Lp 10 Flashcards
(12 cards)
Mechanisms of injury interference w?
- Membrane Fxn
- E production
- Protein synthesis
- Alterations in genetic material
-disintegration of axon & its myelin sheath distal to site of injury
-can occur in both CNS & PNS (mechanisms of repair are different for each)
-mechanism of degeneration:
*deprived of nutrition,distal end disintegrates
*cellular debris accumulates
Wallerian degeneration
-regeneration of structural integrity but loss of Fxn
-macrophages remove debris after axon degeneration
-Astrocyte proliferation leads to structural repair of degenerated axon & myelin sheath *astrocytiv glial scar forms
-no atonal regeneration d/t scar
Regeneration in CNS
-reproduce in response to NGFs released at injury site
-form a regeneration tube
-become active once axon membrane is regenerated
Schwann cells
Effects of degeneration
-loss of n impulse conduction decrease Fxn
-sensory loss
-motor loss
-tropic disturbances d/t decrease nutritional & metabolic activity
-re-establishment of fxnal connections;
*stimulation by NGF
*pseudopodia formation
-n compression more likely to repair than n transection
-axon growth is 1-4 mm/day= rate of atonal transport
-realignment of NMJ- usually reattaches neuron to original m
Peripheral n regeneration
-atonal regeneration usually unsuccessful
-response to injury in CNS
-result of tissue changes
-glial scarring responsible for failure of regeneration
CNS regeneration
Injury to n tissue results in
-neuronal death
-demyelination
Recovery- neural plasticity:
-regain Fxn
-post-injury chances in NS
-mechanism is unclear
Demyelination characteristics:
-partially reversible
-process is sow, never complete
-intermodal areas contain few na+ channels
Effects: deymination slows/blocks n conduction
-demyelination in PNS
-spontaneous remission possible
GuillIan-barre syndrome
Relapse & remission permits impulses to propagate slowly- appears sufficient for snail recovery
Multiple sclerosis- demyination in CNS