An Experimental Study In Rabbits: The Pathogenesis Of Syringomyelia

Objective: 1 To establish two different model of syringomyelia in rabbits: Non-communicating canalicular syringomyelia was induced by Kaolin and non-communicating intramedullary syringomyelia produced by quisqualic acid (QA). 2 To investigate the MRI and ECT changes of two types in different time after injections with Kaolin and QA, and. compare the changes of pathology and ultrastructure caused by two methods in spinal cord tissues. 3 To discuss the pathogenesis of these two kinds of experimental syringomyelia and the role of subarachnoid block in the genesis of syringomyeliaMaterials and methods: 1 Kaolin solution was percutaneously injected into the cisterna magna of animals. A laminectomy of C7-T1 was performed and then the spinal cord was exposed. To establish syringomyelia models, Kaolin was injected into subarachnoid and QA into unilateral intramedullary under direct vision. The rabbits in control group were received a injection of normal saline at the same place. 2 To observe the MRI and ECT performances animals were observed in different time of postoperation. All animals were sacrificed at the 8 week after the operation, and the spinal cord were collected for analysis of pathology and ultrastructure.Results: 1 MRI: In the animals which received a Kaolin injection in cisterna magna, obvious cavitation was not found at 2 weeks after injection and 3 of them were found with hyperintensity in upper cervical cord at the 4^th week, and at 6⁸ weeks, except 1, all animals developed syringomyelia In the animals which received an injection of kaolin into the spinal subarachnoid space, no cysts were seen in all animals. Only 2 rabbits had secund spinal cords. A short thread-like hyperintensity was observed at C7-T1 level of 6 animals inthe quisqualic acid group. The same performance appeared in 7 of 8 animals in the group with quisqualic acid and kaolin, and 2 of these had secund and broaden spinal cords. In control group, no significant changes were seen in 2-8 weeks after the operation. 2 ECD In control group and quisqualic acid group, the subarachnoid below upper cervix was outlined 30 minutes after technetium injection, and the total cerebrospinal fluid circulatory system was seen after 1 hour. In the animals which received cisterna magna kaolin injection, the subarachnoid below cervicothorax was outlined 30 minutes after developer injectioa After another 30 minutes, the developer went rostral to the middle and upper cervical subarachnoid, and this level did not change at 15 hour. In animals injected quisqualic acid with kaolin in spinal cord and animals injected kaolin in subarachnoid, the subarachnoid caudal to the middle thorax was seen, and in 3 of these animals, the developer went rostral to the upper thorax in another 30 minutes. No changes were found in other animals. 3 Microscopec findings: In the animals of control group and those with Kaolin in subarachnoid, there is no intramedullary syrinxe. And the size of central canal is normal. In the animals with QA alone, A small well-defined cyst could be found. The nervous tissues in spinal cord edema, and the perivascular space became larger than normal. In animals with QA and Kaolin, a larger well-defined cyst could be seen in dorsal part of spinal cord. Neurons and gliocytes degenerated, but the endyma is intact In cisterna magna kaolin injection group, the central canal enlarge, and some fissure stretch toward the essence of spinal cord. The endyma became flat and broken. 4 Changes of ultrastructure: In control group and kaolin subarachnoid injection group, electron microscopy revealed that neurons and gliocytes had normal membrane structures, organoids and plentiful Nissl bodies. While, in animals with QA, neurons and gliocytes degenerated, necrosis. Most Nissl bodies disappeared. The markedly enlarged perivascular space could be seen. Myelin sheathbecame edema, and degeneration. In cistema magna kaolin injection group, neurons and gliocytes also necrosis, and Nissl bodies vanished The axonal degeneration and demyelination could be found. The perivascular space became larger than normal.Conclusions: 1 Cistema magna kaolin injection and intramedullary quisqualic acid injection in rabbits may establish two different experimental syringomyelia model. Percutaneously subarachnoid kaolin injection induces the dilation of the central canal ( hydromyelia). There are central canal dilation with intramedullary cavitation in part of these models. These can be used to simulate non-communicating canalicular syringomyelia caused by Chiari I malformation in human. Nevertheless, the syrinx induced by intramedullary quisqualic acid injection under direct vision usually is located in the gray matter of the spinal cord, which is accord with the pathology of post-traumatic syringomyelia in human being. 2 The mechanism of cavitation in cistema magna kaolin injection and that of intramedullary quisqualic acid injection. In the former model, the granuloma is formed and then obstructs the median aparture which increases the CSF pressure. In turn, the pressure in central canal raises, and the central canal from cervix to thorax dilates. Under some circumstances, the rostral CSF flow is blocked, and CSF is forced to enter the peranchymal part of spinal cord through perivascular spaces, leading eventually to intramedullary cavitatioa In the latter model, the excitotoxic effect of quisqualic acid may damage the neuron of spinal cord, and simulate the cavitation caused by secondarily elevated levels of excitatory amino acids after the spinal cord injury. 3 Compare the group with only intramedullary quisqualic acid injection and the group with quisqualic acid and kaolin, excitotoxic cell death induced by quisqualic acid may contribute to the pathologic process leading to the formation of initial cyst Subarachnoid block by arachnoiditis may give rise to abnormal CSF flow, which is likely to be an important factor...