rruscles perlorm normally for nonspeech irclilities and who are able to express language through nonspeech channels (e g , writing). Careful ribserr,ation and analysis of their speech suggests

or

right side by hemiparesis or hemiplegia LA has been more widely accepted in neurology as a distinct clinical entity than has AOS, in spite of approaches to is clinical diagnosis that have been higbly variable and subjective. The psychologic, physiologic, and anatomic bases of LA have been addressed
extensively in the neurologic literlture since before the early part of this century when Liepman68 prcsented his historically dominant and widely acceptcd conceptualization of apraxia A comprehensive review of LA is beyond thc scope of this chaprer.* From lhe theoretical stand point, it is noteworthy that there are important historical and conceptual similarities nd differences between notions of apraxia as it affects the limbs versus speech Anyone interested in in-depth study of AOS should be familiar with theoretical and clinical issues associated with LA. From the clinical standpoint, it is important to recognize that people with left hemisphere pathology may have difficulty organizing movements of both their right and left extremities, sometimes only on fonnal testing, but in some cases during activities of daily living Oi special relevance tbr issues related to communication, LA may interfere with writing as well as with

(or exc the

structures and pathways that plan and program movements for speech. Degenerative neurologic diseases, in general, are not commonly associated with AOS Even condi_ tions in which dysarrhria occurs frequentl such as

at matter) that and often are e,s network of

myoclonus, but other pyramittlrl signs can be evident.Tt Various dysarthria types hve not been well descri are rarcly unilateral, but a documcnt that CJD can announce itself focally as aphasil. Review of these reports suggests that at least sontc of the cases also had AOS. s chal'actcrprogression age impuir-

mos decl and

A few additionaI degenerative conditions deservc mention, because AOS can be prominent or among their presenting sjEns. Creutzf'eldt-Jd.kob diseu; (CJD), ongifurnt _also desig encephalopathy, is a untrcnt_ able, degenerative, in . Median age at onset is approximately 60 years, and death usually occurs within 6 months to several years Its

ical features include cognitivc

d (1
sometimes can bc their 6r.st sign. For example, although the general clinical literature on cr.ti_ cobasal degeneration (CBD)\ suggests that AOS occurs in less than 5Vo of repoiled cases,6 recent
studies that have carefully examined speech and lan_ guage suggest that it occurs in nealv 407o of cases and is sometimes the Rrst or mong t-hc firsr signs of

peri t) hemis
the

tions

th

""il31.:1
of the
lcl.r

asr lor 1r

tlrlt

lricc has come to be called AOS by clinicians and in\cstigators who recognize its distinctiveness, its vrluc in contribuling to our understanding ol the rcLrrology of speech and the localizarion of disease, ;rnd the unique demands it places on patients and cLinicians who tty to minimjze its effects on
romlnuntcatton

sornething is awry with the planning/ rroerarlrling of speech movements. This distur-

T]

NOhISI'EECFT, NONOROMOTOR, ANE}

NOhIL!NGUIs-TIC CHARACTERIST'E5 OF r,ATIENTS WiTFI APRAXEA OF SPEEEH

Physical speech mechanism findings, oromotor

hchaviors, and disorders of language that testify to the prcsence of dominant hemisphere pathology lrerlucntly accompany AOS. These characteristics ae discussed in the section on speech pathology later ir Lhis chapter. Several additional clinical findings cornnronly accompany AOS They usually reflect danlrge to the lefi fiontal or parietal lobe, or to left ruhcorticl pathways and structures associated with the direct and indirect activation pathways.

propositional nonverbal communication (such as pantomime and sign language).r This is an important consideration for people with severe AOS who may be in need of an augmentative or alternative form of
communication-

example oI an uncolntnon, plobable toxic-metbolic cause is the occureDce of AOS as part of promjncnt speech disorder that can emerge following ofhotopic Iiver tlansplantation It has been esrrmated that this speech disturbanc ppoximately lqo

*An

amyotrophic lateral sclerosis (ALS), CJD, cortico nigral degeneration, and, zheinrcr's disease- PPA deserves contcxt. because a significant prop id to havc
PPA may also have had AOS

at

o possibly, no rphasia

a'1ll.11

dug
rThe

of adults undergoing te procedure cyclosporin has been ssoc

cessation of the

speech.ru

improvement of

literature documents cases of MS with aphasia, and several

and among rhe nrs( symptoms in an addirional

?Overviews of theoretical and clinical assessment and diagnostic issues in limb apraxia can be found in a numbcr of sources For example, brief basic summaries can be found in Brooksbierr and Mesulan flMore cletailed reviews and discussion can be found n r DeRenzi,3 Duffy and Duffy,rt Ochipa md Gonzalez Rothi,ei Roy and Square Storer,es md Square Storer ud Roy r12 tAphasia also is related to difficulty in expressing proposional t"o or symbolic meanings througlr pantomirne and sign lungu"ge

cases and occurred

On examination, AOS was isolated in 9Z o[

7,,,1,.

rtrc

with aphasia or dysarthriu, or

Sce Bcn[eLt and Netsellr for a comprehensive discussion of the pr)ssible roes ol the insula in speech and Language

riSht greate than leli hemisphere) prietal lobe dysfrrnctrrrr and neuopsychiatric disoders associated with fronral krbc
dysfunction

*Examples of other asymeric cortical degenerative syndrorrrcs include perceptuomotor deficits associated wirh bilarerl (olic

312

fhe Disorders and Thelr Diagnoses

LnapLer tt

ApfaxtaorJpeecfr

)r)

bt| the AOS was the more prominent decit in 787o of those who also had aphasia and the more prominent deficir in 717o of those who also had dysarthria- Approximately two thirds of the cases received a nonspecific etiologic neurologic diagnosis such as PPA, progressive AOS, irsymmetric cortical degeneration, ot degenerative CNS disease However, 287a rcceived neurologic tliagnoses tied to conditions with prominent motor manitestations, including CBD (i170), CBD versus PSP (37o), and parkinsonism (6Vo). Of interest, because it is unexpected, 9o/o had ALS or motor neuron disease Thus there is accumulating evidence that AOS can be the first, the only, or the most prominent manit'estation of a degenerative neurologic disease When this is the case, the designation
botb. in the remaining 9lVo,

I fl lt-l t
Atferent motor aphasta Anarthria Aphema Apraxic dysarthra Artculatory dyspraxa Ataxic aphasa Broca's aphasia Cortical anarthria Codical dysadhria Efferenl motor aphasia Expressive aphasia Little Broca's aphasia Oral verbal apraxia E

Peripheral motor aphasa Phonematc aphasia Phonetic disintegration Primary verbal apraxia Pure motor aphasia Pure word mutism Secondary verbal apraxia Sensormotor impairment Speech apraxa Speech sound muteness Subcortcal motor aphasia Word muteness

ovefi recognition lo the existence of a molor speech planning/programming deficit.' They do, howeveq descnbe patienls' speech as slow. labored or effor[lul, "dysar1hric," reduced in phrase length, abnormal in prosody, and having poor "articulalory agility" These characteristics are consistent with those of speakers with AOS. If people with Broca's aphasia truly are a/so aphasic, then grammatical and syotactic errors and problems with word retrieval usually also characterize their speech It is reasonable to conclude that people with
Broca's or nonfluent aphasia often have an accompanying AOS. In fact, it has been argued that AOS may be an integral part of the syndrome of Broca's aphasia and that its presence may be required lor its diagno sis.78 However, AOS is not synonymous with Broca's

among people with left hemisphere lesions simply [eflect the blurred boundaries between disorders of language and motor planning/programming and between motor planning/programming and motor execution That is, one "type" of AOS might actually reflect a linguistic phonologic disorder such as that encountered in Wernicke's or conduction aphasia (or an aphasic phonologic disorder plus AOS), and another "type" a dysarthria (or an AOS plus dysarthria). If this is the case, then there may not be types of AOS, only AOS versus aphasia or dysartbria, or AOS plus aphasia or dysarthria. At this time, it thus seems inappropriate to subdivide AOS until the common features of the disorder are betler
delineated and understood

primrtry progre.t:ive AOS,

or

PPAOS'

seems

eppropriate.tt To summarize, AOS encountered in most clinical setlings is usually caused by stroke and sometimes by tumor or lrauma Although uncommon, lbe insidious development ofAOS in the absence of vascular disease, tauma, or tumor may be a presenling or prominent sign of several fbrms of degenerative CNS disease.

aphasia because the aphasic component of the syndrome includes deficits that are not explainable

At the same time, several theories suggest that breakdowns at differen! stages of motor

The debate about the nature of AOS bas lraditionally centered on whether or not it is distinguishable from aphasia The lrequent cooccurrence of aphasia with AOS and the overlap of anatomic
regions that are crucial to language and motor speech planning/programming help drive thts uncertainty. However, there does seem to be general agreement that ( 1) at least some ol the speech sound abnormali-

by AOS. They also are not synonymous because AOS can occur without any manifestations of aphasia Are aLl sounl LeveL errors made by ophasit patients manit'estations of AOS? Again, the answer

is no, but with qualifications This question is motivated by the presence of sound level errors in people

with Wernicke's and conduction aphasia' Their

speech, by definition, is usually perceived as fluent,

SfrEEcFl qrA-rF{OLOGV

Terrninology and Theory

Someone once said, "When krowledge is lacking, a name comes to take its place " Different beliefi about the clinical chacteristics and nature of AOS, efforts to achieve compalibility with embraced models of language, ego, nationalism, and the poli-

ties of some aphasic patients are attributable to

molor planning/ptogramming rather than linguistic/ phonologic decits, and that (2) a disorder of speech motor planning/programming can result from left cerebral lesions that may or may not also cause difficulties with language. Tbe support for these conclusions comes from studies of people with AOS but normal language in nonspeech modalities, careful clinical perceptual descriptions, and acoustic and physiologic studies, sometimes with compar-

tics of academra and medicine have all probably contributed to the abundance of terms that have been applied to the disorder Some ol the terms summarized in Box I1-1 are rarely encountered in clinical

easily produced, and prosodically normal. Many of their sound substitutions, omissions, and addiions probably reflect problerns at the phonologic level of language. That is, their erlors mosl likely represent inadequate selection or ordering of phonologic units, but with subsequent adequate planningi programming of rhem tbr execution by the MSP. Ease of production and normal prosody appear to be major clues to distinguishing aphasic phonologic errors from those attributable to AOS, although some

planning/programming may lead to different types of apraxia For example, Rosenbek, Kent, and LaPointee6 stated, ". we might imagine erors in planning to be distinct from erroLs in serial ordering, whrch in turn could be distinct from ertors in execution or implementation " Square-storer and Roylrt stated " several subtypes of apraxia of speech may exist in that several cortical and subcortical sites appear responsible for the programming of spatial and temporal information requisite for normal motor speech production." More recently, on the basis of
models postulating that normal speech encoding can

be accomplished through different routes (distinct

mechanisms, or strxctures and pathways), it bas been suggested that AOS may include a spectrum of disorders in which, for example, different routes might be impaired independentiy of each other, with subsequent dirtinctire speech churacteristics tied Lo each l2o The incrcasing sophistication ol damaged roule.ll models of speech planningiprogramming and clarification oi their distinction from models of phonologic processing should permit testing of these predictions in people with AOS. If different breakdown patterns are identified, and particularly if they are pe(ceptually salient, then clinically useful subtypes of AOS may be recognized At this time, the greatest practical clinical diagnostic challenge relates to the fact that AOS tiequently occurs simultaneously with dysarthria and, especially, aphasia. As a result, clinicians and reserchers struggle frequently with the interpretation of abnormalities as apraxic versus aphasic or dysarthric. Clinical distinctions between AOS and

people with Wemicke's and conduction apbasia

make detectable phoneticJevel errors.t* Differences, theefore, may be ones of degree, \ryith motor level defrcits predominating in speakers with AOS (and Broca's or nonfluent aphasia), and phonologic deficits, when they are present, predominating in Wernicke's, conduction, and other fluent aphasias Are there subtypes of AOS?' We do not know It may be that different patterns of speech distulbance
*Representative procedurcs tbr jdentitying Broca's aphasia ae included in frequently used tests of aphasia, such as the Borlo, Diagnostic Aphasia Examinatioto and the Wee APhasia

practice today; they survive only as vehicles for

tracing the history of the disorder. A number of labels are still used in addition to AOS. The most cornmon are speech apraxia and otal verbal apraxia, Broca's aphasia, aphemia, and aphasic phonologic impairrnenf Speech apraxia, oral verbaL apraxia, and,

probabll,, aphemia* are synonymous with AOS.

Broca's aphasia usually includes, but encompasses more than, AOS Aphasic phonologic impairment may be confused with, but ls different than, AOS.

isons to aphasic and dysarthric speakers * It is beyond the scope of this chapter to review the details of the literature on the nalure ofAOS, particularly its distinction from aphasia Some basic questions that frequently arise in clinical practice that reflect this debate should be addressed, however, because they bear on differential diagnosis and the use of terminology in clinical practice Fits, s the term AOS sytxonymous with Broca's or nonfuent aphasia? The answer is no Most definitions of Broca's and nonfluent aphasia do not give
+tt is of inlerest lhat questions also have arisen about e distinction between AOS and dysdhria, a distinction that may be as difficult in some respects as that between AOS and aphasia.tesr't6 Perceptual, acoustic, and physiotogic compuisons between AOS and the dysrthr-ias (particully ataxic and unilateral UMN dysuthrias) are necessuy to sort out these distincons witLt
greater cluity

Baltetl.6r
+For example, Fox et al 13 rcpofed a case with aphemia with a small stoke in the lefl precentral gyrus with underculting of tnotor and premotor cortex There was no aphasia in any modality The description of speech chuacleristics was similil to those associ ated with AOS The authos concluded: "Ou patienL's speech apraxia durlng recovery suggests that apbemia c4 present as a
severe

iThis is an important issue, because "it is likely that the majority of the liteature on AOS, and on phonemic paraphasias as well, is seriously confounded by the observtion and quandncation of behaviors implicating both praxis and phonologic mechanisms "80

aphasia and between AOS and dysarthria are addressed in Chapter 15, which covers differential
diagnosis.

iDiscussion of this issue cd

sources

be foutld in

seveal

form of apruia of speech

"

314

The Disorders and Their Diagnoses

Chapter

1.1 Apraxia of

Speech

Il5

frontal lobe. One lefthanded pafient had a right frontal lobe tumor resection and was also aphasic
Degeneratve Traumatc 15%

Vascular (49%) Single left hemisphere stroke (41%) Multple strokes, including left hemisphere (8%) Degeneratve (26%) Unspecified degenerative CNS disease (10%) PPA or AOS, or both (7%) Alzheimer's disease or dementia (3%) CBD

postoperatively; he likely had right hemisphere dominance for speech and language A few patients had sustained a closed head injury (CHI), further establishing that focal motor speech disturbances can result from such traumaFour percent of the patients had a left hemisphere tumor, all including the frontal lobe. In thee of these patients, AOS was among the initial neurologic signs. In one patient, AOS was the only clinically apparent evidence of neurologic disease, the tumor being identified on subsequent computed tomogra-

made,'72Vo had evidence of aphasia. Thus it appear.s that for those in whom AOS is the most promincnl speech or language disturbance, accompanying aphasia is often, but not always, present. Although this percentage also suggests that AOS can occur independent of language disturbance, it is inappropriate to conclude fhat287o of all people with AOS have no aphasia. That is, the sample did not includc patients with AOS in whom aphasia was the primary speech-language disturbance.

How often was dysarthria present? Among thc

155 patients for whom observations about dysarthria were made, dysarthria was present in 297o. As was the case for aphasia, this figure probably underestimates the percentage of people with AOS who also

phy (CT)

scan.

Other: asymmetric cortical degeneration; CBD; ALS:

vs

PSP; CJD; leukoencephalopathy

(7%)

Vascular 49%

Several patients had AOS as the only evidence of neurologic disease, leaving the etiologic diagnosis undetermined. The remaining patients had AOS in association with seizures, liver transplantation, or a combination of disorders.

have dysarthria because the sample did not include patients with AOS in whom dysarthria was

the primary speech-language disturbance. When dysarthria type was specified, it was usually unilateral UMN (UUMN) or spastic in type. The lairly
frequent cooccunence ofAOS and dysarthria is con sistent with the proximity of crucial speech motor

Traumatic (15%)

Tumor resecton, aneurysm or AVM repair, hemorrhage evacuation cHr (1%) Tumor (Left Hemisphere) (4%)

FIGURE 11-1 Distribution of ctologics for t55 quasitandomly seLected cases with a primily speech pathobgy diag nosis of apraxia of spccch at the Mayo Clinic from 1969 1990

Lesions

0ther (6%)
AOS of undetermined etology (3%) causes (2%)
S, Amyotrophtc lateral sclerosis: AOS, apraxa of speech; AyM corticobasal degeneration; CH,' 'rnvenoils maltormation: CBD, closed head iniury CJD, creutzfeldt-Jakob disease; CNS' cenlral neryous system; PP,4, primary progressive aphasia; PSe

Other: seizure disorder; post liver transPlant; multiple

but somewhat similar lo those fbr spastic and unilateral UIVIN dysafhria. Approximately half of the cases were accounted for by strokes alone, and 907 ol the cases were accounted for by stroke, degener-

rtive. and traumatic etiologies.

Single strokes in the left hemisphere bral artery distribution accounted for mo cular causes. This is consistent with the of stroke as an etiology of focal neurologic signs and the localization ol crucial speech planning/ programming functions in the left hemisphere- The i".iind". of the vascula cases had multiple strokes in which at Ieast one o[ the lesions was in the left

The localization of left hemisphere strol(e for people who had CT scans or magnetic resonance imaging (MRI) that identied a lesion was generally consistent with notions about lesion localization in AOS. The fontal lobe was most frequently included in the lesion distribution, though not much more often than the parietal lobe. Wben only a single lobe was implicated, it was most often the frontal lobe, The temporal lobe was sometimes involved but never alone. The lesion was confined to subcortical structures in some cases.

planning/prograrnming structures and pathways to

cortical and subcortical components ofthe direct and

indirect activation pathways. UUMN dysarthria is the expected dysarthria on this basis, with spastic dysarthria usually occurring in those with lesions in mol than just the left hemisphere. How often was AOS the only neurologic communication disorder (i.e., no dysarthria, aphasia, or
nonaphasic cognitive-communication
defi cits)? Data

progressive supranuclear PalsY.

Associoted Deficits"

Associated Deficits in Clinical Practice

Etiologies

Distribution of Etiologies, l-esions, and

Box 11-2 and Figur

rcent had an unsPecified

x Percent of the

cases were
de

AOS was among the initial symptorns of neurologic disease in a significant majority of the patients. This is not surprising because of the high proportion of vascular etiologies in which speechlanguage and motor and sensory deficits usually are present
together at onset

for 155 quasirando

Mayo Clinic with a nosis of AOS.* The
about generalizing these findings to the general population or all speech Pathology practices apply here
as

PPAOS. The remaining cases had Alzheimer's disease. a similar dementing condition, or other conal or asymmetnc ditions that

. Seven Percent had a diagno

or

How often was NVOA present? Among 107 patients for whom relevant data were sought, 6370 of
those

for whom observations about NVOA

were

regarding this were most confidently derived from among the 48 most recently seen of the 155 patients Among them, AOS was the only apparent communication disorder in four patients, or 8.3% Of interest, degenerative disease was the etiology in three ol the four, raising the possibility that "pure" AOS may be more cornmon in degenerative disease than it is in stroke or trauma. It is important to recognize that fhe 8.3Vo figure almost certainly inflates the overall frequency of isolated AOS, because the data arc derived only from patlents in whom AOS was thc primary communication disorder. If all cases witlr AOS were examined (i.e., including those in whonr aphasia or dysarthria were more prominent), this figure. by definition, would have to be lower, prob
ably considerably lower.

well.

(e CBD, CJD)
findings

degeneration, as the only or the

al

of the disorder. Thus consistent with the llterature, there was a frequent but not
made had evidence

The data establish that AOS can result from

initial sign of disease, or it was among the most sig-

number

of medical conditions' the distribution of

which is quite dilferent lrom several dysarthria types

*The distbution of ettoLogies repoed here is Seneralty consrs tent with that reponorl by Wertz' Rosenbek, and Deal'sr28 analysis of ctiologies in a group of 176 adults wilh AOS

nificant deficits at the time ol diagnosis. This illushates that some degenerative neurologic diseases can present as focal disturbances and that AOS can be the rst sign of a slowly progressive degenerative
neurologic disease. Surgical trauma was the etiology in 157o of th^e -[n most instances, surgery involved the left

invaiable cooccurrence of AOS and NVOA. How often was aphasia present? Among the 155 patients for whom observations about aphasia were
*In

Patient Perceptions and Complants

When AOS occurs without aphasia, individuals often say something like "my speech won't come out righL I krow the words I want to say, but they won't come out the right way." Phrases such as "not as fluent as before" and words like "mispronounce" are common descriptors. Complaints nearly always center on articulation and rate and rarely on breathing, phona-

comprehensive review of the literatue, McNeil, Doyle, and found that 4870 to 857o of those wth AOS also had NVOA, an average of 8l7o also had aphasia, and 29Vo to 4'l% also had dysethria
a

Wambaughso

"u..r.

Chapter

'1

Apraxia of Speech

317

tion, or resonnce When AOS is mild, patienrs sometimes note being surprised by enors that intrude into an otherwise fluent narrative Others report having to speak slowly or carefully in order to
prevent eftors. Some predict errors on difficult-topronounce muttisyllabic words, and many recognize
errors when they occur and attempt to correct them. The word "stutter" is used occasionally to describe associated dysfluencies, groping for articulatory postures, and attempts at effor con'ection. Many patients say the problem worsens under conditions of stress or fatigue.

Nonverbol Oral Aproxia A substantial proportion of people with AOS exhibit NVOA,' NVOA is an inability to imitate or follow

$E
Varable Lmb

Common limb, nonverbal oral, other speech-language deficits, and patient complaints associated with A0SFindnqs Right hemiparesis or assocated sensory deficits, or both Babinski sign Hyperactive stretch ref lexes Lmb apraxia, usually bilateral Right lower face weakness Rght lngu3l weakness Nonverbal oral apraxa Oral sensory deficits Aphasa, most often Broca's aphasia when aphasia can be categorized Unilateral Ul\ilN dysarthria "Speech doesn't come out rght" l\ispronuncation Stuttering Must speak slowly to prevent erfors

on adequate auditory f'eedback to speak as well

as

commands

movements of speech structures (e.g,, cough, blow. click tongue)

that cannot be attributed to poor task comprehension

to perlbrm volitional

they do. It is reasonable to conclude that AOS can exist in the absence of auditoly processing difficulties, bur. because AOS usually occurs with aphasia, auditory

Those with isolated AOS do not complain of chewing, swallowing, or drooling difficulties. If such problems are present, they should raise concerns about neuromuscular deficits and an accompanying dysarthria. Patients also deny difficulties with verbal comprehension, reading comprehension, and the
tingurstic aspects of writing Because AOS frequently occurs simultaneously with aphasia, however, all people with su,spected AOS should be considered aphasic until comprehensive longuage assessmenl
prove.s othetwte

or sensory or neuromuscular deficits The lesions leading to it are in the left hemisphere and tend to inciude the fiontal and central (rolandic) opercula, anterior paraventricular white matter, adjacent portions of the first temporal convolution, anterior porrion of the insula, or parietal lobe.'r'8
Commonly used tasks

processing decits are oftcn present in aprlxic speakers Their presence, howeve is not likely to be causally related to their AOS, although such deficirs might serve to exacerbate it
Speech

Nonvefbal

Oral

for

detecting NVOA
Language & other Speech Deficts

include imitating or following commands to cough, click the tongue, smack the lips, blow, or whistle (see Box 3-1, Chapter 3, for a list of tasks and suggestions for evaluating NVOA) " People with NVOA attempt to lespond bul do so awkwardly or with off-target responses, effortful groping for conect movements, or inconsislent trial-and-error attempts.
Sometimes while

Tasks placing demands on the sequencing of various sounds and syllables with varying pattems of stress

are most likely to elicit the salient and distinguishing leatures of AOS Conversational and nnative speech and reading can be revealing tbr this purpose.

Patient

Complaints

if language and reading skrlls ure relatively good and the patient can give more than brief and unelrborated conversational or narratvc
particularly
responses.

trying to perform the act,

they

simultaneously say the command. For example, asked to cougb, a patient may say "cough" and simultaneously attempt to cough Patients usually
are perplexed, frustrated, atnused, or embarrassed by these otT-target responses and otten try to correct

E
with AOS

AOS, Apraxia of speech; UM, upper molor neuron

'None of these deficits/complaints are tnvariably present in people

Imitative tasks assist the clinical hunt for AOS. because they can contain stimuli that challenge speech planning/programming abilities and because

(linical Findings
Nonverbol Orol Mechonism

they circumvent demands on word retrieval

and

lf dysarthria is not presenl, the gag rellex and chewing and swallowing functions may be entirely
normal, and there may be no pathologic oral reflexes. There need not be any right central lingual or facial

weakness However, it is often the case that the causative lesion is large enough to have damaged corticobulbar pathways It is thus common to find a right central facial weakess and sometimes right

lingual weakness. A UUMN dysarthria may be present and related to such weakness. Any speech deficits attributed to unilateral face or tongue weakness are part of the dysarthria and not the AOS,
however.

themselves but with inconsistent success. Many patients may later cough reflexively, lick their lips, or blow out air in an exhausted sigh alter failing to perform the same act on initation or command People with suspected AOS should always be assessed for NVOA becausc its presence is a sign oi left hemisphere pathology, noI because it has a necessary causal relationship with AOS Although AOS and NVOA frequently occur simultaneously, they can be dissociated. The fact that they can occur independently argues against the notion that AOS is simply a reflection of a ntore fundamental disturbance of nonverbal oral movement, at least in some
patrents

Auditory Processing

Skills

There is general consensus that auditory deficits are not present in people with purc AOS and that when they are present in those with AOS and aphasia they do not explain speech errors that are considered apraxic in nature These conclusions are based on a number of studies of apraxic speakers that have demonstrated adequate perception ol stimuli to be produced and, at the least. auditory skills that were superior to speech production skills. In one of the most thorough and convincing investigations of this issue, Square-Store Darley, ancl Sommersrr0 con-

other aspects of language formulation This is important, because aphasia can make assessment of motor speech difficult; it can mask or be difficult to distinguish fiom AOS Speech sequential motion rates (SNIRs). and imitation oicomplex multisyllabic words and sentences

are among the structured tasks most sensitive k) AOS. It is not unusual for suspicion of AOS generated during conversation and simple language tasl<s to blossom into an unequivocal diagnosis after observing attempts to sequence SMRs and repelr
words and sentences like "catastrophe," "statistical

Because motor planning/programming

control is a sensorimotor process, it ask if oral sensation (e g., oral form identiflcation, two-point orl discrimination, mandibular kinesthetic abilities) is impaired A f'ew studies have
addressed this issue, some deficits and a relationship to s others failing to find such defi

and is reasonable to

Limb, nonverbal oral, other

speech-language

cluded that auditory processing abilities can

be

deficits, and patient complaints that may accompany AOS are summarized in Table I I - l.
,Other f'requently used tems that are roughly synonymous with NVOA include oraL nonvebctl apraxia, buccofacaL apruict, linguol apraxia, oral aprua, andJbciaL apruio.

normal in AOS, and that AOS and aphasia are distinguishable deficits from both motor speech and auditory processing perspectives.

analysis," and "the municipal judge sentenced the criminal." This does not mean that speakers with AOS have disproportionate difficulty with repetirion (in fact, imitation can be superior to spontaneous speech in some respects). It simply means that imtation tasks can be specifically designed to elicit the chacteristics of AOS more efficiently than spontaneous speech sampling

It does appear that apraxic speakers are susceptible to the effects of disrupted auditory feedback,
however. For example, delayed auditory feedback (DAF) severely disrupted speech in those with
Broca's aphasia, more so than n speakers with any other aphasia type.'t This effect does not necessarily argue for a causal role for disrupted auditory feedback in AOS, however. That is, it may be that the output decit (in AOS) "is so fragile that any perturbation of the articulatory system seriously affects rhe quality oI their output."rs It mighL be argued that apraxic speakers are particularly reliant

Wertz, LaPointe, and Rosenb their review of such studies that some people with AOS have oral sensory deficits that may or may not be related to AOS severity In general, the available data do not support a primary causative role of oral sensory deficits in AOS Testing for such deficits is
not necessary to diagnose AOS

'Volitional coughing, blowing, and whistling are among the most difficult simple tasks, becuse they require coodination of the

The challenging tasks just described are not always useful for people with marked or severe AOS. For such patients it is more valuable to discover what they are able to do and to contrast that
*Apraxic speakers have relative prescrvation of speech AMRs, at least when their impairment does not preclude the bility to produce a single syllable accuately As a group, thei AMRs ue somcwhat slower than nomal but faster tlm for several groups of dysarthric speakers (due to stroke, CHI, and cerebellar disease), although not those with Pakinson's disease-'r'

breath strearn, laryngeal activity, and oral movements Sequences of nonverbal oral motot movements (e g, click teeth together nd then pucker the lips) are moe difficrtlt than single
5e

discrete movements,usto but performance can be confounded by verbal comprehension deficits on commnded tasks or by shor-ttem retention difficulties on imitation tmks

318

The Disorders and Their Diagnoses proposed a list of features that seem to dist.inguish AOS from aphasic phonemic paraphasias. The validity of many of the salient speech cbaracteristics summarized in Box ll-3 is supported by the results of acoustic and physiologic studies and perceptual studies using narrow phonetic transcription.'* Narrow pbonetic transcription has highlighted the presence of vowel errors and the relative pervasiveness of distortions, helping to establish that what are perceived as substitutionst may be the result of, or at least accompanied by, motor/pbonetic level distortions For example, it appears that apraxic speakers produce more consonant distortions than substitutions and that half ol their perceived substitutions are also perceived as distortions.e2 This is why many of the substitution, addition, and prolongation characteristics listed in Box 11-3 ale characterized as distorted The pervasiveness of distortions among the artic-

Chapter

Apraxia of Speech

tions, or omissions, whereas rale and prosody arc

11-3
Articulaton
Consonant and vowel dstortons (imprecise articulation), with consonant distortions usually predominating Distorted substtutions Distorted pefseveralive substilutons (e 9., "nanana"/ banana) Dstorted anticPatory substtutions (e-9, "popado"/potato) Distorted additons Distorted sound Prolongations Distorted vocing dstinctons (bluring of voiced-voiceless boundaries) Belatively consstent tral tral articulatory enor locaton Relatvely consistent ltial-trial error type Rate and Prosody Altered stress occasionally leads to perception of foreign accent in monolingual sPeakersr Fluency Successful or unsuccessful attempts to self-correct articulatory errors that cross phonemic boundaries False articulatory starts and restarts Effortful visible and audible trial-and-error groping for artculatory postures Sound and syllable rePetitions

usually normal within phonemically on-targct

ities of AOS, considered alone, are similar to thosc in some dysarthria types, such as ataxic, spastic, iln(l unilateral UMN. several possible explanations, including: (l) thcy could represent a fundamental feature of AOS, (2)
they could be a by-product of a fundamental problcnr with articulation (e.g., how could rate and prosody

The rate and prosodic abnormalities in AOS

hLrvc

Slow

overall especiallY length

rate regardless of phonemic accuracy, for utterances more than one syllable n

lnfluential Task Variables Error rates higher for voltonal/purposetul versus automatic/reactive utterances, but automatic/reactive utterances often not perceptually normal Speech S[/]Rs more lkely to be abnormal n phonemic accuracy and rate than Al\,4Rs Error rates hgher for nonsense'syllables/words than
meanngful words

Prolonged but variable vowel duration n multsyllabc words or words in sentences Prolonged but variable nteruord intervals regaldless of
phonemic accuracY Syllable segregation Errors of stress assgnment, wth a tendency to equalze stress across syllables/words Decreased phonemic accuracy as rate increases

Consonant clusters errors more frequent than singleton errors lntation of utterances particularly difficult Errors occur on both lmitative and spontaneous speech
tasks

ulatory characteristics listed in Box ll-3 hetps distinguish the substitutions, additions, and prolongations associated with AOS from the phonologic errors (phonemic paraphasias) tbat can occur
in aphasia; that is, aphasic phonologic substitutions, additions, and prolongations are not perceptually

lmitation errors generally do not exceed spontaneous

speech errors on comparable productions

AMFS Alternate motion rales; SMFS' sequental motlon rates (e g, imprecise articulaton, slow rate' distorted voicng dstinctions) and ^A number of these characteristics oa"u, in.oa" dysarthria types of several characteristics' as well as the aphasa (e g , attempts to self-coect errors, articulaiory groping) lt is otten the clustering fhesedistnclons

distorted. [n contrast, articulatory distortions are not helpful in distinguishing AOS from dysarthria, although other characteristics are: that is, dysarthria is rarely associated with additions or substitutions The rate and prosodic abnormalities lrsted in Box ll-3 are pervasive problems in AOS'and are prob-

possibly be normal in the context of the disordcr's characteristic articulatory deficits?), or (3) they coultl reflect efforts at compensation for a fundamentul deficit in articulation It is probable that all thrcc explanations are valid for many ptients, but it is important to recognize thaf accumukting evidentt suggests that rate and prosodic disturbances ure n defning feanre of AOS'2 and not simply (only) secondary to articulation errors or a by-product oicorn pensatory efforts. This is illustrated by the clinical observation that some apraxic speakers who report that they slow their rate to mainlain accuracy oftcn fail to normalize their rate when instructed to do s0 regardless of errors. Admittedly, howeveq accuracy often suffers when rate can be increased (see Box

absenceolotherabnormatities,lhalnetpsiientityspeecanoimalitiesasapraxic,asopposedtodysarthrcoraphasc
are addressed n Chapter 1 5. rsee Chapter 13 for a more complete descriplon and dscussion of pseudoloregn accenl

ably more important than articulatory errors

in

distinguishing AOS from phonemic paraphasiasThat is, abnormalities of rate and prosody are nearly a.lways present in apraxic speakers, even ibr utterances that are free of perceived substitutions, addiiNmow
phonetic lnscription is not the only perceptul method

1l-3). The abnormal fluency" characteristics associatccl with AOS may be evident in many patients, but thcy may also be present in aphasic patients who mtkc phonologic errors,i thus reducing their value in diitinguishing AOS from aphasia. Nonetheless, with thc
possible exception of hypokinetic dysarthria, lluency abnormalities frequenrly observed in apraxic speukers are uncommon in dysarthric speakers, so they tkr help distinguish AOS t-rom dysarthria or recognizc AOS when it occurs simultaneously with dysarthria Neurologic fluency disorders are discussed in morc detail in Chapter l3 Apraxic speech perforrnance can be influenced by a numberoffactors (see Box ll-3), although aphasic speakers are susceptible to many of the same inRuences. Again, however, such factors are not usually active for dysarthric speakers For example, AOS

witb the nature of the tasks in which performance is

SMRs or even attempt to imitate multisyllabic words is more adequately able (although often not normally) to count, imitate simple consonant-vowelconsonant (CVC) syllables, sing a Familiar tune, and produce spee AMRs because they are highly overlearned, can produced "automatically," ol place minimal or different demands on planning/programming abitities. From this standpoint, examination reflects a search for the threshold at which Patients succeed and fail on (asks reflecting a concinuum of speech planning/programming demands. For some, te theshold is bigh and tasks should be difficult; for

fitr
3.)

Atlults [ABA-2]23 was also discussed in Chapter

Modern descriptions of the perceptual characteristics of AOS were bom with Darley's clinical observations in the late 1960s'?5'z6 and an influential study by Johns and Darley."58 Since then, the features considered salient to the cl inical identification of the disorder have evolved as a product of careful research, refrnements in the definition of AOS, and the influ-

for infemng motor-level problems in AOS For exanrp)e, a less direct phonologic process analysis of apraxic speakels wjth
Broca's aphasia tailed to reveal evidcnce of phonologic impair-

ment aud identified pttems of enors (e g-, prevocalic and postvocalic devoicing) that suggested a motor/phonetic Level
impaiment.sT

ence

of models of phonology and motor

planning/programming on the setting of ior the disorder. The salient perceptual chaacteristics described in Box l1-3 reflect these developments' the author's cllnical experience, and the influence ol recent papers by Mceil and colleagues8os2 that have

speech boundaies

othels, the threshold is

simple any st
respon

low and tasks should be

interest in AOS should read at least "Those with a serious research scveral ofthe historic. theoretic, or clinical overviews ofAOS that Ia33nt)q2a6r7 have been published over the pasl few decades

This may reflect our comon "desire" as listeners to perceive meaningful units and ignoe signal noise (i e , distortiond), as well our being primed to look only for phonologic enors by mmy perceptual studies of AOS tlat used broad transcription and linguistic phonologic process malyses that were not sensitive to distonions Another possibility is rhat some studies that have influenced our thinking may actually have included subjects who had no distolions and were, by today's delinition of AOS, not aPrxic but rather aphasic and mahing phonologic enors
as

'.The use of the tem]fuency in this chapter refers to intemptions speech, such as silent or audible sound syllable repetiuon and prolongaon (dyslluencies), or groping lor

in the nomal flow of

rThe

prosodic abnormalities have functonal consequences For

articulatory manner or position It is not used here to ret'er lo abnomalities that are manifestations of language impairncnL, such as reduced phrase length or agrammatism, chaacteristics that are often associated with so-called nonfluent aphasia

list of
assessing AOS. A published test, the Aprdxia Battery

exmple, it has been shown that listene$ have difficulty idenifying different emotions expressed by apruic spealers through variations in L, duration. md amplitude r'1l

'For examplc, it has been suggested that the notion of efforllul tial and eror groping as a necessary or differential feature (rehve to aphasia) of AOS hs not been cletrly establjshed
s'?

32O

The Disorders and Their Diagnoses

LrrdPrrr

rr

APtd^rd ut JPrsLr

speakers usually have more difficulty with speech

SMRs than AMRs, whereas dysarthric speakers

pe|lbrm about the same on both tasks (or sometimes

istics depart from those described for less severe fbrms The summary is strongly influenced by the
astute observations by Rosenbek,es who pointed out that speech in severe AOS can be limited to a few meaningful or meaningless utterances on imitation. reading, or spontaneous speech tasks. Even attempts to imitate isolated sounds may be in error and the

Summory

even better on SMRs than AMRs!). Volitional/

propositional utterances generate more abnormalities than automatic/reactive utterances, although the latter ofien are not entirely normal; dysarthric
speakers show no such distinctions

What leatures ol AOS help distinguish it from the dysarthrias? Among all of the speech abnormalities that may be detected, distorted sound substitutions and additions, segregation of syllables in multisyllabic utterances, decreased phonemic accuracy with
increased rate, attempts to correct articulatory errors

types

of error

responses

limited When phonetic

Not alt people with AOS display all of the characteristics summarized in Box ll-3, just as not all people with specic dysarthria types have all of the characteristics that bave been reported for their type ol dysarthria The reasons for this are not entirely clear. They probably include natural varrability within the disorder, the possible existence of subtypes ofAOS, various contaminating effects of concomitant aphasia, variability associated with degree ol impairment, or variable methods of description.
Severe Aproxia

of

Speech

repertoire is limited, errors may not approximate the target unless the target happens to resembie sounds or syllables in the repertoire. Automatic speech may not be noticeably better than volitional speech (e.g., a severely impaired patient might produce, slowly and with distortions, "dun, doo, dee, daw, digh," when attempting to count from one tq ve). Singing a lamilia tune may contain the conect number of syllables, with a reasonable approximation of the tune, but contain only a few distorted consonants and a few vowels (e.g., "apee turdee too doo"/"Happy birthday to you"). When only a ew different sounds can be produced, enors are highly predictable, some-

that cross phonemic boundaries, groping for articulatory postures, greater difficulty on volitional versus automatic speech tasks, and greater dilficulty on SMR and multisyllabic word tasks versus AMR and single syllable tasks are the most common distinctive clues to the presence of the disorder. In general,

it is

usually the clustering

of

several

of

these

characteristics lhal help distinguish AOS from he various dysarthria types. What features of AOS help distinguish it from

of voicing before the release of the stop), simultaneous voice onset and stop release, or voice lag (onset of voicing within approximately 20 milliseoonds after the stop release) Voice lag of 40 ms or more characterizes voiceless stops. VOT has been used as an acoustic measure of coordination in studies oI AOS, because it reflects relative timing between supralaryngeal articulators (e.g., the lips and tongue) and respiratory-laryngeal events that are essential to signaling voicing distinctions VOT measures have provided valuable insights about motor programming versus phonologic decits in people with AOS Several studies of apraxic speakers indicate considerable overlap in the distributiot't of VOT valttes lbr voiced and voiceless s/ops. VOT values may fall
onset

in a

People with mild to moderate AOS probably dominate the database from which much of our clinical descriptions of the disorder are based. Unfortunately, there has been little systematic study of marked to severe (hereafter called severe) AOS. This is probably because people with severe AOS tend to have signifrcant and often severe aphasia that contaminates its study. This is unfortunate because severe

times giving the impression that the patient

phonemic paraphasias associated with aphasia? Among all of the speech abnormalities that may be detected, articulato ry disto rt ions, re lalive ly con.s is tent trial-trial phonemic error Localiott and type,
slow rce, proLonged interword interval,s and sylkrble segregation, and equalized stress-and errors in
stress assi|nmet?/ are the most common distinctive clues to the presence of the disorder. Again, it is usually the clustering of several of these characteristics that best help distinguish AOS from aphasic phonologic errors. Distinctions among the speech leatures of AOS, the dysarthrias, and aphasic pbonologic elrors are discussed further in Chapter 15.

runge between normal voiced and voiceless values (i.e, between 25 and 40 ms), and have greater than normal variability even when stop pro-

has

ductions are perceived as accurate. These abnormaliies have also been documented for initial voiced and voiceless fricatives.2 Although apraxic speakers

AOS probably occurs much more frequently than

generally milder pure AOS. It is additionally unfortunate, because the characteristics of severe AOS may not reflectjust a greater magnitude of the chaacteristics that define milder ftrrms Box 1l-4 summarizes the speech characteristics of people with severe AOS whose speech character-

!""

actually "lost" the representations of movements that generate sounds from Lheir motor repertoire. The severity continuum for AOS extends to muteness. Most clinicians agree that the inability to phonate (apraxia of phonation) in pure AOS is an early and transient problem, usually resolving within a few days, at least when the lesion is confined to Broca's area.se lt is rare for muteness due to AOS alone to last for more than 2 weeks. In fact, a gratifying aspect of clinical practice is eliciting the first utterances n a mute apraxic patient a few days after a stroke by having him or her count or sing a familiar tune with clinician cuing Persistence of AOS mutism for more than a few weeks should raise suspicions about a different diagnoss or an additional problem, such as severe aphasia, anarthria, akinetic mutism, or psychogenic mutism. The distinctions among AOS and other forms of mutism are addressed in Chapter 12.

sometimes produce VOT values that suggest a phonologic enor (e.g., a VOT value for a /b/ that clearly falls in the normal VOT range for /p/), the general trend in the data is indicative of a pervasive phonetic rather than phonologic disorder. In fact, VOT values for productions perceived as substitutions tend not to be distributed in a manner consistent with normal productions of the perceived
substituted phoneme. ln general, this overlap

Acoustic and Physiologic Findings

Acoustic and physiologic studies have provided con firmation for many of the disorder's perceptual characteristics and have identified additional features that clinicians should attend to perceptually. Equally important, a substantial body of instrumental data supporting the conclusion thatAOS is a phonetic disorder of motor planning/programming has accumulated. The following somewhat arbitrary subsections summarize the results of a number of representative acoustic and physiologic studies that have helped to

of VOT values or their greater than normal variability generally indicates that corect phonemes (voiced or voiceless) are
selected, but that the timing of articulatory and laryn-

The geal activity is poorly regulated.u'1 pervasiveness of VOT abnormalities suggests that AOS is particularly susceptible to phonetic parameters requiring the integration of activities among diflerent speech structures.
Rote

u 51 54 56 i03 120

Lmited repertore of speech sounds Speech may be limted to a few meaningful or unntellgble utterances lmitation of solated sounds may be in error, and errors limled n variety Errors may be highly predictable Automatic speech may not be better than volitonal speech Error responses may approxmate target if stmuli are chosen carefully /uteness may be presenl but rarely persisls for more than 1 to 2 weeks if other speech, ianguage, or cognitive defcts are not present Usually accompaned by severe aphasia but can occur in the absence of aphasa Usually accompaned by nonverbal oral apraxia

Mute apraxic patients nearly always

make

attempts to speak on request, with attempts charac-

terized by silent gropng attempts to move the jaw, lips, and tongue to articulate, along with gestural and facial expressions of frustration. A severe NVOA is usually present. It is rare that articulation ability significantly exceeds a patient's inability to phonate. That is, apraxia of phonation is nealy always accompanied by severe articulation difficulties.*
*A case study by Milshall, Gandour, and Windsort' represents a drmatic exception Their patient had a selective impaiment of phonation (a laryngeal apruia) for an extended time and was able to speak nomally when using an electolarynx.

characterize the disorder's clinical features and clarify its general underlying nature. These findings
are summarized

in Box ll-5.

Voice Onset Tme

Acoustic and physiologic studies generally support and refine the cllnical perception that slow rate is a near-constant perceived abnormality in AOS, and thcy provide insight into whether slow rate is a core l'eature of the disorder or a compensatory strategy to maintain articulatory control. Studies have consisrlr'l25 r3L They tently quantified slow rate.4e6r'er'i03'l0E

Voice onset time (VOT) is the duration between the articulatory release of a consonant and the onset of

have also documented excessive lengthening of

consonants6''18'26 and increasetl vowel duration in .sylLabtes, multisyllabic words, word strings, and

voicing for a following vowel.

It is

measured

acoustically from the onset of the noise burst reflecting stop release to the onset of periodicity in the waveform reflecting the onset of glottal pulsing. Voiced stops are characterized by voicing lead (the

phrases.+
*References 14.21- 52- 61. 78. 101

I
The Disorders and Their Chapter
1

Apraxia of Speech

la)

11-5

in word strings, but they are less consistent in doing so; this suggests an impaired mechanism for activating and executing motor plans.rlr'r'o Findings of
increased verbal response timesnin apraxic speukers also support this conclusion. It has been difficult to establish if slow rate in AOS is compensatory (i.e., articulatory accuracy may be achieved if rate is "intentionally" slowed) or

Ievel deficits rather than linguistic deficits, especially because apraxic speakers are generally capable til' signaling linguistic distinctions that are dpendcnt on though such studies arguc ag dons for rate decits, they

VOT

Overlap in distributon of VOf values between voiced and voiceless stops and frcatives lncreased variablty and abnormal dstribution of VOT values, even when perceived as phonemically accurate Rate

Uniform syllable durations within utterances, regardless of stress or positon within sentences Equalzed stress on stressed and unstressed syllables within utterances

do

and abnormalities found in certain rypes

dysarthria, particularly ataxic dysarthria.
Prosody

distinctions between AOS

(rt

Articulation and Fluency

Falure to achieve complete vocal tract closure for slops (i e,, spirantization) Abnormal F1 and F2 for vowel producton wth bite block in place Misdirected, exaggerated, or "perseveralive" formant trajectories Reduplicated, aborted, "stuttered," or groping artculatory attempts

Slow overall rate of speech and underlying movements

Excessive lengthening of consonants and vowels in syllables, multisyllabic words, word strings, and sentences lncreased interword interuals and verbal response times Feduced ability to adjust speech rate, especially to rncrease rate-even normally fast rates are sometimes possible Delayed, defcient, or nconsislent coarticulation among

adjusting speech rates, especially increasing rate, even when they are_ sometimes able to produce normally fast rates.8r'sor0t These findings suggest a problem with motor control and argue against the notion that all slowed rate in AOS is compensatory. It has also been pointed out tltat certain temporal parameters in AOS may be artifacts of slow rate,
because even normal speakers show some evidence

primary, fundamental feature of the disorder. However, apraxic speakers are lss fficient in

Prosodic abntrmalities are a core and deJinin feature of AO.L Acoustic data documenting rate
abnormalities are strongly predictive and supportivc of perceived prosodic abnormalities in most apraxic speakers. A numbe of additional acoustic studies have addressed prosody and stress abnormalities

Variability
lncreased variabilty in onset of coarticulaton, formant trajectories (i e, movement transitions), attainment of vowel targets, and vowel duration lncreased varabillty n stop gap duration, VOT, and syllable duration lncreased varablity n the direction, duration, velocty, peak veocity, and amplitude of iaw, lip, tongue, or velar movements, and the temporal and spatial relatonships (coartculatory palterns) among those structures Nonspeech oromotor Control lnstabilty on measures of nonspeech isometric force and static positon control of lips, tongue, and jaw Dfficulty trackng predctable movement patterns with lower lp and jaw movements and modulaton of f"

speech structures Slowed formant trajectories and lengthened steady-state

components in diphthongs

s at slow rates when compared

rates.78

on or increased variability of relative

to

directly. They also are supportive

abnormalities.

of

perceivcd

Longer and more variable movement duratons of lower lp and jaw movements during speech More frequent velocty changes and increased velocity
variability during articulatory movements Prosody and Stress

Excessive temporal regularity and flattenng of intensity envelope (syllable syllable intensity variability) in
phrases and sentences Feduced fo contour within sentences Reduced f" decline over the course of lengthy sentences Reduced final word lengthening, relatve to non-fina words, in sentences lncreased ntersyllabic pauses and pause duraton wthin utterances (i e, syllable segregaton)
AOS, Apraxia ol speecht
fo,

fundamental frequency; Ff, first fotma|, F2, second formant; VOT voice onset tme

Because vowel duration does not canJ specifrc Iinguistic mcaning in many contexts, it is difficult to argue that increased vowel durations reflect an undcrlying linguistic disorder, especially when findings also indicate that AOS speakers follow certain linguistic rules for vowel duralion. For example, like normal speakers, apraxic speakers generally reduce vowel duration in segments as the number of segments in an utterance increases*; for example, the voweI in the syllable "cat" in the word "catapult" is shortened relative to the vowel in the syllable "caf'

protluced

in

speakers obey the

isolation.2l5t "t "6 In addition, AoS "vowel shortening rule" to signal

the voicing feature for syllable final consonants (i e , vowels preceding voiceless final consonants are shorter than vowels preceding the voiced cognate).t'ol7 Thus apraxic speakers vary vowel duration to signal linguistic contrasts even though their vowel durations tend to be longer than in

Acoustic studies have found evidence of delaved, or inconsistent coorticulotion aong Iaryngeal, velar, lingual, or labial speech gestures, making it difficult for listeners to predict upcoming articulatory events.t'''tt'tt Abnormally slowed foi mant trajectores and long steady-state portions within diphthongs have also been identified.116 Kinematic measures of lower lip plus jaw movements during word repetition in apraxic speakers have identified normal peak velocity (the maximum speed attained) but longer and more variable movement durations and more frequent velocity changes and greater vebcity variabili4,.7e These results suggest that lip movements are not fundamentally slower an normal, even though lip gestures take longer to acbieve.+ It has been speculated that movements take longer because some are larger (involve greater displacement) or because there are a greater number of aberrations over the course of movement (dysmetrias). It has also been noted that such dysmetrias are not dissimilar to those observed in ataxic

deficienr,

tence utterances.4e'6L 1rr'rrr This generlly means tht unstressed syllables are produced with relatively greater duration and intensity than normal, thus blurring their distinction from stressed syllables. This tendency toward temporal and amplitude uniformity seems correlated with the perception of neutraliztion of stress and dysprosody.TE

ity and reduced intensity variation from syllable to syllable within polysyllabic word, phrase, or sen-

Apraxic speakers tend to show temporal regular-

normal

Aco ic analyses also demonstrate increased interword interuals, a finding that supports the perception of syllable segregation This suggests that apraxic speakers engage in independent (syllable-

eakers.

dysarthria, although they might be an artifact of slow speaking rate because some normal speakers can look dysmetric when speaking at slow rates.?e In summary, speech rate in AOS is generally slower and more variable than normal. Acoustic and physiologic lindings generally support a conclusion that these rate aberrations reflect motor or phonetic

Documentation of reduced funclamental frequency (f") contour in sentencestoo has confirmed the frequent perception of reduced pitch variability within sentences. Other abnormalties in regulati,n off. can also occur. In normally spoken declarative sentences, f. tends to decline in a linear fashion over the course of an utterance, with the greatest and most rapid decline occurring at the end of the utterance. In addition, the terminal words of declarative sentences tend to be lengthened, also signaling the end of the utterance. Speakers with Broca's aphasia (and, presumably, AOS), while demonstrating a decline in f. at the end of simple sentences, may not do so over longer utterances. In addition, duration of fnal word.s in utterances are not clearly longer (antJ sometimes are shorter) than initial or medial words: this lack of durational distinction might reflect an increase in the length of nonfinal words rather than articulation or d.ifficulty with syntax, reflecting a smaller scope ol linguistic or motor planning, or
both.

a shortening of final words.2a Danly and Shapiro suggested tbat this occurrence could reflect effortful

*Similarly, apraxic speakers can generare high peak lip velocities when asked to speak mpidly and when a bite block is in place, and eir peak lip velocities do not diffe between perceptually
accurate and inaccuate word productions.ea Howevcr, othe kine matic malyses indicate rhat apraxic speakers may need increased tirne to reach peak velociry 76

This is not always the case has bccn observed that some apraxic spekers actuallv increase vowel dutation in segnents s word lgngth inceses,tr a phenomen that could reflect motol
phnning/progromming constraints

Ii

xf,:IJ
they ve to

:"f,Tij::
nterwold intervals

Acoustic studies have also documented increased intersyllabic pauses within utterances,t3 I suggesting

that each syllable is being programmed independently. Acoustic findings of longer pause time, increased number of pauses within utterq.nces,

324

The Disorders and Their Diagnoses

Chapter normal Jorce and positiott instabilin on measures of nonspeech isometric force and static position control of the lips. tongue, and jaw, although the patern of

Apraxia ot speech

325

bles, sLower overaLL rate, .shorter phrases,

quent perception of prosodic and stess

A few studies have documented the occurrence of syllaand. events that support the perception of dysfluencies, uniform syllabLe durations reganlless of stress or aborted articulatory attempls, and attempt at error senLence positionaer all provide support for the frerevision For example, electromyogram (EMG),

\tre\.\ on euch syllabLe incLuding nonslressed

Although nor included in tbis review, it should be noted that some speakers with conduction aphasia and Wernicke's aphasia have displayed acoustic and physiologic abnormalities similar to rhose found in AOS. Such abnormalities are usually of lesser magnitude than those lound in AOS, and they do nr argue for linguistic explanations of AOS. They suggest, however, that some degree of motor plan,

simplification of motor planning/programming in AOS. That is, the perception that each syllable is attempts to revise errors, ",\tuttered" initial stressed or produced as a single unit, rather than consonant segments, and aIed movements and merged with other syllables and words in a phrase, groping.416o'6ettttte'tz6t3o suggests thal some speakers (must) approach the planning/programming of speech in a sylLable-by.ryllabLe manner; normal stress and prosodic

ities. Taken together, these findings imply a

abnormal- kinematic, acoustic, and

perceptual studies have documented reduplicated aftempts during the initial segments of words, abtrted articulatory attempts,

instability is not consistent across all structures

tested or all AOS subjects tested.76 Apraxic speakers have also had dfficulty on nonspeech visuomotor tracking asks in which lower lip, jaw, and f" are used to track a visually displayed signal. This difficulty might reflecr deficirs in rerrieving or developing an internal plan for intended movement pattems.sl

ning/programming difhculty may

be presenr

in

people with aphasia who do not display perceptual evidence of AOS

flow

are

lost in the process.

Voriobility

Articulotion ond Fluency

Many of the acoustic and physiologic findings already discussed carry an implication that articulation is imprecise, if not inaccurate, in place, manner, and voicing. A few additional ndings add to such evidence. They also provide support tbr perceived tlysffuencies in AOS
Regarding articulatory imprecision, there is acoustic evidence that Broca's aphasic or AOS speakers may fail to achieve complete vocal tract
stops.to6"6 The resulting noise (spirantizaton), inslead of silence reflecting closure, suggests distortion rather lhan true fricative for stop
cLo.sure

Variability is considered by many to be a hallmark of AOS, at least at less than severe degrees of impairment. Acoustic and kinematic studies have provided considerable evidence of greater than normal variability in AOS These studies are theoretically important, because abnorml variability has been identified within productions perceived as phonologically accurate, making it difficult to argue that such disturbances are linguistically
based.

(ases

A 68-yeu-old

woman awoke one moming unable to speak and with righrsided weakness Emergency department examination confimed these deficits and also noted

Speech therapy was undertaken.

At the time of

dis-

r rigbt central lacial

Several studies of vowel formant trajectories have

weakess Speech evaluation the following day demonstrated

chuge 6 weeks later she was producing most sounds within single syllables, although slowly md with syllable segregation when she attempted to string syllables
together When reassessed 2 months late she was speaking laboriously in sentences, with moderately sJowedrate md segregated syllables, deliberate articulation, and pervasive mild aficulatory distortions When reassessed 2 years later, speech was funcional but chtracterized by moderately slowed ate and occasional perceived articulatory substitutions, especially on multisyllabic words She had consistent difficulty with /s/, /zl, Al, nd all consonant clusters.

documented reduced rate

r0r r0r r:6
132

for

normal variability on indices of coarticulation,

rate of change, and attanment of proper
voweL

but also greater

thatl

nomal oral movements with the exception of limited

tongue excursion to the right She produced only offtarget groping movements ofherjaw and lips when asked
to clear her throat, click her tongue, blow, or whistle. Her

substitution. Imprecision extends to vowels With a bite block in place, normal speakers are able to achieve normal fbrmant positions for targeted vowels, often at the lirst glottal pulse of their initial eftbrt. In contrast, speakers with Broca's aphasia (and, presumably, AOS), attempting to produce /i/ with a bite block in place, have abnormally high rst tbrmant (Fl) and low second formant (F2) values, indicative of undershooting of tongue elevation and fronting "t At the least, this suggests that AOS is associated with dif'ficulties in making onJine adjustments for compensatory articulation, including vowels Acoustic studies yield evidence of misdirected formant trajectories within connected speech. For exampie, rather than lormants following a normal monotonic course, they sometimes initially rise and then fall. Formant trajectories may also be exaggerated (indicative of exaggerated movement), in which

Similarly, studies ofsingle syl lable, multisyllabic, and phrase productions have generally found greater than normal variability in r01 10s 126 vowel duration.r43r'52 Increased variability in stop-gap durtion, VOI duration of consonanttargets83ee

reflexive cough was normal Slre produced only

awkwrd, groping, off-targer jaw and lip movements when asked to count, sing a familiu tune, or imitate
simple sounds or syllables. She could awkwarclly produce the vowel "ah" md with effort imitated the vowels /ou/ and /u/ She was able to produce /m/ in isosounds She achieved correct atliculatory place for /f/ but could not simultaneously move air to produce trication Verbal antl reading comprehension were normal, even for difficult comprehension tasks. Writing with her pre f'ered nght hand was awkward because of wea-kress, but

vowel syllables, and between-word duration has also

been documented.
lo3

Commentary,

(l)

Stroke is the most common cause

rtl

Abnormal variability, as well as temporaL and spatal dyscoordfutttion within and among articulators, has been demonstrated through acoustic, kine47 ll5 o0 For example, have several studies fbund markeil variability in the height and segmental duration of velar movements across repetitions of the same stimuli, in spite of the fact that a lairly normal pattern of velar movement is maintainedi this variability in velar timing can lead

lation but could imitate no other isolated

matic. and EMG measures

of AOS, md AOS may be the only or most prominent manifestation of stroke (2) AOS may be chracterized by muteness at onset, although people mute from AOS usually attempt to speak. (3) Alrhough AOS usually occurs with aphasia, even severe AOS can exist wiout any evidence of language impaiment (4) AOS is frequently accompanied by an NVOA. (5) When caused by
stroke, AOS tends to improve over time, sometimes dramatically Prognosis may be best when there is little or no language impairmenr.

to a perception of nasal subslrtution errorstotttt Highly variable coarticulato,j ptterns for labial
and velar movements during speech, especially for measures of spatial displacement, have also been

spelling, word choice, and grammar were nomal A CT scan 5 days after onset identified a lesion in the left hemisphere at the junction of the posterior frontal and anterior parietal lobes. The neurologic diagnosis was

lefl hemisphere stroke.

the frequency change

in a

formant transition is

identified.60 Similarly, studies

ol lip and jaw

greater than normal. Finally, perseverative trajectories, in which formant transitions resemble those in preceding syllables, may occur.'2u Each of these

movements have identified greater than normal variabilty in peak velocity, velocity changes, and relationships between movement amplitude and
veIocity.a2le

observations imply imprecision

or

inaccuracy of

articulatory movements during speech. Of interest, it has been observed that some of these characteristics are ataxic-like in character, while others might reflect effort at compensation.r26

There is also some evidence that nonspeech oromotor movemeDts in people with AOS may not be normal. That is, some apraxic individuals (and some people with ataxic dysahria) have greater than

t_

The Disorders and Their Diagnoses

Cha

Apraxia of Speech

327

A 63-year-old man was hospitalized following a left cilotid endaferectomy at another institution 6 weeks
previo

proble
noted

facial weakness and a nonfluent aphasia " Speech-language evaluation revealed mild difculty with verbal md reading conprehension and inability to write intelligibly because of right hemipaesis- Speech was telegaphic and chuacterized by numerous articula-

etal region. He underwent sur8ery for gross total removal of a meningioma. Reassessmet 2 days postoperatively indicated that the aphasia had resolved Mild AOS and unilateral L\lfN dysarthria remained but were improved He received therapy for 1 week before his discharge' At the time of dischrge, he wm able to carry on a conversation without significant dfficulty His AOS was most apptrent when he was anxious or attempting to speak at

An

year-old man was admittel to a rehabilitation unit linb control difficulties of 2 yers' duration, presumably the result of a left hemisphere stroke A CT scan revealed mild cerebral atrophy but was ohemise nomal An electroencephalogram was suggestive of a leti hemsphere lesion He was refened for
because of speech md

8l

a-nomal rate. Reassessment by his neurologist several

months later suggested that he had continued to improve,

tory

revisions, hesitancy, and repetitions, as

well

as

but that residual speech difficulty remained'

Commentary. (1) AOS often occurs simultaneously with aphasia and unilateral IJMN dysathna' In this case' all thee disorders were present initialty, with AOS being

reduced loudness, mild hoaseness, md consistent mild articulatory distortions' A right central facial weakness was pfesent. The clinician concluded that tbe patient had "an AOS' which is the major vriable contributing to his comunication disorder; a nonfluent (Broca's-like) aphasia; aud a unilateral UMN dysarthda." SpeechJanguage therapy was recommendedA CT sian and cerebral mgiogram the following day identified the presence of a mass in the left frontopri-

the most evident deficit (2) Etiology of AOS may include vasculr dislubmces, as well as tumor In is

speech-Janguage assessmenI and recomendations. During initial interyiew the patient reported that his speecb had been deteriorating slowly Oral mechanism examination revealed a mild rigbt central tacial weakness and an NVOA characteriz-ed by difficulty voluntarily clicking his tongue and coughing, with associated groping, oft -targel movements He had mild to moderate dilf culties comprehending complex spoken or wrilten sentences He made several selt'-conected semantic enors when nming pictures

together" He was unable to write and had signicmt difficulty coordinating movements of bis righi arm He had had a brief period of speech tberapy following bis bospital dischrge but did not fee.l it helped Examination again tevealed a signif,cmt NVOA His AOS was simila' in character but clearly worse thm dudng initial evaluation. There was little evidence of worsening of his
aphasia, The clirician concluded that he "continues to exhibit a mrked AOS that is worse thm 6 months ago He also

has a significant NVOA (md upper limb apraxia). His behavior during examination is quite characterjstic of

case, stroke initially appeared to be the etiology, although ibilof a tumor subse ated e AOS. (3) ity th velY ln this cas with

mild and improved significantlY.

A 5l-yeu-old womm was admitted to the bospital

a11er

several hous of progressive speech and writing dif6culty, difficulty counting change, md not knowing how to stat her cm. Emergency depalment evaluation revealed a right central facial weakness, disorientation, limb apraxia, and difficulty wi verbal expression Comprehension appemed normal. A cerebral algiogram conducfed 4 days later identified occlusion of two ascending

She was mildly telegaphic, but the clinician wondered if it reflected compensaon for the AOS' She had o

difficulry with pictme namiog, but rapid word retrieval

frontal-pmietal bmches of ttle left middle cerebral artery A CT scm was negative. A diagnosis of Ieft frontoparietal stroke was made Speech-language examiDation a few days later revealed AOS as her most prominent communcation

abilities fell outside the normal range. Reading comprehension for sentnces md short Pilagraphs was adequate. Writilg was linguistically adequate, but she had sme difficully with letter formation, suggestive of limb apraxia. There was no evidencs of NVOA' The clinician concluded that tbe patient had moderately sevete AOS md mild aphasia. Therapy was rec-

ommended. She improved significantly by the time of her discharge a few days laler. For example, during a 10minute conversation she exhibited only three perceived substitutions and one instance of gropilg tbr uticulatory

with increasing.wcird- or uttermce length. Speech AMRs wee slow, and She had difficulty with SMRs' She had a right central facial weakness and equivocal tongue weakness The clinician felt she rught also bave had a unilat eral UMN dysarthria. She had good comprehension for single comands but perfomed poorly on the chailenging comprehension tasks Linguistically, verbal expression was quite good

dischuge.

Commentary.

(l)

AOS nd aphasia are frequently

(2)

e initial mmifestations of left hemisphere stroke

Conversational speech was slow and chtracterized by short phrases lht were occasionally telegraphic and infrequell semantic enors thal he usualJy conected He made numerous spelling enors when writing to dictation. Flis sell'-generated written sentences were lelegraphic, with self-couected gramatical enors and some ucorrecled spelling enors Motor speech evaluation revealed: reduced rte ( 2); iregultr aticulatory breakdowns (1,2); distofied substilutions, with associated groping lbr articuJalory postures and dysprosody (2,3) Speech AMRs were slow (-1), md SMRs were poorly sequenced He had considerable dil'fi culty repeating mulrisyllabic rvords Intelligibility was mildly impaired The clinician conc.luded that the patient hd a "mod erately severe AOS, perhaps with accompanying unilal eral UMN dysrria, both suggestive of lelt hemisphere posterior fronral dysfunction " He also had a "mild ro moderate aphasia affecting all language modalities, allhough expressive functions were more impaired thar receptive This is also suggestive of left perisylvian. predominmtly prerolmdic dysfunction " The clinicim was concemed about lhe patient's report of slow progression of symptoms and raised the possibility of a slowly progressive degencrative condition rather than stroke as the etiology for his problems Subsequently, behavioral neurology consultation concluded thal the patient might have an asymmetric cortical degenerative disease such as primay progressive aphasir The patient made some equivocal functional gains in speech during his hospital stay When seen 6 monlhs later lbr follow-up, he reporred that his speech had worsened and said, "I can't read very much words run

people with significant AOS and mild to moderate aphasia I observed no evidence of behavior which is more typical of patients with generalized cognitive impaiment." Because e patient felt strongly that he would not benefit from speech lherapy and because he had benefited minimally fron lherapy in the past, continued
therapy was not pursued. He was advised, however, that therapy might be beneficial if his speech deterioated to a poiot where functional verbal communication was difficult. Augmentalive means of communication were discussed

Neuropsychological assessment evealed little evi dence of difficulty beyond the speech md lmguage realm. A single photon emission computed tomography (SPECT) scm showed diffusely decreased uptake in the left parietal region and somewhat less decreased uptake ir the left frontal region. It was concluded that the patient had m asymetric degenerative process with the left prietal and left lrontal regions being predominmtly affecled- The patient was not seen again for foJ.low-up, but a phone call to the patient's wife 2 yetrs later establisbed that he was mule and had no functional use of his fight upper extremity His wit'e believed that his verbal comprebension md use of tbat his left upper extremity were good. Commentary. (l) AOS md aphasia cm be amoog the firsl md, for an extended lime, most prominent signs of an asymmetric cortical degenerative process The nature of the AOS md language disturbance nay be indistinguishable from that seen in stroke. (2) AOS sometimes occurs simultmeously with significart LA. LA can mike
a\sessmenl of the linguistic aspecls of wtiting d nonverbal inte.uectual abilities diffrcult (3) Issuei ielated to the management of AOS ir people with degnerave disease differ from lhose for nndegenerative etiologies. These ue discussed in the chapters on managemenl.

deflcir in Y mild at

t
occur without evidence of NVOA

Aos t"n

328

The Disorders and Their Diagnoses

Chapter

Apraxia of Speech

329

A 68-yer-old, left-hmded man was seen for speechlanguage assessment 6 weeks following a left hemisphere stroke. MRI showed a small area of increased signal in the left frontal lobe consistent with snoke. The patieni reported that he could produce only a few unintelligible sounds at the time of onset. He felt that his thoughts and the words in his mind were adequate, and he denied difficulty with verbal comprehension. As bis speech begaa to improve, he felt thal he had an accent that resembled Gernant as be continued to improve, it seemed more Norwegian in character. These accents resolved. He did feel tbat his reading rate had slowed, although he had never been a good reader or speller He noted that he had always had difculty in school and 'Just got by." At the time of examination, he felt that be had recovered to approximately 80% normal and was not having significant frustrations becuse of his speech

dence of phonenic or semantic puaphasias. Conftontation nming ability and rapid word retrieval ability on a word fluency task was reduced. Readirg mte was mildly slowed, semanticerors were evident, and he made occasional word reversals. With bis prefered left hand, his errors, but his own generated sentence w6 adequate. It was felt that at least a portion of his reading and writing difficulty reflected longstanding problerrs related to erly learning. The clinician concluded that the patient had a mild AOS and, perhaps, mild aphasia. The patient was pleased witb his recovery and stated he was not frustrated with his residual speech difficulties. It wil felt that the prognosis for significant fufher recovery was good. Therapy was not recomended. He was counseled, however, that if his difficulties persisted md became a source of frustration for hin reassessment and consideration of therapy would be appropriate. Commentary. (I) AOS is frequently caused by stroke

sound prolongations, and trial-and-enor groping for

correct place ofarticulaion. These difficulties were more evident during spech SMRs and repetition of multisyllabic words. Intelligibility was normal. The clinician concluded that the patient had a mild to

writing to dictation contained frequent spelling

moderate AOS plus, on the basis of problems with wriften lmguage, mild aphasia- Therapy was recommended but not stafed, because the patient underuent a left caotid endarterectomy 2 days later. His gpeech was described by his surgeon as normal at the time ofdischage shortly thereafte. He was not seen for formal speech-language reassessment or therapy postopera-

tively, however

difculty. He denied difficulty witb chewing or

swallowing. Oral mecbanism examination was normal. There

Commentary. (1) AOS is frequently associated with Iesions in e left posterior frontal lobe' When the lesion is small, the AOS may be isolated or associaed with less prominent impaiments of language, sometimes confined to expressive modalities. (2) Oral mechanism examination may be entirely normal in people with AOS. (3)
Recovery from initially miid AOS following stroke is often quite good (although the true degree ofrecovery is this case was not formally established).
FIGURE 1 l -2 Magnelic resonance image of a 59-yer-old rao with mild to moderate apraxia of speech md mild ptoblems with written language (see Case ll-6). The mow identifles a relatively small lesion in the left posteor frontal operculum.

in the left

was no evidence

nonverbal oral apraxia. Voice md resonance were normal Occasional vowel and consonant distortions, with vowel distortions being somewhat more prominent, characterized aficulation.
Infrequendy, he produced distorted substitutions or additions. Overall speech rate was mildly slowed, paficularly when he produced nultisyllabic words. Speech AMRs were normal, but he had difficulty with SMRS at rapid rates. Language examination revealed normal verbal comprehension and retenon. Cooversational lmguage was normal in gramm and synt, and there was no evi-

of

posterior frontal lobe, even in lefthanded people (2) AOS cm be the dominant communication impaiment resulting from stroke, and it cm occur with minimal evidence of aphasic language impairment. (3) Prosodic abnormalities associated with AOS sometimes lead to perception of a (pseudo) foreign accent. (4) In
general, when lesions are small and language impairment is not signicant, prognosis for significant recovery from

AOS due to soke is considered good. (5) Not all

patients with AOS require speech therapy. Decisions to recommend therapy need to consider, at the least, patient attitudes, judgments, and desircs, as well as examination findings and prognosis.

A 73-yea-old womaJl was seen for

speechlanguage assessment as part of a workup addressing a 1-

fo Z-year history of progressive neurologic difficulies,

idenfi ed elsewhere as parkinsonism. She described her speech difculty by saying "I say what I'm gonna say, and I say the opposite," meaning that she made word choice enors md frequently substi-

she was asked to imitate or perform on command; sbe also groped for conect postures. Speech was characterized by strained-harsh-house

A 59-year-old, right-handed man was

admitted

to the hospital after developing visual difficulties and headache, followed several hours later by the onset of
"expressive aphasia." Neuologic examinaon was normal, witb the exception of a "prominent expressive aphasia chaacterized by hesitant speech with frequent
word finding pauses ald frequent errors and revisions." He had no obvious difficulties following simple md complex commands. The remainder of his neurologic examination was normal. MRI the day after admission (Figure 11-2) identified ar early subacute infarct in the left posterior fronal operculum.

Spech pathology consultation 3 ys after onset revealed a normal oral mechanism md no evidence of nonverbal oral apraxia. Lalguage examination revealed normal verbal comprehension md retention- Reading comprehension was also nomal, but reading aloud contained occasional semantic enors, mild hesitation, and occasional initial sound prolongations Expressive language was normal in grammr and syntax, dnd there were no remntic or phonologic enors. Writing was difficult, with several semantic ad spelling erors noted.

hrted yes/no or vice versa. She denied difficulty with verbal comprehension but admitted to reading difficulty. She was unable to write because of right band motor difficulties. She ad her son agreed that she was able to cornnunicate her basic needs quite adequately, if given enough time Oral mechanism examination was essenally normal in size, strength, and symmetry. She had a signifrcant nonverbal oral apraxia, characterired primarily by verbalization or v<icazation during orofacial movements

voice quality (1), articulatory imprecision (1), grolng for aticulatory postures, occasional variable distortions and distorted substitutions, and difculty with the sequeocing dernands of multisyllabic word production. She had some false stats ad occasional initial sound./syllable repetitions. Speech AMRs were mildly slow. She was unable to sequence sounds for SMRsLanguage examination revealed mild impairrnent of verbal comprehension Delays for word retieval efforts and occasional semantic enors were appuent during conversation, and she occasionally deleted a function word. Word definions and proverb explanations werc concrete- Oral spelling was poor. She was able to ead
Continued

Speech was characterized by equivocally straired voice quality, occasional, brief hesitations and initial

-'I
330 The Disorders and Their Diagnoses documented a number of additional acoustic and movement faits that characterize the disorder In general, they provide strong support for the notion that AOS is a problem of motor speech pla nning/programmi n g.
References

Apraxia of Speech
l

lilge print words, but semantlc and syntactic enors were evident when she read sentence level materials aloud. Her writing was not assessed because of significant limb
apraxia and lremulousness The clinicim concluded that the patient had AOS, NVOA, possibly a mild spastic dysafhria, mild to moderate aphasic language impaiment, and some cognitive difficulties that could not cleilly be attributable to her aphasia. He stated: "The patient's apraxia of speech, nonverbal oral apraxia, equivocal spastic dysuthria, md aphasia would be very unusual in Parkinson's disease but arc not unusual in CBD, in my experience." Both the patient and her son felt that she was getting along quite well in terms of functional communication in her everyday envionment She did not desire therapy' She and her son were couseled that if she developed increasing comunication difftculties, speech-language therapy could be of assistance in developing compensatory strategies to facilitate functional colmunication Subsequent MRI showed mrked cerebral atrophy, most prominent in the frontal and parietal lobes bilateally. SPECT scan showed decreased perfusion in the frontal, prietal, and temporal lobes bilaterally but rela-

tively worse in the left parietal lobe. Neuropsychologiassessment confimed the presence of moderate dementia, with cortical and subcortical features. Tbe final clinical neurologic diagnosis was probable CBD Commentary. (1) AOS cm occur in association with degenerative neurologic disease, in this case probable CBD. (2) Although it can be the most prominent communication disorde aphasia, dysafhria, and nonaphasic cognitive deficits cm accompmy it. The presence of all of these deficits may provide some clues for neuro-

cal

20 Cohen L et al: Pure progressve aphemia, I Neurol Neurosurg Psychiatry 56:923, 1993 2t Coltins M, Rosenbek JC, Wertz RT: Spectrographc analysis of vowel arul worcl duration in apraxia of speech, J Speech Hear Res 26:224, 1983

ti ,t
IL

22

Croot

K: Diagnosis of AOS: tleJinition anl. criteriq.

Tex,

l
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Semin Speech Lang 23:267, 2002

2l
24

I Alexander MP et aL 2 -J 4

Dabul B: Apraxia battery for adults, ed 2, Austin,

2000, Pro-Ed Danly M, Shapiro
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logic diagnosis in people witlr degenerative neurologic disease. In this case the constellation of difculties was consiiiered unusual for Pukinson's disease but not
unusual for some other degenerative neurologic conditions, such as CBD. (3) Not all patients with neurologic

NeuropsychoLogical antJ neu roanatomcal dimenions of ideomotor opruia, Brain 115:87,1992 Baum SR et aL: Temporal dmensons of utnsonant anrl votuel productiott: an acouslic and CT scan analyss oJ aphasic speech, Brain Lang 39 3J, 1990. Bennett S, Net,ell Rlil: PoysbLe roles of the insula t
research, J Med Speech-Lang Pqthol 7:253, 1999 Bergeron C et al: Unu,yual clinutl presento!ons of cortical bosal gangl.iottic degeneration, Ann Neurol 40:893,

: Speech prosocly in B roca's aphasia,

speech and language processing: directions for

communication disorders desire

therapy, and their lack

of desire is often

speech-language based on a

t996
syndromes, Bren Cogn 3l:188, 199 6 Bluntstein SE et a[: Prrduction deJicits in aphasa: a voice-on,tet tme anaLysis, Bruin Lang 9:153, 1980 7. BLumstein SE et a[: The perception and producrtn of voce onset tinle in aphasia, Neurop,tychologa )5:371, I 977 8 Boeve B el dl: Ptogressive nonfuent aphasa and subsequetil aphasic denrentia assocated wth atypicaL prcgressive suprarutclear puLsy pathology, Eur Neurol 49:72, 2003 9 Boeve BF et aL: D),satthria antl apruxt of speech assocued with FK-506 (tucrolimts), ldyo CLtu Proc 7l:969 1996 l0 Bronster DJ et aL: Los,s oJ ryeech aJler orthototic Liver lranlplontatidx, TrunspL ltrt 8:234, 1995 I I Brookshte RH: ltrln)uenon n neurogeilr comnuuti( 0 tion disorders, ed 6, St Louit,2003, Mosby. 12. Brrussolle E et al: Slowly progressive anartfuia vtith letc anerior opercular s.vntlronte: a varitutt form oJ liontal cortcql il,ophv syntlrone,t, J Neurcl Sci I44:11,
I 996

5 Black SE: Focal cortcal atrophy

judgment that thei functional communication abilities

ile

adequate for thei needs The clinician's responsibilsuch cases is to inform the patient and his or ber significant others aboul what therapy might accomplish

Brain Lang l6:171, 1982. 25, Darley FL: Aphasa: nput crnd. outpuL dstarbance,s n speech and language processing Presented dt the meeting of the American Speech and Hearing Associa tion, Chicago, IIl, 1969 26 Darley FL: Apruia of speech: 107 years oJ termno ktgical confusion. Presened at the nveting of thc American Speech ond Heoring Association, Denver, Colo, 1968 27 Darley FL: Incunae and research approaches to them In MilLiken C, Dorley FL, edtors: Bran mechanisms underlying speech and ktnguage, New York, 1967, Crune & Statton. 2ll De Renzi E: Merhods of linb apraxia examination anl
their bearng on lhe interpretalion of the dsorder In Roy EA, editor: Neuroprychologiccrl studies of cLpruia arul relalel disorders, New York, 19E5, North-Holland. Dettsch SE: OraL form identifcqtion as a meuure oJ cortical sensory dysfunction n apruio of speech antl aphasia, J Commun Disord 11:65, l98l Devere TR, Trotter JL, Cross AH: Acute aphosa n mul tiple sclerosis, Arch Neurol 57:1207, 2000

ity in

and to facilitate the provision of such services wben

desired.

29 30

STJMMARV
I

thria Oral sensation may be impaired, but such

impairments do not have a clear causal relationship with AOS. People with AOS but no evi dence ol aphasia generally have normal auditory processing skills Deviant spebch characteristics associated with AOS inctude a number of abnormlities of articulation, rate, prosody, and fluency. The characteristics that best distinguish it from other motor speech disorders (the dysarthrias) are distorted

3l i2

Dronkers NF:

A new brain region for coordinathg

AOS is a motor speech disorder resulting from

an impaired capacrty to plan or program the sensorimotor commands that dilect movements that

speech articulation, Nature 384;159, 1996 Dufu JR: Apruia of speech in de7enerqtive neurologit: cli,tease ( in preptraton)

33 Duffy lR: Aprmo of

taL

speech: hstorical oveniew and

result in phonetically and prosodically normal speech. Its clinical characteristics are not attributable to the physiologic disturbances that explain the dysarthrias nor to the language processing disturbances that explain aphasia.
2

cli,lcqL manifeslqlions oJ thc ctcquired and developmen-

ceedings

forms ln Shriberg LD, Campbell TF, editors: Proof the 2002 Childhood Apruia of Speech

Symposium, Carhbatl, Cal$, 2003, The Hendri

Foundalion.

lJ
I

AOS is nearly always the result of pathology

sound substitutions and additions, decreased

phonemic accuracy with increased rate, atlempts to correct articulatory errors that cross phonemic boundaries, groping for articulatory postures, greater ditficulty on volitional than automatic speech tasks, and geater difficulty on SMR and multisyltabic word tasks than AMR and single syllable tasks. People with severe AOS may have a limited phonetic repertoire, little difference between voluntary and automatic speech utterances, and a highly consistent pattern of perceived speech errors. Articulatory distortions, reduced rate, and various prosodic abnor-

in the left (dominant) cerebral hemisphere lt

occurs as the primary speech pathology diagnosis at a rate comparable to that for several of the major single dysarthria types. It is also often a secondary speech pathology diagnosis in people with left hemisphere damage and aphasia.

4.

Buckngham HW: ExpLanation in apraxia with consequences for lhe concept oJ apraxia of speech, Bruin Lang 8:202, J979 C aLig iuri M P, Ti Ll J A : Ac o us t ic al ana Iy s is of vo we I tlura Iion n apraxia of speech tt cuse stutly, FoLia Phoniatr

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Slowly progressive apha,sitL.

In

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RH, editor: CLncol apha.siology, lllinneapoLis, 1987,

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BRK Publshers Dttffy J R, Duffy RJ : The assessment of Lmb apruia: the Lintb aproxia test h GE Hammond, editor: Cerebral. control oJ speech and limb movements, New York, I 990,
ELsevi.er Science

It

frequently occurs with other motor and

an

sensory signs of left hemisphere damage, but it can occur as the only evidence of neuropathol-

ogy. Some people with AOS also have

4

NVOA and LA, but the three conditions can

occur independently AOS is usually caused by stroke and sometimes by tumor or trauma It occasionally is the presenting sign of a degenerative CNS disease AOS can occur in association with dysarthria, most often UUMN dysarthria or spastic dysar-

l8
19

malities help distinguish AOS from aphasic

phonologic errors. A number of acoustic and physiologic studies

have provided confimation for the clinical

42:1462,1992 Chapin C, Blumsten SE, Meissner B: Speech production mechanisms in tphasr: u deLayed auditory feedback srudy, Brqin Lang l4 106, l98l Chapman SB e al: Aub[onrtl domnutt prcgressive syndrome of notor-speech loss withou denentia,
Neurology 49: I 298, I 997.

Duffy JR, Duffy Rl: The limb apraxia te\: an imitatvc measure of upper Limb apruia In Ptescott TE, elitor: Clinical aphasiology, vol 18, Boston, 1989, CollegeHII. 37. Duffy JR, Gawle CA: Apraxic speakers' vowel duratiorr n consonant-voweL-consonant syllabLes. In Rosenbek C, McNeiL MR, Atonson AE, edtors: Apraxa of speech: physioLogy, acou\tics, lnguistics, management, Sdn Diego, 1984, CoLLege-H ill 3ti Duffy, JR, Watt JR, Duffl RJ: Path anab,sis: a stratc3y lor westigating the mlltvarate causaL relatonships in communcation disorder., J Speech Hecrr Res 24:471,
t9t

36

perceptual characteristics

of AOS and have