Acquired Apraxia of Speech: Features,

Accounts, and Treatment

Richard K. Peach

The features of apraxia of speech (AOS) are presented with regard to both traditional and contemporary descriptions of
the disorder. Models of speech processing, including the neurological bases for apraxia of speech, are discussed. Recent
findings concerning subcortical contributions to apraxia of speech and the role of the insula are presented. The key fea-
tures to differentially diagnose AOS from related speech syndromes are identified. Treatment implications derived from
motor accounts of AOS are presented along with a summary of current approaches designed to treat the various sub-
components of the disorder. Finally, guidelines are provided for treating the AOS patient with coexisting aphasia. Key
words: apraxia, apraxia/di [diagnosis], apraxia/th [therapy], neuromuscular control, speech disorders, speech therapy

“T he management of individuals with AOS

(assessment, treatment, prognosis) takes
a decidedly different form from those of
Features of Apraxia of Speech

its closest clinical neighbors. The failure to make
this differentiation has important consequences
for both theory and patient care.”1 The essential
reasons for critically reviewing the literature on
apraxia of speech (AOS) are certainly represented
in this quote. Indeed, more than 30 years ago,
Darley2 appealed to speech-language pathologists
to recognize the differences among aphasia, aprax-
ia, and dysarthria in the interests of improving
clinical services to each of these communicatively
disordered patient groups. Although the literature
concerning apraxia of speech has seen a continu-
ous debate since Darley’s original contribution
regarding the essential nature of the disorder, it
has nonetheless offered an increasingly detailed
account of the disorder that has had a substantial
impact on the treatment of the disorder. In this
article, the features of apraxia of speech are pre-
sented with regard to traditional and contempo-
rary descriptions of the disorder. Models of speech
processing, the neurological bases for apraxia of
speech, and recent findings regarding the subcor-
tical contributions to apraxia of speech and the
role of the insula are discussed. Treatment impli-
cations derived from motor accounts of apraxia of
speech are presented along with a summary of
current approaches designed to treat the various
subcomponents of the disorder. Finally, guidelines
are provided for treating the AOS patient with
coexisting aphasia.
Articulatory characteristics
The articulatory errors in apraxia of speech are
characterized by perceived substitutions, distor-
tions, omissions, and repetitions.3,4 Substitutions
predominate but may reflect or include distortions
if narrow transcription is used. Distinctive feature
analyses demonstrate that errors involving the
place of articulation are most frequently followed
by errors of manner, then voicing, and then those
with oral/nasal distinctions. With regard to place
errors, those involving bilabial and lingual-alveo-
lar phonemes occur more often than those involv-
ing other places of articulation. When patterns are
analyzed according to manner of production,
errors in affricates and fricatives appear most
often. Substitutions are anticipatory or regressive
(later occurring phonemes influence earlier tar-
gets), reiterative/perseverative (earlier phonemes
are maintained downstream), or metathetic
(phoneme exchanges).
More errors are also observed on consonant
clusters than singletons. When singletons are
involved, the errors or distortions may appear in
Richard K. Peach, PhD, is Professor, Departments of
Otolaryngology, Neurological Sciences, and Communication
Disorders & Sciences, Rush University Medical Center,
Chicago, Illinois.
Top Stroke Rehabil 2004;11(1):49–58
© 2004 Thomas Land Publishers, Inc.
www.thomasland.com
49
50 TOPICS IN STROKE REHABILITATION/WINTER 2004
either consonants or vowels or both. Consonant
errors predominate when both error types are
present. Consonant substitutions are perceived
sometimes as complications rather than simplifi-
cations of the target sounds. Distortions and per-
ceived substitutions tend to be close to the dis-
tinctive features of the target phoneme.3,4
Influences on error productions
The position of the target sound within words
may not exert a strong influence on error frequen-
cy, but when it does, the initial position tends to
be the most difficult. Errors are greater for infre-
quently occurring sounds. Patients with AOS pro-
duce more errors in nonsense syllables than in
meaningful words. Phoneme errors also increase
as the length of the target word increases. More
errors are observed as the distance between suc-
cessive points of articulation increases.
Error rates are higher for volitional/purposive
utterances than automatic/reactive utterances.
Phoneme errors also tend to be inconsistent, that
is, the same sounds are not always in error and the
error types are not always the same in specific
utterances. Errors appear in both imitative and
spontaneous speech, although errors in sponta-
neous speech will exceed imitative errors. Patients
with AOS are not only aware of their articulatory
errors but can sometimes predict them and will
often attempt to correct them.3,4
Speech prosody in AOS is characterized by a
tendency toward equal stress. Other features
include inappropriate intersyllabic pauses and
restricted and altered intonational and loudness
contours. Patients demonstrate effortful, groping,
and repetitive attempts to produce sounds accu-
rately. Speech rate is usually slow. Occasionally, a
foreign accent is perceived in speakers with
AOS.3,4
Recent Accounts
The study of brain damage and the behaviors
that result have provided researchers with numer-
ous opportunities to study and clarify
brain–behavior relationships. Damage to the lan-
guage mechanism has comprised one such area of
interest, particularly with regard to the motor
speech production.
Phases in speech processing
Darley, Aronson, and Brown5 described a three-
level model of motor speech programming con-
sisting of a central language processor (CLP), a
motor speech programmer (MSP), and the down-
stream motor cortex. For language, the CLP
selects the words and word sequences that trans-
form meaningful content into language. For
speech, the CLP identifies the phonemes and
meaningful sequences of phonemes for language
transmission. The CLP then converts these
phoneme sequences into a neural code that drives
the MSP. The MSP activates the appropriate mus-
culature to produce the desired speech sounds in
their proper order. The MSP then projects directly
to the motor cortex.
Darley et al. attributed AOS to a disturbance in
the programming of movements for speech. That
is, the linguistic plans (syntactic, phonologic) for
an intended message are assembled accurately but
the speaker is unable to program the musculature
for its motor expression. The difficulty then is not
related to deficits in the neuromotor execution of
speech (i.e., disturbances to the basic motor
processes involved in muscular control of the
speech mechanism), but rather to an inability to
transform phonologic plans into a code that is rec-
ognized by the speech motor system.
More recently, Van der Merwe6 has described a
four-phase model of speech sensorimotor control
that makes explicit the planning and program-
ming stages described by Darley. In Van der
Merwe’s first phase, phonologic representations
(i.e., phonemes) are activated and transformed to
motor code during the motor planning or second
phase of speech production. Motor planning
involves activating and organizing the temporal
and spatial specifications for the production of
sequences of phonemes. Core motor plans for par-
ticular phonemes are adapted to the specific
speech contexts in which they will appear and are
entered into subroutines that enable movement of
the articulatory structures. In the third phase, the
motor plan subroutines are fed-forward to the

motor programming system where muscle-specif-
ic motor programs for articulatory movements are
selected and sequenced. Motor programs specify
spatiotemporal and force dimensions such as
muscle tone, movement direction, force, range of
movement, and rate. In the last phase, the plans
and programs of the preceding phases are trans-
formed to muscle movements. Following from
this model, Van der Merwe conceived AOS as a
motor planning disorder, because (a) AOS is not
attributable to deficits of muscle tone or reflexes
and (b) motor programming deficits allow for
alterations in muscle tone, force, direction, speed,
and timing. The latter characteristics would
instead be encompassed within the group of
speech disorders known as the dysarthrias.
Neurological bases of AOS
Close inspection of these models reveals an
important difference between the two with regard
to AOS. For Darley et al.,5 the linguistic and
phonemic planning functions associated with the
CLP show little or no impairment while selective
activation of the programming routines for the
speech musculature is deficient. In the Van der
Merwe6 approach, the fundamental deficit of AOS
is found in the planning rather than the program-
ming stage of speech motor production, that is, at
the point in Darley et al.’s CLP where neural codes
are computed for specifying the spatial and tem-
poral characteristics of the output. Accordingly,
AOS is a motor programming disorder for Darley
that results from damage to the hierarchically lat-
er motor speech programmer but is a motor plan-
ning disorder for Van der Merwe that follows from
damage to the earlier motor planning phase of
speech motor production.
These accounts are important for identifying the
neurological foundations of AOS. Both Darley et
al.5 and Van der Merwe6 assume that the specifica-
tion and programming of motor speech output are
mediated by the cortical association areas — the
premotor cortex, the supplementary motor area
(SMA), the prefrontal areas, and the posterior
parietal areas. Both accounts also suggest that AOS
should result from lesions to the cortical associa-
tion areas and dysarthria should result from
Acquired Apraxia of Speech 51
lesions to the basal ganglia and other lower seg-
mental structures.
Peach and Tonkovich,7 however, provide evi-
dence that suggests that the basal ganglia and
frontal white matter are involved in the functional
systems responsible for motor speech processing
and production.8,9 Motor speech appears to be
governed by several functionally distinct cortical
motor areas including primary motor (Brodmann’s
area 4) and nonprimary motor areas (premotor
areas 44 and lateral 6 and mesial supplementary
motor area 6) and the parietal lobe. Square and
her colleagues8,9 have suggested that the nonpri-
mary motor cortex is involved in movement
preparation and sensory guidance and the primary
motor cortex is involved in the execution of move-
ments. The parietal lobe appears to mediate the
integration of sensory input for the preparation of
motor behavior. These cortical areas relate to the
basal ganglia through their projections to specific
subcortical nuclei that send reciprocal projections
to the supplementary and primary motor areas.
The primary and nonprimary motor areas project
to the putamen, which then projects to the globus
pallidus and substantia nigra. Globus pallidus and
substantia nigra project to the supplementary
motor areas by way of their thalamic connections.
Projections from prefrontal, parietal, and temporal
association areas project to the caudate and then
to the globus pallidus and substantial nigra, which
project via the anterior thalamus to the lateral pre-
motor area.8 The basal ganglia, therefore, contain
structures that are central to the integration of
afferent and efferent impulses associated with per-
ception and skilled motor movement.
Some studies have observed apraxia of speech
from isolated damage to the anterior portion of the
insula.10,11 In fact, Dronkers10 adheres to a strong
hypothesis that states that the insula must be dam-
aged in order for apraxia of speech to occur.
Furthermore, researchers have also reported insu-
lar involvement in several cases of Broca’s apha-
sia.12,13 These findings are not without dispute.
Earlier studies, as well as several recent studies,
have demonstrated that apraxia of speech occurs
in the absence of insular damage.14–16
Jones, Peach, and Schneck17 examined the
extent to which insular damage was found in a
52 TOPICS IN STROKE REHABILITATION/WINTER 2004
group of participants with apraxia of speech. Only
3 of 11 participants in this retrospective analysis
were found to have brain damage involving the
insula of the dominant hemisphere. Two of these
participants were diagnosed with Broca’s aphasia
and accompanying apraxia of speech; the third
demonstrated pure apraxia of speech. In the latter
case, the site of lesion was not isolated to the insu-
la. Damage to the frontal cortex was identified in
8 of the 11 participants. The frontal lobe was the
area most consistently damaged in these partici-
pants. However, the frontal lesions were also
accompanied by extension into the parietal, tem-
poral, insular, and temporo-occipital areas.
Damage in two of the participants was isolated to
the frontal cortex. In addition to the areas men-
tioned thus far, infarction limited to the basal gan-
glia was identified in two participants. The latter
finding supports recent work that has attempted
to characterize AOS secondary to subcortical
lesions.7 No common neuroanatomical structure
was damaged among all 11 participants. These
results are consistent with recent notions concern-
ing a distributed network of anatomical sites
underlying speech production.18
Contemporary definitions
Based on an extensive review of this literature,
McNeil, Robin, and Schmidt19 provide a contem-
porary definition for AOS. According to these
authors, AOS is a phonetic-motoric disorder of
speech production that is caused by inefficiencies
in translating phonologic frames to kinematic
parameters for carrying out intended movements.
This produces intra- and interarticulator temporal
and spatial segmental and prosodic distortions
that result in extended durations of consonants,
vowels, and time between sounds, syllables, and
words. These distortions are perceived as sound
substitutions, misassignment of stress, and other
prosodic abnormalities. Errors are relatively con-
sistent in location and invariable in type.
These views have definite implications for treat-
ing the disorder. Since AOS is currently assumed
to be a motor control problem, treatment should
incorporate principles of motor control and learn-
ing. The objective should be to improve the
patient’s ability to specify the kinematic parame-
ters necessary for adequate production of speech
sounds and prosody. Treatment for pure AOS does
not need to involve techniques to facilitate phono-
logical frame building or sound selection.
Differential diagnosis
Traditionally, AOS has been distinguished from
other acquired phonological disturbances (i.e.,
dysarthria and phonemic paraphasia) on the basis
of the hypothesized levels of impairment within
the speech processing system and the anatomical
locus of the brain damage associated with these
impairments. Recent advances with regard to
these issues have challenged these assumptions.
Dysarthria and AOS
Dysarthria has most often been defined as a dis-
turbance of basic motor processes involved in the
execution of speech. This definition may be inad-
equate to distinguish it from AOS given recent
descriptions of AOS as a phonetic-motoric disor-
der.19 The latter definition assumes that motor
planning and programming are essential phases of
motor processing (see previous definitions) and
that impairments to these levels are motoric in
nature. The traditional definition lacks this speci-
ficity and suggests that motor processing encom-
passes only the final stages of speech output.
The description of a unilateral upper motor neu-
ron (UUMN) dysarthria has also complicated the
traditional anatomical distinctions between
dysarthria and AOS.19 Previously, dysarthria (i.e.,
spastic) was associated only with bilateral upper
motor neuron lesions. Unilateral lesions involving
motor cortex that were sufficient to produce
speech disturbances were assumed to cause AOS.
Dysarthria and AOS after unilateral lesions of the
motor cortex make specification of the nature of
the articulatory errors problematic in patients with
these lesions. For example, irregular articulatory
breakdown, irregular AMRs, and slow rate are
associated with both UUMN dysarthria and AOS,
as well as ataxic dysarthria for that matter, making
differential diagnosis of dysarthria versus AOS dif-
ficult in such cases. Co-occurrence of AOS and

UUMN after left-hemisphere damage may make it
difficult to attribute specific errors or characteris-
tics to one disorder rather than the other.20
Phonemic paraphasia and AOS
Similarly, attempts to differentiate AOS and
phonemic paraphasia have been based on partici-
pants selected for either lesion location or aphasia
type. Yet studies that use CT scans to investigate
the neuroanatomical characteristics of AOS have
found no relationship between site of lesion and
presence of AOS.21 Similar patterns of speech
errors have also been found in patients with pos-
terior lesions and with anterior lesions.22 Patients
with phonemic paraphasia therefore may present
clinical characteristics that are thought to be
salient in AOS and include effortful trial and error
articulatory movements with attempts at self-cor-
rection, articulatory inconsistency on repeated tri-
als, and difficulty initiating utterances. These
results may suggest that AOS and phonemic para-
phasia cannot be distinguished from one another
simply by patterns of phonological errors.
Tonkovich and Peach23 suggest that phoneme
sequencing errors may provide one basis for dis-
tinguishing AOS from phonemic paraphasia. In
AOS, errors tend to involve transitionalization fol-
lowed by occasional anticipatory errors. In phone-
mic paraphasia, errors are not only of the antici-
patory type, but include perseverative and
transposition (metathesis) errors as well.
Sound sequencing errors appear to be worth-
while candidates for distinguishing between these
disorders, because it is difficult to assign such
errors to the motor level of speech production.
Sequencing errors are theoretically consistent
with a breakdown that causes the phonological
buffer to be misconstructed or filled with misse-
lected phonemes. Only intrusive schwa and
abnormal prosody belong exclusively to the indi-
vidual with AOS.
Treatment for Apraxia of Speech
Motor-based perspectives
Because AOS is viewed currently as a phonetic-
Acquired Apraxia of Speech 53
motoric disorder of speech production,24 the prin-
ciples of motor skill learning that have been devel-
oped for nonspeech skilled acts should be appli-
cable to the treatment of AOS. Wertz et al.3
provide the following list of principals:
1. Establish maximal patient motivation.
2. Briefer rather than lengthier practice sessions
should be scheduled and distributed over a
longer period of time.
3. Although massed and distributed practice lead
to similar retention, distributed practice has
been found to produce superior immediate
effects.
4. Whole practice is favored for simple or well-
organized tasks, whereas part practice is more
efficient for complex tasks.
5. Mental practice is more effective in learning
motor skill than no practice at all.
6. Practice performance conditions should simu-
late the actual performance conditions with
respect to the speed and accuracy of the move-
ment.
7. The first and last events that are learned are
retained best from a sequence comprising an
activity.
8. Drill or problem solving can be equally effec-
tive.
9. Programmed self-learning encourages inde-
pendent and individual rates of work.
10.Highly prompted learning is expedient for a
new task; discovery learning is better for reten-
tion and generalization.
11.Overlearning (above criterion) leads to better
retention.
McNeil et al.19 suggest that, as precursors to
motor learning, clinicians should consider the
patients’ attentional capacity as well as their long-
term memory abilities to ensure that they are suf-
ficient to support a successful treatment outcome.
Clinicians should also consider the following
“prepractice” principals:
• Establish motivation
• Simplify instructions to promote understand-
ing of task
• Provide observational learning (modeling and
demonstration)
• Provide verbal pretraining (exposure to all tar-
geted stimuli)
54 TOPICS IN STROKE REHABILITATION/WINTER 2004
• Provide knowledge regarding movement (e.g.,
graphic representations)
• Establish reference for correctness, especially
when shaping target production
Singer (as cited in Wertz et al.3) asserts that
motivation influences selection of a preference for
an activity, persistence, effort, and adequacy of
performance relative to a set of standards. Four
dimensions of motor activity relating to motiva-
tion are complexity, physical demands, appeal,
and meaningfulness. Some activities or programs
that ensure maximal motivation include develop-
ing systems of rewards and reinforcers, using
knowledge of results of performance, setting goals
(specific level of expected performance) and
involving the patient in goal setting, exhibiting
high levels of clinician enthusiasm, and demon-
strating the relationship between tasks and
improved speech.3,19
Motor learning is achieved through practice and
experience. Frequent and intensive practice with
careful structuring is necessary to improve effi-
ciency. Systematically controlled variability is rec-
ommended to improve motor control. Random
(versus blocked) practice facilitates adaptation to
the sequences of movements that constitute
speech.25 Mental practice (focus during movement
task, imaging) also enhances learning.19,24
However, according to McNeil et al.,19 use of con-
trolled feedback and manipulation of the intervals
for providing feedback may constitute the most
important consideration for motor learning.
McNeil and his colleagues1,19 describe two types
of feedback: knowledge of results (KR) and
knowledge of performance (KP). KR concerns
feedback about the correctness or incorrectness of
the movement. The KR-delay interval is the peri-
od between the response and KR. McNeil et al.19
advocate short delays to facilitate learning. They
also advise clinicians to avoid filling the delay with
extraneous activity. The post–KR-delay interval is
the period between KR and the subsequent
response. Because this is a time of active informa-
tion processing, McNeil et al.19 suggest no less
than 3 seconds before the next response is initiat-
ed. Shorter (versus longer) intervals of post–KR-
delay help maintain motivation and decrease the
demands on memory.
McNeil et al.19 also believe that summary rather
than immediate KR better promotes motor learn-
ing. In their view, immediate KR may provide too
much information while summary KR promotes
response variability. They suggest that summary
KR be provided for AOS over three trials initially
followed by greater response summary feedback.
KR should include information about any errors
but in a fairly general way. Reduced feedback
appears to be more facilitative than frequent KR
(e.g., bandwidth training).
KP is feedback about the specific aspects of the
patient’s performance. Examples of KP include
biofeedback (e.g., visipitch) and verbal feedback
(e.g., position of lips or tongue). Similar con-
straints apply to providing KP as to governing KR.
McNeil and his colleagues1,19 conclude their dis-
cussions of treatment for AOS by offering the fol-
lowing six clinical principals based on motor
training:
1. Treatment should be intensive (massed prac-
tice over long time periods).
2. Large numbers of repetitions (e.g., no fewer
than 20) of speech or nonspeech movements
are needed.
3. A neutral position should be established
between attempts.
4. Speech tasks should be used unless nonspeech
movements are necessary to achieve some
degree of success.
5. A hierarchical approach should be used. For
example, work on syllables in isolation versus
words and motorically simple phonemes
(vowels, frequently occurring or visible conso-
nants) before advancing to more complex
phonemes and voicing contrasts. (See also
Maas, Barlow, Robin, & Shapiro26 regarding
treatment of more complex targets prior to less
complex items.)
6. There should be a focus on prosody (e.g., con-
trastive stress drills).
Treatment programs
Wambaugh27 notes that the arrays of treatments
that have been developed for AOS over the years
have generally targeted improved accuracy of
articulatory positioning and transitioning within

and across sounds in utterances of various lengths.
These correspond to what Square-Storer28
described as treatments that enhance spatial tar-
geting and “phasing” at the segmental and syllable
levels and that McNeil et al.1 referred to as articu-
latory/kinematic approaches to treatment.
Wambaugh27 distinguishes another group of treat-
ments that address the rhythmic, temporal, or
prosodic aspects of speech production. For
Square-Storer,28 these are treatments that facilitate
the temporal schemata of speech and the sequenc-
ing of segments in longer utterances; for McNeil et
al.,1 they facilitate rhythm, rate, and stress.
Wambaugh27 also identifies a final group that
includes the use of alternative and/or augmenta-
tive communication strategies for treating patients
with AOS.
Approaches targeting improved accuracy of articula-
tory positioning and transitioning
Imitation, phonetic derivation or progressive
approximation, phonetic placement, integral stim-
ulation, and the key word technique comprise the
first group of approaches in this category. Wertz et
al.3 recommended that these approaches be used
in the treatment of patients with severe AOS.
Imitation of course consists of the patient simply
watching and listening as the clinician provides a
model and then trying to reproduce it as closely as
possible. Phonetic derivation consists of using
sounds or movements that the patient can make to
teach the production of sounds or movements that
the patient cannot make. In phonetic placement,
sounds are taught by describing how they are
made using graphs, drawings, or associations
while physically manipulating the articulators. In
integral stimulation, the clinician provides a mod-
el for imitation and exaggerates the presentation to
make the stimulus as salient as possible. The key
word technique promotes generalization of sound
production to many environments by practicing
target sounds in a few key words.
Rosenbek, Lemme, Ahern, Harris, and Wertz29
developed an eight-step task continuum that
incorporated many of the aforementioned tech-
niques. The approach incorporates modeling, imi-
tation, integral stimulation, and repetition using
Acquired Apraxia of Speech 55
both auditory and visual cues leading up to role
playing of the target stimulus. For Square-Storer,28
this technique encourages volitional control of
speech.
Imitation of phonetic contrasts (minimal pair
contrasts) is another approach in this category.
Wertz et al.3 advocate this approach for speakers
with moderate AOS. Generally, the method con-
sists of imitation of carefully selected speech
sound contrasts at various levels of production
(i.e., word, phrase, sentence). McNeil and col-
leagues have summarized1,27 the results of their
systematic investigations of the effects of this treat-
ment in speakers with AOS.
Approaches addressing the rhythmic, temporal, or
prosodic aspects of speech production
Three primary methods are included under this
grouping: melodic intonation therapy (MIT),
vibrotactile stimulation, and prompts for restruc-
turing oral muscular phonetic targets (PROMPT).
These are discussed in order.
Despite Sparks and Holland’s30 claims that the
emphasis in MIT is on recovery of prepositional
language expression rather than the motor aspects
of speech, MIT has become a popular technique
for treating AOS. The primary elements of melod-
ic intonation include slow tempo, precise rhythm,
and distinct stress. Sparks and Holland suggested
that the slower and more lyrical tempo of intoned
speech should result in more precise speech
rhythm and accentuated points of stress that facil-
itate articulation. Unfortunately, reports attesting
to the effects of this approach with AOS are large-
ly anecdotal.1
Rubow, Rosenbek, Collins, and Longstreth31
used vibrotactile stimulation to provide sensory
cues to a patient with AOS regarding the rhythm
and stress of multisyllabic words. Vibrations of
varying intensities are provided to the patient’s
index finger for each syllable the clinician speaks
in polysyllabic words. The patient then repeats the
words without the auditory model but with the
vibrations signaling the rhythm and stress patterns
of the word.
The PROMPT system32 is a tactile-kinesthetic
oral-facial cueing system that uses tactile cues
56 TOPICS IN STROKE REHABILITATION/WINTER 2004
about the face and neck of the patient to represent
the various positions of the articulators during
speech. Proprioceptive, pressure, and kinesthetic
cues are provided to the patient with AOS to sig-
nal various aspects of speech production includ-
ing the relative timing of speech segments. Freed,
Marshall, and Frazier33 investigated the outcome
of PROMPT treatment on a core vocabulary of
functional words and phrases in a patient with
severe AOS and aphasia. Strong acquisition and
maintenance effects were observed for the trained
items but generalization to untrained items was
not observed. In another study, Bose, Square,
Schlosser, and van Lieshout34 found evidence for
heightened awareness of movement trajectories
and sequences in a young individual with Broca’s
aphasia and apraxia of speech after PROMPT
treatment. Unlike the study of Freed et al., gener-
alization of improved speech precision and
sequencing of speech movements was found for
untrained sentences.
Additional treatment approaches that address
the rhythmic aspects of speech production include
pacing techniques using finger counting, hand
tapping, and/or a metronome. Speech prolonga-
tion is another technique that promotes rhythmic
control. Finally, electromagnetic articulography
has also been used to provide visual feedback
regarding real-time movements of the tongue tip
during speech production.35
Alternative and/or augmentative communication
strategies
The final group of techniques utilizes gestural
training alone or in combination with spoken
word training. In the latter approach, the gestures
are viewed as intersystemic symbolic/linguistic
facilitators, that is, relatively intact nonverbal abil-
ities that help reorganize speech output.
Communication boards provide one type of ges-
tural system to improve communication. Simple
gestures that are translated directly into a word or
phrase constitute another gestural approach.
Amer-Ind,36 a gestural system based on American
Indian Sign, uses manual illustrators to communi-
cate information that can be used with or without
verbal accompaniment.
What to treat
It is clear from the foregoing discussion that
numerous approaches are available for the treat-
ment of AOS. However, few if any treatment stud-
ies have been reported where the patients who are
the focus of the investigation were diagnosed with
pure AOS. In most instances, patients with AOS
also demonstrate a coexisting aphasia. Treatment
approaches therefore will be influenced by the
presence of an accompanying aphasia (e.g.,
Broca’s aphasia, global aphasia).
Tonkovich and Peach23 describe three primary
types of intervention procedures for the
aphasic/apractic speaker: (a) those promoting
reacquisition of syntactic form only, (b) those pro-
moting articulatory precision or sequencing only,
and (c) those purporting to do both. There are
myriad programs in the aphasia literature that
address improved syntactic form, including
Matrix Training,37–39 the Helm Elicited Language
Program for Syntax Stimulation,40,41 Mapping
Therapy,42,43 and Treating Underlying Forms.44 A
number of programs were identified previously
that address articulatory precision and sound
sequencing, including the eight-step task continu-
um and PROMPT treatment. Finally, MIT and
minor hemisphere mediation would be examples
of programs that address both syntactic form and
articulatory precision.
Tonkovich and Peach23 also describe some gen-
eral principles for treating apractic–aphasic
patients. First, train basic comprehension skills
before production. In the patient for whom basic
comprehension is retained, higher level compre-
hension skills should be treated concurrently with
production skills. Second, determine the relative
contribution of each disorder with regard to the
patient’s overall communicative impairment.
Patients for whom the apraxic component of the
disorder precludes the development of syntactical-
ly accurate phrases of increasing length will
receive treatment for their AOS before attention is
given to syntactic accuracy. Third, clinicians
should be realistic about the maximal recovery
status of their patients. This will influence when
and how long to pursue verbal, verbal plus ges-
tural, or gestural treatment programs. Fourth, cli-

nicians should encourage self-evaluation and self-
cueing in their patients at an early time to support
recovery and generalization of treatment. And
finally, clinicians should use patient behaviors,
rather than static programs, to develop hierarchies
for training.
Odell45 also provides guidance for selecting the
targets for treatment in the individual with AOS.
Similar to Tonkovich and Peach’s second princi-
ple, her first decision concerns which aspect of
general communication to target (i.e., speech
behaviors, attitudes, emotional adjustment).
When the decision concerns speech behaviors, the
clinician focuses on articulatory errors versus
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