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目的 建立马尾神经综合征的实验模型 ,进一步探讨马尾神经综合征形成的机制。方法 纯种健康雄性封闭群清洁级新西兰兔 80只 ,应用改良的EirenToh的马尾神经的实验压迫模型 ,进入椎管矢状径的 1 9、2 9、1 2 ,造成马尾神经压迫产生神经症状 ,对症状、骶神经功能检测 ,并进行定量分析 ,马尾神经、神经根、骶髓作组织病理学和免疫组织化学的研究 ,并进行定性分析。结果 模型 2较模型 1同等条件下 ,易导致马尾神经损害 ;各实验组马尾神经综合征发病 1 2d ,其马尾神经组织均出现广泛的炎性反应 ,骶髓前角细胞出现凋亡 ;骶神经功能评分模型A各组 ,A1 、A2 、A3( 1.7± 0 .5、2 .0± 1.6、6 .3± 2 .1)B1 、B2 、B3( 4 .3± 1.9、6 .4± 3 .0、9.6± 2 .7)同对照组和其他时间段比较 ,差异有显著性 ( P <0 .0 5 )。结论 压迫马尾神经导致马尾神经损害 ,双节段压迫比单节段压迫更易出现广泛马尾神经损害 ;马尾神经压迫点的病理改变向头、尾两端扩散 ,形成广泛病理损害。骶髓前角细胞出现凋亡。
Objective To establish an experimental model of cauda equina syndrome and to further explore the mechanism of the formation of cauda equina syndrome. Methods Totally 80 male New Zealand white rabbits were enrolled in this study. The experimental model of EirenToh’s cauda equina was used to compress the model into the sagittal diameter of vertebral canal at 19, 29, and 12, resulting in neurological symptoms caused by compression of cauda equina. Symptoms, sacral nerve function tests, and quantitative analysis, cauda equina, nerve root, sacral bone for histopathology and immunohistochemistry, and qualitative analysis. Results Compared with model 1, model 2 could easily lead to cauda equina injury. In each experimental group, cauda equina syndrome developed extensive inflammatory reaction and apoptotic sacral anterior horn cells in cauda equina neurons at 12 days after onset. Function score model A, B1, B2, B3 (4.3 ± 1.9, 6.4 ± 3, 1.7 ± 0.5, 2.0 ± 1.6, 6.3 ± 2. .0,9.6 ± 2 .7) compared with the control group and other time periods, the difference was significant (P <0. 05). Conclusions The cauda equina nerve resulted in cauda equina nerve injury. Compared with the single segment compression, the cauda equina nerve injury was more likely to occur in the cauda equina. The pathological changes of the cauda equina compression point diffused to the head and tail to form extensive pathological lesions. Sacral anterior horn cells appear apoptosis.