马尾神经综合征实验模型的建立及其形成机制(英文)

Establishment of an animal model of cauda equina syndrome and its formative mechanism

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:将纯种健康雄性封闭群清洁级新西兰兔80只随机分为3组:对照组、模型1加压组、模型2加压组,应用改良的EirenToh马尾神经实验压迫模型,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、骶髓做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;骶神经功能综合测定,A1,A2,A3(1.8±0.9,2.0±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,差异有显著性差异意义(P<0.05)。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,且骶神经损伤症状出现1/2d时达到高峰。

AIM:To establish an animal model of cauda equina syndrome simulate the actual clinical condition to study pathology of cauda equina syndrome. METHODS:Eighty normal adult male New Zealand rabbits were divided into control group, model 1 and 2 groups with compression injury in the cauda equina and spinal nerve root (groups A and B). Nerve compression was applied to the dural matter and the nerve roots after partial laminectomy in the vertebral canal (1/9, 2/9, 1/2). The specimens were sampled at different time points after the compression for pathological and immunohistochemical study with the nerve functions assessed. RESULTS:Significant neurological changes were observed with 75% restriction of the cauda equina, sacral nerve function grade 1/2 d after the compression in comparison with other time points (P< 0. 05).Neural tissue damage included inflammatory response in the cauda equina, and axonal and wallerian degeneration followed by Schwann cell proliferation,axonal bud regeneration and necrosis of the pseudounipolar neurons in the nerve root ganglion.Apoptosis of the anterior horn cells occurred in the conus medullaris.