OVERVIEW

OF
APRAXIA

SUBMITTED TO : MS .Shewtha Prabhu

SUBMITTED BY : Mohamed Roshan A.V
Apraxia is a neurological disorder . The diagnostic term “Apraxia” can be used to classify
the inability of a person to perform voluntary and skillful movements of one or more body
parts , even though there is no evidence of underlying muscular paralysis , in-coordination ,
or sensory deprivation.
• Additionally, motor performance in response to commands, imitation tasks, and use
of familiar objects may be equally difficult.
• These types of disturbance result from injuries , illness, or diseases of different
regions of the brain normally responsible for regulating such abilities.
• Disturbance in carrying out skilled acts , caused by a lesion in the cerebral cortex ,
motor power capacity remain intact.
• Apraxia is a disorder of learned movement in which the patient is unable to carry

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 out, at will, a complex or skilled movement that they were previously able to
perform(Geschwind, 1975).

ETIOLOGIES OF AOS
• AOS can be caused by any process that damages dominant hemisphere structures
involved in motor speech programming. Because inflammatory and toxic metabolic
diseases usually produce diffuse effects, only rarely are they associated with an
isolated form of AOS.
• Tumors and trauma are more likely to cause focal unilateral signs, mostly when
they affect the left hemisphere, AOS may result.
• Vascular lesions are the most common cause of AOS. There is nothing unique about
the nature of the vascular disturbances that cause AOS, except that they are
localized to dominant hemisphere speech programming structures and pathways.
• Degenerative neurological diseases are uncommonly associated with AOS, but
sometimes they present as focal motor disturbances, one of which can be AOS. For
example - AOS can occur in multiple sclerosis.
• Duffy and Peterson (1992) concluded from their review of 54 cases that PPA can be
at least sometimes accompanied with AOS. Also, review of cases with Creutzfeldt-
Jakob disease suggests that some of the patients probably can have AOS.
PREVALANCE
• Vascular (58%)
• Single left hemisphere stroke (48%)
• Multiple strokes including left hemisphere (10%)
• Degenerative (16%)
• Unspecified degenerative CNS disease (9%)
• Alzheimer disease or dementia (4%)
• Other-PPA (3%)
• Traumatic (26%)
• Neurosurgical (12%)
• Tumor (6%)
• Closed head injury (6%)
Undetermined etiology (2%)

Neuro-Anatomical Sites Of Lesions Associated With AOS

• AOS is most frequently due to stroke in the hemisphere dominant for language,
usually left hemisphere.
• The area most frequently cited as being associated with apraxia has been
Boardman's area 44 (3r frontal convolution). Other sites of lesion frequently noted
with AOS include the parietal lobe, sub-cortical structures such as thalamus, basal
ganglia and insula (Duffy, 1995).
• All individuals with apraxia showed lesions in a discrete region of the left pre-
central gyrus of the insula, a cortical area beneath the frontal and temporal lobes.
The more diffuse the damage the more likely other cognitive and linguistic
disorders will occur along with the apraxia.

Anatomy & Basic

functions of the

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motor speech Programmer :

• Motor speech control involves the interactive participation of all components of the
motor speech system, as well as higher level activities related to conceptualization,
language and motor planning. The motor programming component of these
activities is sometimes referred to as the motor speech programmer (MSP) (Darley,
Aronson and Brown, 1975).
• The MSP is influenced by sensory feedback, the basal ganglia and cerebellar
control circuits, the reticular formation and thalamus, the limbic system, and the
right hemisphere. From this perspective, motor speech programming involves
widespread areas of the CNS.
• The MSP has a primary role in establishing the motor program for achieving the
cognitive and linguistic goals of spoken messages. It organizes the motor commands
that ultimately result in the production of temporally sequenced sounds, syllables,
words and phrases at particular rates and patterns of stress and rhythm.
• When a phonologic representation of a portion of verbal message has been
formulated, the MSP must be activated to organize and activate a plan for its motor
execution.
• This seems to involve the transformation of the abstract phonemes to a neural code
that is compatible with the operations of the motor system. Execution of this motor
program results in the activation of muscles in patterns that generate an acoustic
signal compatible with the speaker's linguistic and communicative goals.
• It is reasonable to assume that the MSP selects , sequences, activates and controls
pre-programmed movement sequences that through learning and practice, can be
run off somewhat automatically.
• This inturn permits rapid speech rates and greater allocation of resources of the
more conscious formulation and monitoring of the cognitive and linguistic goals of
communication.
• The MSP relies heavily on pre-motor areas(PMA).
• The supplementary motor area (SMA) is also involved in the activities of the MSP.
It has connections with the primary motor cortex and Broca's area, and also to the
basal ganglia by way of the thalamus and the limbic system
• The parietal lobe, somatosensory area and the supramarginal gyrus are also
implicated in the activities of MSP and may be particularly important in integrating
sensory information necessary for skilled motor activity.
• In addition the insula appears to play a role in motor speech programming and
appears to be a frequent site of lesion in patients with AOS (Dronkers, 1993).
• The basal ganglia, consistent with its known role in motor control, seem active in
the activities of the MSP; lesions of the striatum have been associated with AOS
(Kertesz, 1984).

Neurophysiology of Apraxia
• The presence of apraxia was taken as evidence for damage in premotor cortex,
regarded as the centre for motor planning.
• Buckingham (1979) has postulated two different models for apraxia: the Center
model and the disconnection model.

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 • According to the center model apraxia is caused by damage to the cortical Center
of praxis.
• According to the disconnection model apraxia is caused by disconnections of those
parts of the left hemisphere that can comprehend spoken commands from those
parts that can plan and carry out responses to the commands.
• The key difference between both the types of apraxia is in their response to
nonverbal requests for movements of the apraxic body parts.
• Patients with center apraxia are unable to execute requested movements whether
movements are requested verbally or nonverbally because the center for planning
the movements is damaged.
• Patients with disconnection Apraxia on the other hand are unable to perform
movements in response to verbal requests, but will be able to do them if the request
is made nonverbally, because making the request nonverbally bypasses the
pathways involved in transmission of the request from the language comprehension
area.
• The relationship between dominance and unilateral apraxia is explainable by a
connectionist model. According to this , the left hemisphere pathways from the
primary auditory cortex to Wernicke's area and via the arcuate fasciculus to the
premotor and motor cortex are crucial for performing motor movements in response
to spoken commands.
• According to this model, the spoken request for movements is processed at the
primary auditory cortex . The message then goes to Wernicke's area where its
meaning is deduced. A response to the message then goes, via the arcuate fasciculus
to the premotor cortex, where the plan for the requested movement sequence is
drawn up.

• If the patient has to carry out the movement sequences with right hand and arm, the
plan is sent from the premotor cortex to the primary motor cortex in the left
hemisphere. If the patient has to carry out the movement sequence with left hand
then the plan is sent from the left hemisphere premotor cortex across the corpus
callosum to the motor cortex in the right hemisphere . Destruction of Wernicke's
area, interruption of the pathway that carries information from Wernicke's area to
the premotor area or destruction of the left premotor area causes bilateral limb
apraxia, because the motor cortex in both hemispheres is cut off from the message.
• If the pathways from the left primary auditory cortex through the left premotor
cortex are intact, but the crossing fibers that connect the premotor cortex in the left
hemisphere with the motor cortex in the right hemisphere are interrupted then it
results in unilateral apraxia of the left hand , because the left hand is isolated from
both the meaning of the instructions and the motor plans for the response.

CLASSIFICATION:

• Richard Liston & Raymond Tallis et al (2003) gave a classification system which
was based on the higher level gait disorders in patients with cerebral multi-infarcts

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 states.
• They proposed a simplified classification of these gait disorders and related the
clinical phenomenon to possible locations of infracts within the pathways
controlling the motor programming of gait ignition. This classification was referred
as the vascular - HLGDS i.e. Higher Level Gait Disorder.

Ignition Apraxia

• Patients with vascular -HLGD with predominantly movement ignition difficulties

i.e. gait ignition failure, shuffling, difficulty with turns and freezing-have infarcts in
the basal ganglia/thalamus/SMA pathways and / or ischemic lesions in their
connections in the periventricular white matter.
• These patients have difficulties primarily with automatic movements which are
internally driven.

Equilibrium Apraxia

• Patients with vascular - HLGD with predominantly disequilibrium have infarcts in

the sensory/PMA pathways and/or ischemic lesions in their connections in the
periventricular white matter.
• These patients have difficulties primarily with externally cued \ movements; the
automatic internal cueing mechanism is normal. The patients gait characteristics
will not improve when externally cued.

Ideational Apraxia
• It is a disorder gestural behavior which involves the loss of ability to formulate the
ideational plan for the execution of the components of a complex act. In this
disorder the individual component movements of a complex act cannot be
synthesized into a purposeful plan, even though the simple isolated component
movements may be performed normally. In some cases individual component
movements may be performed in a faulty sequence or portions of the complex act
may be performed. Occasionally the patient with ideational apraxia may perform an
action similar to but not the same as the one required.

• Ideational apraxic stand out as being abnormal in everyday activities. Patients with
ideational apraxia are able to imitate an action, in such situations the plan of action
is provided to them from outside.

• Ideational apraxia is always manifested bilaterally and rarely occurs as an isolated

phenomenon. Clinically it is most often observed as a manifestation of diffuse brain
disorders although in some cases it has been reported secondary to focal brain
lesions (Poeck and Lehmkuhl, 1980). Ideational apraxia may also co-occur with
other types of apraxia making it difficult to distinguish clinically.

Mixed Gait Apraxia

• Since lesions may affect the connections of both SMA and PMA, it is to be

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 expected that there will be patients with both disequilibrium and gait ignition
difficulties as proved in practice.

Limb-Kinetic Apraxia

• This disorder was first described by Leipmann (1908) and is characterized by an

inability to execute fine acquired motor movements. The disturbance is often
confined to one limb and in most cases affects the finer movements of the distal
portions of one upper extremity. Furthermore, the impairment is present in
automatic as well as volitional acts. Movements affected include those required for
tasks such as writing, doing up buttons etc.
• Commonly seen as a part of Broca's aphasia, limb-kinetic apraxia is associated with
lesions in the pre-motor area of the cerebral cortex. Consequently, it manifests
unilaterally on the side contra-lateral to the corresponding lesion. It may occur with
ideomotor apraxia.
• Leipmann (1908) suggested that limb-kinetic apraxia results from the loss of the so-
called kinetic memories for a single limb. More recently, however, several authors
have excluded it from the true apraxias (Kerschensteiner, Poeck and Lehmkuhl,
1975). Most contemporary authors regard it as a pyramidal movement disorder
rather than an apraxia.

Constructional Apraxia
• In this type of apraxia, first described by Kleist (1992), the patient is unable to form
a construction in space. Miller (1986) defined constructional apraxia as a disorder
of planned movement for any kind of task involving the structuring or arranging of
objects, parts of objects or lines in two and three dimensional space. Patients with
this disorder therefore, are unable to copy simple geometric figures.

In majority of cases constructional apraxia is associated with lesions in

either of the parietal lobes, although constructional deficits have occasionally been
secondary to frontal lobe lesions. As an isolated disorder, it is more common
following lesions of the non dominant hemisphere (right), in which case the
disturbance associated with this condition also tend to be more severe.

• Warrington et.al (1996) concluded that constructional apraxia following right

hemisphere damage were due to a defect in visuo-spatial perception. Performance
did not improve with learning during the test procedure. The constructional apraxia
following left hemisphere damage was due to a defect in motor executor control, a
defect in programming the action. Visual cues appear to compensate for the deficit
by providing a program for the action.

Dressing apraxia is a disturbance in which patients cannot dress because they are unable
to relate the parts of the garment to the parts of their body. This disturbance is seen most
frequently in association with lesions in the parietal lobe of the non dominant hemisphere
although it has also been reported to follow left parietal lesions. Dressing apraxia is often

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accompanied by constructional apraxia and may co-occur with aphasia. In some case
dressing apraxia is further complicated by the presence of a hemiplegia, hemi-neglect and
visual field defects.

Oral Apraxia
Nonverbal apraxia of the oral mechanism can be defined in a number of ways.
Einson (1954) view apraxia as a defective volitional use of tools and when these
tools are tongue, lips, and velum, oral apraxia is the result. Geschwind (1965)
characterized the condition in the following way: « The patient usually does most
poorly in carrying out facial movements to verbal commands.
• * He may simply fail to perform at all or may make an incorrect
movement. E.g. he may open his mouth when asked to protrude the
tongue
He may make movements with one of his limbs to carry out the demanded task
• E.g. he may pretend to stub a match in an ash tray or stamp on it with his feet when
asked how he would blow out a match. » Patient may also echo the command
• E.g. when asked to blow out a match he may say 'blow'

Whole Body Apraxia

• Apraxia of gait is often accompanied by what has been referred to as 'trunko-pedal'
apraxia, i.e. apraxia of whole body movements, such as lying down, sitting,
standing up or roll over. Geschwind (1965) prefers the term frontal gait disturbance
to apraxia of gait, since he believes that the gait disorder that follows frontal lesions
reflects impairment of motor mechanisms and therefore should not be defined as an
apraxia. He stressed the preservation of whole body movements in apraxic patients.
He suggested that the corpus callosum is not necessary for integration of these types
of movements and that whole body movements may be controlled as integrated acts
at the level of the brainstem.

Apraxia of Speech (AOS)

• The clinical manifestations of AOS are believed to reflect a disturbance in the
programming of movements for speech. Unlike the dysarthria , AOS can exist
without clinically apparent impairments in the speech muscles for non speech tasks.
• Unlike aphasia, in which there are nearly always multimodality impairments of
language, AOS can exist independent of impairments in verbal comprehension,
reading comprehension, and writing as well as independent of verbal errors that are
unrelated to articulation and prosody. Although AOS can co-exist with
• Although AOS can co-exist with dysarthria or aphasia, the distinctiveness of its
clinical characteristics, its apparent nature as a motor programming disturbance and
its occasional emergence as the only disturbance of speech justify its identification
as a unique type of speech disorder.
• Its distinction from other motor speech disorders is additionally warranted because
it is nearly always the result of pathology in the left cerebral hemisphere.
CHARACTERISTICS OF AOS

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 • Tasks placing demands on the volitional sequencing of a variety of sounds are most
likely to elicit the salient and distinguishing features of AOS. Among the task most
sensitive to APS are sequential motion rates (SMR) and imitation of complex
multisyllabic words and sentences. Patients repeated attempts at such tasks not only
demonstrated apraxic errors but also highlight the inconsistency and variety of
errors that are characteristics of many apraxic speakers.
But performing these tasks is not always useful for patients with AOS. It is more
valuable to discover what they are able to do and to contrast with the nature of the
tasks in which performance breaks down. Thus, it may be discovered that a patient
who cannot converse intelligibly and cannot perform SMR is able to count, imitate
simple C-V-C syllables, sing familiar tunes because they are highly over-leamed,
can be produced automatically or place minimal demands on sequencing abilities.

Articulation:
• Perceived substitutions, distortions, omissions, additions, and repetition.
Substitutions more frequently perceived than other' error types.
• Perceived substitutions tend to rank from highest to lowest frequency as follows:
place> manner> voicing> oral/nasal.
• Bilabials and lingual -alveolar consonants less frequently in error than other place
of articulation.
• Fricatives and affricates more frequently in error than other manner of productions.
• Some but not many perceived substitutions are anticipatory or regressive
(nanana/banana), some are reiterative/perseverative (popado/potato) and some
metathetic (dofter ducky/doctor duffy)
• Consonants clusters more frequently in error than singletons.
Vowel errors/distortions occur
• Consonant substitutions sometimes perceived as complications rather than
simplifications of target sounds.
• Sound position within words may not influence error frequency; when it does initial
position is most difficult
• Error rates are higher for infrequently occurring sounds
Error rates higher for non sense words and syllables Error
rates increased with increasing word length
• Error rates increase as the distance between successive points of articulation
increase (SMR is more difficult than AMR)
• Error rates higher for volitional/purposive utterances vs automatic/reactive
utterances Inconsistent errors; same sound not always in error; error types not
always the same in specific utterances
• Speakers are often aware of articulatory errors, can sometimes also predict them
and often attempt to correct them

Development Apraxia of speech (DAS)

• Some individuals oppose the diagnosis of apraxia of speech in children because
they theoretically disagree with the explanation for the disorder implied by the use
of the term.
• Some authors are reluctant to associate the term apraxia with speech disorder unless
a skill has been lost thus rejecting the concept of development apraxia (Bankson,

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 1988).
• In children with DAS, the reduced capacity to form systematic mappings between
articulatory movements and auditory consequences might underlie the oral motor
and early speech learning difficulties in DAS and put the child at a disadvantage for
the acquisition of motor aspects of phonology, i.e. phoneme specific mapping.
• There is strong evidence that delayed or deviant motor development and perceptual
motor learning play a role in many children with DAS. The first clinical evidence is
reduced babbling.
• The second clinical evidence is the high incidence of concomitant dysarhtria and
oral motor dyspraxia (Rosenbek and Wertz, 1973; Yoss and Darley, 1974).
• The third piece of evidence is the frequently reported clumsiness, mild mental
retardation or difficulty with coordinating alternating hand movements.
 
DAS: TWO VIEWS:
A review of various ways to look at interaction of articulatory problems and language in children
will clarify the strength that resides in separating these behaviors when using the diagnosis of
apraxia. One view sees language and articulation as a single entity. Much of the research to date
reinforces the idea that the speech and language components of the child's communication disorder
are inseparable.

Green (1967) discussing articulatory dyspraxia reported that there was always an accompanying
language disorder. Aram and Glasson (1979) reported that developmental apraxia of speech is not
confined to the articulatory or motor aspects of speech. Aram adopted the term developmental
verbal apraxia because it denotes that the expressive disorder is not confined to speech, but includes
all other aspects of verbal expression. Crary (1982) referred to developmental verbal dyspraxia as a
term used to describe children presenting expressive language disorder encompassing both
phonology and syntax. Crary, Landess and Towne (1984) report that an analysis of phonological
error patterns in a group of children with symptoms consistent with DVD confirms the observation
that this clinical entity is an expressive linguistic disturbance. The linguistic problems described
may be related to underlying sensory motor deficits responsible for limitations and motor planning.
A second view of the relationship between DAS and language is a held by a group of authors who
discuss DAS and separate apraxic features from other behaviors that may accompany it. Morley,
Court and Miller (1954) state that the condition may or may not be associated with delayed
development of language. Thus, the diagnosis of DAS should be based on the child's speech
production and the performance of the speech mechanism during attempts at speech production.
Other behaviors, though they may co-occur, are not a part of DAS.

SPEECH MOTOR LEARNING AND DAS-

Infant speech development begins with babbling and vocal play. There is a continuous
developmental progression from oral motor behavior during the 1 st year of life to early speech in 2 nd
year of life. 1st year of speech development is dominated by motor learning, which remains
important during the years to follow but in normal development is gradually replaced by more
phonological orientation.

In children with DAS, the reduced capacity to form systematic mappings between articulatory
movements and auditory consequences might underlie the oral motor and early speech learning

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difficulties in DAS and put the child at a disadvantage for the acquisition of motor aspects of
phonology, i.e. phoneme specific mapping.

There is strong evidence that delayed or deviant motor development and perceptual motor learning
play a role in many children with DAS. The first clinical evidence is reduced babbling. The second
clinical evidence is the high incidence of concomitant dysarhtria and oral motor dyspraxia
(Rosenbek and Wertz, 1973; Yoss and Darley, 1974). The third piece of evidence is the frequently
reported clumsiness, mild mental retardation or difficulty with coordinating alternating hand
movements.

Clinically, a central issue in the discussion of DAS is the actual speech characteristics the children
exhibit in their attempts at oral communication. There is much information in the literature
concerning the speech characteristics of the disorder. However, the literature includes
inconsistencies and contradictions.

SPEECH CHARATERISTICS OF DAS

Speech Sound Errors

The literature contains descriptions of many different types of speech errors being produced by
children exhibiting DAS. The speech of any single child with DAS could contain a number of
different types of errors.

i) Errors in sound class and manner of production

Phoneme acquisition has been found to have~ a general developmental pattern in normal children
(Ross and Milisen, 1942). Rosenbek and Wertz (1972) found that the 50 children they studied erred
most frequently on fricatives, affricates and consonant clusters. Crary (1984 b) reviewed a series of
studies focusing on speech sound characteristics of developmental verbal dyspraxia. He reported
most errors were made in the sound classes involving the more complex oral gestures. Subjects
made more errors on clusters, followed by fricatives, affricates, stops and nasals.

Jackson and Hall (1987) conducted a retrospective longitudinal study of the changes occurring in
the speech of four individual children exhibiting DAS. Variability in the children's performance
across the years was noted, but individual trends were present within their error patterns. Errors in
stops and nasal reduced in number during the second year and were no longer present during the
final evaluation. Errors in later learned sound classes, such as fricatives, affricates, liquids, glides
and vacalics also reduced in number over the time period studied (3yrs 1 mnth -5yrs 3mnths). At the
age of 5 yrs and 3 mnths errors occurred only with fricatives and affricates.

The data indicates that the pattern generally seen as normal children develop classes of
speech sounds is also present in the children with DAS. However, Jackson and Hall longitudinal
study illustrated that the apraxic children may be acquiring these sounds at a much slower rate at
older ages and possibly only with the assistance of fairly intensive remedial services.

Unusual errors

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Studies looking closely at the speech production of children with DAS report ypes of errors
typically not seen in the productions of children with speech sound disorders.

Addition errors: children with DAS may make speech more complicated for themselves
>----------------——
by producing extra phonemes in their speech attempts. Such errors were reported by Rosenbek and
Wertz (1972) and Yoss and Darley (1974a) they noted that addition errors occurred in both
repetition tasks and in spontaneous speech tasks. They also noted that another type of addition error,
that of syllable addition occurred during production of polysyllabic words. E.g. /keloud/ for
cloud, /klaet/ for cat
Prolongation errors: Yoss and Darley found that this occurred during imitated speech
tasks consisting of subject repetition of the investigator's models of C-V-C, nonsense
words, real words and three syllable words placed in a three word carrier phrase speech
task. E.g. /s:an/ for sun, /hae;pe/ for happy

Repetition of sounds & syllables: this was also noted to occur in the context of imitated
speech tasks. Ararriatid~TjTassoTr-fT979) also noted trial and error groping kinds of repetition.
E.g. /s steirz/ for stairs

Non-phonemic productions: children with DAS occasionally make errors that seem to
defy accurate transcription using typical phonetic systems, even when using narrow
transcriptions. Aram and Glasson (1979) noted the presence of glottal plosives and bilabial
fricatives. In addition, Yoss and Darley (1974a) cited nasal assimilation and distortions
described as subtle voicing and devoicing errors that were not overt substitution errors.

Difficulties sequencing phonemes and syllables

A problem in correctly sequencing a speech production has been identified as a characteristic of

DAS. Sequencing errors are disruptions in the production of the correct sequencing of phonemes
and syllables .
The apraxic child may have difficulties in correctly producing phonemes in their appropriate order.

• Morley (1972) noted that some children with DAS may be able to accurately imitate
phonemes in isolation but unable to use them in more complex speech tasks or may
be able to produce a syllable or isolated word correctly but unable to produce the
word in phrases or sentences.
• McGinnis (1963) described DAS child as having pronounced difficulty in
sequencing the sounds within words, even though the individual phonemes were
within the child's repertoire.

Intelligibility
• Rosenbek and Wertz (1972) stated that connected speech was more unintelligible

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 than would be expected on the basis of single word articulation test results.
• Edwards (1973) noted that imitation of single words and of short automatic phrases
may be reasonable but stretches of spontaneous creative speech may be
unintelligible.
• Aram and Glasson (1979) noted variability in speech intelligibility which was
dependent on the length and complexity of utterances. The least intelligible context
was conversational speech.
 

Groping Behaviors
• Yoss and Darley (1974) stated that this behavior was present only in the older
subjects occurring most noticeably during the production of three syllable words.
• Occasionally, apparently out of desperation with their failure to achieve correct
articulatory postures, children with DAS have been observed to manipulate their
articulators with their fingers in an attempt to produce the sound correctly.
• Perhaps the groping increases after the implementation of remediation when the
child's awareness of the articulatory placement and the child's desire to perform
correctly increases.

Voicing errors
Yoss and Darley (1974a) noted that voicing errors during imitated speech tasks
occurred more than twice as often for the presumed DAS subject group than for the
comparative group of articulation disordered subjects. Aram and Glasson (1979) reported
that voicing errors were variable with prevocalic voiceless consonants often becoming
voiced while final voiced stops became devoiced.

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