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Neuromuscular PT 1 > Neuroplasticity > Flashcards

Neuroplasticity Flashcards

1
Q

What is neuroplasticity

A
  • refers to the ability of the NS to change
  • plasticity that occrs in the absence of injury is learning
  • plasticity that occurs in response to injury is recovery
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2
Q

What does neuroplasticity encompass

A
  • habituation
  • experience-dependent plasticity
  • cellular recovery post injury
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3
Q

What is habituation

A
  • learned suppression of a response to a repeated non-noxious stimulus
  • simplest form of neuroplasticity
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4
Q

What happens when habituation occurs

A
  • decrease in presynaptic activity
  • decrease in release of excitatory NT
  • decrease in free intracellular Ca++
  • ie: clothing on skin
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5
Q

What happens with habituation over time

A

will see structral changes over time

  • decrease in number of synpatic connections
  • decrease in number of receptors on post synpatic neurons
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6
Q

Clinical examples of habituation and what they are

A
  1. vestibular rehab with UVH/BVH: learning to suppress the response
  2. tactile defensiveness: sensitive to things that are non-noxious (foot on carpet)
  3. amputation: getting use to a prosthetic by applying pressure there
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7
Q

Learning and memory

A
  • declarative and procedural learning requires awareness and attention
  • procedural learning: involved cerebral cortex, cerebellum and basal ganglia
  • declarative learning involved cerebral cortex and hippocampus
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8
Q

Mechanisms of experience dependent learning

A

protein synthesis

  • promotes growth of new synpatic connections
  • alters neuron excitability

long term potentiation

  • increased synpatic activity
  • increased efficiency of cell firing
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9
Q

Long term potentiation

A
  • formation of new memories
  • recovery after an injury
  • may have negative effects such as chronic pain syndromes or aberrant learning (addictive behaviors)
  • unmasking/conversion of silent synpases to active synpases
  • structural changes in post-synaptic membrane
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10
Q

Unmasking of silent synapses

A
  • inactive synapes that are still there
  • lack functional glutamate AMPA receptors
  • mobile AMPA receptors cycle between cytoplasm and synpatic membrane attach to silent synapse to activate it
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11
Q

LTP - unmasking of silent synpases

how does this happen

A
  • Ca++ enters cell through channels assoicated with NMDA glutamate receptors
  • results in insertion of AMPA receptors into memebrane
  • new dendritic spine forms
  • presynpatic new synpases form with learning
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12
Q

morphological changes in cell LTP

A
  • requires genetic alteration in neurons (during the learning process)
  • Ca++ regulates gene activity
  • nucleus contains Ca++ ion channels
  • allows for changes in gene expression and changes that occur due to learning
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13
Q

Astrocytes and experience dependent plasticity

A
  • astrocytes increase their contact with neurons in enriched environments
  • transmission of info through glia may be important in learning
  • astrocytes can release gliotransmitters (like glutamate) to signal neighboring neurons
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14
Q

Transcranial magnetic stimulation

A
  • used to enhance or inhibit motor learning (LTP) and memory
  • magnetic stimulation of local neurons
  • effects can last several days
  • may benefit CNS lesions
  • TMS for depression as well
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15
Q

Results of NS injury

A
  • interruption of axonal projections from the injured area
  • denervation of neurons innervated by injured neurons
  • in CNS may get cascade of degeneration or anterograde transneuronal degeneration
  • need proteins for learning
  • with Diffuse TBI there is axonal injury which can cause quick axon degeneration
  • survival of cytoplasm related to connection with nucleus otherwise degeneration occurs
  • may cause atrophy or cell death
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16
Q

Cell body damage (CNS vs PNS)

A

in CNS microglia act as phagocytes

  • astrocytes proliferate and replace neuron with glial scaring

in PNS tissue macrophages act as phagocytes

  • fibroblasts replace neuron with scar tissue
17
Q

result of NS injury

neuronal shock/diaschisis

A
  • short term loss of function in neuronal pathways at a distance from lesion
  • penumbra: salvagable brain area - over time this area decreases
18
Q

cellular recovery post injury

sprouting

A
  • occurs mainly in PNS

collateral sprouting

  • axonal growth from neighboring intact axons

regenerative sprouting

  • axon and target cell are damaged
  • regrowth of original axon
  • either can lead to synkinesis (unintended movements)
19
Q

cellular recovery post injury

collateral sprouting rate and process

A
  • grows slowly about 1.5 mm/day
  • new axon will be smaller in diameter
  • motor axon may innervate more fibers than before
  • giant motor unit action potentials
  • most sucessful in crush injuries when endoneurial sheath remains intact
  • can act as a conduit into which axon can regrow to reach its target
20
Q

cellular recovery post injury

collateral sprouting when is it less effective

A
  • nerves are completely severed (neurotmesis)
  • nerves are spearated by more than a few millimeters
  • mixed nerve is severed
  • infection is present
  • patient does not receive PT
21
Q

cellular recovery post injury

sprouting in CNS vs PNS

A
  • axonal sprouting occurs mainly in the PNS
  • less sucessful in CNS

due to

  • lack of growth factor
  • glial scars => nogo: neurite outgrowth inhibitor oligodendrocytes) inhibits neural growth
22
Q

cellular recovery post injury

Synpatic changes following injury

A
  1. recovery of synpatic effectivness: edema that is compressing a nerve ie CTS
  2. denervation hypersensitivity: death of presnyaptic cell
  3. synpatic hypereffectiveness: loss of some presynpatic terminals
  4. unmasking of silent synpases
23
Q

cellular recovery post injury

unmasking of silent synpases - translation

A
  • synpase that was previously not used jumps in to take the place of injured neurons
  • develops silent synpases during learning
24
Q

cellular recovery post injury

changes due to ischemia

A
  • lack of blood flow and oxygen to area
  • accumulation of glutamate
  • leads to excitotoxicity
  • changes in somatotopic representation
  • thought to be cause of ALS
25
Q

cellular recovery post injury

increase in intracellular Ca++ causes problems

A
  • results in an efflux of K+
  • Na-K pump works overtime
  • glycologsis = breaks down cell membrane
26
Q

cellular recovery post injury

ischemia: Ca++ influx also causes

A
  • influx of water
  • release of proteases and other enzymes detrimental to mitochondria
27
Q

how are

Cortical maps

modified

A

modified by

  • experience
  • learning: skilled musicians
  • sensory input: amputations (phantum pain), blindess, hearing loss
  • brain injury
28
Q

role of rehabiltation

A
  • waiting for natural recovery = brain repesentation shrank after injury
  • if they are rehabed and forced to use affected hand = function improves, decrease loss of representation
  • shows plasticity in CNS
29
Q

Negative plasticity

A
  • there is evidence in animals models that negative plasticity or loss of cortical representation can be caused by noxious stimuli or disuse
  • ie someone chewing gum really loud
30
Q

brain changes in humans

with aging

A

with aging the human brain tends to

  • have less gray matter
  • decreased levels of NT
  • changes in cognitive function
31
Q

Negative plasticity theory applied to aging, auditory perception and memory

A
  • disuse: people are less active as they age
  • noisy processing: harder to tune out background noise
  • weak modulatory control
  • negative learning

together these result in cognitive decline, demonstrated as memory impairments

32
Q

negative learning with age

A
  • adults may experience decreases in sensation, strength, ROM and falls

falls may result in

  • decreased interest in physical activity
  • gait changes such as looking down to see floor
  • decreased use to surroundings visual input
  • increased risk for falls and even less physically activity
  • loss of ability to walk over time
33
Q

How to promote neuroplasticity after brain injury

A
  1. use it or lose it
  2. use it nad improve it
  3. specificity
  4. repetition matters (requires reps for function change)
  5. intensity matters
  6. time matters
  7. salience matters (must be important to patient)
  8. age matters
34
Q

Experience-dependent Neuroplasticitiy

Transference

A
  • Neuroplasticity and the change in function that results from one therapy can augment the attainment of similar behaviors
35
Q

Experience-dependent Neuroplasticitiy

Interference

A

plasticity in response to one experience can interfere with acquisition of other behaviors

35
Q

Prognostic imaging: PET adn fMRI

A
  • the activation pattern used by a patient after a stroke is well-correlated with level of recovery and outcomes
  • patients who demonstrate activation maps similar to controls have fewer residual impairments
  • if area lights up = it is still giving and getting signals = can help with recovery
36
Q

Functional reorganization

A
  • the brain is able to reorganize and make connections
  • can take two years
37
Q

drugs affecting neuroplasticity

A
  • amphetamines
  • dopamine
  • Acetyl cholinesterase inhibitors-arousal and attention
  • growth factor
38
Q

research and methods to reduce effects of neuronal injury

A
  • use of steriods to reduce swelling
  • inducing hypothermia: mild to help pH of body
  • schwann cell transplants
  • introduction of peripheral neurotrophic factors into CNS
  • infusion of antibodies at site of injury

Neuromuscular PT 1 (32 decks)

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