This article reviews the pathophysiology of spinal cord injury. The fo
cus is on the role of post-traumatic membrane lipid changes, including
lipid hydrolysis with enzymatic lipid peroxidation (ie, eicosanoid pr
oduction) and nonenzymatic, free radical-induced lipid peroxidation in
the secondary autodestruction of injured spinal cord tissue. A specul
ative etiopathogenesis of secondary injury is presented in an attempt
to explain the importance and order of the pathophysiologic events tha
t result in tissue death and the apparent effectiveness of diverse pha
rmacologic agents in the treatment of experimental spinal cord injury.