Apraxia Flashcards

1
Q

Ideational apraxia

A

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

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2
Q

Neuroanatomical correlate of ideational apraxia

A

L parietal lobe or diffuse cortical involvement (dementia)

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3
Q

Conduction apraxia

A

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

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4
Q

Ocular apraxia

A

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

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4
Q

Four broad categories of errors seen in ideomotor apraxia

A

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

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5
Q

Neuroanatomical correlate of ideomotor apraxia

A

LH, anywhere w/i perisylvian region

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6
Q

Limb-kinetic apraxia

A

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

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7
Q

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

A

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

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8
Q

What are innervatory patterns (in relation to apraxia)?

A

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

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9
Q

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

A

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

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9
Q

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

A

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

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9
Q

Weintraub says that ideational apraxia may represent a primary distrubance of

A

Attention or executive functions

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12
Q

Dressing apraxia

A

Difficulty with dressing following RH lesions; not seen in isolation

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14
Q

Ideomotor apraxia

A

Defective execution of individual components of an action

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15
Q

Goodglass defective symbolization model of apraxia

A

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

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15
Q

Conceptual apraxia

A

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)

16
Q

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

A

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

17
Q

Buccofacial apraxia

A

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

18
Q

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

A

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

19
Q

Optic apraxia/optic ataxia

A

Apraxia of ocular searching movements affecting visually-guided hand mvmt

20
Q

Gait apraxia

A

Disorder of gait seen in diseases affecting the frontal lobe

21
Q

3 types of spatial errors seen in ideomotor apraxia

A

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

22
Q

Disconnection hypothesis of apraxia

A

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

23
Q

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

A
  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)
25
Q

Representational (or praxicon) hypothesis of apraxia

A

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

26
Q

Buccofacial apraxia is common with type of aphasia?

A

Broca’s

27
Q

Neuroanatomical correlate of limb-kinetic apraxia

A

CL premotor area or subjacent WM

28
Q

Liepman’s neuroanatomical model of apraxia

A

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

29
Q

Proglems with Liepman’s Neuroanatomical Model

A

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

30
Q

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

A

Arcuate fasciculus

31
Q

Apraxia

A

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

32
Q

Representational hypothesis of apraxia (Heilman)

A

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