Excitotoxic model of post-traumatic syringomyelia in the rat

Study Design. A rat model was developed to elucidate the role of excitatory amino acids and spinal subarach-noid block in the genesis of post-traumati c syringomyelia This excitotoxic model produces intramedullary. cavities ra ther than the dilation of the central canal (canalicular syringomyelia) cre ated by previous animal models. Objectives. To produce extracanalicular cysts in the rat spinal cord with q uisqualic acid, a potent agonist of multiple excitatory amino acid receptor s, and to compare the effects of excitotoxic injury only with that of excit otoxic injury and subarachnoid block with kaolin. Summary of Background Data. In post-traumatic syringomyelia, primary injury and excitotoxic cell death secondary to elevated levels of excitatory amin o acids may initiate a pathologic process leading to the formation of spina l cavities. Subarachnoid block by arachnoiditis may promote enlargement of the cavities. Methods. Three control rats received a unilateral injection of normal salin e into the spinal cord, and another five rats received an injection of kaol in into the spinal subarachnoid space. Quisqualic acid was injected unilate rally into the spinal cord of 20 rats, and 13 additional rats received a un ilateral injection of quisqualic acid into the, spinal cord after injection of kaolin into the subarachnoid space. Histologic and immunocytochemical a ssessments were undertaken. Results. in the control groups, no, parenchymal cyst developed in any of th e animals. Spinal cord cyst formation was observed in 16 of 19 animals in t he quisqualic acid groups, but no cysts exceeding two segments in the lengt h of the spinal cord developed in any of the, rats. Much larger cavities we re seen in 9 of 11 animals in the group with quisqualic acid and kaolin, an d cysts exceeding two segments developed in all 9 of these (9/11; 82%). Conclusions. In post-traumatic syringomyelia, excitotoxic cell death occurr ing secondarily to elevated levels of excitatory amino acids may contribute to the pathologic process leading to the formation of spinal cord cysts. S ubarachnoid block by arachnoiditis is likely to cause enlargement of the ca vity.