Ultrastructural pathology of nerve fibers in calcium-induced myelopathy.
Calcium has been proposed as a mediator of nerve fiber degeneration following traumatic injury of the spinal cord. It induces a spongy, necrotizing myelopathy similar in its evolution to that observed in experimental spinal cord trauma. The current study was undertaken to determine the ultrastructural changes in the central nervous system (CNS) nerve fibers associated with calcium-induced myelopathy. A 10% calcium chloride (CaCl2) solution (pH 7.4) was slowly dripped on the dorsal surface of the surgically exposed lower thoracolumbar spinal cord of adult male Sprague-Dawley rats. The posterior and lateral columns of the spinal cords were fixed and processed for electron microscopy. Controls consisted of tissue from normal and sham-operated animals, as well as those receiving equal volumes and osmolarities of sodium chloride (NaCl), magnesium chloride (MgCl2), and potassium chloride (KCl) at the same pH. In the CaCl2 treated animals, spongiosis of increasing severity developed in white matter, as the result of periaxonal, adaxonal and intramyelinic swelling. Vesicular demyelination was consistently observed, beginning within one hour (h) and progressing with increasing severity up to 24-72 h. Axonal changes included pleomorphic spheroids, granular degeneration and intra-axonal calcification. The ultrastructural changes in the nerve fibers provoked by calcium were indistinguishable from those previously reported in experimental spinal cord trauma. These observations strengthen the hypothesis that calcium initiates the nerve fiber degeneration following spinal cord injury.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D008297:Male; D009412:Nerve Fibers / Q000032:analysis / Q000648:ultrastructure*; D051381:Rats; D011919:Rats, Inbred Strains; D013116:Spinal Cord / Q000378:metabolism / Q000648:ultrastructure*; D013118:Spinal Cord Diseases / Q000378:metabolism / Q000473:pathology
D002118:Calcium