Following injury to the CNS, highly reactive free radicals may produce
secondary or delayed tissue damage via peroxidation of lipids in cell
ular membranes. This extensive generation of free radicals appears to
overwhelm natural defence mechanisms, dramatically reducing the levels
of endogenous antioxidant compounds. In numerous studies utilising mo
dels of CNS injury, treatment with a synthetic antioxidant, the nongrl
ucocorticoid 21-aminosteroid (lazaroid) tirilazad, has been shown to m
aintain the level of endogenous antioxidants, improve neurological out
come, decrease cell loss, reduce cerebral oedema formation and improve
survival. As a result of these encouraging results, clinical trials h
ave been initiated to evaluate the utility of tirilazad in the treatme
nt of subarachnoid haemorrhage, spinal cord injury, traumatic brain in
jury and stroke.