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PTRS 852 - Neuro PT I Midterm > Neuroplasticity > Flashcards

Neuroplasticity Flashcards

1
Q

Term: The ability of neurons to change their functions, chemical profile, or structure for longer than a few seconds

A

Neuroplasticity

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2
Q

3 Mechanisms of Neurplasticity

A
  1. Habituation
  2. Experience-dependent plasticity
  3. Recovery following injury
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3
Q

Term: Decrease in response to a repeated, benign stimulus due to a decrease in synaptic activity between sensory neurons and interneurons

A

Habituation

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4
Q

Describe the effect of absence of the stimulus on habituation

A

After a period where the stimulus is not applied, the effect resolve or diminish, once the stimulus is reapplied the response will return

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5
Q

Describe the effects of prolonged, repeated stimulus on habituation

A

Can result in more permanent, structural changes – the number of synaptic connections decreases

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6
Q

Term: Allows other types of learning to occur by letting people pay attention to important stimulation but “tune out” stimulation that is less important

A

Habituation

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7
Q

Term: Involved with learning and memory

A

Exeperience-dependent plasticity

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8
Q

Term: Persistent, long-lasting changes in the strength of synaptic connections between neurons and within neural networks

A

Exeperience-dependent plasticity

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9
Q

Describe the mechanisms behind Experience-dependent plasticity

A
  1. synthesis of new proteins
  2. growth of new synaptic connections
  3. modification of existing synapses
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10
Q

2 types of Experience-dependent plasticity

A
  1. long-term potentiation (LTP)
  2. long-term depression (LTD)
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11
Q

Describe how presynaptic and postsynaptic sysnapses change with Experience-dependent plasticity

A

Pre: through changes in NT release

Post: through changes in receptor density/efficiency

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12
Q

Term: “What fires together wires together”

A

LTP

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13
Q

Term: Prolonged stimulus results in growth of new cells/synapses

A

LTP

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14
Q

Term: Receptors englufed resulting in the synapses becoming inactive

A

LTD

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15
Q

Describe the role of astrocytes in Experience-dependent plasticity

A

Astrocytes modulate NT release and receptor expression at the post-synaptic membrance via the release of gliotransmitters, they may also be responsible for new synapse formation

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16
Q

Term: Remembering the 3 things you need to pick up at the store

A

Working memory

17
Q

Term: Remembering a new phone number 5-10 minutes later

A

Short-term memory

18
Q

Term: Recall of facts

A

Long-term memory – Delcarative – Semantic

19
Q

Term: Recall of events

A

Long term memory – Declarative – Episodic

20
Q

Term: Recall of facts and events

A

Delcarative Memory

21
Q

Term: Recall of motor skills

A

Non-declarative – Procedural memory

22
Q

Describe what an injury to an axon in the PNS looks like physiologically

A
  • cytoplasm leaks out
  • segments retract from one another
  • distal Wallerian degeneration
  • glia clean up debris
  • cell body undergoes central chromatolysis
  • potential synapse degeneration and death
23
Q

Term: degeneration of axon and myelin distally along with mm atrophy

A

Wallerian degeneration

24
Q

Term: cell body degenerative changes

A

Central chromatolysis

25
Q

Describe regeneration of axons in the PNS

A

Regeneration occurs in the form of sprouting of damaged axons which is guided by nerve growth factor produced by Schwann cells and by Bands of Bungner

Recover is slow – 1 mm/day, but can be stimulated by exercise

26
Q

Term: maladaptive rewiring; either alterned/crossed sensations or mm co-contraction

A

Synkinesis

27
Q

Describe the post injury response in the CNS

A

The majority of the damage takes hours to days to evolve due to the cascade of cellular events which is why it can take time to see how a pt. will present

  • white fiber tract damage leads to increased Ca influx
  • leads to the disruption of axonal transport and results in build up
  • leads to axonal swelling
  • leads to axonal retraction ball
  • leads to chromatolysis and Wallerian degeneration
28
Q

Describe the difference between the physiology behind SCI and TBI

A

SCI: extent of deficit depends on damage of white tracts and level

TBI: interial forces can cause widespread tearing and stretching which can cause diffuse axonal injury (stretched/torn fibers) and widespread neuron disconnect

29
Q

Describe the ability of the CNS to recover

A

Doesn’t occur as well as in the PNS

Regeneration is limited by glial scars which release neurite outgrowth inhibitor (Nogo)

30
Q

2 Promising tx for CNS axonal injury

A
  1. Drugs to inhibit Nogo
  2. Stem cells
31
Q

4 CNS synaptic changes following injury

A
  1. Recovery of synpatic effectiveness
  2. Denervation hypersensitivity (increase in receptors)
  3. Synaptic hypereffectiveness (increase NT release)
  4. Unmasking/disinhibition of silent synapses
32
Q

Describe Cortical Reorganization

A

Cortical represenation can be modified by sensory input/experience/learning/injury. Performing a motor skill task regularly can enlarge that area of cortical representation

33
Q

Describe the impact of genetics on cortical reorganization

A

Those with a BDNF gene have a decreased ability to learn a motor task and had poorer recovery following subarachnoid hemorrhages

The implications for PT include: could help direct plan to accomodation or rehabiliation, could also limit the pt. potential due to a stigma of inability to improve

34
Q

2 areas in the adult brain where new neurons are produced

A

Hippocampus and the wall of the lateral ventricles

35
Q

Describe the issue with naturally occuring neurogenesis

A

The new neurons/stem cells produced in the brain move to the area of injury but do not survive long enough to resolve the problem

36
Q

Describe how rehabilitation can promote plasticity

A
  1. Intensity (too much to soon can be damaging)
  2. Type (task specific!)
  3. Amount (early and frequent)

PTRS 852 - Neuro PT I Midterm (15 decks)

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