There is evidence from both clinical and experimental studies that the spinal cord suffers both primary and secondary damage after acute spinal cord injury. The pathophysiology of secondary injury involves a multitude of cellular and molecular events which progress over the first few days after injury, the most important of which are systemic and local vascular insults, electrolyte shifts, oedema and excitotoxicity. These secondary processes contribute to the evolution of the pathological changes which in the severe injuries progress from central haemorrhagic necrosis involving mainly the grey matter to infarction of both the white and grey matter at the injury site and for a considerable distance proximally and distally. Less severe injuries show a variety of axonal and myelin changes. The concept of secondary injury is consistent with the results of therapeutic approaches to improve outcome.