Yang L, Jones N R, Stoodley M A, Blumbergs P C, Brown C J
Department of Surgery (Neurosurgery), University of Adelaide, Australia.
Spine (Phila Pa 1976). 2001 Sep 1;26(17):1842-9. doi: 10.1097/00007632-200109010-00004.
A rat model was developed to elucidate the role of excitatory amino acids and spinal subarachnoid block in the genesis of post-traumatic syringomyelia. This excitotoxic model produces intramedullary cavities rather than the dilation of the central canal (canalicular syringomyelia) created by previous animal models.
To produce extracanalicular cysts in the rat spinal cord with quisqualic acid, a potent agonist of multiple excitatory amino acid receptors, and to compare the effects of excitotoxic injury only with that of excitotoxic injury and subarachnoid block with kaolin.
In post-traumatic syringomyelia, primary injury and excitotoxic cell death secondary to elevated levels of excitatory amino acids may initiate a pathologic process leading to the formation of spinal cavities. Subarachnoid block by arachnoiditis may promote enlargement of the cavities.
Three control rats received a unilateral injection of normal saline into the spinal cord, and another five rats received an injection of kaolin into the spinal subarachnoid space. Quisqualic acid was injected unilaterally into the spinal cord of 20 rats, and 13 additional rats received a unilateral injection of quisqualic acid into the spinal cord after injection of kaolin into the subarachnoid space. Histologic and immunocytochemical assessments were undertaken.
In the control groups, no parenchymal cyst developed in any of the animals. Spinal cord cyst formation was observed in 16 of 19 animals in the quisqualic acid groups, but no cysts exceeding two segments in the length of the spinal cord developed in any of the rats. Much larger cavities were seen in 9 of 11 animals in the group with quisqualic acid and kaolin, and cysts exceeding two segments developed in all 9 of these (9/11; 82%).
In post-traumatic syringomyelia, excitotoxic cell death occurring secondarily to elevated levels of excitatory amino acids may contribute to the pathologic process leading to the formation of spinal cord cysts. Subarachnoid block by arachnoiditis is likely to cause enlargement of the cavity.
建立大鼠模型以阐明兴奋性氨基酸和脊髓蛛网膜下腔阻滞在创伤后脊髓空洞症发生过程中的作用。这种兴奋性毒性模型产生的是髓内空洞,而非先前动物模型所造成的中央管扩张(管型脊髓空洞症)。
用多种兴奋性氨基酸受体的强效激动剂喹啉酸在大鼠脊髓中产生管外囊肿,并仅比较兴奋性毒性损伤与兴奋性毒性损伤加高岭土蛛网膜下腔阻滞的效果。
在创伤后脊髓空洞症中,原发性损伤以及兴奋性氨基酸水平升高继发的兴奋性毒性细胞死亡可能引发导致脊髓空洞形成的病理过程。蛛网膜炎引起的蛛网膜下腔阻滞可能促使空洞扩大。
3只对照大鼠单侧脊髓注射生理盐水,另外5只大鼠蛛网膜下腔注射高岭土。20只大鼠单侧脊髓注射喹啉酸,另有13只大鼠在蛛网膜下腔注射高岭土后单侧脊髓注射喹啉酸。进行组织学和免疫细胞化学评估。
对照组动物均未形成实质囊肿。喹啉酸组19只动物中有16只观察到脊髓囊肿形成,但所有大鼠均未出现长度超过两个节段的囊肿。喹啉酸加高岭土组11只动物中有9只出现大得多的空洞,其中所有9只(9/11;82%)出现了长度超过两个节段的囊肿。
在创伤后脊髓空洞症中,兴奋性氨基酸水平升高继发的兴奋性毒性细胞死亡可能促成导致脊髓囊肿形成的病理过程。蛛网膜炎引起的蛛网膜下腔阻滞很可能导致空洞扩大。