Plasticity Flashcards
Neural Plasticity
• Lifelong ability of the brain to reorganize neural pathways and neural activities based on new experiences • Ongoing process of change, in response to new experiences • Brain level: glial/vascular • Network: reorganization of cortical maps and patterns • Inter/intracellular • Biochemical • Genetic
Neural plasticity after injury can be
•Restorative: Direct; Resolution of temporary changes and recovery of the injured tissue. •Compensatory: Indirect; Different neural circuits enable the recovery of lost or impaired function.
How does CNS respond to damage?
•Early: depress brain function; local response (edema and diaschisis); synaptic effectiveness •Intercellular responses: denervation supersensitivity, etc •Changes in cortical maps Remapping after peripheral lesions (amputations)
Early Transient Events
oEdema •Cytotoxic: accumulation of fluid •Vasogenic: leakage of proteins and fluids •Compression of axons, affects conduction oDiaschisis •Temporary disruption/depression of function in an intact brain area •Affects neuronal process far from the primary site of lesion •Caused by reduced blood supple, reduced metabolism, edema oSynaptic Effectiveness •Spontaneous recovery/resolution of neural shock because of Reduction of edema Resolution of diaschisis Absorption of necrotic tissue
Denervation supersensitivity
• Occurs when critical # of neurons destroyed • Postsynaptic membrane of a neuro becomes hyperactive to a released transmitter • Supersensitive because it doesn’t get the normal amount of stimulus. Increases number of available receptors, increases their responsiveness Parkinson’s causes a loss of dopamine producing neurons in the substantia nigra. Due to the denervation, the postsynaptic target neurons become hypersensitive to the dopamine that is released.
Recruiting/Unmasking of silent synapses
o Normally not functioning, masked under normal conditions o Facilitated by injury, drugs, experiences
Synaptic Hypereffectiveness
Presynaptic changes •Increased release of NTs Postsynaptic changes • Changes in postsynaptic membrane sensitivity Ex: increased sensitivity to Acetylcholine
Neural Regeneration (regenerative synaptogenesis)
o Seen in PNS o Begin sprouting 3-7 days after injury o Can travel long distances, but grows 1 mm per day
Collateral Sprouting (Reactive Synaptogenesis)
o 4-5 days after injury o Neighboring normal axons sprout to innervate synaptic sites that were previously activated by the injured axons
Experience Dependent Plasticity
o Cortical maps w/in one brain area are DEPENDENT o Can be modified by activity and experience • Learning an instrument at a young age change the strength of neural connection o Experience can also change the strength of neural connections between brain areas.
Experience Dependent Plasticity and Motor Learning
o At first, practice sequential finger tapping skill increases activation of sensory and motor cortical areas M1, M2, S1, S2 o When they get better, activation of motor area decreases, activation of thalamic pathways to other brain regions increases. o Constant shifting of which tasks require the most intense activation in which brain areas
Changes in Cortical Maps after Lesions: Peripheral
o Occurs after Peripheral nerve lesions, amputation, prolonged immobilization o Cortical maps are use dependent, if not used it will be replaced
· Changes in cortical maps after CNS Lesions
o Brain reorganization can occur following deafness or blindness
§ These area can be reprogrammed to respond to other sensory stimuli
§ Area still performs original function but responds to different mode of stimulation
o Reorganization of affected hemisphere through:
§ Redundant pathways OR
§ New regions taking over function of damaged area
§ Damage to primary motor causes activation of secondary motor areas
ú PMC, SMC, Cingulate Cortex
· Changes in Cortical maps after lesion: Contributions of Ipsilateral Pathways
o Uncrossed pathways play an important role
o Contralateral primary motor cortex (cortex on the side opposite to affected area) may play a role
· Changes in Cortical maps after lesions: Cerebellar contributions to Recovery from Ctx. Injury.
o Cerebellum enhances motor learning
o Generates new pathway b/w cerebellum and CTX that support more automatic performance of skilled movement
o Contralateral cerebellum is important
Clinical Implications
o Experience is very important in shaping cortical maps
o Effect of training
§ Reorganization of sensorimotor cortex can result from training
§ Optimal timing and intensity of training to maximize neural plasticity
§ Cortical stimulation through behavioral changes may facilitate motor recovery.
Effects of Age
[*] The brain reacts differently to injury at different stages of development
–Adult brains are less plastic than child
[*] The younger the age, the greater the plasticity of the nervous system
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–Lesion during early ages causes fewer deficits than damage in the adult years
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[*] Animal studies
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[*] Language function following lesion in the dominant hemisphere
[*] Several factors must be taken into consideration:
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–The area of the brain where the injury had occurred
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–The maturity of the brain region rather than the age of the individual
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–The loss of other behaviors
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–Maturational status of the damaged area
[*] Functionally mature area
–Comparable deficits as seen in adults
[*] Functionally immature related area
–It might take over the function of damages area
Gender
[*] Male versus female
–No evidence
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[*] Female may be better!
–Female brain is less lateralized in cortical functions
–Effects of hormones on the formation of edema
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Characteristics of the Lesion
[*] Severity of the injury
–Evidence shows strong correlation between severity of injury and long-term functional outcomes
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[*] Lesion size
–The smaller the lesion, the greater the recovery
–Remember: depends on the area of the brain involved
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[*] Re-occurrence of injury
–After having sufffered brain damage (e.g., stroke), another stroke usually has significantly larger detrimental effects
[*] - Plastic reserve has been drained
How quickly does the injury occur? Slow vs. rapid lesions
[*] Slowly developing lesions create less disruption of function than sudden lesions
[*] Tumor versus gunshot or stroke
–Brain tumors or slowly develping hydrocephalus à slow destruction of brain matter, time for adaptive / plastic changes
–Brain tumors can be large before any symptoms are noticed
–Stroke: sudden loss of areas, drastic behavioral / cognitive effects
[*] Autopsy studies of people who functioned well even near death
[*] Serial small lesions in animals VS one large lesion
–For serial lesion phenomenon consider:
[*] Amount of tissue damage in each stage
[*] Time difference
[*] Age
[*] Experience
Pre-Injury Neuroprotective Factors
Exercise
[*] Pre-injury exercise protects against deficits
[*] Animal studies:
–Prestroke exercises reduces infarct size
–Animal studies show that exercises may:
[*] Promote neuroplasticity
[*] Increase angiogenesis to support collateral
[*] Decrease apoptosis and edema
PINPF
Environmental Enrichment
[*] Improved performance?
–Enriched infant crib
–Enriched maze for rats[*] Enrichment before brain damage
–Protects the individual from the usual results of brain damage
Post-Injury Factors (PIF)
Effects of pharmacology
[*] Medications are used to …
1.Reduce nervous system’s reaction to injury
2.Promote recovery of function
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[*] The effects of drugs include:
–Prevention of scaring
[*] Affect trophic factors, and promote regeneration
–Prevention of neurotoxicity
[*] Toxic substances released by dead or dying cells
–Restoring blood circulation
–Replacing neurotransmitters lost by cell death
–Stimulating growth
PIF
Neurotrophic Factors
[*] Growth factors regulate:
–Synapse formation
–Neurotransmitter release
Neuronal excitability
