Selective axonal calcification has been consistently observed in experimental spinal cord trauma in laboratory animals as well as in human spinal cord injury. A hypothesis of calcium influx resulting in activation of proteolytic and/or lipolytic enzymes has been proposed as a major mechanism of nerve fiber degeneration. The current study was undertaken to determine the effects of calcium influx into nontraumatized spinal cord tissue, utilizing 10 per cent calcium chloride at a pH of 7.4 slowly dripped onto the dorsal surface of the surgically exposed spinal cord of adult male Sprague-Dawley rats. Controls consisted of animals similarly treated with solutions of sodium chloride, magnesium chloride, and potassium chloride at the same pH and osmolarity. Sham-operated and normal animals were also observed. The experimental animals that received calcium chloride consistently developed paraplegia that was evident within 24 hours after treatment. The initial spinal cord lesion consisted of discrete areas of spongiosis in posterior and lateral columns in the segment beneath the application of calcium. The spongiosis progressed in severity and was accompanied or followed by necrosis. The gray matter was relatively spared; however, the posterior horns became consistently necrotic. Calcium was observed histochemically in the areas of spongiosis/necrosis but not in spared areas. Although the topography of the calcium-induced myelopathy differs from that of spinal cord injury, the progression of the clinical and pathologic changes is consistent with the calcium-mediated hypothesis of necrosis in the latter.