Class 2 - Motor and Action 2 Flashcards

(50 cards)

1
Q

Cerebellar damage

A

Cerebellar ataxia
• Difficulty of coordinating movements (ex. coordinate muscles)
• Dysarthria (symptom)
Affects recalibration of movement after visual distortion
Eyeblink conditioning

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2
Q

Dysarthria

A

cerebellar ataxia of speech output

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3
Q

Test of cerebellar damage

A

Nose test
(touch nose, touch other finger, and back, looking for patterns of activity, and how muscles of arm are working together vs should work)
in cerebellar ataxia - can be overshoot

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4
Q

Action tremor

A

tremors occurring during performance of action

tend to overshoot the movement of the hand`

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5
Q

Eyeblink conditioning

A

when making a blinking response to something being blown in eye - normally eyes close - if tone before than close eyes before air puff happen
timing of a conditioned response

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6
Q

Parkinson’s Disease

A
  • Dopamine deficiency: Damage to substantia nigra (projects to striatum )
  • Overactivity of indirect pathway as a result of lack of inputs to the striatum
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7
Q

Positive symptoms of PD

A
  • Tremors - there because other systems are trying to compinase for high level of indirecct pathway of inhibiton
  • Rigidity - high actvaton of indirect pathway - blocks movemtn
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8
Q

Negative symptoms of PD

A
  • Akinesia/bradykinesia

* Disturbance in posture

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9
Q

Huntington’s Disease

A

• Selective loss of projections from striatum to GPe
• Damages indirect route
- hereditary neurodegenerative disorder (autosomal Dominate)
Chorea
Dystonia

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10
Q

Chorea

A

rapid, jerky, involuntary sequences of movements

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11
Q

Dystonia

A

abnormal posturing due to involuntary muscle contractions

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12
Q

Apraxia

A

Apraxia typically results from lesions of left parietal or frontal lesions, but can result from lesions to multiple areas

• Inability to do skilled, sequential, purposeful movement
Low-level motor processes intact
• Bilateral deficit instead of just contralateral to damage
Thought to be due to damage to the ventrodorsal stream

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13
Q

Callosal apraxia

A
  • Disconnection syndrome
  • Inability to follow verbal command with left hand
  • Corpus callosum severed, so right motor cortex cannot receive commands
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14
Q

Can ipsilateral cortex take over for contralateral loss?

A

potently in PFC

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15
Q

Akinesia/bradykinesia

A

slowness of movements
trouble walking steadily, write, etc.
cueing can help with movement (lines on floor, sound beep, etc) along with medication

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16
Q

Biomarkers promessing when the assemsent is prefromed after the paitent has recoverd from the critical inital post stroke period

A
  • integerty of the corticospinal tract mesured with DTI

- presence of uper limb MEPs in response to TMS

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17
Q

peri-infarct cortex

A

tussie surrounding the lesion

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18
Q

if peri-infarct cortex is intact (after stroke)

A

mice show a degree of recovery

- if use TMS here, accelerates recovery process

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19
Q

increase of __ in peri-infarct zones post stroke

A

GABA

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20
Q

GABA post stroke

A

reduces the efficasy of sensory imputs and in turn leads to neural hypoactivity

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21
Q

long term neuroprosteic control leeds to the formation of a

A

remarkably stable cortical map that is preadily recalled and resistant to the stroage of a second mab

22
Q

BMI bipasses the

23
Q

Problems with BMI

A

repeated surgeries, recording devices fail over time

operate in an open loop mode, do not take in sensory information

24
Q

a reward or the antisapaton of a reward triggers

A

firing of DA neurons

25
dull effect of direct (encoring selected actions) an indirect pathway (discouraging non-selected actions) makes it more likely that
the same response will be initated when the rewared input patern is reactivated in the future.
26
HD progression
rapid progression, usually die within 12 years of onset
27
Hyperkinesia
excessive movements
28
Striatal changes in HD primaraly occour in
inhibatory neurons that form the indirect pathway
29
Atrophy in HD is most prominate in
the basal ganla, death rate is as high as 90% in the striatum
30
PD results from the loss of
DA producing neurone in the SNc
31
Hypokinesia
reduced ablility to initate volentary movements (PD)
32
Bradykinesia
slowing in the rate of movemtn
33
akinesia
absence of volentary movement
34
visual targets, cane, etc. help __ paitents
PD
35
in PD, paitnet may be able to ___ movment but __
plan movements, but without normaly functioning BG the ablility to quickly initate a movement is comprimaised
36
l-dopa can help
PD paitents | considerably improves motor problems
37
l-dopa is
a syntheic precurer for DA can cross BBB replacement therapy
38
with l-dopa neurons become
sensatizedm ammount of meducation tends to increase, additional sympoms form this inclde drug induced hyperkenesa, (may be from acting on other normal areas of the brain that becaome overdosed)
39
PD paitents have trouble shifting
mental states, similar to movment
40
Learning is
non-cognative
41
first effects of learning are likely at a __ level
more abstract
42
sea legs are a form of
sensorimotor adaptation
43
snesorimotor learning
introduction of perturbation lare increase in many cortical areas, with practives activation in these areas is reduced, returning to state before pertubation
44
Voxels in motor areas show
directional tuning
45
Tuning of voxels ni visual cortex
remained faithful to the stimulus location,retained retnotopic maping
46
tuning of voxels in paretia cortex
changed durring the course of adaptation
47
Posterior paretal neurons learned the
new sensiormotor nap, retaining the new assocations between the visual imput and required motrt output
48
patients with cerbellular damage have sever imparments in
learning to move in novel enviorments
49
cerebellar tDCS leads to
faster learning
50
___ essencal for leanring new map, but __ essencal in consoldating new map ( and __ imporant for storing new map)
cerebellum, M1 | parietal cortex.