Class 2 - Motor and Action 2 Flashcards

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

A

spinal cord

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
Q

dull effect of direct (encoring selected actions) an indirect pathway (discouraging non-selected actions) makes it more likely that

A

the same response will be initated when the rewared input patern is reactivated in the future.

26
Q

HD progression

A

rapid progression, usually die within 12 years of onset

27
Q

Hyperkinesia

A

excessive movements

28
Q

Striatal changes in HD primaraly occour in

A

inhibatory neurons that form the indirect pathway

29
Q

Atrophy in HD is most prominate in

A

the basal ganla, death rate is as high as 90% in the striatum

30
Q

PD results from the loss of

A

DA producing neurone in the SNc

31
Q

Hypokinesia

A

reduced ablility to initate volentary movements (PD)

32
Q

Bradykinesia

A

slowing in the rate of movemtn

33
Q

akinesia

A

absence of volentary movement

34
Q

visual targets, cane, etc. help __ paitents

A

PD

35
Q

in PD, paitnet may be able to ___ movment but __

A

plan movements, but without normaly functioning BG the ablility to quickly initate a movement is comprimaised

36
Q

l-dopa can help

A

PD paitents

considerably improves motor problems

37
Q

l-dopa is

A

a syntheic precurer for DA
can cross BBB
replacement therapy

38
Q

with l-dopa neurons become

A

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
Q

PD paitents have trouble shifting

A

mental states, similar to movment

40
Q

Learning is

A

non-cognative

41
Q

first effects of learning are likely at a __ level

A

more abstract

42
Q

sea legs are a form of

A

sensorimotor adaptation

43
Q

snesorimotor learning

A

introduction of perturbation lare increase in many cortical areas, with practives activation in these areas is reduced, returning to state before pertubation

44
Q

Voxels in motor areas show

A

directional tuning

45
Q

Tuning of voxels ni visual cortex

A

remained faithful to the stimulus location,retained retnotopic maping

46
Q

tuning of voxels in paretia cortex

A

changed durring the course of adaptation

47
Q

Posterior paretal neurons learned the

A

new sensiormotor nap, retaining the new assocations between the visual imput and required motrt output

48
Q

patients with cerbellular damage have sever imparments in

A

learning to move in novel enviorments

49
Q

cerebellar tDCS leads to

A

faster learning

50
Q

___ essencal for leanring new map, but __ essencal in consoldating new map ( and __ imporant for storing new map)

A

cerebellum, M1

parietal cortex.