Neuroplasticity Flashcards
What is neuroplasticity
- 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
What does neuroplasticity encompass
- habituation
- experience-dependent plasticity
- cellular recovery post injury
What is habituation
- learned suppression of a response to a repeated non-noxious stimulus
- simplest form of neuroplasticity
What happens when habituation occurs
- decrease in presynaptic activity
- decrease in release of excitatory NT
- decrease in free intracellular Ca++
- ie: clothing on skin
What happens with habituation over time
will see structral changes over time
- decrease in number of synpatic connections
- decrease in number of receptors on post synpatic neurons
Clinical examples of habituation and what they are
- vestibular rehab with UVH/BVH: learning to suppress the response
- tactile defensiveness: sensitive to things that are non-noxious (foot on carpet)
- amputation: getting use to a prosthetic by applying pressure there
Learning and memory
- declarative and procedural learning requires awareness and attention
- procedural learning: involved cerebral cortex, cerebellum and basal ganglia
- declarative learning involved cerebral cortex and hippocampus
Mechanisms of experience dependent learning
protein synthesis
- promotes growth of new synpatic connections
- alters neuron excitability
long term potentiation
- increased synpatic activity
- increased efficiency of cell firing
Long term potentiation
- 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
Unmasking of silent synapses
- 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
LTP - unmasking of silent synpases
how does this happen
- 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
morphological changes in cell LTP
- 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
Astrocytes and experience dependent plasticity
- 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
Transcranial magnetic stimulation
- 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
Results of NS injury
- 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
Cell body damage (CNS vs PNS)
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
result of NS injury
neuronal shock/diaschisis
- short term loss of function in neuronal pathways at a distance from lesion
- penumbra: salvagable brain area - over time this area decreases
cellular recovery post injury
sprouting
- 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)
cellular recovery post injury
collateral sprouting rate and process
- 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
cellular recovery post injury
collateral sprouting when is it less effective
- 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
cellular recovery post injury
sprouting in CNS vs PNS
- 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
cellular recovery post injury
Synpatic changes following injury
- recovery of synpatic effectivness: edema that is compressing a nerve ie CTS
- denervation hypersensitivity: death of presnyaptic cell
- synpatic hypereffectiveness: loss of some presynpatic terminals
- unmasking of silent synpases
cellular recovery post injury
unmasking of silent synpases - translation
- synpase that was previously not used jumps in to take the place of injured neurons
- develops silent synpases during learning
cellular recovery post injury
changes due to ischemia
- lack of blood flow and oxygen to area
- accumulation of glutamate
- leads to excitotoxicity
- changes in somatotopic representation
- thought to be cause of ALS
cellular recovery post injury
increase in intracellular Ca++ causes problems
- results in an efflux of K+
- Na-K pump works overtime
- glycologsis = breaks down cell membrane
cellular recovery post injury
ischemia: Ca++ influx also causes
- influx of water
- release of proteases and other enzymes detrimental to mitochondria
how are
Cortical maps
modified
modified by
- experience
- learning: skilled musicians
- sensory input: amputations (phantum pain), blindess, hearing loss
- brain injury
role of rehabiltation
- 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
Negative plasticity
- 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
brain changes in humans
with aging
with aging the human brain tends to
- have less gray matter
- decreased levels of NT
- changes in cognitive function
Negative plasticity theory applied to aging, auditory perception and memory
- 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
negative learning with age
- 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
How to promote neuroplasticity after brain injury
- use it or lose it
- use it nad improve it
- specificity
- repetition matters (requires reps for function change)
- intensity matters
- time matters
- salience matters (must be important to patient)
- age matters
Experience-dependent Neuroplasticitiy
Transference
- Neuroplasticity and the change in function that results from one therapy can augment the attainment of similar behaviors
Experience-dependent Neuroplasticitiy
Interference
plasticity in response to one experience can interfere with acquisition of other behaviors
Prognostic imaging: PET adn fMRI
- 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
Functional reorganization
- the brain is able to reorganize and make connections
- can take two years
drugs affecting neuroplasticity
- amphetamines
- dopamine
- Acetyl cholinesterase inhibitors-arousal and attention
- growth factor
research and methods to reduce effects of neuronal injury
- 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
