Neuroplasticity Part 2 Flashcards

1
Q

Who compared changed in cortical motor representations post Stroke?

A

Nudo

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2
Q

What were results for spontaneous group in nudos post-stroke study?

A

Hand and digit cortical areas surrounding the lesion decreased compared to control

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3
Q

What were results for rehab group in Nudos post-stroke study?

A

Hand and digit cortical areas did not differ from control

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4
Q

Nudo suggests rehab training prevented

A

loss of cortical area.

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5
Q

What is another change that occurs after cortical lesion?

A

modifications of intracortical pathways.

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6
Q

What was Jeff Kleims Novelty intervention?

what did it do?

A

Use of drugs to promote plasticity

increased cortical area

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7
Q

In using drugs for plasticity, what is the only way it worked?

A

if accompanied by motor skill training.

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8
Q

What happened to animals who received TMS

A

they improved faster and reached a higher end point.

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9
Q

What happened to brain areas around infarct in animals who received TMS?

A

They were preserved with change in cortical maps.

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10
Q

What did Frackowiak + Chollert do?

A

Used PET to look at changes in regional blood flow.

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11
Q

What was result of Frackowiak + Chollert’ study?

A

Showed increased bloodflow (activity) in ipsilateral side during recovered finger mvmt. Showed opposite side took over.

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12
Q

What are 10 Principles of Experience in dependent neural plasticity.

A
  • Use it or lost it
  • use it improve it
  • Specificity
  • Repitition Matters
  • Intensity Matters
  • Time matters
  • Salience Matters
  • Age Matters
  • Transference
  • Interference
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13
Q

Spontaneous recovery after stroke is .

who thought this?>

A

Highly Variable

Kramer

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14
Q

Recovery of motor function post-stroke cannot be directly explained by ____.

What else has influence?

A

lesion type, location, or extent.

genetics

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15
Q

a protein growth factor involved in neuroplasticity and neuroprotection
and is identified as a key mediator of motor learning after stroke.

A

Brain derived Neurotrophic factor

BNDF

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16
Q

What happens with ppl who have val66met allele?

A

they have decreased levels of brain derived from neurotophic factor

17
Q

Decreased levels of BNDF associated with

A

decreased ability to recover from CNS injury

18
Q

What increases levels of BNDF?

A

aerobic exercise

19
Q

there is a relationship between dopamine levels and

A

exercise

20
Q

What are strategies for repairing Spinal cord lesions?

A

Replace cells
Re-grow axons
Retrain circuits

21
Q

Who introduced SC plasticity treadmill training

A

Barbeau and Rossignol

22
Q

What did they do in Treadmill Training?

A

cat got SC in Tspine cut. trained hindleg walking on Treadmill.
at first PWB and tail was pinched for extension response.

23
Q

What were results of TM training ?

A
  • Coordinating locomotion developed.
  • eventually walked faster and FWB
  • had better locomotion than control
24
Q

What happened to cats when provided trunk support, manually assisted loading and facilitation of stepping kinematics?

A

they generated hindlimb stepping response w/ absence of supra spinal control.

25
Q

What was hodgsons TM study

A

each group learned to stand or hindlimb walk

26
Q

What were results of hodgsons study?

A

each group learned task but couldn’t perform opposite task.

task specificity

27
Q

What is paradigm shift of SCI rehab?

A

compensation for deficits -> rehab for walking recovery

28
Q

What did Dobkin do?

A

compared SCI its who got TM training and no TM training

29
Q

What is result of Dobkin study?

A

Pts. with TM training showed increase walking ability.

30
Q

What were the results from the LEAPS trial?

A

locomotor training not superior to progressive exercise

31
Q

What were results of ICARE RCT?

A

no difference b/w task-oriented UE training and dose equivalent.

32
Q

In addition to dosing, what affects outcomes?

A

timing and duration of interventions