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

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
What was hodgsons TM study
each group learned to stand or hindlimb walk
26
What were results of hodgsons study?
each group learned task but couldn't perform opposite task. | task specificity
27
What is paradigm shift of SCI rehab?
compensation for deficits -> rehab for walking recovery
28
What did Dobkin do?
compared SCI its who got TM training and no TM training
29
What is result of Dobkin study?
Pts. with TM training showed increase walking ability.
30
What were the results from the LEAPS trial?
locomotor training not superior to progressive exercise
31
What were results of ICARE RCT?
no difference b/w task-oriented UE training and dose equivalent.
32
In addition to dosing, what affects outcomes?
timing and duration of interventions