TAILIEUCHUNG - CNS injuries : cellular responses and pharmacological strategies

Three distinct sequential cellular responses characterise the reaction of the adult spinal cord and brain to injury. An acute haemorrhagic phase immediately ensues after wounding, in which haematogenous cells flood the lesion site. This is followed by a subacute period during which macrophages clear necrotic debris, glial cell reactions are mobilised, the clot becomes organised, and scarring is initiated. Finally, the scar tissue contracts during a consolidation phase . Superimposed on the above primary inflammatory/scarring responses are secondary neuronal degenerative and regenerative reactions to injury, accompanied by demyelination and remyelination. The interrelations between primary and secondary responses are not understood. It was once thought that scarring arrested axon regeneration in the central nervous system (CNS), but. | Cellular Responses to Penetrating CNS Injury Martin Berry Arthur Butt and Ann Logan CONTENTS Introduction Inflammation Scarring Responses to Injury in the Adult CNS Acute Haemorragic Phase 0 to 3 Days Postinjury Subacute Phase 3 to 8 Days Postinjury Reaction of Astrocytes to Injury Reaction of Oligodendrocytes to Injury Reaction of Microglia to Injury Consolidation Phase 8 to 20 Days Postinjury Inflammation Scarring Responses to Injury in the Foetal Neonatal CNS Responses of Neurons to Injury References INTRODUCTION Three distinct sequential cellular responses characterise the reaction of the adult spinal cord and brain to injury. An acute haemorrhagic phase immediately ensues after wounding in which haematogenous cells flood the lesion site. This is followed by a subacute period during which macrophages clear necrotic debris glial cell reactions are mobilised the clot becomes organised and scarring is initiated. Finally the scar tissue contracts during a consolidation phase. Superimposed on the above primary inflammatory scarring responses are secondary neuronal degenerative and regenerative reactions to injury accompanied by demyelination and remyelination. The interrelations between primary and secondary responses are not understood. It was once thought that scarring arrested axon regeneration in the central nervous system CNS but more recent experimental data indicate a contrary proposition that regenerating axons actually prevent scarring possibly by protease release and thus scarring could be a consequence rather than a cause of the failure of axons to regenerate in the CNS. Pharmacological strategies for the control of the cellular injury responses after CNS injury aim to 1999 CRC Press LLC Modulate acute inflammation to reduce oedema and necrosis in the neuropil about the wound Decrease the density of deposition of the glia collagen scar to create an environment favourable for the regrowth of .

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