Ilrl I)lorrk'rs

nd Their Diagnoses

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tr r

tt

Weismer C et

()

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175, Young IvlC: Communication disorders

in

systemic

CHAPTER OUTLINE

Unlikc the dysarthrias,,' AOS can exist withour

I. Anatomy nd basic functirurs of the motor speech

pr0grammer
A Functions of the motor speech programmer

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

D Clinical ndings
E Acoustic and physiologic

findings

V. Cases

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.

clinically apparent impairments in the

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

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

Chapter

The Disorders and Their Diagnoses

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

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

*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

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

fit with notions

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.

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.

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

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

Functions of the Motor

Speech Programmer
The MSP has a leading role in establishing

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

in

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-

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

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

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

peripheral feedback either belore the program is

readicd for movement or during movement execu-

Apraxia of Speech

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

construct programs anew

for each syllable to

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

well-estblished subroutines; or "nacros-" to borow computer

teminology

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

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

'Cogent, comprehensive discussions of

*Other tems that might apply include generalized motor programs; verbal motor memories; engrams; movement gestalts;

309

motor

speech

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

planning/programming

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

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

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

tlrlt

sornething is awry with the planning/

rroerarlrling of speech movements. This distur-

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

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.

Sce Bcn[eLt and Netsellr for a comprehensive discussion of the

pr)ssible roes ol the insula in speech and Language

Chapter

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

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

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-

ETIOTOGIES

'l

Apraxia of Speech

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

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

Stroke is ilxe most conlmon cause ofAOS.Therc

is nothing unique abour thc nature of rhe vascular

(or
exc
the

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

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

mos
decl
and

ical features include cognitivc

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-

d
(1

tions

th

peri
t) hemis
the

""il31.:1
of the

tAphasia also
is related to difficulty in expressing proposional
t"o
or symbolic meanings througlr pantomirne and sign lungu"ge

lcl.r

asr lor 1r

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

*An

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

of adults undergoing te procedure

cyclosporin has been ssoc

dug

speech.ru

rThe

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

cessation of the

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

somc

On examination, AOS was isolated in 9Z o[

cases and occurred

7,,,1,.

rtrc

with aphasia or dysarthriu, or

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

riSht greate than leli hemisphere) prietal lobe dysfrrnctrrrr

and neuopsychiatric disoders associated with fronral krbc
dysfunction

LnapLer tt

fhe Disorders and Thelr Diagnoses

312

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,

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.

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-

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

Ifl 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

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-

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-

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

+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

+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

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.

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

aphasia because the aphasic component of the

syndrome includes deficits that are not explainable

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,

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

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

Baltetl.6r

severe

form of apruia of speech

"

greater cluity

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

iDiscussion of this issue cd

sources

be foutld in

seveal

ApfaxtaorJpeecfr

)r)

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

At the same time, several theories suggest

that breakdowns at differen! stages of motor

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

aphasia and between AOS and dysarthria are

addressed in Chapter 15, which covers differential
diagnosis.

Chapter

The Disorders and Their Diagnoses

314

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%)

phy (CT)

Unspecified degenerative CNS disease (10%)

PPA or AOS, or both (7%)
Alzheimer's disease or dementia (3%)

Other: asymmetric cortical degeneration; CBD; ALS:

vs

PSP; CJD; leukoencephalopathy

Vascular
49%

(7%)

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

Traumatic (15%)

Tumor resecton, aneurysm or AVM repair, hemorrhage evacuation

cHr (1%)
Tumor (Left Hemisphere) (4%)

0ther (6%)

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-

AOS of undetermined etology (3%)

Other: seizure disorder; post liver transPlant; multiple

causes (2%)

rtive. and traumatic etiologies.

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

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

progressive supranuclear PalsY.

Distribution of Etiologies, l-esions, and

Associated Deficits in Clinical Practice

x Percent of the

Etiologies

PPAOS. The remaining cases had Alzheimer's

disease. a similar dementing condition, or other conal or asymmetnc
ditions that

or

Mayo Clinic with a

nosis of AOS.* The

about generalizing these findings to the general population or all speech Pathology practices apply here

well.

The data establish that AOS can result from

de

. Seven Percent had a diagno

for 155 quasirando

as

cases were

rcent had an unsPecified

Box 11-2 and Figur

(e
CBD, CJD)
findings

al

degeneration,
as the only or the

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

which is quite dilferent lrom several dysarthria types

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

*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

neurologic disease.
Surgical trauma was the etiology in 157o of th^e
-[n
most instances, surgery involved the left

number

of medical conditions' the distribution of

"u..r.

scan.

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.

Degeneratve (26%)

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-

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.

Associoted Deficits"

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

How often was NVOA present? Among 107

patients for whom relevant data were sought, 6370 of

for whom observations about NVOA

were

of the disorder. Thus consistent

with the llterature, there was a frequent but not
made had evidence

invaiable cooccurrence of AOS and NVOA.

How often was aphasia present? Among the 155
patients for whom observations about aphasia were
*In

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

Speech

Il5

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

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

Lesions

those

1.1 Apraxia of

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

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.

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-

Chapter

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.

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

(linical Findings

$E

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

Varable

Findnqs

that cannot be attributed to poor task comprehension

Lmb

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

commands

to perlbrm volitional

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

for

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.

Because motor planning/programming

and
is reasonable to

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

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

Oral

trying to perform the act,

Patient

Complaints

they

simultaneously say the command. For example,

asked to cougb, a patient may say "cough" and
simultaneously attempt to cough Patients usually
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

Limb, nonverbal oral, other

Language & other

Speech Deficts

AOS, Apraxia of speech; UM, upper molor neuron

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

with AOS

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-

cluded that auditory processing abilities can

speech-language

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.

'Volitional coughing, blowing, and whistling are among the most

difficult simple tasks, becuse they require coodination of the

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

Apraxia of Speech

317

as

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

complaints associated with A0S-

detecting NVOA

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

Nonvefbal

on adequate auditory f'eedback to speak as well

Common limb, nonverbal oral, other

speech-language deficits, and patient

A substantial proportion of people with AOS exhibit

NVOA,' NVOA is an inability to imitate or follow

are perplexed, frustrated, atnused, or embarrassed by

these otT-target responses and otten try to correct

Nonverbol Orol Mechonism

not necessary to diagnose AOS

Nonverbol Oral Aproxia

'1

be

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

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

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

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.

if language and reading skrlls ure

relatively good and the patient can give more than
brief and unelrborated conversational or narratvc
particularly

responses.

Imitative tasks assist the clinical hunt for AOS.

because they can contain stimuli that challenge
speech planning/programming abilities and because

they circumvent demands on word retrieval

and

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

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

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'

Chapter

The Disorders and Their Diagnoses

318

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

Slow

overall
especiallY
length

rate regardless of phonemic accuracy,

for utterances more than one syllable n

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

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

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

Consonant clusters errors more frequent than singleton

errors
lntation of utterances particularly difficult
Errors occur on both lmitative and spontaneous speech
tasks

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

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

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

othels, the threshold is

fitr

respon

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

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

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-

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, addi-

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

3.)

iNmow

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

ence

of models of phonology and motor

speech
boundaies

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

low and tasks should be

simple
any st

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-

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

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

Apraxia of Speech

tions, or omissions, whereas rale and prosody arc

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.
The rate and prosodic abnormalities in AOS

hLrvc

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

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

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

as

rThe
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

phonetic lnscription is not the only perceptul method

prosodic abnormalities have functonal consequences For

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

'.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

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

'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

LrrdPrrr

The Disorders and Their Diagnoses

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

propositional utterances generate more abnormalities than automatic/reactive utterances, although

the latter ofien are not entirely normal; dysarthric

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

speakers show no such distinctions

types

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.

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-

even better on SMRs than AMRs!). Volitional/

Severe Aproxia

of

Speech

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

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-

!""

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

of error

responses

limited When phonetic

times giving the impression that the patient

has

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.

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.*

increased rate, attempts to correct articulatory errors

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,

usually the clustering

of

several

these

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.

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

characterize the disorder's clinical features and

clarify its general underlying nature. These findings

in Box ll-5.

Voice Onset Tme

Voice onset time (VOT) is the duration between the

articulatory release of a consonant and the onset of

voicing for a following vowel.

*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.

of

characteristics lhal help distinguish AOS from he

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

are summarized

APtd^rd ut JPrsLr

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

Summory

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

it is

rr

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

in a

runge between normal voiced and voiceless

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

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

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

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 larynu 51 54 56 i03 120

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

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

have also documented excessive lengthening of

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

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

I
The Disorders and Their

Chapter

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

11-5

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

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

speech structures
Slowed formant trajectories and lengthened steady-state
components in diphthongs

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,

Uniform syllable durations within utterances, regardless of

stress or positon within sentences
Equalzed stress on stressed and unstressed syllables
within utterances

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

Ii

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

primary, fundamental feature of the disorder.

However, apraxic speakers are lss fficient in

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

on or increased variability of relative

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"

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'

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

protluced

in

isolation.2l5t "t "6 In addition, AoS

"vowel shortening rule" to signal

speakers obey the

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

normal

eakers.

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-

xf,:IJ
they
ve to

:"f,Tij::
nterwold
intervals

s at slow rates when compared

to

rates.78

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,

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

*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

Apraxia of Speech

la)

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

do

distinctions between AOS

and abnormalities found in certain rypes

(rt

dysarthria, particularly ataxic dysarthria.

Prosody

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

directly. They also are supportive

of

perceivcd

abnormalities.

Apraxic speakers tend to show temporal regular-

ity and reduced intensity variation from syllable to

syllable within polysyllabic word, phrase, or sen-

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

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

a shortening of final words.2a Danly and Shapiro

suggested tbat this occurrence could reflect effortful

articulation or d.ifficulty with syntax, reflecting a

smaller scope ol linguistic or motor planning, or
both.

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

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),

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

quent perception of prosodic and stess

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

\tre\.\ on euch syllabLe incLuding nonslressed

bles, sLower overaLL rate, .shorter phrases,

abnormal- kinematic, acoustic, and

ities. Taken together, these findings imply a

perceptual studies have

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

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

flow

are

lost in the process.

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

for

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

the frequency change

in a

formant transition is

t_

based.

Several studies of vowel formant trajectories have

documented reduced rate

but also greater

thatl

normal variability on indices of coarticulation,

rate of change, and attanment of proper
r0r r0r r:6

voweL

132

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

vowel syllables, and between-word duration has also

been documented.

lo3

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

matic. and EMG measures

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

identified.60 Similarly, studies

ol lip and jaw

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

observations imply imprecision

veIocity.a2le

or

inaccuracy of

pattems.sl

Apraxia ot speech

325

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,

ning/programming difhculty may

be presenr

in

people with aphasia who do not display perceptual

evidence of AOS

Voriobility

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

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

instability is not consistent across all structures

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

(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

r rigbt central lacial

weakess
Speech evaluation the following day demonstrated

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

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 iso-

lation but could imitate no other isolated

sounds
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

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.

Speech therapy was undertaken.

At the time of

dis-

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.

Commentary,

(l)

Stroke is the most common cause

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.

Cha

The Disorders and Their Diagnoses

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-

tory

revisions, hesitancy, and repetitions, as

well

as

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-

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

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

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

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

a-nomal rate. Reassessment by his neurologist several

months later suggested that he had continued to improve,

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

the most evident deficit (2) Etiology of AOS may

include vasculr dislubmces, as well as tumor In is

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.

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

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

dischuge.

Commentary.

(l)

AOS nd aphasia are frequently

e initial mmifestations of left hemisphere stroke

(2)

deflcir in
Y mild at

t
occur without evidence of NVOA

Aos t"n

8l

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

An

because of speech md

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

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

Apraxia of Speech

327

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

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.

328

The Disorders and Their Diagnoses

Chapter

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

difculty. He denied difficulty witb chewing or

swallowing.
Oral mecbanism examination was normal. There

was no evidence

of

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-

writing to dictation contained frequent spelling

moderate AOS plus, on the basis of problems with

wriften lmguage, mild aphasia- Therapy was recom-

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

mended 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

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)

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

in the left

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

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.

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.

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-

"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.

329

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

fo Z-year history of progressive neurologic difficulies,

admitted

Apraxia of Speech

sound prolongations, and trial-and-enor groping for

speechlanguage assessment as part of a workup addressing a 1-

to the hospital after developing visual difficulties and

headache, followed several hours later by the onset of

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

A 73-yea-old womaJl was seen for

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

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.

Speech was characterized by equivocally straired

voice quality, occasional, brief hesitations and initial

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

she was asked to imitate or perform on command; sbe

also groped for conect postures.
Speech was characterized by strained-harsh-house

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

-'I
Apraxia of Speech

The Disorders and Their Diagnoses

330

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-

AOS is a motor speech disorder resulting from

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

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

AOS is nearly always the result of pathology

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.

It

frequently occurs with other motor and

sensory signs of left hemisphere damage, but it

can occur as the only evidence of neuropathol-

ogy. Some people with AOS also have

an

NVOA and LA, but the three conditions can

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

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-

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2
-J

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I 996

malities help distinguish AOS from aphasic

phonologic errors.
A number of acoustic and physiologic studies

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5 Black SE: Focal cortcal atrophy

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-

NeuropsychoLogical antJ neu

roanatomcal dimenions of ideomotor opruia, Brain
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speech and language processing: directions for

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I Alexander MP et aL

logic diagnosis in people witlr degenerative neurologic

disease. In this case the constellation of difculties was
consiiiered unusual for Pukinson's disease but not

thria Oral sensation may be impaired, but such

STJMMARV

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.