Neurological Recovery Flashcards

This deck tests your knowledge of the theory of neuroplasticity.

1
Q

Following a neural injury, what are the possible outcomes?

A
  1. Resolution of reversal damages
  2. Neuroplasticity
  3. Neurogenesis
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2
Q

Why is neurogenesis not common in neural injury?

A
  • Minimal self-repair capacity (most regions have no SCs)
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3
Q

What are the two mechanisms of neuroplasticity?

A
  1. Altering synaptic efficacy
  2. Regeneration / Sprouting
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4
Q

What are the mechanisms for altering synaptic efficacy?

A
  1. LT potentiation / depression = stronger / weaker synapse
  2. Activity-dependent unmasking (repeat activity can cause previously ineffective synapses to become active)
  3. Denervation HS (when one neuron is damaged, surrounding connected neurons become hypersensitive to signals (network plasticity), thus preserving function
  4. Delayed decline in neurons
  5. Change in number and type of receptors
  6. Change in NTs released and taken up
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5
Q

What is the mechanism for regeneration / sprouting?

A

In order to compensate for lost neurons, regeneration / collateral sprouting may occur

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6
Q

What does regeneration / sprouting need?

A
  1. Angiogenesis + gene expression of products for cell viability, growth, and remodeling + dendritic spine remodeling
  2. Signalling molecules + inhibition of growth cone extension
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7
Q

What are two examples of maladaptive neuroplasticity?

A
  1. Neuropathic pain (abnormal neuroplastic reaction to sensory nerve damage, leading to dysesthesia + allodynia)
  2. Spasticity (abnormal neuroplastic reaction to stretch reflex injury, usually causing inhibition to be removed from descending motor input)
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8
Q

Detail some diseases where neuroplasticity has positive effects.

A
  1. Multiple Sclerosis - patients w/ good clinical recover show increased functionality of affected hemisphere’s primary SMC, instead of using unaffected hemisphere’s primary SMC
  2. Spinal Cord Injury - patients have functional redundancy; collateral + interneuron sprouting; spontaneous remyelination of unaffected but demyelinated axons; etc.
  3. Aphasia - treatment with melody and rhythm improve expressive language, by engaging language-capable regions in unaffected hemisphere
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9
Q

What is neuroplasticity therapy affected by?

A
  1. Age
  2. Lesion size / site
  3. Medications
  4. Premorbid conditions
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10
Q

What are the six principles of neuroplasticity therapy?

A
  1. Use it or lose it
  2. Quantity of training - need sufficiently intense reps of the activity, but past a certain limit = no effect + reinforces undesired behaviours
  3. Quality of training - directly do the task you want to train
  4. Feedback - intrinsic (sensory) and extrinsic (results and performance) helps improve learning, correct errors, and reestablish disrupted sensorimotor loops
  5. Suitable environment (motivation, physical activity)
  6. Time - earlier rehab. prevents maladaptive neuroplasticity
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