Apraxia

Question 1

Ideational apraxia

Answer 1

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

Question 2

Neuroanatomical correlate of ideational apraxia

Answer 2

L parietal lobe or diffuse cortical involvement (dementia)

Question 3

Conduction apraxia

Answer 3

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

Question 4

Four broad categories of errors seen in ideomotor apraxia

Answer 4

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

Question 5

Neuroanatomical correlate of ideomotor apraxia

Answer 5

LH, anywhere w/i perisylvian region

Question 6

Limb-kinetic apraxia

Answer 6

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

Question 7

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

Answer 7

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

Question 8

What are innervatory patterns (in relation to apraxia)?

Answer 8

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

Question 9

Weintraub says that ideational apraxia may represent a primary distrubance of

Answer 9

Attention or executive functions

Question 10

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

Answer 10

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

Question 11

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

Answer 11

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

Question 12

Dressing apraxia

Answer 12

Difficulty with dressing following RH lesions; not seen in isolation

Question 13

Ocular apraxia

Answer 13

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

Question 14

Ideomotor apraxia

Answer 14

Defective execution of individual components of an action

Question 15

Conceptual apraxia

Answer 15

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)

Question 16

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

Answer 16

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

Question 17

Buccofacial apraxia

Answer 17

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

Question 18

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

Answer 18

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

Question 19

Optic apraxia/optic ataxia

Answer 19

Apraxia of ocular searching movements affecting visually-guided hand mvmt

Question 20

Gait apraxia

Answer 20

Disorder of gait seen in diseases affecting the frontal lobe

Question 21

3 types of spatial errors seen in ideomotor apraxia

Answer 21

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

Question 22

Disconnection hypothesis of apraxia

Answer 22

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

Question 23

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

Answer 23

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)

Question 24

Goodglass defective symbolization model of apraxia

Answer 24

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

Question 25

Representational (or praxicon) hypothesis of apraxia

Answer 25

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

Question 26

Buccofacial apraxia is common with type of aphasia?

Answer 26

Broca’s

Question 27

Neuroanatomical correlate of limb-kinetic apraxia

Answer 27

CL premotor area or subjacent WM

Question 28

Liepman’s neuroanatomical model of apraxia

Answer 28

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

Question 29

Proglems with Liepman’s Neuroanatomical Model

Answer 29

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

Question 30

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

Answer 30

Arcuate fasciculus

Question 31

Apraxia

Answer 31

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

Question 32

Representational hypothesis of apraxia (Heilman)

Answer 32

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