• Final will have 4 questions on mechanisms of recovery
• Two main types of brain injury are stroke and TBI
• Usually some recovery but it is usually incomplete after years
• Objective of todays lectures:
• Neural mechanisms of recovery
• Describe behavioural compensations
• Neural mechanisms
• Brain simutaltion o Internal, natural drug assisted o Internal means activity from one area going to another o Natural means sensory mediates o Drug assisted: drugs that increase activitiy or reduce (GABA) inhibition o Phenomenon: After brain damage a function is lost and the comes back fairly quickly
• Usually a function that isn’t supposed to be loacalized to area of damage
• Can include function localize to penumbra o neurons need a lot of input to fire, sometimes that input os lost so thresholds adapt! Adjust sensitivity to new input levels and then they work again. o ***Distas***** review lecture notes
• Regrowth of axons o Mammals VERY different from amphibians
• Regrowth of axons studied in frogs and newts just doesn’t happen in mammal brain o In mammals PNS myelin sheath act as guide for axon regrowth o If nerve CRUSHED axon regrows back to target o If nerve CUT axons might grow back in incorrect targets o Eye muscles controlled by cranial nerves whish are in the PNS o If nerve cut and separated- no regrowth (usually) o Regrowth in PNS Not CNS o In CNS of mammals damaged axons regenerate
• But only briefly (1-2mm) ineffectively o Axon regrowth in CNS is NOT a key factor in recovery o STUDY NOTE be careful not to confuse what happens in CNS wof humans with what happens in pns of humans and cns of frogs
• Axon Sprouting o When an input dies its connection sites stay open o Nearby inputs come in and form new connections
• Collateral sprouts^ o shown to contribute to behavioral recovery after damage to hippocampus IN RATS o chemical treatments o help sprouting and recovery
• gangliosides aid recovery after several kinds of damage(in rats)
• Progesterone may be a factor helping recovery
• Denervation o After denevation or disuse, post-syncell becomes supersensitive to transmitter
• 1)Supersensitvity follows loss of input axons
• A)Disue supersensitivity follows inactivity inputs
• 2)Due to ^ # of receptors or change inside post-synaptic cell
• Reorganization of sensory representation in cortex o Problem: phantom limb o Old idea: active nerves in stump -> solutions: amputate more limb o NEW idea: remaining afferents expand into vacated region
• Representation of body on somatosensory cortex
• Brain remains plastic throughout life
• Cortex re-organized in response to change input
• Alt. Mechanism: Learned adjustment in behaviours o Main source of recovery is use of residual functions learning it use hwat is left to accomplish same goal o Sometimes use of impared function is avoided after brain injury
• Behavioural therapy primary treatment o Concentrate on remaining abilities o Usual focus on compensatory abilities o Some attempt to retrain lost abilities
• Questions asking to distinguish the best means of recovery and best stratergies o Means = way it happens
• Studying tips:
• Entire course more emphasis on 2nd half material more how 1st half relates o 2nd half
• Rat analogy from notes, train rat to go to white door, damage visual cortex, they then don’t tend to