Progress in neuropathology has made possible the description of local responses of neural tissue in early stages after traumatic spinal cord injury (SCI). The recent identification of multiple factors responsible for secondary spinal cord damage and for potential regenerative abilities has not resulted in the development of a standard for neuroprotective therapy in SCI patients. The paper reviews current knowledge concerning the sequence of biochemical events in the injured spinal cord and gives an overview of therapeutic possibilities for preventing the spread of secondary injury. The literature survey has led to the following conclusions: 1. The primary zone of traumatic damage enlarges due to local vascular disturbances, hypoxia, and the resulting inflammation. 2. Inflammation in the region of secondary injury, apart from having a destructive impact, is the source of substances which may induce neural tissue repair. 3. The administration of methylprednisolone and surgical decompression of the spinal cord within several hours after SCI improves functional and neurological outcomes in patients with incomplete neurological deficits. Currently there is no sufficient scientific evidence to support the safety and efficacy of other neuroprotective methods in humans.