The incidence of spinal cord injury in the United States is between 50 and 55 million per year. The personal and societal costs have been an impetus for experimental studies that defined the posttraumatic pathological and biochemical changes from which the hypothesis has arisen that a portion of the resulting neurological deficit is caused by the response of the spinal cord to the injury. Alteration in this response has been a therapeutic goal. Clinical series over a number of years with varied treatment regimens have failed to show any significant difference in neurological outcome. A single randomized clinical trial of 'high dose' 'low dose' steroid treatment failed to support the secondary injury response hypothesis. The experimental studies and lack of therapeutic effectiveness of present treatment both support the concept of further experimental studies and further randomized clinical trials. It is important to test the hypothesis of secondary injury since, if it is a cause of a portion of the resultant loss of neurological function, the benefit of its control would extend beyond spinal cord injury to other central nervous system injuries.