1. A Review o~ Fifty Cases
of Developmental Apraxia o~ Speech
John C. Rosenbek and Robert T. Wertz
ii~~' ~:~:~
Rosenbek
A commonly diagnosed communication disorder in children, in which
the child has little or no intelligible speech, is expressive aphasia
(McGinnis, 1963; Myklebust, 1952). Wilson (1964) describes the char-
acteristics of childhood expressive aphasia as: lack of expressive speech
and language; adequate understanding of speech and language; speech
confined to one- and two-syllable utterances; partial or complete in-
ability to imitate tongue, lip, and jaw actions; inability to imitate sounds
and words; adequate intelligence; and absence of facial and lingual
paralysis.
Since Wilson's description better fits an articulatory or motor speech
disorder rather than a central language disorder, such a child might more
correctly be said to have an apraxia of speech or a developmental apraxia
of speech, if the lesion occurs before the onset of speech development.
His partial or complete inability to imitate tongue, lip, and jaw actions
during nonspeech activities, if such inability is not due to paralysis,
paresis, or ataxia, might more correctly be called an oral apraxia. The
term aprctxia, by emphasizing the articulatory or motor programming
deficit in these children, differentiates them from children with a central
language impairment-aphasia-and suggests efficacious therapeutic pro-
cedures. With the exception of Morley's (1965) review of 12 children
demonstrating developmental dyspraxia and Weiner's (1969) discussion
of the speech and language performance of eight children diagnosed as
having "congenital aphasia" and dyspraxia, the literature on this disorder
is somewhat barren.
The purpose of this review is to present the neurological, including
Requests for reprints should be directed to John C. Rosenbek, A,~sistant Professor,
Department of Speech Pathology and Audiology, University ol Colorado, Boulder,
Colorado 80302. He is also director of the University Speech and Hearing Clinic. Robert
T. Wertz is an associate professor in the same department and assistant professor of
physical medicine and rehabilitation in the University of Colorado School of Medicine.
23
2. electroencephalographic, and speech and language findings which char-
acterize a group of children diagnosed as having apraxia of speech with
no prior history of cortical insult; in other words, children with develop-
mental, rather than acquired, apraxia of speech. Such a review, besides
supplementing existing information about the developmentally apraxic
child, should reveal similarities and differences between developmental
and acquired apraxia, differentiate developmental apraxia from other
articulatory disorders in children, and suggest a hypothesis about cortical
control of voluntary movement in children.
Subjects
Fifty children with a diagnosis of apraxia of speech and with no history
of trauma, cerebral vascular accident, tumor, or other disease process
served as subjects in this study. Children whose apraxia of speech could
be associated with postnatal trauma of any kind were excluded because
we were interested in only those children whose speech problem could
be considered developmental or congenital, not acquired. In all cases,
the diagnosis was made by both a consulting neurologist and a speech
pathologist. The 50 children, 12 females and 38 males, ranged in age
from 2 years, 9 months, to 14 years with a mean of 4 years, 9 months,
and a standard deviation of 5 years, 10 months. Twenty-one of the chil-
dren were right-handed, 4 were left-handed, 6 had mixed handedness, and
handedness was not reported in 19. All 50 children showed developmental
apraxia of speech. Some displayed apraxia in combination with aphasia
and/or dysarthria. No effort was made to exclude children with language
delay or mental retardation.
Method
The medical and speech histories of 45 children evaluated for speech
or language deficiency by the section of speech pathology, Mayo Clinic,
and diagnosed as presenting apraxia of speech were reviewed by three
doctoral speech pathologists. Five additional children were seen in the
University of Colorado Speech and Hearing Clinic and were tested with
a battery of articulation, language, and oral movement tests. Because the
45 children from the Mayo Clinic series had been seen over a period of
years by three different speech pathologists, no standard speech and
language tests were available for statistical comparison. A review of the
speech reports on the 45 and of the test results for the five, however,
does reveal consistent features of developmental apraxia of speech. Be-
24
3. cause our results are descriptive and in large part retrospective, they can
only be considered as hypotheses to be tested, and not as experimentally
documented results capable of supporting conclusions.
Results
Neurological Findings. A pediatric neurological examination was com-
pleted on 36 of the 50 children. This examination included a parental
report on the child's birth and development; evaluation of cranial and
peripheral nerve integrity; sensory integrity; and general observations
of his alertness, mentation, and coordination. In all cases, a consulting
neurologist made some evaluation of the child's speech, although the
neurologist's speech evaluations were always brief-usually in response
to the speech pathologist's request for confirmation of a diagnosis of
apraxia of speech.
The major finding, based on 36 complete neurological examinations,
was that 22 of these children presented an "essentially normal" neuro-
logical examination, except for the presence of either a generalized ap-
raxia, including an oral apraxia (N=12) or an apraxia confined to
orofacial musculature (N-7). In three cases, the examining neurologist
did not indicate whether the apraxia was generalized or limited to oro-
facial musculature.
This high incidence of isolated apraxic signs is different from the
situation in adults who demonstrate acquired apraxia of speech; one
usually discovers the presence of a right hemiparesis or paralysis, espe-
cially in those adults whose apraxia of speech results from lesions to
Broca's area and the sensorimotor cortex of the left hemisphere. One
implication of this finding, and one that is suggested by the electroen-
cephalographic findings as well, is that praxis centers for speech move-
ments in the child's cortex may be quite diffuse. In other words, greater
areas of both frontal and posterior cortex may be necessary to a child's
successful development and volitional performance of skilled speech
movements. In the adult, on the other hand, praxis centers for the speech
musculature may be more focal, involving only the senorimotor strip and
inferior-posterior portion of the third frontal convolution.
In 14 children, the apraxic condition was accompanied by other neuro-
logical deficits. For example, apraxia was accompanied by muscle weak-
ness in three patients, by hyperreflexia and spasticity in eight, by hypore-
flexia and muscle weakness in one, and by hyperkinesia in two. Another
positive neurological sign of nervous system involvement was excessive
drooling, present in 11 of the 50 children. While drooling is a common
25
4. accompaniment of paralysis or paresis of facial musculature, six children
whose only other sign of neurological dysfunction was either a generalized
or focal apraxia also drooled. So, while drooling is not of differential
diagnostic significance in dysarthria and apraxia, its presence in the
absence of paralysis or paresis should prompt the examiner to test for
an apraxia of the oral musculature. Trouble in feeding during infancy
was frequently reported both in children with apraxia plus dysarthria
and in those with apraxia but no dysarthria.
It would appear, then, that apraxia of speech may occur in isolation,
a condition confirmed by speech and language testing, or it may be part
of a general picture of neurological deficit.
Electroencepkalographic Findings. Electroencephalographic data were
available on 26 of the 50 children. Eleven (42%) had normal EEG's;
15 (58%) had either focal or generalized abnormalities. While it is impos-
sible to draw any conclusions about the localization of lesions resulting
in developmental or congenital apraxia because of the limited number
of abnormal records available for analysis, certain observations may be
emphasized and tentative hypotheses advanced. Ten (67%) of the ab-
normal EEG records showed a generalized cortical disturbance, and the
records were without lateralizing or localizing significance. Five records
(33%) are suggestive of focal abnormalities. Two children had focal
bilateral abnormalities, in one instance involving the motor strips and
in the other, the Sylvian and parietal regions. The three remaining chil-
dren had loci of disruption confined to the right hemisphere. One record
suggested a right temporal-parietal lobe lesion. One showed a focus in
the right temporal lobe and reduction of cortical activity in the right
hemisphere. One record demonstrated a right parietal and posterior
temporal focus.
In light of classical notions that apraxia of speech results from Broca's
area lesions in the left or dominant hemisphere (Denny-Brown, 1965),
the EEG localization data on the children with focal right hemisphere
lesions are of some theoretical importance. It may be that young children
have large areas of cortex in both hemispheres essential to the develop-
ment of volitional, skilled performance. At some point, praxis centers
for skilled movements may lateralize, usually to the left hemisphere, and
become more discretely localized. Before such lateralization and locali-
zation take place, any of a variety of left-right, anterior-posterior lesions
may result in apraxia of speech. After lateralization and Iocalization take
place, apraxia of speech results from Broca's area lesion or from lesions
in tracts connecting this area with visual, auditory, and tactile-kinesthetic
centers. However, apraxia of speech following right hemisphere lesions
in adults has been reported (Wertz, Rosenbek, and Deal, 1970).
26
5. Speech and Language Characteristics.The following list shows 13 char-
acteristics of children with developmental apraxia of speech. Certain of
these characteristics are similar to those of aquired apraxia. Differences
are to be expected, of course, because the lesions in these 50 children
were presumed to be present before the onset of speech development.
1. May occur in isolation or in combination with aphasia and/or
dysarthria.
2. Speech development is delayed and deviant.
3. Receptive abilities are inordinately superior to expressive abilities.
4. Oral nonverbal apraxia often, but not always, accompanies apraxia
of speech.
5. Prominent phonemic errors: omissions (errors are more often omis-
sion of sounds and syllables than substitution of sounds and syllables),
substitutions, distortions, additions, repetitions, prolongations.
6. Frequent metathetic errors.
7. Errors increase as words increase in length.
8. Repetition of sounds in isolation is often adequate; connected speech
is more unintelligible than would be expected on the basis of single-
word articulation test results.
9. Errors vary with the complexity of articulatory adjustment; most
frequent errors are on fricatives, affricatives, and consonant clusters.
10. Misarticulations include vowels as well as consonants.
11. Errors are highly inconsistent.
12. Prosodic disturbances: slowed rate, even stress, and even spacing,
perhaps in compensation for the problem.
13. Groping trial-and-error behavior manifested as sound prolongations,
repetitions, or silent posturing which may precede or interrupt im-
itative utterances.
A primary characteristic is that developmental apraxia of speech, like
the acquired variety in adults, may occur in isolation or in combination
with aphasia or dysarthria. Nine (18%) of the children were diagnosed
as having apraxia of speech without aphasia or dysarthria. Twenty (40%)
had both aphasia and apraxia of speech. Thirteen (26%) had apraxia
and dysarthria. Eight (16%) had apraxia, aphasia, and dysarthria. The
presence of nine children with an isolated apraxia of speech may be
spuriously high. This number may well have been influenced by the
difficulty in measuring aphasic involvement in children, both because
the behaviors to be called aphasia in children are not agreed upon by
all speech pathologists and because language testing is difficult in chil-
dren with severe output disturbances.
27
6. Whether the apraxia of speech occurs in isolation or is accompanied
by other deficits, a common characteristic seems to be delayed or abnormal
speech development. All 50 of these children were slow to develop speech
competence. Nineteen were referred to the Mayo Clinic solely for a speech
appraisal and diagnosis, and five were referred to the University of
Colorado Speech and Hearing Clinic for the same reason. As a typical
example, one child did not attempt words until age three. Prior to this
time, his speech had consisted primarily of grunts and a limited number
of consonant-vowel syllables. The speech attempts which his parents had
labeled as words were unintelligible to all except his parents.
Another cardinal characteristic of these children, if they are free of
language deficits, is that their receptive abilities are inordinately superior
to their expressive ones. Such children may function normally or near
normally when asked to point and make nonverbal responses to two-
and three-step commands, but be unable to make intelligible verbal re-
sponses on command. We suspect that this is not the case with all such
children, however, and suggest research on the sensory, including auditory
and tactile-kinesthetic, systems of children thought to be developmentally
apraxic.
The next characteristic is that these children often present an ac-
companying oral nonverbal apraxia manifest as an impaired ability to
perform on command such tasks as puffing out their cheeks, licking their
lips, and protruding their tongues. Three children used their fingers
during the performance of oral nonverbal movements seemingly in an
effort to guide their tongues and lips to the requested positions. The
exact incidence and severity of oral nonverbal apraxia in this sample was
not determined but is assumed to be very high, as the examining clinicians
were reluctant to diagnose apraxia unless an oral nonverbal apraxia was
present. In this regard, Eisenson (1968) reserves the label expressive
aphasia (presumably a synonym for apraxia of speech) only for children
with oral nonverbal movement difficulties, on the assumption that pro-
duction problems otherwise are explainable on the basis of higher audi-
tory deficits.
DeRenzi, Pieczuro, and Vignolo (1966), reporting on adults, demon-
strated that apraxia of speech without oral apraxia is possible, probably
because the muscle coordinations necessary to speech are more complex
than those involved in opening the mouth, protruding the tongue, smil-
ing, and the like. Because of the previously mentioned reluctance of the
examining speech pathologists to label a child's speech as apraxic unless
an oral nonverbal apraxia was discovered, our developmentally dyspraxic
children cannot be compared directly with DeRenzi, Pieczuro, and Vig-
nolo's apraxic adults. On the other hand, 2 of our 50 children had a very
28
7. mild articulatory deficit in the presence of a severe oral nonverbal
apraxia. This condition is somewhat similar to one discussed by DeRenzi,
Pieczuro, and Vignolo. They discovered four adult patients with an oral
apraxia and no apraxia of speech. Taken together, these findings suggest
that centers for oral nonverbal movements and for speech movements may
exist separately in the cortex. Cortical lesions may impair one and spare
the other.
As in acquired apraxia of speech, phonemic errors predominate in
developmental apraxia. They include omissions, substitutions, distor-
tions, additions, repetitions, and prolongations. While there is predictable
variance in these children's speech disorders, most had severely reduced
phoneme repertoires. The speech of 11 was classified as 100% unintel-
ligible. The articulation defect was described as mild in only two chil-
dren. In these two, errors were confined to fricatives, affricatives, and con-
sonant clusters. Several children were reported to have had no obvious
speech defect until they began combining words into phrases. This find-
ing is confirmed by Morley (1965) in her sample of 12 subjects.
Unlike the apraxic adult, the child seems to make more sound and
syllable omission errors. Characteristically, initial sounds and syllables
are present especially if they are stressed, and medial and final sounds
and syllables are omitted. Like the adult, the child's errors are some-
times metathetic, such as [f~rg] for [frog] and [fir] for [fiJ']. A series of
studies is needed to determine the patterns of phonemic errors in such
children. It is unlikely that these patterns will resemble those of the
adult because of the differences between these two groups in the temporal
relationships of speech development and occurrence of the lesion. It was
our impression that the child's age is an important determinant of his
error pattern. The older children's error patterns, especially on imitative
speech tasks, had much the flavor of the adult apraxics'. The younger
children's performances did not. Their productions, when they could be
classified as substitutions, were often grossly off target, resembling jargon,
and omissions predominated, as previously mentioned.
Phonemic errors in developmental apraxia are related to a variety of
response variables. The first (and in this, children with developmental
apraxia resemble apraxic adults) is that articulatory inaccuracy increases
with response length. For example, it appears that these children are
often capable of correct single-sound productions appropriate for their
age, but they make articulation errors on these same sounds when they
are combined into longer units such as words and phrases. This char-
acteristic may be of some differential diagnostic significance when the
developmentally apraxic child is compared to one with a functional
articulation disorder. The latter child often requires several integral
29
8. stimulations if he is to correct an error sound even in isolation. Also, the
developmentally apraxic child's score on a single-word articulation test
may grossly overestimate his intelligibility in connected speech. These
observations are to be expected in disorders of programming or sequenc-
ing of articulatory movements; therefore, the pattern of errors as a func-
tion of response length may differentiate the apraxic child from those
whose articulation errors have a different etiology.
The apraxic child's articulatory errors vary with the complexity of
articulatory adjustment. The apraxic child resembles the adult apraxic
in that fricatives, affricatives, and consonant clusters are more frequently
in error than are the plosives. In this regard too, the apraxic child is not
distinguishable from the child with functional misarticulations. Un-
like the adult and the functional case, however, apraxic children, es-
pecially the younger ones, tend to make errors on vowel sounds. These
errors are frequently either substitutions or distortions and may be of
differential diagnostic importance.
The apraxic child's phonemic errors are inconsistent, but probably
not so inconsistent as the apraxic adult's. For example, [lif] may become
[fif], [wif], and [lif] on three consecutive repetitions of this word. These
inconsistencies may be independent of stimulus length as in the previous
example. They seem more closely related to attempted self-correction,
especially in older children.
Like the adult apraxic, the developmental apraxic's speech may be
characterized by prosodic disturbances. Adult apraxics, however, present
a consistent pattern of prosodic disturbance which Darley (1969) has
suggested may be the result of compensatory efforts. The apraxic child
does not display this consistency. Disturbed prosody is seen most fre-
quently on imitative speech tasks and is characterized by slowed rate,
even stress, and inappropriate pauses. Frequently in spontaneous speech,
however, there are no prosodic problems, and the child may be fluent but
unintelligible. Possibly the prosodic disturbance reflects the child's effort
to compensate, as appears to be the case in acquired apraxia. However,
this disturbance disappears when there is no obvious environmental
premium on intelligibility.
The final characteristic of children with developmental apraxia of
speech, and the one that may be of uppermost diagnostic significance, is
the presence of groping trial-and-error behavior manifested as sound
prolongations, sound repetitions, and silent posturing preceding or within
imitative utterances. This characteristic and the previously mentioned
presence of oral nonverbal apraxia are of importance in differentiating
developmental apraxia of speech from functional articulation deficits.
The apraxic child appears to be struggling mightily, but often in vain,
30
9. to position his articulators for correct speech production. Such is not
the case with a functional articulation disorder.
Discussion
In this review, we have outlined certain neurological and speech char-
acteristics of a group of children whom both neurologist and speech
pathologist have diagnosed as presenting developmental apraxia of
speech. Certain theoretical, diagnostic, and therapeutic implications arise
from these data, especially as they are compared to what is known about
acquired apraxia of speech and, to a lesser extent, functional articulation
:lisorders.
Our data demonstrate that developmental apraxia may occur as part
of a generalized picture of neurological and speech and language dys-
function, or it may occur in isolation. Therefore, developmental apraxia
of speech may be the only sign of cerebral dysfunction, especially in
younger children. Our neurological data, including the EEG's on five
children, suggest that praxis centers in children may involve large cortical
areas of both hemispheres. In order to reconcile this suggestion with clas-
sical notions about centers for speech praxis in adults, we hypothesize
that with maturation, praxis centers lateralize and become more focal.
This hypothesis needs considerably more investigation, of course, but it
is supported, at least indirectly, by Penfield and Roberts' (1959) con-
clusion that ideational speech centers undergo progressive lateralization,
perhaps until age six.
Also, there are similarities and differences between acquired apraxia
of speech and developmental apraxia of speech. The similarities are most
obvious in the oral nonverbal performance of the two groups, in the
groping trial and error behavior, and in the relationship of articulatory
accuracy to a variety of response variables, the most potent of which
appears to be stimulus length. Apparent differences in the pattern of
phonemic errors and in prosodic disturbance are to be expected, given
the difference in the temporal relationship of speech development and
time of insult in the two groups. The exact differences in phonemic
error pattern and the possible influence of age on articulatory integrity
must be explored experimentally.
Perhaps of greatest diagnostic significance, especially to the clinician
who treats articulatory disorders in children, are the suggested differences
between children with developmental apraxia of speech and those with
a functional articulation disorder. We have made such comparisons
sparingly, suggesting only that vowel errors, presence of oral nonverbal
31
10. apraxia, groping trial and error behavior, and more errors on longer
responses differentiate the developmentally apraxic child from the child
with a functional articulation disorder. Our conservatism grew out of
the descriptive nature of this review and, as importantly, out of the sus-
picion that many children labeled in previous reports as functional articu-
lation defectives may indeed have been developmentally apraxic. While
it is impossible to document our suspicion about previous reports, it is
possible and necessary to undertake research aimed at differentiating these
two groups of speech-defective children.
The therapeutic significance of differentiating the apraxic child from
the one with a functional articulation disorder is difficult to determine
because so little is known about proper articulatory training procedures
with apraxic children. Characteristics of their speech performance, how-
ever, provide certain clues. With young children, McDonald's approach
(1964) to therapy seems especially appropriate. Emphasis should be on
the syllable rather than the sound, and exercises using duplicative syl-
lables such as /papapa/ or ]bababa/ with systematic variation in stress
and intonation appear especially appropriate. Classical reliance upon
auditory discrimination training is probably inappropriate with such
children.
For older children, meaningful words, phrases, and sentences are prob-
ably the appropriate stimuli. Self-monitoring and the learning of com-
pensatory behaviors such as equal stress and the use of pauses to break up
phrases and sentences may be appropriate. Special attention to polysyl-
labic word production, again emphasizing equal stress, and the use of
pauses as compensatory behaviors will be necessary. The intrusive schwa
can be taught as an addition in consonant clusters to aid in the production
of individual phonemes and insure proper ordering. For example, the
clinician may suggest /stv-rAk! for ]strAk]. The intrusive schwa is
dropped after production has been stabilized. Results of experimental
therapy with these children are badly needed.
Summary
The neurologic, including electroencephalographic, and speech and
language findings on 50 children demonstrating developmental apraxia
of speech have been presented. Thirteen characteristics typify the speech
of developmentally apraxic children. These characteristics reveal simi-
larities and differences between developmental apraxia and acquired
apraxia. Further, they assist in differentiating developmental apraxia of
speech from other articulatory disorders in children. Finally, we have
32
11. suggested a hypothesis about cortical control of voluntary movement in
children.
Acknowledgment
This article is based, in part, on information gathered during two pre- and postdoc-
toral fellowships in the Mayo Clinic supported by the National Institute of Neurologic
Diseases and Stroke. Additional support was provided by a Research and Training
Center Grant (16-P-56815) from the Social and Rehabilitation Service, Department of
Health, Education, and Welfare, Washington, D.C. Parts of the material were presented
as a paper during the Colorado Speech and Hearing Association Convention, Gunnison,
Colorado, May 1971.
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MCDONALn, E. T., Articulation Testing and Treatment: A Sensory-Motor Approach.
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McGINNIs, M. A., Aphasic Children. Washington, D.C.: Alexander Graham Bell Asso-
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MORLEY, M. E., The Development and Disorders of Speech in Childhood. London: E.
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MYKLEBUST,H. R., Aphasia in children. Except. Child., 19, 9-14 (1952).
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33
