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Neuromotor Function 1 > Lecture 21 - Neuroplasticity > Flashcards

Lecture 21 - Neuroplasticity Flashcards

1
Q

Define neuroplasticity.

A

The ability of your brain to reorganize itself, both physically and functionally, throughout the lifespan. (influenced by environment, thinking, emotions, and behavior).

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2
Q

T/F: With neuroplasticity the brain reorganizes itself by forming new neural connections.

A

True (it DOESN’T make new nerves)

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3
Q

In what 3 ways do neurons change when acted upon by neuroplasticity?

A

Change their:
`1. function
2. chemical profile
3. structure

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4
Q

Ultimately, neuroplasticity can compensate for injury and disease leading to _____ of ______.

A

recovery of function

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5
Q

The ability to generate neurons stops at the age of __.

A

5

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6
Q

What are the 3 overall factors affecting recovery of function?

A
  1. Nature of the Injury
  2. Premorbid conditions
  3. Adequate stimulation
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7
Q

What are 3 characteristics you would think of when analyzing the nature of the injury?

A
  1. size of the lesion (harder to compensate for larger size)
  2. structures involved (some structures are harder to recover function for, depending on their function)
  3. rate of onset (slow developing lesions can be compensated for easier)
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8
Q

What are 3 characteristics you would think of when analyzing a person’s premorbid conditions?

A
  1. general health
  2. genetics
  3. age
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9
Q

T/F: If the pt doesn’t continue to stimulate the part of the brain where neuroplasticity is trying to compensate for losses then recovery of function will be slower.

A

True (pt needs to keep stimulating the area in order for permanent neurplastic changes to result)

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10
Q

List and define the 2 main types of recovery.

A
  1. Spontaneous recovery – from repair processes occurring early after injury
  2. Function-induced recovery – ability of the nervous system to modify itself as a result of changes in activity and the environment
    •from increased use of the involved body segments
    in relevant tasks
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11
Q

Your pt suffered an ischemic stroke 4 days ago and you are amazed to see the progress in motor and coordination. You think that this is most likely due to ______ (spontaneous/function) recovery.

A

spontaneous

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12
Q

What are the 3 attributable mechanisms leading to spontaneous recovery?

A
  1. resolution of the initial response of the body to the “shock” of the injury
  2. reduction of edema
  3. unmasking of existing (but silent) synapses
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13
Q

The mechanism of early recovery following an injury is termed as _________ recovery

A

spontaneous

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14
Q

How does edema impact recovery?

A

It is a build up of fluid extracellularly which puts pressure on certain structures and inhibits their function. Once the edema recedes the structure is able to function better.

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15
Q

What are silent synapses?

A

Synapses in areas of the brain that are not functional because of competition within neuronal pathways

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16
Q

T/F: The process of unmasking of existing (but silent) synapses is always a spontaneous mechanism.

A

False (can be either induced or spontaneous)

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17
Q

T/F: Functional recovery is a short term mechanism of recovery.

A

False (long term)

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18
Q

Functional recovery targets the ____ on the nerve cell and occurs in ____ neurons.

A

axon; PNS

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19
Q

What type of glial cell is involved in the functional recovery mechanism?

A

Schwann

20
Q

T/F: Schwann cells are able to regrow the PNS nerve using nerve growth factors.

A

False (helps in the re-growth of AXONS, not the entire nerve cell/neuron)

21
Q

How do Schwann cells participate in the functional recovery mechanism?

A
  • provides an environment that support the re-growth of damaged axons
  • has nerve growth factor
22
Q

T/F: Functional recovery of the nerve is still possible when the cell body is damaged b/c of Schwann cells.

A

False (Schwann cells can only regrow the axon)

23
Q

Can axonal re-growth occur in PNS and CNS?

A

No, only in PNS (in CNS the glial cells form a plaque around the damaged axon)

24
Q

How fast is axonal growth during recovery?

A

1mm/day

25
Q

Th ability for axonal regrowth occurs through what 2 mechanisms?

A
  1. collateral sprouting

2. regenerative sprouting

26
Q

Describe collateral sprouting.

A

Branches of intact axons close to the area of the lesion sprout to re-innervate denervated targets (nerves)

27
Q

What happens to a nerve cell over time if it doesn’t receive any input?

A

It will die

28
Q

Describe regenerative sprouting.

A

occurs when an axon and its target cell (neuron, muscle, gland) have been damaged
injured axons sends out side sprouts to a new
target

29
Q

Can regeneration of dendrites occur?

A

No, b/c Schwann cells act on axons not dendrites.

30
Q

T/F: Collateral and regenerative sprouting occur in the CNS too.

A

False (only occur in the PNS - b/c axons can be regenerated in the PNS but not the CNS)

31
Q

What 2 factors prevent axonal regeneration in the brain & spinal cord?

A
  1. glial cells (astrocytes and microglia) form scars (plaques) on the damaged axon
  2. lack of nerve growth factors (astocytes and microglia release INHIBITORY factors)
32
Q

** BRAIN BREAK**

What do you call a row of rabbits hopping away?

A

A receding hare line!

:)

33
Q

List the 4 types of synaptic changes that occur with neuroplasticity.

A
  1. Long-term potentiation
  2. Recovery of Synaptic effectiveness
  3. Denervation hypersensitivity
  4. Synaptic hypereffectiveness
34
Q

Define Long Term Potentiation (LTP).

A

A cellular mechanisms producing lasting changes (several minutes to months) in synaptic connections with motor learning

35
Q

How is Long Term Potentiation possible?

A

Through conversion of silent synapses to active synapses.

36
Q

Describe how silent synapses become active synapses.

A

silent synapses lack functional glutamate AMPA receptors, with LTP these AMPA receptor sites are inserted into the post-synaptic cell membrane rendering the synapse active

37
Q

Describe how recovery of synaptic effectiveness works.

A

Occurs with the reduction in local edema that occurred with injury and interfered with AP conduction. (before the edema was pressing on the axon and preventing the AP from reaching the synapse)

38
Q

Describe how denervation hypersensitivity works.

A

occurs when pre-synaptic axon terminals are destroyed, depriving post-synaptic neurons of an adequate supply of neurotransmitter
The post-synaptic neurons develop new receptor
sites in response to transmitter released from other
nearby axons (does this to attract new collaterals
b/c it needs to receive stimulation or else it dies)

39
Q

Where can you often see denervation hypersensitivity?

A

Neuromuscular Junction

40
Q

Describe how synaptic hypereffectiveness works.

A

results when some branches of presynaptic axon are damaged, neurotransmitter accumulates in the undamaged axon terminals, resulting in larger than normal amounts of neurotransmitter being released at the remaining terminals onto the post-synaptic receptors

41
Q

Cortical maps (aka homunculi) can be altered by what 4 things?

A
  1. sensory input
  2. experience
  3. learning
  4. BRAIN INJURY
42
Q

What happens to the cortical area related to the injury?

A

With time neighboring areas of the cortex take over the area of the cortical map that is no longer being used (ex: finger amputation)

43
Q

Explain cross-modal plasticity in response to severe unimodal sensory deprivation.

A

Ipsilateral motor pathways (the less dominant pathways) begin to play an important role in the control of movement when the contralateral (dominant) motor pathways have been affected
(translation: a pathway that runs along the same track as the damaged pathway will be refined so that it can now carry out the function of the damaged pathway)

44
Q

T/F: Neuroplasticity can take place indefinitely.

A

False (neuroplasticity is less effective with re-occurence of injury - so recovery following a 2nd stroke won’t be as good as recovery following the initial stroke, you will see larger detrimental effects)

45
Q

To target neuroplasticity, rehabilitation techniques need to have what characteristics?

A
  1. focus on functional and meaningful skilled activities
  2. the pt needs to pay attention to somatosensory (proprioception and kinesthetic) aspect of the task
  3. appropriate intensity
  4. need to take place in a timely manner following the injury (you want to intervene before the movement is learned in a wrong way and synapses are created for this faulty movement pattern)
46
Q

Who is awesome?

A

YOU GUYS!
Thank you all so much for the hard work you’ve put into making these cards. I hope they were all helpful for everyone and we can take it to the bank, cash it in, and get a shiny 100%! Remember, you know more than you think you know, it’s just hidden very, VERY well sometimes. Good luck on the final everyone!
~ Julietta

Neuromotor Function 1 (21 decks)

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