Neuroplasticity: Exam 1 Flashcards
(84 cards)
CNS pathology
what happens?
- damaged area OR areas connected by damaged path. STOP working normally
- Result depends on what part is damaged
Recovery
what happens?
-
Sparing
- lack of observable deficit
-
Compensation– a way to get better
- accomplish goal in NEW and DIFF way
-
True Recovery–neuroPT’s goal!!!
- gradual return of lost function
- end result==> accomp. goal in same manner as was done prior to CNS injury
What contributes to recovery ?
- Plasticity—reorg. of CNS
-
reversal of Neural Shock
- shock is right after injury
- Denervation hypERsensitivity
- activation redundant systems
Capacity of the CNS to adapt to functional demands and therefore to the system’s capacity to reorganize
Neural Plasticity
Neural Plasticity
Capacity of the CNS to adapt to functional demands and therefore to the system’s capacity to reorganize
Capacity for Neuroplasticity:
2 types
- Functional–Short-term
- Structural–Long-term
Capacity for Neuroplasticity:
Functional (short-term)
changes in efficiency or strength of synaptic connections
*short term because just affects the already existing conections
Capacity for Neuroplasticity:
Structural (Long-term)
changes in organization and numbers of connections among neurons
*long term because changes in the numbers and organization
Plasticity:
2 types
- ReACTIVE Synaptogenesis
- Regenerative Synaptogenesis
Plasticity:
Reactive Synapto.
Think Sprouts!!!
- collateral sprouting
- axons sprout NEW synapses
- sprouts typ. from SAME neural system

Plasticity:
Regenerative Synapto.
*Think Neuron heals!!!
- neural regen.
- occurs when injured axons sprout NEW dendrites

Research on Neuroplasticity
3 conclusions:
- Phys rehab after stroke is a potent modulator of plasticity process
- happens because of DEMAND
- demand leads to angiogenesis and synaptogenesis
- new blood vessels
- new neural connects.
- Int of training shown to INC recovery!!!
Neural Shock
Explain…
- Temp abolition of excitability in areas related to damaged area from:
- dec blood flow
- reduction in metabolism
- Lesion==swelling==dramatic LOSS of function==rapid RETURN of function
Therapeutic implication of Neural Shock
- Goal of early PT:
-
disinhibit system
- STOP inhibition and let system function again
-
disinhibit system
Denervation Hypersensitivity
occurs when neuron loses normal input, results in hypersensitivity of post-synaptic membrane to neurotransmitters
*Injury==rapid LOSS function==function restored because neurons become MORE sensitive
occurs when neuron loses normal input, results in hypersensitivity of post-synaptic membrane to neurotransmitters
*Injury==rapid LOSS function==function restored because neurons become MORE sensitive
Denervation Hypersensitivity
Ischemic Penumbra
- cells bordering ischemic region
- neurons are viable, but NOT functional
- lost connects OR insuff. blood flow
- improved thru tx w/ amphetamines and PT

System Redundancy
- recruitment of previously silent/unused synapses
- suggests presence of synapses that do not normally function due to neuronal competition
- training may lead to unmasking these silent synapses ALONG W/ amphetamines
- facilitates activation
Recruitment of previously silent/unused synapses
System redundancy
*includes neuronal competition
What happens during recovery?
COMBO of processes occurring simultaneously OR sequentially
*NOTE: PT’s must understand these processes!!!
CNS Pharmacologic interventions
*remember goal to DISinhibit system
- prevent scarring
- prevent swelling
- stimulate growth
- Disinhibit inhibited regions
Spontaneous recovery occurs due to _______ when?
Nat. processes AFTER lesion
When is recovery considered spontaneous?
- Much of the recovery in first 3-4 wks after insult are spont.
- normalize edema, circ, and/or neural shock
NOTE: changes after 3-4wks are due to other mech’s
Spontaneous recovery and PT research?
was it the PT intervention OR spont. recovery that was going to happen anyway?
Need control vs. experimental groups





