Pathology of experimental spinal cord trauma. I. The necrotic lesion as a function of vascular injury.

Adult Sprague Dawley rats were subjected to spinal cord trauma at the lower thoracic-lumbar levels utilizing a weight dropping technique onto the surgically exposed dorsal surface. The experimental conditions of trauma consistently produced severe paraplegia without spontaneous movement of the hindlimbs, a sensory level, and neurogenic bladder dysfunction. Changes in blood vessels and the development of tissue necrosis were studied in a posttrauma time sequence by light and electron microscopy. Fibrinoid necrosis and disruption of major arteries as well as veins were observed immediately after impact, antedating the evolution of parenchymal necrosis. A fusiform zone of spinal cord necrosis, involving the complete cross-sectional area beneath the site of impact, evolved over a period of 8 to 24 hours, being initially complete in the gray matter by 4 hours and thereafter in the white matter. Ultrastructural observations revealed that the evolution of necrotic cellular constituents was piecemeal. Except for the occurrence of intracellular calcification and heterophagocytosis in the traumatized tissue, the electron microscopic features of cellular necrosis were comparable to those of postmortem spinal cord autolysis, studied in parallel. The observations are consistent with trauma producing ischemic necrosis, resulting from major blood vessel disruption occurring at the moment of impact.