Plasticity

neuroplasticity

brain’s lifelong ability to change, adapt and reorganize itself by forming new neural connections and pathways in response to learning, experience or injury

• microlevel

• marcolevel

(can be adaptive or maladaptive)

microlevel

cellular/network level

• NEURAL plasticity

macrolevel

behavioral/system level

• BEHAVIORAL plasticity 

microlevel recovery 

restoration of the function within an area of the cortex that was initially lost after injury 

microlevel compesnsation

when a different neural tissue takes over the function lost after injury

macrolevel recovery

the capacity to preform a previously impaired task in the same manner as before the injury

macrolevel compensation

the use of a new strategy to preform that same task

macro and micro connection

they influence each other

• micro allows brain to learn new behavioral skills

• behavior itself can alter the brain, which reinforces the behavior 

mechanisms of recovery

• reduction of edema

• reperfusion

• resolution of diaschisis

reduction of edema

swelling will go down → areas that were temporarily malfunctioning due to pressure can now function normally again

reperfusion

blood flow is restored to areas of hypoperfusion

• with refreshed blood, brain tissues becomes more functional

resolution of diaschisis

functions associated with brain structures remote from the area of damage that had been initially impaired improved overtime 

can be precursor to neuralplasticity

mechanisms of neuroplasticity

• neuronal regeneration

  • dendritic branching

  • collateral sprouting

• long-term potentiation (LTP)

• unmasking of preexisting pathways

• cortical reorganization

neuronal regneration

components of injured neurons can be restored (not cell bodies who died)

• dendritic branching 

dendritic branching

an increase in dendritic connections and thus the number of synapses that can be made per neuron

collateral sprouting

an increase in axonal receptivity per neuron to other neurons through the growth of new axonal branches in uninjured axons near injured cells

long-term potentiation (LPT)

the persistent strengthening of synapses between neurons resulting from recent patterns of activity

• efficiency of transmission at the synaptic level is increased in surviving neurons, which compensates for reduced transmission from others

synaptic plasticty

unmasking preexisting pathways

neural connections that already existed before injury that were not active, may be activated to help compensate for connections lost through injury

cortical reorganization

basic brain behavior relationships are modified as areas of brain tissue that were not centrally involved in certain functions prior to injury take over those functions

recovery based on behavior concepts

1. compensation may occur which may show a change in strategy or the substitution of a new behavior for the lost one

• partial restoration of the original behavior

• complete restoration of behavior d

timeline of recovery

1. acute: immediately following trauma: short period of shock when functions may be affected

2. subacute: within a few hours - days with period of rapid recovery then steady improvement over several weeks

3. chronic: improvement gradually decreases as the months and tears go by

reperfusion

happens within hours after stroke and means blood flow is restored to tissue

reperfusion: acute

physical repair of penumbra cells happen during initial days as wounds heal and disturbed physiological functions improve

reperfusion: subacute

neural processing mechanisms reorganize impaired areas by taking advantage of intact brain regions spontaneously 

reperfusion: chronic

new learning mechanisms govern the extent to which the person can be retrained to perform a specific skills

recovery

• once physiological repair and restitution take place, organisms may still be functionally impaired

• only option for further improvement is to use strategies to bypass lesion site

• using new strategies may prompt further physiological changes and encourage further structural changes

left and right hemisphere roles

• acute stage there is global breakdown of the language network (weak left hemisphere activation)

• in the subacute stage, we see mild improvement in language function (bilateral cerebral activation with stronger activation in the right)

• in chronic stage we see normalized of activation pattern (shift back to left hemisphere)

prognostic factors of language recovery

• etiology of injury

• lesion size

• site of lesion

• severity of cognitive symptoms

• type of aphasia

• age

• education

• handedness (left handed people have better prognosis)

• psychologica; and emotional issues

• time since stroke onset

early physiologic recovery

day or weeks after stroke

• reduction of edema, reperfusion and resolution of diaschisis temporarily improve neural function around lesion

• isn’t true neuroplasticity yet

recruitment of perilesional tissues (LH)

• areas surrounding lesion in left hemisphere begin to take over lost functions

• surviving neurons show

  • dendritic branching and collateral sprouting

  • long term potentiation

• interhemispheric reorganization

activation of right hemisphere areas

• right hemisphere become more active if left hemisphere have extensive damage

• areas support and compensate for some language functions

• excessive activation can interfere with efficient processing

network level reorganization

brain forms new communication pathways between distant regions 

• unmasking of preexisting connections and strengthening of secondary language networks 

behavioral and therapeutic influence

• speech-language therapy drives plasticity by stimulating repeated, meaningful language use

• repeated activation of language circuits strengthens synaptic efficiency and supports cortical reorganization through experience-dependent learning

• intensity, timing and task-specificity of tehpay influence how effective;y the brain reorganizes