INFLAMMATION AFTER AXONAL INJURY HAS CONFLICTING CONSEQUENCES FOR RECOVERY OF FUNCTION - RESCUE OF SPARED AXONS IS IMPAIRED BUT REGENERATION IS SUPPORTED

Neural injury leads to tissue damage beyond that caused by the initial lesion, mainly as a result of a chain of autodestructive events trigg ered by the trauma. These events apparently include the activation of immune-derived cells and their products, as treatment with anti-inflam matory agents, such as corticosteroids, limits the damage and thus imp roves recovery. On the other hand, immune-derived substances, such as cytokines, are thought to play an important role in post-traumatic axo nal regeneration. Thus, the need to reduce inflammation to limit the s pread of damage appears to be in conflict with the need to permit infl ammation to promote regeneration. Comprehension and resolution of this apparent conflict may lead to the development of treatment protocols aimed at rescuing axons spared by the initial injury, without hamperin g the potential regeneration of directly and indirectly injured axons. In this study, carried out on rats with crushed optic nerves, daily i ntraperitoneal injections of dexamethasone commencing prior to the inj ury significantly attenuated the injury-induced decrease in electrophy siological activity and reduced the area of tissue damage. On the othe r hand, dexamethasone treatment reduced the permissiveness of the inju red nerves to neural adhesion and regrowth in vitro. This latter pheno menon was also observed in injured peripheral nerves. Results are disc ussed with respect to the possible establishment of an appropriate pro tocol for corticosteroid treatment of nerve injuries aimed at promotin g neuronal rescue without compromising neuronal regeneration.