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Flashcards in Apraxia Deck (32):

Ideational apraxia

Failure to perform sequential motor movements though each individual component can be performed in isolation


Neuroanatomical correlate of ideational apraxia

L parietal lobe or diffuse cortical involvement (dementia)


Conduction apraxia

Pt can pantomime movements to command, but has difficulty imitating transitive movements


Ocular apraxia

Inability to perform purposeful ocular movements Component of Balint's syndrome


Four broad categories of errors seen in ideomotor apraxia

1) perseverative 2) sequencing error 3) spatial 4) timing


Neuroanatomical correlate of ideomotor apraxia

LH, anywhere w/i perisylvian region


Limb-kinetic apraxia

Loss of deftness including ability to make finely graded, precise, individual but coordinated finger movements


According to the ideomotor apraxia model, lesions of the left inferior parietal lobe will lead to 

Inability to recognize gestures b/c damage to representations of learned, skilled mvmts; gesture discrimination problem


What are innervatory patterns (in relation to apraxia)?

Heilman's theory: the specific motor plan used for praxis. The supplementary motor cortex is responsible for translating praxicons into innervatory patterns.


Patients with ideomotor apraxia have the greatest difficulties when asked to make what type of movements?

Transative (to use a tool) However, is also seen with intransitive movements


2 causes of ideomotor apraxia, as postulated by the representational hypothesis

Damage to the praxicons (believed to be in either L supramarginal or angular gyrus) OR connection b/t this area & primary motor cortex


Weintraub says that ideational apraxia may represent a primary distrubance of

Attention or executive functions


Dressing apraxia

Difficulty with dressing following RH lesions; not seen in isolation


Ideomotor apraxia

Defective execution of individual components of an action


Goodglass defective symbolization model of apraxia

Because the LH seems involved in both apraxia & aphasia, this is the idea that the L is involved in symbolization (apraxia being a loss of nonverbal symbolization). Counter argument: not all individuals with apraxia have aphasia


Conceptual apraxia

Pt can make transitive movements, but use the wrong one (ex hammering motor for screwdriver) Assoc. w/ posterior L lesions (Liepman says caudal L parietal)


According to the ideomotor apraxia model, lesions of the connections between the left inferior parietal lobe & the supplementary motor area will lead to

Bilateral ideomotor apraxia but can comprehend & discriminate gestures; movement memories not destroyed, just can't interact with anterior areas responsible for motor implementation


Buccofacial apraxia

Difficulty making movements with face, larynx, pharynx, etc. Assoc. w/ lesions in frontal & central opercula, anterior insula, 1st temporal gyrus


According to the ideomotor apraxia model, lesions of the supplementary motor area will lead to

Bilateral ideomotor apraxia with an inability to comprehend & discriminate gestures; innervatory patterns can't gait access to motor area


Optic apraxia/optic ataxia

Apraxia of ocular searching movements affecting visually-guided hand mvmt


Gait apraxia

Disorder of gait seen in diseases affecting the frontal lobe


3 types of spatial errors seen in ideomotor apraxia

1) posture 2) spatial orientation 3) spatial movement (movement at wrong joints)


Disconnection hypothesis of apraxia

Disconnection b/t language areas & visuokinesthetic engrams; fibers either cross from Wernicke's area to the CL association area or from the L premotor area to the R premotor area


Ansher & Benson (1993) - potential sites of damage associated with apraxia

1.  Lesion to L parietal lobe can damage arcuate fasciculus, interrupting flow of into anteriorly, prevents motor system from receiving direction to act

2.  Large lesion to L premotor area interferes w/ motor execution

3.  Lesion to anterior CC (only seen w/ L hand)


Representational (or praxicon) hypothesis of apraxia

Heilman argues for existence of 'visuo-kinesthetic engrams' or 'praxiconx' in the inferior parietal lobe

Based on idea that newrvous system learns & stores skilled  mvmt; disconnection b/t the area that stores this info & premotor/motor areas will result in poor implementation of skill mvmts


Buccofacial apraxia is common with type of aphasia?



Neuroanatomical correlate of limb-kinetic apraxia

CL premotor area or subjacent WM


Liepman's neuroanatomical model of apraxia

Suggested that the L parietal area is critical for control of complex mvmt; mediated by the L frontal lobe & area 4 for the R side of the body; disruption anywhere in this system would produce R-sided apraxia; control of the L limbs was proposed to be mediated via CC


Proglems with Liepman's Neuroanatomical Model

Does not recognize involvement of BG & thalamus in movement

Patients w/ circumscribed cortical lesions do not typically demonstrate chronic abnormalities on standard clinical tests of apraxia


Geschwind's model of apraxia involves impairment of what tract?

Arcuate fasciculus



Acquired disorder of skilled purposeful movement (may still do automatically)


Representational hypothesis of apraxia (Heilman)

The brain stores "praxicons" (visuo-kinesthetic engrams) in the inferior parietal lobe