Handbook of Clinical Neurology, Vol.

88 (3rd series)
Neuropsychology and behavioral neurology
G. Goldenberg, B.L. Miller, Editors
# 2008 Elsevier B.V. All rights reserved

Chapter 13

Apraxia of speech

WOLFRAM ZIEGLER*

Entwicklungsgruppe Klinische Neuropsychologie, Munich, Germany

13.1. History and terminology
The term apraxia of speech dates back to the 1960s,
when F.L. Darley borrowed it from the ideas of H. Liep-
mann to describe an impairment of the capacity to pro-
gram the movements of the articulators for the purpose
of speaking (Darley, 1968). Liepmann (1900, p. 129)
used the term ‘Apraxie der Sprachmuskeln’ (apraxia
of the language muscles) to characterize the ‘motor
aphasia’ of his patient ‘T.’ The history of this disorder
is characterized by terminological confusions and theo-
retical disputes, mainly originating from strong dissents
concerning relationship and interface between the lin-
guistic and motor aspects of speaking.
Broca had studied several patients who, after left
inferior-frontal lesions, were unable to speak, but had
normal or virtually normal comprehension, normal
intelligence, and whose speech muscles were not signif-
icantly paretic. He coined the term aphemia to describe
this disorder, and characterized it as a loss of the faculty
of articulate language, i.e., an inability to coordinate the
movements pertaining to the articulation of syllables
and words (Broca, 1861; 1865). On another occasion
Broca characterized the syndrome as a loss of ‘the mem-
ory of the processes required for the articulation of
words’ (‘. . .le souvenir du procédé qu’il faut suivre pour
articuler les mots’; cf. Liepmann (1913, p. 490)). Later,
in Wernicke’s and Lichtheim’s theory, the terms motor
aphasia and Broca’s aphasia were used to refer to this
disorder, which was then considered to result from a
destruction of speech motor images (‘Sprechbewe-
gungsbilder’) located in the left anterior perisylvian
region (Lichtheim, 1885). Associating the motor with
the linguistic aspects of speech was not a sacrilege in
these times, and a few terminological relicts from this
era, such as the labels pure motor aphasia or subcortical
motor aphasia, have survived until more recently
(cf. Kertesz, 1985, in the latest issue of this Handbook).
At the beginning of the twentieth century P. Marie
introduced the term anarthria to underscore his convic-
tion that the impairment initially described by Broca is a
motor syndrome which must strictly be kept separate
from aphasia (cf. Alajouanine et al., 1939). This position
more or less anticipated the theoretical stance prevailing
in the second half of the last century, when aphasia was
seen as a dysfunction of the ‘linguistic module’ and, as
such, entirely independent of cognition, perception,
and motor functions. In this view, disordered language
production could be either aphasic (i.e., linguistic), or
dysarthric (i.e., motor), and the proponents of this dual-
ism consequently used the terms dysarthria or cortical
dysarthria when they referred to Broca’s aphemia
(e.g., Bay, 1957; Schiff et al., 1983). As a consequence,
the disorder—which had been the starting point of mod-
ern aphasiology—disappeared from the screen of the
new aphasiology school, because, in a strict sense, it
was no longer related to the ‘language organ’ proper.
A source of confusion within the syndromal theory of
these days was that ‘articulatory agility’ nonetheless
constituted an important criterion for the differential
diagnosis of the aphasic syndromes, especially for the
diagnosis of Broca’s aphasia (Kaplan et al., 1983).
Darley’s understanding of the disorder, on the
contrary, emerged from a neurological taxonomy of
movement disorders which distinguished between ‘ele-
mentary’ motor syndromes, such as paresis, ataxia, or
akinesia, and an impairment of hierarchically higher
aspects of motor planning or programming, i.e., ideo-
motor apraxia (Darley et al., 1975). His introduction
of the term apraxia of speech was guided by phenom-
enological similarities of the speech disorder with limb
apraxia, such as its attribution to left-hemisphere

*
Correspondence to: Wolfram Ziegler, PhD, Entwicklungsgruppe Klinische Neuropsychologie, Dachauer Strasse 164, D 80992.
München, Germany. E-mail: wolfram.ziegler@extern.lrz-muenchen.de, Phone: þ49-89-1577474, Fax: þ49-89-156781.
270 W. ZIEGLER
damage, its error inconsistency, or the helpless appear-
ance and groping behavior of apraxic patients who
are confronted with a (speech or motor) task they are
unable to perform (see Chapter 16). On clinical
grounds, Darley’s taxonomic distinction between the
dysarthrias and apraxia of speech stood the test of time,
since in many clinical respects, including therapeutic
approaches, dysarthric patients are fundamentally
different from patients with apraxia of speech.
13.2. Definition
A definition relating apraxia of speech to theories of
spoken language production postulates that it is an
impairment of the phonetic encoding of words and sen-
tences. Accordingly, apraxic speakers have (a) a pre-
served knowledge of the phonological form of the
words they intend to produce (i.e., ‘how the words
sound’), and (b) no significant paresis, ataxia, akinesia,
or other motor execution problem which would prevent
them from performing the required speech movements.
Instead, their problem is to transform the more abstract
representations of word forms into the motor commands
that guide the articulators, or, in the terms used by Darley,
to program the positioning of speech organs and the
sequencing of articulations (Darley, 1968; Code, 1998).
This definition suffers from the drawback that it
relies on model-based terms, such as phonetic encoding
or motor programming, whose semantics is not suffi-
ciently clear to make the definition clinically useful.
Instead, an operational definition of the disorder would
focus on the most salient symptoms of apraxia of
speech, i.e., disfluent, groping, and effortful speech with
phonetic distortions and phonemic paraphasias, and a
frequent occurrence of false starts and restarts (see
13.3). Effortful and phonetically distorted speech are
considered suggestive of the motor nature of the disor-
der, the presence of silent groping movements and of
self-initiated corrections indicates that the patient strug-
gles for the realization of some stable phonological tar-
get he/she has in mind, and the fact that the symptoms
are variable and inconsistent is taken as evidence
against more elementary, dysarthric pathomechanisms,
such as paresis, ataxia, akinesia, dyskinesia/dystonia,
etc. However, these symptoms are far from unequivocal
and clinicians do not always agree on their presence or
absence, which often creates uncertainty in the differen-
tial diagnosis of apraxia of speech vs. aphasic phonolo-
gical impairment or vs. dysarthria.
Within the ICF classification system of the World
Health Organization (2005), apraxia of speech is listed
among the disturbances of ‘specific mental functions of
sequencing and coordinating complex, purposeful
movements’ (World Health Organization, 2005, b176).
13.3. Clinical presentation
Patients with apraxia of speech may present with a broad
variety of clinical signs, depending on the severity of
their speech impairment and the pattern of accompany-
ing aphasic symptoms.
In its most severe form, apraxia of speech may result
in a total inability to voluntarily produce even a single
word, syllable, or speech sound (apraxic mutism). In
stroke patients this stage is frequently confined to the first
few hours or days postonset and is then followed by a
transition into the characteristic pattern of apraxic speech
(see below). In rare cases, apraxic mutism after a left
hemisphere lesion may extend over several weeks
(Lecours and Lhermitte, 1976; David and Bone, 1984).
Persisting mutism combined with oral–facial apraxia
was observed in patients with bilateral opercular lesions
(Groswasser et al., 1988; Pineda and Ardila, 1992). Since
the complete loss of speech in these cases was not ascrib-
able to paresis of the speech musculature or to severe
linguistic impairment, a speech-apraxic mechanism has
been considered as the underlying cause.
In less severe cases, patients with apraxia of speech
are able to pronounce isolated syllables or words or
even short phrases. They produce many speech errors,
both of a phonemic and a phonetic type (see
Table 13.1). The term phonemic error refers to substi-
tutions, omissions, or additions of speech sounds, such
as *gog for dog, *cocodie for crocodile, or *clat for
cat. (An asterisk indicates that the linguistic form that
follows is not a real word.) Typically, these aberrations
sound well-articulated, as if the patient had erroneously
created a nonexistent string of sounds, but pronounced
the wrong form smoothly and adequately. Most often
the resulting nonword is phonemically close to the
intended word, and substituted phonemes share many
features with their target phonemes; e.g., if cow is pro-
nounced as *gow, the target phoneme /k/ and its substi-
tute /g/ are both produced by forming a complete
closure with the back of the tongue in the posterior
palatal region, and they differ only by their timing of
the laryngeal gesture (adduction of the vocal folds
occurring earlier in /g/ than in /k/). Another frequent
type of phonemic error is deletion of a consonant in
consonant clusters, such as *fog for frog or *tone for
stone, most often at the onset of a word or a syllable
(Aichert and Ziegler, 2004). The mechanism causing
these errors has usually been described as articulatory
simplification (Romani and Calabrese, 1998).
The term phonetic distortion, on the other hand,
refers to an error type in which the integrity and well-
formedness of speech sounds is destroyed (Table 13.1).
For instance, a phonetically distorted /f/ neither sounds
like a proper /f/, nor like a /v/ or /p/ or like any other
 APRAXIA OF SPEECH 271
Table 13.1
The symptoms of AOS

Segmental impairment: Errors concerning the segments (phonemes) of words

Phonetic distortions Phonemic paraphasias
gradual aberration from target phoneme categorical aberration from target phoneme
phonemes sound awkward, ill-formed phonemes sound well-articulated
Error variability
Errors are inconsistent: a patient may produce the same sound accurately or inaccurately, and multiple inaccurate productions
may have different qualities.
Islands of unimpaired speech: Even severely impaired speakers may at times produce entirely accurate words or phrases.
Prosodic impairment: Disturbances concerning the flow and melody of speech
Speech is hesitant and halting, with many pauses between syllables or words, with false starts, repairs, and repetitive
attempts at initiating speech. Pauses are often accompanied by prolonged articulatory groping. Disfluent articulation corrupts
the regular rhythm and melody of speech.

consonant of the patient’s native language. Likewise,
transitions between phonemes or syllables may sound
awkward, as if the patient had lost the ability of
smoothly moving from one articulatory position to
the next. The fact that phonetically distorted sounds
no longer pertain to the phoneme inventory of the
patient’s native language is taken as evidence for an
obvious motor basis of phonetic distortions.
On closer inspection of the error patterns of apraxic
speakers, a structural relationship can often be
observed between gradual (phonetic) and categorical
(phonemic) errors, which suggests that the two types
of errors may result from a common motor mechanism
(Ziegler and Cramon, 1986; Ziegler, 1987; Table 13.2).
For instance, phonetic denasalizations of nasal conso-
nants (i.e., /m/ or /n/ sound as if the nasal passage were
obstructed) often go together with a frequent occur-
rence of nasal-to-oral phoneme substitutions (i.e., /m/,
/n/ or /ng/ are substituted by /b/, /d/ or /g/), suggesting
a problem with the interplay between velar adjustments
and the articulations of the lips and the tongue in both
error types. Alternatively, audible over-aspiration of
voiceless plosives (e.g., /t/ sounds like /thhh/) often co-
occurs with a prominence of voiced-voiceless parapha-
sias (substitutions of /b/by /p/, /d/ by /t/, or /g/ by /k/),
indicating an impairment of the appropriate timing of
laryngeal adductory and abductory movements relative
to supralaryngeal articulations as the mechanism
underlying both gradual and categorical voicing aber-
rations. Table 13.2 lists more examples to illustrate
similar relationships between phonetic and phonemic
errors. However, it must be admitted that more com-
plex phonemic errors may also occur in apraxia of
speech, which cannot be traced back straightforwardly
to such simple motor mechanisms.
A salient property of apraxic speech is that the
pattern of phonetic impairment lacks any apparent con-
sistency. As an example, the consonant /s/ may be
produced correctly in one instance, sound like a voiced
/z/ in another instance, hover somewhere between /s/
and /sh/ on a third occasion, or even be completely uni-
dentifiable in a fourth incidence. Or, the transitions from
/s/ to /a/ to /m/ in the word some may sound fluent and
smooth on one occasion, but laborious and clumsy on
the next. The variability of the error pattern may even
go so far that severely distorted stretches of speech are
sometimes interspersed by ‘islands’ of entirely fluent
and well-formed articulation. During administration of
a word repetition test, for instance, a patient who is vir-
tually unable to pronounce any of the test tokens, may
unexpectedly come out with a fluent and completely
intelligible comment or with a clearly articulated
expression of her frustration (Table 13.1).
The phonetic and phonemic aberrations in apraxic
speech are usually overarched by a halting and disflu-
ent manner of speaking. Patients often require several
attempts at initiating an utterance, they may produce
off-target onsets and re-starts and may separate the syl-
lables of a word by pauses or by vocalic intrusions
(Table 13.1). Hesitations are often accompanied by a
visible groping or by sounds resulting from searching
movements of the larynx and the articulatory organs
(Hoole et al., 1997). These events interrupt the flow
of speech in a way that orderly rhythmical and intona-
tional patterns are no longer recognizable. In less
severe cases speech may be reasonably fluent and only
retain some scanning, syllable-by-syllable rhythm with
occasional phonemic and phonetic errors (McNeil
et al., 1997; Croot, 2002).
13.4. Etiologies
The primary cause of apraxic speech impairment is left
hemisphere stroke. The great majority of patients with
apraxia of speech have suffered from infarction or hemor-
rhage of the left middle cerebral artery (central cortical
272 W. ZIEGLER
Table 13.2
Phonetic vs. phonemic errors: examples of common articulatory-based error mechanisms

Phonetic distortions* Phonemic paraphasias

Oral–nasal distinction (elevation vs. lowering of the soft palate)

ball ! mball, bmall, ~ball
(b sounds partly or completely nasalized, but still sounds different from m) ball ! mall
insufficient, ill-timed, or missing elevation movement of the soft palate
nail ! dnail, ndail, ~dail
(n sounds partly or completely de-nasalized, but still sounds different from d) nail ! dail
insufficient, ill-timed, or missing lowering movement of the soft palate
Voiced–voiceless distinction (adduction vs. abduction of vocal folds)
dull ! dull
_ insufficiently voiced, but still sounds different from t)
(d sounds dull ! tull
insufficient adduction or premature abduction of glottis
tail ! dail
_ insufficiently unvoiced, but still sounds different from d)
(t sounds tail ! dail
insufficient abduction or premature adduction of glottis

*While phonemic paraphasias can be transcribed orthographically, a formal description of phonetic distortions requires phonetic transcription
symbols. Here, a simplified transcription style was chosen for the sake of readability.

branch) and its perforating arteries, or of the left lateral
lenticulostriate arteries. A few cases of apraxia of speech
after right hemisphere strokes have also been reported,
both in right-handers (‘crossed apraxia of speech’;
Delreux et al., 1989; Balasubramanian and Max, 2004)
and in left-handed persons (Tanji et al., 2001).
Other etiologies can also cause apraxia of speech, e.g.,
traumatic brain injury (Pellat et al., 1991), hematoma
caused by arteriovenous malformation (Ruff and Arbit,
1981), or brain tumor (Mori et al., 1989). Moreover,
apraxia of speech may be among the initial symptoms
of primary progressive aphasia (Nestor et al., 2003) and
of frontal cortical atrophy syndromes (Broussolle et al.,
1996), including Pick’s disease (Sakurai et al., 1998).
13.5. Localization
Broca’s attempt at localizing the ‘faculty of articulate
language’ has often been considered as the birth of mod-
ern neuropsychology. His examinations of the brains of
several patients with aphemia had led him to postulate
that (a) speech, like other skilled motor activities, is in
most people controlled by the left hemisphere (Broca,
1865), and (b) the seat of this faculty is the posterior part
of the (left) inferior frontal convolution—the region
which later was named after Broca (Broca, 1861). Since
then, the classic model has repeatedly been challenged,
mainly by case studies demonstrating that circumscribed
lesions to Broca’s area did not result in persisting speech
problems (Alexander et al., 1990). For instance, a number
of patients were reported who, after complete ablation of
the posterior part of left inferior frontal cortex, had no or
virtually no speech or language impairment (see Hecaen
and Consoli (1973), for a review). It was also noted that
the patients originally described by Broca had large
lesions which included far more than the posterior part
of the inferior frontal convolution (Mohr et al., 1978).
Basing on such considerations, several alternative models
have been proposed during the course of time.
13.5.1. Subcortical white matter
In Dejerine’s view, the pure motor form of Broca’s
aphemia, which he had termed subcortical motor apha-
sia, resulted from lesions to fibers connecting Broca’s
area with the motor centers in the brainstem (Dejerine,
1891) (‘. . .rupture des fibres qui relient la circonvolu-
tion de Broca aux noyaux bulbaires. . .’ (Dejerine
1891, p. 161)). Dejerine’s interpretation nowadays is
at odds with the widely accepted view that the
cortico-bulbar projections implicated in speaking are
organized bilaterally and that one-sided lesions to this
system can be compensated for within short time
(Muellbacher, Artner, and Mamoli, 1999). However,
the hypothesis of a subcortical mechanism has been
upheld until very recently. For instance, in their review
of 13 cases from the literature and their presentation of
four new cases, Schiff et al. (1983) identified the white
matter deep to the inferior motor strip and the opercular
part of the inferior frontal gyrus, including the anterior
limb of the internal capsule of the dominant hemi-
sphere, among the regions responsible for the ‘org-
anization of simultaneous and sequential motor
actions into well-articulated speech’ (p. 726). In a
 APRAXIA OF SPEECH
comprehensive analysis of the subcortical pathways
implicated in severe non-fluency in aphasia, Naeser,
Palumbo, Helm-Estabrooks, Stiassny-Eder, and Albert
(1989) postulated a significant role of two distinct sub-
cortical regions in the genesis of persisting articulatory
impairment, i.e., (1) the ‘medial subcallosal fascicu-
lus’ area, located deep to Broca’s area, and (2) the
middle portion of the periventricular white matter area,
located deep to the mouth and face area of primary
sensory-motor cortex, both in the left hemisphere. In
a recent fMRI-study of four patients with severe per-
sisting nonfluent speech, presumably including verbal
apraxia, Naeser et al. (2005) suggested that white mat-
ter lesions in these areas may be responsible for a trans-
callosal disinhibition of right motor cortical and right
SMA activity causing severe nonfluency and speech
motor problems. The idea that deep-reaching lesions
may prevent recovery of speech functions through
transcallosal (as well as intrahemispheric) mechanisms,
however, is much older, and originally goes back to
Kleist (for a discussion cf. Mohr et al., 1978; Ruff
and Arbit, 1981).
13.5.2. The ‘lenticular zone’
Pierre Marie, after a re-examination of Broca’s most
prominent cases and a review of several new cases,
denied that the left posterior inferior frontal gyrus plays
any specific role in language. Marie ascribed the syn-
drome he called anarthria to lesions within the ‘lenti-
cular zone,’ i.e., a rectangular area, extending—on a
horizontal brain section—from the anterior to the pos-
terior aspect of the insula and comprising the insular
cortex and the subcortical structures deep to it (extreme
capsule and claustrum, caudate and lenticular nuclei),
in either the left or the right hemisphere (Alajouanine
et al., 1939; Lecours and Lhermitte, 1976). This
hypothesis, which—at least in its most general form—
was disproved by numerous observations reported later
on (Liepmann, 1907), is no longer valid. However, the
‘lenticular zone’ in the left hemisphere includes brain
structures which are still considered relevant in apraxia
of speech today, i.e., the white matter areas discussed
above, the anterior insular region (see 13.5.4), or,
according to a small number of single case reports, the
basal ganglia (Peach and Tonkovich, 2004).
13.5.3. Left inferior motor cortex
In several case studies, lesions to the inferior portion of
the left precentral gyrus, i.e., the face, mouth, and larynx
region of left primary motor cortex, were mentioned as a
potential cause of apraxia of speech (Lecours and Lher-
mitte, 1976; Tonkonogy and Goodglass, 1981; Schiff
273
et al., 1983, cases 1, 2; Kushner et al., 1987; Mori
et al., 1989; LeRoux et al., 1991; Tanji et al., 2001).
According to the classical model, left motor cortical
lesions should result in a unilateral upper motor neuron
syndrome (Urban et al., 2001). Consequently, Bay
(1957) suggested that the syndrome (which he termed
cortical dysarthria) results from a spastic movement
disorder. Yet, the symptoms characterizing apraxia of
speech are not explainable by the mechanisms underly-
ing the spastic syndrome, i.e., increased tone, reduced
force, and reduced dexterity. Moreover, the severity
and persistence of the disorder in many apraxic speakers
cannot be reconciled with the fact that important parts of
the corticobulbar system are organized bilaterally and
that unilateral lesions to this system can usually be com-
pensated for within a few days or weeks (Muellbacher
et al., 1999).
In a different view, the left inferior precentral region
(together with the opercular portion of the inferior fron-
tal gyrus and underlying white matter) is considered
part of a specialized motor network which integrates
‘simultaneous and sequential motor actions into well-
articulated speech’ (Schiff et al., 1983). It is known that
prerolandic motor cortical regions are functionally
reorganized during long-term practice of specific motor
skills (Karni et al., 1995; Elbert et al., 1995; Ungerlei-
der et al., 2002). Since adult speech is the result of
extensive long-term motor learning, such mechanisms
may account for a specific role of the left inferior motor
cortex and the regions immediately anterior to it in
speaking. Destruction of this network would produce
a complex disturbance of the interplay between articu-
latory gestures rather than merely a hemiparesis of the
oral and facial muscles of the right side.
13.5.4. Left anterior insular cortex
Left insular cortex, which is part of P. Marie’s ‘lenticu-
lar zone’ (see above), has often been mentioned as a
potential locus of speech motor impairments (Mohr
et al., 1978; Shuren et al., 1995). A comprehensive
lesion study was conducted by Dronkers (1996), who
compared overlaps of CT- or MRI-documented focal
lesions of 25 patients with apraxia of speech (AOS) with
those of 19 patients who were not apraxic. All patients
had suffered single left-hemisphere infarcts and were
more than one year post-onset. The lesions of the AOS
patients overlapped in a small region within the left pre-
central gyrus of the insula, and, at the same time, this
region was spared in the overlap of the 19 non-apraxic
patients. In the years following publication of Dronkers’
investigation several single case studies of patients with
apraxia of speech after left anterior insular lesions were
reported (Kumabe et al., 1998; Nagao et al., 1999;
274 W. ZIEGLER
Duffau et al., 2001; Nestor et al., 2003). More recently,
Dronkers and Ogar (2004) extended their findings by
reporting on 23 patients with left anterior insular
lesions, all of whom had apraxia of speech. A role of left
anterior insular cortex in articulation was also corrobo-
rated by functional imaging studies (Wise et al., 1999;
Riecker et al., 2000) and by an MEG-study (Kuriki
et al., 1999). However, the fMRI data reported by
Riecker et al. (2000) suggested that the implication of
left anterior insular cortex is confined to the actual
execution of speech movements (‘overt performance’)
and is absent during covert speech. The conclusion that
AOS might result from a lesion to this area is not compa-
tible with the view that the apraxic speech impairment
extends to covert articulation as well, especially that it
also abolishes the covert rehearsal processes involved
in verbal short-term memory tasks (Waters et al.,
1992; see 13.8.3).
13.5.5. Broca’s area, revisited
More recently the pendulum swung back again towards
Broca’s original model. Hillis et al. (2004) studied 80
patients with left hemisphere, non-lacunar strokes, 40
with and 40 without insular damage. One crucial aspect
of their approach was that they examined patients with
acute infarcts, i.e., within 24 hours after stroke, with
the aim of identifying patients with transient speech
impairments after small infarcts—a group which
may have gone unnoticed in lesion studies of patients
with chronic AOS. A second specialty of this study
was that Hillis et al. (2004) used diffusion- and
perfusion-weighted MRI methods, with the hope of
identifying—over and above the structurally lesioned
brain regions—those areas which may be dysfunctional
as a consequence of hypoperfusion. No association was
found between the occurrence of AOS and left anterior
insular lesions in the large patient sample of this inves-
tigation. However, there was a statistically significant
association between the presence of AOS and a hypo-
perfusion or structural lesion of Broca’s area, as well
as a strong association between the absence of AOS
and the absence of infarcts or hypoperfusion in Broca’s
area. Hillis et al. (2004) speculated that the association
of AOS with anterior insular damage reported by Dron-
kers (1996)—though statistically reliable—was not
causative, but was rather due to the fact that chronic
apraxia of speech usually results from large MCA
infarctions, and that—by virtue of the distribution of
cerebral blood flow—the insula is very likely within
the overlap region of large MCA strokes. Basing on
the presumed validity of their combined diffusion/per-
fusion-weighted imaging method and their inclusion
of patients with and without AOS early after onset,
Hillis et al. (2004) claimed that the left posterior infer-
ior frontal gyrus is crucially involved in articulation.
Their findings were consistent with the results of three
earlier PET experiments examining oral reading and
word repetition in normal subjects (Price et al., 2003),
in which speech-related activation was found in Bro-
ca’s area, but not in the anterior insula. The results of
a PET study of patients with recovered apraxia of
speech suggested that it is especially the posterior por-
tion of the left pars opercularis which is responsible for
motor control aspects of speech production (Blank
et al., 2003).
Indirect neurobiological evidence for a role of
Broca’s area in speech motor control has only recently
been presented by Petrides et al. (2005). These authors
showed that, in macaque monkeys, the cortical region
lying anterior to the ventral part of premotor cortical
area 6 is cytoarchitectonically comparable to dysgranu-
lar human cortical area 44, and that the cytoarchitec-
tonics of its bordering cortical regions is comparable,
rostrally, to human cortical area 45 (granular) and, caud-
ally, to human cortical area 6V (agranular). Most impor-
tantly, intracortical microstimulation within this area
elicited complex oral–facial, lingual, and respiratory
movements, suggesting that BA 44 might have evolved
as an area exercising high-level control over the motor
system involved in spoken language communication.
13.5.6. The localization of apraxia of speech:
tentative conclusions
The inconsistency of the neuroanatomic findings related
to apraxia of speech may be attributable to several
sources, such as (1) divergent taxonomies or inconsis-
tent definitions of the speech impairment in the reported
cases (Mohr et al., 1978), (2) individual variability in
gyral patterning and a lacking reliability of sulcal con-
tours as cytoarchitectonic landmarks in left anterior
perisylvian cortex (Amunts et al., 1999), or (3) indivi-
dual variability in structure–function relationships in
this region (Hillis et al., 2004). Despite these uncertain-
ties, a few tentative conclusions can be drawn. It is safe
to say that AOS is a syndrome of the dominant hemi-
sphere and that it occurs after lesions to the anterior peri-
sylvian region. Within this region, parts of Broca’s area
and eventually also its caudally neighboring primary
motor cortical region seem to play an important role,
at least initially. A causative role of left anterior insular
cortex still waits to be proven. One might speculate that
the process of speech motor learning, which extends
over more than the first decade of our life, creates
a large, left-lateralized representation area dedicated
to the planning and/or programming of speech
movements. This region extends anteriorly from the
 APRAXIA OF SPEECH
face/mouth/larynx region of left rolandic motor cortex
to premotor cortex and potentially also includes insular
cortex. The different parts of this network may subserve
specific functions in speech motor control, and lesions
to different subunits may create subtypes of speech
impairment which we have so far been unable to differ-
entiate. Small cortical lesions alone are probably not
sufficient to cause severe, persisting AOS. Involvement
of a larger part of the network or of communicating
fibers may aggravate the problem and prevent a func-
tional reorganization of articulation, eventually through
mechanisms of transcallosal disinhibition.
13.6. Differential diagnosis
13.6.1. Apraxia of speech vs. dysarthria
The dysarthrias comprise speech disorders whose under-
lying pathomechanisms correspond to one of the neuro-
motor pathologies known from limb motor control, such
as paresis, akinesia, rigidity, ataxia, dyskinesia/dystonia,
etc. Accordingly, the speech patterns of dysarthric
patients are characterized by predictable and virtually
constant disturbances of speech breathing, phonation,
and articulation, causing symptoms such as increased fre-
quency of inspirations, deviant voice quality, altered
pitch or loudness, undershooting articulation, hypernasal-
ity, reduced articulation rate, etc. Unlike apraxic speakers
with their variable articulatory skills, patients with mod-
erate or severe dysarthria constantly demonstrate the
same quality of their phonetic distortions, and their out-
put is never entirely symptom-free. Moreover, as a conse-
quence of their constant symptom pattern, dysarthric
patients rarely make attempts at correcting themselves
or repairing their vocal or articulatory deviations. Hence,
they do not show disfluencies and initiation problems
related to self-initiated repairs—a symptom which is
typical of apraxic speech. Another important clinical cri-
terion is that persisting dysarthric conditions of a signifi-
cant degree have rarely been observed after unilateral
hemispheric lesions (Urban et al., 2001).
13.6.2. Apraxic mutism vs. akinetic or paralytic
mutism
In the absence of any verbal utterances, the apraxic nature
of a mutistic state cannot be diagnosed with certainty.
Mutism may also occur as a sign of complete akinesia,
e.g., after mesodiencephalic or after left or bilateral med-
ial–frontal lesions (Alexander, 2001; Nagaratnam et al.,
2004), where it is seen as a consequence of reduced cor-
tical ‘arousal’ or as an impaired activation of the speech
motor system (Choudhari, 2004). A behavioral sign
which can be useful to distinguish apraxic from akinetic
275
mutism is that the former is usually associated with
effortful struggling and a visible groping for articulation,
whereas patients with akinetic mutism often make no for-
ceful attempts at speaking. Recovery from akinetic mut-
ism after left ACA-infarction is often characterized by
transient hypophonia and hypokinetic articulations,
sometimes also by stuttering, and by transcortical motor
aphasia (Kumral et al., 2002).
Mutism may also result from a complete bilateral
paralysis of the speech muscles, e.g., in patients with
a Foix–Chavany–Marie or bilateral anterior operculum
syndrome, but this state is distinguishable from apraxic
mutism by visible signs of increased tone or a general-
ized paresis of the oral and facial muscles. The full-
blown syndrome of pseudobulbar mutism is often also
accompanied by pathologic laughter or crying (Mao
et al., 1989).
13.6.3. Apraxia of speech vs. phonological
impairment
The distinction between apraxia of speech and phono-
logical impairment (as it is seen, for instance, in con-
duction aphasia) may cause considerable problems in
clinical diagnosis. Confusions will usually not occur
in patients who present with a fluent phonemic jargon,
i.e., who produce severely distorted, often unrecogniz-
able word forms and create new words (‘neologisms’),
and whose output nonetheless sounds well articulated
and comes out fluently. Phonemic jargon, which can
be part of a severe Wernicke’s aphasia, has no similari-
ties with the clinical pattern of apraxia of speech (see
Chapter 14).
Other aphasic patients may produce fewer phonemic
errors and generate word forms which are much closer
to their targets. When articulation in these patients
sounds accurate and when they speak fluently, without
demonstrating the typical groping and self-correcting
behavior of apraxic speakers, they are diagnosed as
phonologically impaired. Phonological impairment
may be part of any aphasic syndrome, and it is the
major symptom of conduction aphasia (see Chapter
14). Confusion with apraxia of speech may result
from the fact that disfluencies resembling those seen
in apraxic speakers may also occur in patients with
aphasic–phonological problems, where they indicate
word finding difficulties or a phonological ‘conduite
d’approche’—behavior rather than a speech motor
problem.
It has been speculated that phonological impairment
afflicts word and syllable endings more than word and
syllable onsets, whereas the reverse is true for apraxia
of speech (Aichert and Ziegler, 2004), but there is still
too little empirical evidence for such a distinction.
276 W. ZIEGLER
According to a more traditional criterion, patients
with apraxia of speech ‘know what they want to
say and how it should sound.’ Despite their speech
impairment they should therefore be able to resolve
silent meta-phonological tasks, e.g., recognize rhymes,
estimate word lengths, or dissect syllables or words
into their phonemes. However, in clinical practice this
is not a safe diagnostic indicator (see 13.8.3).
Another criterion which has often been mentioned
in the traditional literature is based on the claim that
patients with phonological impairment, in addition to
their speech problem, also have a writing impairment,
whereas patients with ‘pure’ apraxia of speech have
preserved writing. As a matter of fact, in some of the
AOS patients reported in the literature writing was con-
siderably better than speech, or was even completely
preserved (e.g., Lecours and Lhermitte, 1976). How-
ever, brain lesions causing apraxia of speech may, by
virtue of their size and location, also destroy the circui-
tries specific to writing, hence impaired writing can
certainly co-occur with apraxia of speech. Moreover,
since written language can be produced along multiple
separate routes, preserved writing is not necessarily
incompatible with phonological impairment (e.g.,
Mohr et al., 1978; Ellis et al., 1983).
13.6.4. Other related syndromes
Foreign accent syndrome (FAS) is a rare condition of
acute onset, mostly after stroke, in which a patient
speaks with an audible foreign accent, as if she/he were
non-native. Often, the accent cannot unambiguously be
assigned to some specific foreign language (Christoph
et al., 2004), but in some of the reports listeners agreed
in saying that the accent was French, German, Irish,
etc. The first case description was of a young Czech
butcher who, after a stroke, sounded as if he were Polish
(Pick, 1919). A further prominent case was a Norwegian
woman who, during a German bomb attack in World
War II, suffered traumatic brain injury and developed
a German accent (Monrad-Krohn, 1947). Many of the
patients reported in the literature have never been
exposed to the particular language their accent was
reminiscent of, or even to any other foreign language
earlier in their life, while in others a language learned
during childhood reappeared as a foreign accent (e.g.,
Roth et al., 1997).
The syndrome is distinct from apraxia of speech in
that FAS patients do not primarily make phonemic or
phonetic errors, except for the relatively constant devia-
tions characterizing their accent. These deviations,
which have sometimes been characterized as dysarthric,
afflict the segmental aspects and the prosody of the
patients’ speech output in a specific and constant
manner, thereby causing the impression of a foreign
accent (Pick, 1919; Ingram et al., 1992; Kurowski
et al., 1996). Mild aphasic impairment such as word-
finding difficulties or agrammatism may also contribute
to this impression (Roth et al., 1997; Christoph et al.,
2004). In several cases, FAS occurred as a transient or
a persisting state during recovery from a global aphasia
or a Broca’s aphasia, or from muteness (e.g., Monrad-
Krohn, 1947; Avila et al., 2004). Reported etiologies
are ischemic or hemorrhagic stroke (Roth et al., 1997;
Fridriksson et al., 2005), traumatic brain injury (Moonis
et al., 1996; Lippert-Gruener et al., 2005), or multiple
sclerosis (Bakker et al., 2004). FAS may also be asso-
ciated with schizophrenic psychosis (Reeves and Nor-
ton, 2001). Most cases had left hemisphere lesions,
either of the inferior perirolandic cortex and its underly-
ing white matter (Graff-Radford et al., 1986; Blumstein
et al., 1987; Takayama et al., 1993; Christoph et al.,
2004; Avila et al., 2004) or of the basal ganglia (Kur-
owski et al., 1996; Gurd et al., 2001; Fridriksson et al.,
2005). Callosal infarction was also reported as the cause
of a foreign accent syndrome (Hall et al., 2003).
Acquired neurogenic stuttering (ANS) denotes a
speech disorder, secondary to some acquired neurolo-
gic condition, which is predominantly characterized
by disfluent articulation, most typically with frequent
involuntary repetitions of phonemes or syllables rather
than with prolongations or cessations of sound. The
ANS syndrome can be distinguished from apraxia of
speech by the absence of visible groping behavior and
by the observation that the disfluencies seen in ANS,
unlike those occurring in AOS, are not related to pho-
nemic or phonetic errors or to the self-initiated repairs
of such errors.
The major etiologic condition leading to ANS is
stroke (Grant et al., 1999), but stuttering can also be
caused by traumatic brain injury (Ludlow et al., 1987)
or by Parkinson’s disease (Hertrich et al., 1993); it
may occur with epileptic seizures (Michel et al., 2004)
and during migraine attacks (Perino et al., 2000), and
it has been observed after application of pharmacologi-
cal agents (Movsessian, 2005). ANS usually occurs in
patients with left-hemisphere lesions, with or without
concomitant aphasia (Helm et al., 1978), but has also
been described in right-handers with right hemisphere
infarctions (Fleet and Heilman, 1985; Ardila and Lopez,
1986), or after bilateral lesions (Helm et al., 1978; Bala-
subramanian et al., 2003). A great variety of different
intrahemispheric lesion sites have been suggested as
being responsible for ANS, such as left anterior medial
cortex (Ackermann et al., 1996; Ziegler et al., 1997;
Chung et al., 2004), left parietal cortex (Turgut et al.,
2002), the basal ganglia and thalamus (Ludlow et al.,
1987; Sorokeret al., 1990; Andy and Bhatnagar, 1991;
 APRAXIA OF SPEECH
1992; Carluer et al., 2000; Ciabarra et al., 2000; Van
Borsel et al., 2003), or the corpus callosum (Hamano
et al., 2005).
It is not sufficiently clear if the observations of ANS
in all these cases pertain to a unique syndrome, or if they
constitute different pathological conditions. Helm-
Estabrooks et al. (1986) explained stuttering by a lack
of unilateral dominance in the control of the speech
musculature, Soroker et al. (1990) by a disturbance of
the cross-talk between hemispheres. The fact that a
remarkable number of cases with subcortical lesions
were observed may suggest that the striatal–thalamocor-
tical motor circuit plays a role in the genesis of acquired
neurogenic stuttering. An important diagnostic detail is
if a patient has already been stuttering during childhood,
since in this case the symptom may be explainable by a
decompensation of a developmental disorder which had
been compensated for successfully until the brain lesion
occurred (Mouradian et al., 2000).
Developmental apraxia of speech (DAS) occurs dur-
ing speech development in early childhood. It resembles
AOS in that it is characterized by a corruption of the
phonological make-up of spoken words, with distorted
articulation, phonemic errors, and severe disfluency
(Shriberg et al., 1997). A comparison between AOS
and DAS is hampered by the problem that DAS inter-
feres with the early motor learning stage of speech
acquisition, with the consequence that a normal devel-
opment of speech perception and of phonological, lexi-
cal, or syntactic aspects of language is prevented
(Maassen, 2002). A retrospective analysis of speech
acquisition in children with DAS often reveals that they
had delayed or reduced babbling and reduced oral motor
capabilities during infancy. Hence, the contributions of
auditory–perceptual, general oral motor, and speech-
specific factors to the genesis of the disorder cannot
easily be disentangled (Groenen et al., 1996). Although
a neurogenic basis of the disorder is assumed, there are
no consistent findings regarding the localization of a
potentially underlying structural lesion, and in many
cases neuroanatomical findings were unremarkable
(Horwitz, 1984). Today, a genetic origin of DAS is
hypothesized, basing on the discovery of a mutation of
the FOXP2 gene in the DAS-afflicted members of a
family which, over three generations, has shown a high
incidence of the disorder (Vargha-Khadem et al.,
2005). Variants of this mutation have meanwhile been
discovered in DAS patients originating from other
families (MacDermot et al., 2005).
Oral–facial apraxia describes a condition in which a
patient is unable to perform nonverbal movements of the
facial, oral, or laryngeal muscles on imitation or on
command (see Chapter 16). It is, by definition, different
from apraxia of speech, since its diagnosis is tied to
277
impaired performance on nonverbal motor tasks,
whereas AOS is a speech disorder (Ziegler, 2003;
2006). Most patients with apraxia of speech also have
face apraxia, but the two conditions often show different
clinical courses (Alajouanine and Lhermitte, 1960).
Apraxic speakers who have no or a completely recov-
ered oral–facial apraxia have repeatedly been described
(Lecours and Lhermitte, 1976; Ruff and Arbit, 1981;
Kushner et al., 1987; Mori et al., 1989; Tanji et al.,
2001). The reverse condition, i.e., facial apraxia with
preserved speech, has been reported less frequently,
but it occurs as well (Alajouanine and Lhermitte,
1960; Kramer et al., 1985; Bizzozero et al., 2000). In
a study of 33 patients with left intracerebral hemorr-
hage Maeshima et al. (1997) found no differences in
speech impairment between patients with and without
oral–facial apraxia.
13.7. Natural course and treatment
Systematic observations of the natural course of apraxia
of speech have, to my knowledge, not yet been pub-
lished. Probably depending on the size and the site of
the lesion (see 13.5), AOS may occur as a transient syn-
drome in some patients, and as a persisting, severe
speech problem in others.
The treatment of persisting apraxia of speech is a
notorious therapeutic challenge. In clinical practice,
speech therapists dispense a variety of well established
treatment techniques, but there is only little empirical
support for their effectiveness. In a recent Cochrane
meta-analysis of non-drug interventions for apraxia of
speech after stroke, no studies fulfilling the criteria of
a randomized controlled trial were found (West et al.,
2005). However, the results of several studies with small
patient groups suggest that behavioral treatments based
on speech motor exercises may lead to substantial
improvements in these patients (Wambaugh, 2002;
Brendel and Ziegler, in press).
Pharmacological trials on patient groups characterized
as ‘nonfluent aphasic’ may also be relevant to the issue
of AOS treatment. Several trials have been made with
bromocriptine (Gupta et al., 1995; Bragoni et al., 2000)
and with amphetamine (Walker-Batson et al., 2001),
though without any convincing, or even consistent,
results.
13.8. Theoretical accounts
13.8.1. AOS and the task-specific nature of speech
motor control
One of the theoretical questions relating to apraxia of
speech is whether the disorder is confined to the control
278 W. ZIEGLER
of speech movements, or if volitional oral motor con-
trol is afflicted more generally, i.e., for nonlinguistic
purposes as well. If a strongly dualistic distinction
between linguistic and motor processes is drawn,
speaking is viewed as one out of many different activ-
ities of a multipurpose motor apparatus, and the rela-
tion of speech motor control to the linguistic domain
is solely determined by the circumstance that it con-
sumes the input provided by a linguistic (i.e., phonolo-
gical) apparatus. Assuming that apraxia of speech is a
motor impairment this model would predict that it is
not confined to the act of speaking, but that its underly-
ing mechanism afflicts all skilful motor actions of the
involved muscles, verbal or nonverbal. Ballard et al.
(2000) claimed that a co-incidence of verbal and non-
verbal apraxic impairment can be demonstrated if
nonverbal motor skills are examined whose motor
demands are comparable to speaking. In their view,
the observation that some apraxic speakers have only
little or no oral–facial apraxia is ascribable to the fact
that the motor tasks probed in examinations of oral
apraxia are not sufficiently demanding. As mentioned
above, however, there is no close relationship between
oral–facial apraxia and speech impairment in patients
with left hemisphere lesions (Maeshima et al., 1997),
and there are also no convincing experimental data in
support of such a relationship (for a review see Ziegler,
2003).
The assumption of a strong dualism between lin-
guistic and motor components of language production
raises the problem of how a strictly linguistic, nonmo-
tor system can get its information across to a strictly
nonlinguistic motor processing device. Therefore, an
alternative view was proposed by Liberman and Wha-
len (2000) in which the organization of the speech
motor system is considered to be shaped significantly
by the specific task it subserves, i.e., speaking. The
idea that the motor system implied in speaking is not
a multipurpose tool, but is specific to the production
of language, is based on a number of fundamental
properties distinguishing speech motor control from
all other motor skills of the facial–oral–laryngeal motor
apparatus (Ziegler, 2003). Two of them are theoreti-
cally most important, namely (1) speech movements
are organized within an acoustic reference frame, and
(2) speaking is an outstandingly skilful motor activity
which is practiced extensively throughout lifetime.
With respect to the idea that speech movements,
unlike mouth movements elicited in imitation or visual
tracking tasks, are guided by an auditory–acoustic refer-
ence frame was already contained in Wernicke’s and
Lichtheim’s theory, which assumed that the motor
images of speaking are closely connected to the acoustic
images of words (Lichtheim, 1885). Liepmann (1913)
emphasized that the role played by an ‘acoustic scheme’
in speaking is similar to that of an ‘optical scheme’ in
hand movements. Meanwhile, this thinking is formu-
lated rather explicitly in computational phonetic models
of speech production and is supported by a considerable
amount of experimental evidence (Guenther et al.,
1998). A neurophysiological basis of the close integra-
tion of auditory–sensory and articulatory–motor pro-
cesses is seen in the ‘dorsal stream’ of the perisylvian
language area, a structure linking auditory cortical
regions in the superior temporal lobe with inferior parie-
tal cortex and with premotor regions in the posterior
inferior frontal cortex of the left hemisphere (Hickok
et al., 2000; Hickok and Poeppel, 2004; Watkins and
Paus, 2004). The neurons in the anterior target region
of the dorsal stream can be considered to specifically
subserve motor functions which are guided by auditory
linguistic goals. They may therefore be specific to the
motor task of speaking, and destruction of these neuron
pools may impair speech, but leave other oral motor
functions unimpaired.
With respect to the link between auditory and motor
regions of left perisylvian cortex, this also forms the
basis of vocal learning in children. The capacity to imi-
tate acoustic patterns by vocal tract movements is spe-
cific to humans and to very few other species, e.g.,
songbirds, but is absent in nonhuman primates (Fitch,
2000). Imitation of the vocal patterns of adult speech
starts early in infancy (Kuhl and Meltzoff, 1996), and
the emerging speech movements are exercised exten-
sively throughout childhood and early adolescence. It
is known from other motor domains, e.g., string instru-
ment playing (Elbert et al., 1995) or juggling (Dra-
ganski et al., 2004), that such learning processes lead
to alterations in the size and the organization of cortical
areas implied in motor control. An extensive amount of
literature has meanwhile been accumulated which
demonstrates that motor practice has a structural sub-
strate and that one and the same movement may have
different neural representations, depending on whether
it is part of a learned or an unlearned motor activity
(Ungerleider et al., 2002). Although the evidence relat-
ing to learning-induced brain plasticity was obtained
from studies of hand motor control and is therefore
not directly related to the vocal motor system, it sug-
gests by analogy that speech motor control in adults
must be based on a highly specific neural organization
and can be impaired differentially. Hence, it appears
plausible to assume that the pathomechanism underly-
ing apraxia of speech may leave other face and mouth
movements unimpaired (Ziegler, 2006).
The bifurcation of the developmental course of ver-
bal and nonverbal motor skills occurs rather early in
childhood (Moore, 2004). Nonetheless, this does not
 APRAXIA OF SPEECH
necessarily entail that a neural network specifically
devoted to speech motor control exists from birth on.
On the contrary, data from patients with genetically
based developmental apraxia of speech suggest that
mutation of a specific gene, FOXP2, results in an
abnormal development of volitional oral motor control
more generally (Alcock et al., 2000) and that, probably
on the basis of this, a development of normal speech is
prevented as well. Hence, the acquisition of speech
motor skills presumably depends on the genetic endow-
ments underlying general oral motor capacities and
vocal learning potentials.
13.8.2. Psycholinguistic models of AOS and the
units of phonetic encoding
Levelt et al. (1999) proposed a model of spoken lan-
guage production which, on a coarse-grained scale, dis-
tinguishes between a conceptual level comprising
prelinguistic, semantic, and syntactic aspects of the for-
mulation of a verbal message, and a motor level com-
prising the different processing stages by which the
phonological form of words and sentences is retrieved
and transformed into motor commands (Fig. 13.1; see
Levelt (2000) for this particular view). On an early stage
Fig. 13.1. Left: organization of spoken language production
at an early stage of language development. Each concept is
associated with a holistic speech motor pattern, e.g., the con-
cept ANIMAL with the articulatory gestures for ‘dog.’ Right:
tripartite model of the phonological–motor component in
adults: phonological encoding (unfilled), phonetic encoding
(shadowed), and motor execution (hatched). After Levelt
(1998; 2000).
279
of language acquisition, one-to-one relationships exist
between a small number of concepts in the child’s reper-
toire, on the one hand, and an equally small number of
holistic motor patterns to articulate them, on the other.
When, in a later developmental stage, the child’s lexi-
con undergoes a dramatic ‘spurt,’ this principle can no
longer be maintained, and the speech motor system is
reorganized by fractionating the holistic motor patterns
of words into smaller, sublexical building blocks
(Levelt, 1998). When a word is articulated, its motor
program must be assembled from the precompiled
motor programs pertaining to these smaller bits. Such
a generative principle allows, among other things, for
a fast acquisition of new words and for a flexible adapta-
tion of spoken words to their environment. Levelt’s the-
ory postulates that, in the mature system, the primitives
of speech motor programs are of the size of syllables
(Levelt et al., 1999; Cholin et al., 2006). Most languages
typically consist of several thousands of syllables, and a
relatively small proportion of them suffice to generate
the major part of the lexical repertoire of a language
(e. g., in English and German, less than 200 syllables
make up more than 70% of the vocabulary used in
everyday communication). Since these high-frequency
syllables are used over and over again during a lifetime,
the Levelt model assumes that they attain the status of
precompiled motor routines which are stored in a repo-
sitory of motor programs. During speaking these rou-
tines must be retrieved and buffered sequentially while
they are being articulated (Fig. 13.1). If, in the case of
low-frequency syllables, no ready-made motor program
exists, a syllabic program must be assembled from smal-
ler, sub-syllabic units (e.g., phonemes). The store of
motor programs, the process of their retrieval, and
their short-term buffering are subsumed under the term
phonetic encoding (Cholin et al., 2006).
Long-term storage of the motor patterns of words in a
word form lexicon is, in Levelt’s theory, based on more
abstract representations, with phonemes as their basic
underlying units. Phonological representations of words
provide a link between sensory (auditory) and motor
(articulatory) processes, and their specifications are suf-
ficiently abstract to allow for diverse morphological
adaptations, for gesturally different, but functionally
equivalent articulations, and for rhythmical adaptations
to the specific context in which a word occurs. Several
processing steps are required for these representations
to hook up with the rhythmical units of speaking, i.e.,
the motor programs of syllables. These processing steps
are referred to by the term phonological encoding
(Fig. 13.1).
The tripartite organization of the processes trans-
forming words and sentences into audible speech, as
sketched in Fig. 13.1, suggests allocation of the different
280 W. ZIEGLER
syndromes of impaired speech production to the three
components of this model: aphasic–phonological impair-
ment to the phonological encoding component, apraxia
of speech to the phonetic encoding component, and
the dysarthrias to the motor execution or articulation
component (Code, 1998). Regarding apraxia of speech,
Broca’s early assumption that ‘the memory of the pro-
cesses required for the articulation of words’ is lost
(see 13.1), translates, in this theory, into a loss of the
‘memory’ of syllabic motor routines, or of a disturbance
of their retrieval or their short-term buffering.
Whiteside and Varley (1998) proposed that a corrup-
tion of stored syllabic speech motor programs forces
apraxic speakers to circumvent the syllable lexicon and
assemble syllables from smaller programming units.
Since their hypothesis was based on weak empirical
grounds, Aichert and Ziegler (2004) examined whether
the distorted speech output of AOS patients contains
any clues indicating if syllabic units still play a role in
their speech. This study revealed that syllables with par-
ticularly high frequencies of occurrence were relatively
preserved in patients suffering from apraxia of speech,
and that the apraxic error mechanism was constrained
by the between-syllable boundaries in a word. In a
further investigation of a large sample of speech materi-
als from AOS patients it was found that these patients’
probability of failing on a word was strongly influenced
by the word’s hierarchical, nonlinear architecture (Zieg-
ler, 2005). According to this model, the motor programs
conducting the articulation of words decompose, in a
tree-like architecture, into rhythmical units (i.e., metri-
cal feet), syllables, subsyllabic units (such as syllable
rhymes), and phonemes (Fig. 13.2). The error profiles
of apraxic speakers reflect that their words are not disin-
tegrated into linear sequences of phonemes. Instead,
these patients obviously rely on integration mechanisms
above the level of the segment. A clinical consequence
of this finding is that preserved suprasegmental motor
mechanisms should be exploited in the treatment of
apraxic speakers (Ziegler, 2005; Brendel and Ziegler,
in press).
13.8.3. AOS and ‘inner speech’
From early on, discussions about the nature of the syn-
drome which is now termed apraxia of speech were
dominated by questions about the status of internal lan-
guage. Broca had already made a clear distinction
between general linguistic capabilities independent of
any specific modality of expression, on the one hand,
and the ‘faculty of articulate language’ on the other,
by underscoring the fact that his aphemic patients had
normal language comprehension and only their speech
was affected. Lichtheim made this point more explicit
when he distinguished between aphasic patients whose
‘inner words’ are either preserved or impaired
(Lichtheim, 1885). He probed the preservation of the
sound patterns of words by asking aphasic patients to

Fig. 13.2. Units of phonetic encoding/speech motor programming of the word ‘prestigious.’ Inserts (A) and (B) illustrate linear
models with a sequential ordering of (A) phonemes or (B) syllables as the primitives of encoding. The nonlinear model, (C) on
the opposite, parses the word’s phonetic code (Wd) into a nested sequence of hierarchically ordered subunits: prestigious decom-
poses into a ‘trochaic foot’-program, tigious, and a syllable-program, pres, the phonetic code of the trochaic foot is composed
of two syllable-sized codes, ti and gious, each syllable consists of an onset- and a rhyme-program (e.g., pres of pr and es)
and rhymes are composed of phonetic codes for a vocalic nucleus and (eventually) a consonantal coda (e.g., e and s in the syl-
lable pres). Wd: word, Ft: foot, Sy: syllable, Rh: rhyme, On: onset, Nc: nucleus, Cd: coda. A modelling of apraxic error-data
from a field of 72 words with different phonological structures and from a large number of testings (N ¼ 100) yielded signifi-
cantly better results for model (C) as compared to linear models, such as (A) and (B), suggesting that apraxic speakers dispose of
hierarchically nested motor representations of words. Double lines indicate representational levels where a particularly strong
integration of phonetic subunits was found in apraxic speakers. Adapted from German; after Ziegler (2005).
 APRAXIA OF SPEECH
tap the number of syllables of an object name with their
unimpaired hands (‘Lichtheim probe’). If a patient with
impaired speech performed this task accurately, he con-
cluded that only the motor images of words, but not the
‘inner words’ themselves, are lost. This was probably
the first example of a task measuring ‘phonological
awareness,’ i.e., the capacity of processing phonological
information without overt speech. A number of different
tasks have later been introduced to measure phonologi-
cal awareness, such as rhyme or onset decision tasks
(‘do the names of two objects rhyme/begin with the
same phoneme?’) or inversion tasks (‘cap’ is converted
into ‘pack’). A similar diagnostic role was always
ascribed to writing, with the idea that written language
production is parasitic of the phonological processing
steps implied in speech, but uses a different motor sys-
tem (for a discussion see Mohr et al., 1978). The concept
of ‘pure anarthria’ or ‘pure apraxia of speech’ (e.g.,
Lecours and Lhermitte, 1976) was based on the assump-
tion that although speech is severely impaired, the capa-
city to perform metaphonological tasks or to write
words should be preserved.
This thinking is faced with several theoretical pro-
blems. First, the tasks probing metaphonological skills,
with the inclusion of writing, comprise a multitude of
processing requirements which are not necessary for
speaking. For instance, most of these tasks have a high
working memory load, e.g., when the names of two
objects must be buffered for a certain period during
which their phonological information is compared for
rhyming. Moreover, skills which are crucial to solve
explicit phonological tasks like ‘first phoneme dele-
tion’ (e.g., break is transformed into rake) can hardly
be imagined to be part of the chain of implicit, automa-
tized phonological encoding steps implied in speaking.
As a matter of fact, it is known that performance on
such tasks is strongly dependent on specific skills,
some of which are more related to literacy than to
speaking. In a recent study of illiterate, partly literate,
and literate healthy adults, Loureiro et al. (2004) found,
for instance, that the ‘readers’ included in their study
differed from ‘non-readers’ on a number of metapho-
nological tasks, e.g., rhyme identification or initial
phoneme deletion, although the two groups obviously
did not differ in their speaking skills. Similarly, com-
parative studies of children who have acquired alpha-
betic or logographic writing systems have revealed
that these groups differed systematically in their
phonological awareness, although all of them were
good speakers (Cheung et al., 2001). From the results
of a brain imaging study of illiterate adults Castro-
Caldas et al. (1998) concluded that with the acquisition
of alphabetic script a new language processing network
is established which subserves metaphonological
281
functions (including nonword repetition), but there is
no reason to assume that this network also influences
the natural, automatized functions of the language
production apparatus. As a consequence, the fact that
an aphasic patient is impaired on metaphonological
tasks does not allow us to infer that the phonological
encoding system required for speaking is impaired
as well.
Second, even if one assumes that the processes
implied in speaking overlap with some of the processing
steps implied in writing or in rhyme decisions etc., their
temporal requirements may vary considerably between
these tasks. In speaking, phonological representations
are necessarily short-lived, and a slowing of phonologi-
cal encoding processes will have dramatic implications
for the quality of a patient’s speech. Writing and meta-
phonological tasks, on the contrary, are based on a
‘frozen’ phonology and are performed within a larger
time-frame (see Berg (2005), for the case of writing).
A slowing of such processes in aphasic patients will
therefore have less dramatic consequences for these
tasks than it has for speaking. Hence, if writing, rhyme
decisions, segmentation, etc. are relatively preserved
in a patient with impaired speech, we cannot conclude
with certainty that the patient’s phonology is preserved
in speaking.
Third, the fact that metaphonological tasks avoid
overt speaking does not necessarily entail that speech
motor representations are not implicated in such tasks.
It has already been mentioned that most of these tasks
draw on working memory resources. In the model devel-
oped by Baddeley (1998) the phonological loop of the
working memory system is based on speech motor
representations of words, since it uses articulatory
rehearsal processes to refresh the information held in a
phonological store. The inferior part of Broca’s area
(BA 44/6), which is assumed to play a role in speech
motor planning, is also part of the neuroanatomical sys-
tem subserving verbal working memory (Paulesu et al.,
1993). Hence, phonological tasks which depend on
working memory resources can be infiltrated by speech
motor impairments if one assumes that these impair-
ments also afflict covert articulation. The mechanism
underlying apraxia of speech is known to interfere with
verbal working memory (Rochon et al., 1990; Waters
et al., 1992). Therefore, tasks probing phonological
awareness may also be impaired in apraxic speakers,
even though no overt speech production is required.
In conclusion, there is currently no clinically useful
method which would allow us, on the basis of ‘inner
speech tasks,’ to distinguish safely between distur-
bances of the phonological and the phonetic encoding
stage of speech production, i.e., between phonological
impairment and apraxia of speech.
282 W. ZIEGLER
References
Ackermann H, Hertrich I, Ziegler W, et al. (1996). Acquired
dysfluencies following infarction of the left mesiofrontal
cortex. Aphasiology 10: 409–417.
Aichert I, Ziegler W (2004). Syllable frequency and syllable
structure in apraxia of speech. Brain Lang 88: 148–159.
Alajouanine T, Lhermitte F (1960). Les troubles des activités
expressives du langage dans l’aphasie. Leurs relations avec
les apraxies. Rev Neurol (Paris) 102: 604–629.
Alajouanine T, Ombredane A, Durand M (1939). Le Syn-
drome de Désintégration Phonétique dans l’Aphasie.
Masson, Paris.
Alcock KJ, Passingham RE, Watkins KE, et al. (2000). Oral
dyspraxia in inherited speech and language impairment
and acquired dysphasia. Brain Lang 75: 17–33.
Alexander MP (2001). Chronic akinetic mutism after mesen-
cephalic-diencephalic infarction: Remediated with dopa-
minergic medications. Neurorehabil Neural Repair 15:
151–156.
Alexander MP, Naeser MA, Palumbo C (1990). Broca’s area
aphasias: Aphasia after lesions including the frontal oper-
culum. Neurology 40: 353–361.
Amunts K, Schleicher A, Bürgel U, et al. (1999). Broca’s
region revisited: Cytoarchitecture and intersubject variabil-
ity. J Comp Neurol 412: 319–341.
Andy OJ, Bhatnagar SC (1991). Thalamic-induced stuttering
(surgical observations). J Speech Hear Res 34: 796–800.
Andy OJ, Bhatnagar SC (1992). Stuttering acquired from
subcortical pathologies and its alleviation from thalamic
perturbation. Brain Lang 42: 385–401.
Ardila A, Lopez MV (1986). Severe stuttering associated
with right-hemisphere lesion. Brain Lang 27: 239–246.
Avila C, Gonzalez J, Parcet MA, et al. (2004). Selective
alteration of native, but not second language articulation
in a patient with foreign accent syndrome. Neuroreport
15: 2267–2270.
Baddeley A (1998). Recent developments in working-mem-
ory. Curr Opin Neurobiol 8: 234–238.
Bakker JI, Apeldoorn S, Metz LM (2004). Foreign accent
syndrome in a patient with multiple sclerosis. Can J Neurol
Sci 31: 271–272.
Balasubramanian V, Max L (2004). Crossed apraxia of
speech: A case report. Brain Cogn 55: 240–246.
Balasubramanian V, Max L, Van Borsel J, et al. (2003).
Acquired stuttering following right frontal and bilateral
pontine lesion: A case study. Brain Cogn 53: 185–189.
Ballard KJ, Granier JP, Robin DA (2000). Understanding the
nature of apraxia of speech: Theory, analysis, and treat-
ment. Aphasiology 14: 969–995.
Bay E (1957). Die corticale Dysarthrie und ihre Beziehungen
zur sog. motorischen Aphasie. Dtsch Z Nervenheilkd 176:
553–594.
Berg T (2005). A structural account of phonological parapha-
sias. Brain Lang 94: 104–129.
Bizzozero I, Costato D, Della Sala S, et al. (2000). Upper and
lower face apraxia: Role of the right hemisphere. Brain
123: 2213–2230.
Blank SC, Bird H, Turkheimer F, et al. (2003). Speech pro-
duction after stroke: The role of the right pars opercularis.
Ann Neurol 54: 310–320.
Blumstein SE, Alexander MP, Ryalls JH, et al. (1987). On the
nature of the foreign accent syndrome: A case study. Brain
Lang 31: 215–244.
Bragoni M, Altieri M, Di P, et al. (2000). Bromocriptine and
speech therapy in non-fluent chronic aphasia after stroke.
Neurol Sci 21: 19–22.
Brendel B, Ziegler W (in press). Effectiveness of
Metrical Pacing in the Treatment of Apraxia of Speech.
Aphasiology.
Broca P (1861). Remarques sur le siège de la faculté du lan-
gage articulé; suives d’une observation d’aphémie. Bull
Assoc Anat (Nancy) 6: 330–357.
Broca P (1865). Sur le siège de la faculté du langage articulé.
Bull Mem Soc Anthropol Paris 6: 377–393.
Broussolle E, Bakchine S, Tommasi M, et al. (1996).
Slowly progressive anarthria with late anterior opercular
syndrome—a variant form of frontal cortical atrophy
syndromes. J Neurol Sci 144: 44–58.
Carluer L, Marie RM, Lambert J, et al. (2000). Acquired and
persistent stuttering as the main symptom of striatal infarc-
tion. Mov Disord 15: 343–346.
Castro-Caldas A, Petersson KM, Reis A, et al. (1998). The
illiterate brain—learning to read and write during child-
hood influences the functional-organization of the adult
brain. Brain 121: 1053–1063.
Cheung H, Chen H-C, Lai CY, et al. (2001). The development
of phonological awareness: Effects of spoken language
experience and orthography. Cognition 81: 227–241.
Cholin J, Levelt WJ, Schiller NO (2006). Effects of syllable
frequency in speech production. Cognition 99: 205–235.
Choudhari KA (2004). Subarachnoid haemorrhage and aki-
netic mutism. Br J Neurosurg 18: 253–258.
Christoph DH, Freitas GRd, Santos DPd, et al. (2004). Differ-
ent perceived foreign accents in one patient after prerolan-
dic hematoma. European neurology 52: 198–201.
Chung SJ, Im JH, Lee JH, et al. (2004). Stuttering and gait
disturbance after supplementary motor area seizure. Mov
Disord 19: 1106–1109.
Ciabarra AM, Elkind MS, Roberts JK, et al. (2000). Subcorti-
cal infarction resulting in acquired stuttering. J Neurol
Neurosurg Psychiatry 69: 546–549.
Code C (1998). Models, theories and heuristics in apraxia of
speech. Clin Linguist Phon 12: 47–65.
Croot K (2002). Diagnosis of AOS: Definition and criteria.
Semin Speech Lang 23: 267–280.
Darley FL (1968). Apraxia of speech: 107 years of terminolo-
gical confusion Paper presented at the Annual Convention
of the ASHA.
Darley FL, Aronson AE, Brown JR (1975). Motor Speech
Disorders. W.B. Saunders, Philadelphia.
David AS, Bone I (1984). Mutism following left hemisphere
infarction. J Neurol Neurosurg Psychiatry 47: 1342–1344.
Dejerine MJ (1891). Contribution à l’étude de l’aphasie
motrice sous-corticale et de la localisation cérébrale des
 APRAXIA OF SPEECH
centres laryngés (muscles phonateurs). Compte Rendu des
Séances de la Société de Biologie 43: 155–162.
Delreux V, Partz MPd KL, Callewaert A (1989). Aphasie
croisée chez un droitier. Rev Neurol (Paris) 145: 725–728.
Draganski B, Gaser C, Busch V, et al. (2004). Neuroplasticity:
Changes in grey matter induced by training. Nature 427:
311–312.
Dronkers N (1996). A new brain region for coordinating
speech articulation. Nature 384: 159–161.
Dronkers N, Ogar J (2004). Brain areas involved in speech
production. Brain 127: 1461–1462.
Duffau H, Bauchet L, Lehéricy S, et al. (2001). Functional
compensation of the left dominant insula for language.
Neuroreport 12: 2159–2163.
Elbert T, Pantev C, Wienbruch C, et al. (1995). Increased cor-
tical representation of the fingers of the left hand in string
players. Science 270: 305–307.
Ellis AW, Miller D, Sin G (1983). Wernicke’s aphasia and
normal language processing: A case study in cognitive
neuropsychology. Cognition 15: 111–144.
Fitch WT (2000). The evolution of speech: A comparative
review. Trends Cogn Sci 4: 258–267.
Fleet WS, Heilman KM (1985). Acquired stuttering from a
right hemisphere lesion in a right-hander. Neurology 35:
1343–1346.
Fridriksson J, Ryalls J, Rorden C, et al. (2005). Brain damage
and cortical compensation in foreign accent syndrome.
Neurocase 11: 319–324.
Graff-Radford NR, Cooper WE, Colsher PL, et al. (1986). An
unlearned foreign ‘accent’ in a patient with aphasia. Brain
Lang 28: 86–94.
Grant AC, Biousse V, Cook AA, et al. (1999). Stroke-asso-
ciated stuttering. Arch Neurol 56: 624–627.
Groenen P, Maassen B, Crul T, et al. (1996). The specific
relation between perception and production errors for
place of articulation in developmental apraxia of speech.
J Speech Hear Res 39: 468–482.
Groswasser Z, Korn C, Groswasser-Reider I, et al. (1988).
Mutism associated with buccofacial apraxia and bihemi-
spheric lesions. Brain Lang 34: 157–168.
Guenther FH, Hampson M, Johnson D (1998). A theoretical
investigation of reference frames for the planning of
speech movements. Psychol Rev 105: 611–633.
Gupta SR, Mlcoch AG, Scolaro C, et al. (1995). Bromocriptine
treatment of nonfluent aphasia. Neurology 45: 2170–2173.
Gurd JM, Coleman JS, Costello A, et al. (2001). Organic or
functional? A new case of foreign accent syndrome. Cortex
37: 715–718.
Hall DA, Anderson CA, Filley CM, et al. (2003). A French
accent after corpus callosum infarct. Neurology 60:
1551–1552.
Hamano T, Hiraki S, Kawamura Y, et al. (2005). Acquired
stuttering secondary to callosal infarction. Neurology 64:
1092–1093.
Hecaen H, Consoli S (1973). Analyse des troubles du langage
au cours des lesions de l’aire de Broca. Neuropsychologia
11: 377–388.
Helm NA, Butler RB, Benson DF (1978). Acquired stutter-
ing. Neurology 28: 1159–1165.
283
Helm-Estabrooks N (1986). Diagnosis and management of
neurogenic stuttering in adults. In: KO St Louis (Ed.),
The Atypical Stutterer. Principles and Practices of Rehabi-
litation. Academic Press, Orlando, pp. 193–217.
Hertrich I, Ackermann H, Ziegler W, et al. (1993). Speech
iterations in Parkinsonism: A case study. Aphasiology 7:
395–406.
Hickok G, Erhard P, Kassubek J, et al. (2000). A functional
magnetic resonance imaging study of the role of left pos-
terior superior temporal gyrus in speech production: Impli-
cations for the explanation of conduction aphasia. Neurosci
Lett 287: 156–160.
Hickok G, Poeppel D (2004). Dorsal and ventral streams: A
framework for understanding aspects of the functional
anatomy of language. Cognition 92: 67–99.
Hillis AE, Work M, Barker PB, et al. (2004). Re-examining
the brain regions crucial for orchestrating speech articula-
tion. Brain 127: 1479–1487.
Hoole P, Schröter-Morasch H, Ziegler W (1997). Patterns of
laryngeal apraxia in two patients with Broca’s aphasia.
Clin Linguist Phon 11: 429–442.
Horwitz SJ (1984). Neurological findings in developmental
verbal apraxia. Semin Speech Lang 5: 111–118.
Ingram JCL, McCormack PF, Kennedy M (1992). Phonetic
analysis of a case of foreign accent syndrome.
J Phonetics 20: 457–474.
Kaplan E, Goodglass H, Weintraub S (1983). The Boston
Naming Test. Lea & Febiger, Philadelphia.
Karni A, Meyer G, Jezzard P, et al. (1995). Functional MRI
evidence for adult motor cortex plasticity during motor
skill learning. Nature 377: 155–158.
Kertesz A (1985). Aphasia. In: JAM Frederiks (Ed.), Hand-
book of Clinical Neurology, Vol 1(45): Clinical Neuro-
psychology. Elsevier, Amsterdam, pp. 287–331.
Kramer JH, Delis DC, Nakada T (1985). Buccofacial apraxia
without aphasia due to a right parietal lesion. Ann Neurol
18: 512–514.
Kuhl DE, Meltzoff AN (1996). Infant vocalizations in
response to speech: Vocal imitation and developmental
change. J Acoust Soc Am 100: 2425–2438.
Kumabe T, Nakasato N, Suzuki K, et al. (1998). Two-staged
resection of a left frontal astrocytoma involving the oper-
culum and insula using intraoperative neurophysiological
monitoring—case-report. Neurol Med Chir (Tokyo) 38:
503–507.
Kumral E, Bayulkem G, Evyapan D, et al. (2002). Spectrum
of anterior cerebral artery territory infarction: Clinical
and MRI findings. Eur J Neurol 9: 615–624.
Kuriki S, Mori T, Hirata Y (1999). Motor planning centre for
speech articulation in the normal human brain. Neuroreport
10: 765–769.
Kurowski KM, Blumstein SE, Alexander MP (1996). The
foreign accent syndrome: A reconsideration. Brain Lang
54: 1–25.
Kushner M, Reivich M, Alavi A, et al. (1987). Regional cer-
ebral glucose metabolism in aphemia: A case report. Brain
Lang 31: 201–214.
Lecours AR, Lhermitte F (1976). The ‘pure form’ of
the phonetic disintegration syndrome (pure anarthria):
284 W. ZIEGLER
Anatomo-clinical report of a historical case. Brain Lang 3:
88–113.
LeRoux PD, Berger MS, Haglund MM, et al. (1991). Resec-
tion of intrinsic tumors from nondominant face motor cor-
tex using stimulation mapping: Report of two cases. Surg
Neurol 36: 44–48.
Levelt WJM (1998). The genetic perspective in psycholin-
guistics or where do spoken words come from. J Psycholin-
guist Res 27: 167–180.
Levelt WJM (2000). Producing spoken language: A blueprint of
the speaker. In: CM Brown, P Hagoort (Eds.), The Neurocog-
nition of Language. University Press, Oxford, pp. 83–122.
Levelt WJM, Roelofs A, Meyer AS (1999). A theory of lexi-
cal access in speech production. Behav Brain Sci 22: 1–38.
Liberman AM, Whalen DH (2000). On the relation of speech
to language. Trends Cogn Sci 4: 187–196.
Lichtheim L (1885). Ueber Aphasie. Aus der medicinischen
Linik in Bern. Dtsch Arch Klin Med 36: 204–268.
Liepmann H (1900). Das Krankheitsbild der Apraxie (‘motor-
ischen Asymbolie’) auf Grund eines Falles von einseitiger
Apraxie (II). Monatsschr Psychiatr Neurol VIII: 102–132.
Liepmann H (1907). Zwei Fälle von Zerstörung der unteren
linken Stirnwindung. Psychol Neurol IX: 279–289.
Liepmann H (1913). Motorische Aphasie und Apraxie.
Monatsschr Psychiatr Neurol XXXIV: 485–494.
Lippert-Gruener M, Weinert U, Greisbach T, et al. (2005).
Foreign accent syndrome following traumatic brain injury.
Brain Inj 19: 955–958.
Loureiro CS, Braga LW, Souza LN, et al. (2004). Degree of
illiteracy and phonological and metaphonological skills in
unschooled adults. Brain Lang 89: 499–502.
Ludlow CL, Rosenberg J, Salazar A, et al. (1987). Site of
penetrating brain lesions causing chronic acquired stutter-
ing. Ann Neurol 22: 60–66.
Maassen B (2002). Issues contrasting adult acquired versus
developmental apraxia of speech. Semin Speech Lang 23:
257–266.
MacDermot KD, Bonora E, Sykes N, et al. (2005). Identifica-
tion of FOXP2 truncation as a novel cause of developmen-
tal speech and language deficits. American journal of
human genetics 76: 1074–1080.
Maeshima S, Truman G, Smith DS, et al. (1997). Buccofacial
apraxia and left cerebral haemorrhage. Brain Inj 11:
777–782.
Mao C-C, Coull BM, Golper LAC, et al. (1989). Anterior
operculum syndrome. Neurology 39: 1169–1172.
McNeil MR, Robin DA, Schmidt RA (1997). Apraxia of
speech: Definition, differentiation and treatment. In: MR
McNeil (Ed.), Clinical Management of Sensorimotor Speech
Disorders. Thieme, New York, Stuttgart, pp. 311–344.
Michel V, Burbaud P, Taillard J, et al. (2004). Stuttering or
reflex seizure? A case report. Epileptic Disord 6: 181–185.
Mohr JP, Pessin MS, Finkelstein S, et al. (1978). Broca apha-
sia: Pathologic and clinical. Neurology 28: 311–324.
Monrad-Krohn GH (1947). Dysprosody or altered ‘melody of
language.’ Brain 70: 405–415.
Moonis M, Swearer JM, Blumstein SE, et al. (1996). Foreign
accent syndrome following a closed head injury: Perfusion
deficit on single photon emission tomography with normal
magnetic resonance imaging. Neuropsychiatry Neuropsy-
chol Behav Neurol 9: 272–279.
Moore CA (2004). Physiologic development of speech pro-
duction. In: B Maassen, R Kent, H Peters, P van Lieshout,
W Hulstijn (Eds.): Speech Motor Control in Normal and
Disordered Speech. Oxford University Press, Oxford,
New York, pp. 191–209.
Mori E, Yamadori A, Furumoto M (1989). Left precentral
gyrus and Broca’s aphasia: A clinicopathologic study.
Neurology 39: 51–54.
Mouradian MS, Paslawski T, Shuaib A (2000). Return of
stuttering after stroke. Brain Lang 73: 120–123.
Movsessian P (2005). Neuropharmacology of theophylline
induced stuttering: The role of dopamine, adenosine and
GABA. Med Hypotheses 64: 290–297.
Muellbacher W, Artner C, Mamoli B (1999). The role of the
intact hemisphere in recovery of midline muscles after
recent monohemispheric stroke. J Neurol 246: 250–256.
Naeser MA, Martin PI, Nicholas M, et al. (2005). Improved
picture naming in chronic aphasia after TMS to part of
right Broca’s area: An open protocol study. Brain Lang
93: 95–105.
Naeser MA, Palumbo CL, Helm-Estabrooks N, et al.
(1989). Severe nonfluency in aphasia. Role of the medial
subcallosal fasciculus and other white matter pathways in
recovery of spontaneous speech. Brain 112: 1–38.
Nagao M, Takeda K, Komori T, et al. (1999). Apraxia of
speech associated with an infarct in the precentral gyrus
of the insula. Neuroradiology 41: 356–357.
Nagaratnam N, Nagaratnam K, Ng K, et al. (2004). Akinetic
mutism following stroke. J Clin Neurosci 11: 25–30.
Nestor PJ, Graham NL, Fryer TD, et al. (2003). Progres-
sive non-fluent aphasia is associated with hypometabo-
lism centred on the left anterior insula. Brain 126:
2406–2418.
Paulesu E, Frith CD, Frackowiak RSJ (1993). The neural cor-
relates of the verbal component of working memory. Nat-
ure 362: 342–345.
Peach RK, Tonkovich JD (2004). Phonemic characteristics of
apraxia of speech resulting from subcortical hemorrhage. J
Commun Disord 37: 77–90.
Pellat J, Gentil M, Lyard G, et al. (1991). Aphemia after a
penetrating brain wound: A case study. Brain Lang 40:
459–470.
Perino M, Famularo G, Tarroni P (2000). Acquired transient
stuttering during a migraine attack. Headache 40: 170–172.
Petrides M, Cadoret G, Mackey S (2005). Orofacial somato-
motor responses in the macaque monkey homologue of
Broca’s area. Nature 435: 1235–1238.
Pick A (1919). Über Änderungen des Sprachcharakters als
Begleiterscheinung aphasischer Störungen. Z Gesamte
Neurol Psychiatr 45: 230–241.
Pineda D, Ardila A (1992). Lasting mutism with buccofacial
apraxia. Aphasiology 6: 285–292.
Price CJ, Winterburn D, Giraud AL, et al. (2003). Cortical
localisation of the visual and auditory word form areas: A
reconsideration of the evidence. Brain Lang 86: 272–286.
 APRAXIA OF SPEECH
Reeves RR, Norton JW (2001). Foreign accent-like syndrome
during psychotic exacerbations. Neuropsychiatry Neurop-
sychol Behav Neurol 14: 135–138.
Riecker A, Ackermann H, Wildgruber D, et al. (2000). Oppo-
site hemispheric lateralization effects during speaking and
singing at motor cortex, insula and cerebellum. Neuro-
report 11: 1997–2000.
Rochon E, Caplan D, Waters G (1990). Short-term memory
processes in patients with apraxia of speech: Implications
for the nature and structure of the auditory verbal short-
term memory system. J Neurolinguistics 5: 237–264.
Romani C, Calabrese A (1998). Syllabic constraints in the
phonological errors of an aphasic patient. Brain Lang 64:
83–121.
Roth EJ, Fink K, Cherney LR, et al. (1997). Reversion to a
previously learned foreign accent after stroke. Arch Phys
Med Rehabil 78: 550–552.
Ruff RL, Arbit E (1981). Aphemia resulting from a left fron-
tal hematoma. Neurology 31: 353–356.
Sakurai Y, Murayama S, Fukusako Y, et al. (1998). Progres-
sive aphemia in a patient with Pick’s disease: A neuropsy-
chological and anatomic study. J Neurol Sci 159: 156–161.
Schiff HB, Alexander MP, Naeser MA, et al. (1983). Aphemia.
Clinical-anatomic correlations. Arch Neurol 40: 720–727.
Shriberg LD, Aram DM, Kwiatkowski J (1997). Developmen-
tal apraxia of speech: I. Descriptive and theoretical per-
spectives. J Speech Lang Hear Res 40: 273–285.
Shuren JE, Schefft BK, Yeh H-S, et al. (1995). Repetition and
the arcuate fasciculus. J Neurol 242: 596–598.
Soroker N, Bar-Israel Y, Schechter I, et al. (1990). Stuttering
as a manifestation of right-hemispheric subcortical stroke.
European neurology 30: 268–270.
Takayama Y, Sugishita M, Kido T, et al. (1993). A case of for-
eign accent syndrome without aphasia caused by a lesion of
the left precentral gyrus. Neurology 43: 1361–1363.
Tanji K, Suzuki K, Yamadori A, et al. (2001). Pure anarthria
with predominantly sequencing errors in phoneme articula-
tion: A case report. Cortex 37: 671–678.
Tonkonogy J, Goodglass H (1981). Language function, foot
of the third frontal gyrus, and rolandic operculum. Arch
Neurol 38: 486–490.
Turgut N, Utku U, Balci K (2002). A case of acquired stutter-
ing resulting from left parietal infarction. Acta Neurol
Scand 105: 408–410.
Ungerleider LG, Doyon J, Karni A (2002). Imaging brain
plasticity during motor skill learning. Neurobiol Learn
Mem 78: 553–564.
Urban PP, Wicht S, Vukurevic G, et al. (2001). Dysarthria
in acute ischemic stroke. Lesion topography, clinicoradio-
logic correlation, and etiology. Neurology 56: 1021–1027.
285
Van Borsel J, van der Made S, Santens P (2003). Thalamic
stuttering: A distinct clinical entity? Brain Lang 85:
185–189.
Vargha-Khadem F, Gadian DG, Copp A, et al. (2005). FOXP2
and the neuroanatomy of speech and language. Nat Rev
Neurosci 6: 131–138.
Walker-Batson D, Curtis S, Natarajan R, et al. (2001). A
double-blind, placebo-controlled study of the use of
amphetamine in the treatment of aphasia. Stroke 32:
2093–2098.
Wambaugh JL (2002). A summary of treatments for apraxia
of speech and review of replicated approaches. Semin
Speech Lang 23: 293–308.
Waters GS, Rochon E, Caplan D (1992). The role of high-
level speech planning in rehearsal: Evidence from patients
with apraxia of speech. J Mem Lang 31: 54–73.
Watkins K, Paus T (2004). Modulation of motor excitability
during speech perception: The role of Broca’s area.
J Cogn Neurosci 16: 978–987.
West C, Hesketh A, Vail A, et al. (2005). Interventions for
apraxia of speech following stroke. Cochrane Database
Syst Rev: Issue 4. Art. No.: CD004298. DOI: 10.1002 /
14651858. CD004298.pub2.
Whiteside SP, Varley RA (1998). A reconceptualization of
apraxia of speech: A synthesis of evidence. Cortex 34:
221–231.
Wise RJS, Greene J, Buchel C, et al. (1999). Brain-regions
involved in articulation. Lancet 353: 1057–1061.
World Health Organization (2005). The International Classi-
fication of Functioning, Disability and Health—ICF http://
www3.who.int/icf/.
Ziegler W (1987). Phonetic realization of phonological con-
trast in aphasic patients. In: JH Ryalls (Ed.), Phonetic
Approaches to Speech Production in Aphasia and Related
Disorders. College Hill Press, Boston, pp. 163–179.
Ziegler W (2003). Speech motor control is task-specific. Evi-
dence from dysarthria and apraxia of speech. Aphasiology
17: 3–36.
Ziegler W (2005). A nonlinear model of word length effects
in apraxia of speech. Cogn Neuropsychol 22: 603–623.
Ziegler W (2006). Distinctions between speech and non-
speech motor control. A neurophonetic view. In: M
Tabain, J Harrington (Eds.), Speech Production. Psychol-
ogy Press, Oxford.
Ziegler W, Cramon DYv (1986). Timing deficits in apraxia of
speech. Eur Arch Psychiatry Neurol Sci 236: 44–49.
Ziegler W, Kilian B, Deger K (1997). The role of the left
mesial frontal cortex in fluent speech: Evidence from a
case of left supplementary motor area hemorrhage. Neu-
ropsychologia 35: 1197–1208.