中国临床康复
中國臨床康複
중국림상강복
CHINESE JOURNAL OF CLINICAL REHABILITATION
2003年
29期
3954-3955
,共2页
史建刚%贾连顺%李家顺%蔡凯华%刘颜玲%贾宁阳
史建剛%賈連順%李傢順%蔡凱華%劉顏玲%賈寧暘
사건강%가련순%리가순%채개화%류안령%가저양
模型,动物%解剖%马尾%前角细胞
模型,動物%解剖%馬尾%前角細胞
모형,동물%해부%마미%전각세포
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Eiren Toh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1/2 d时达到高峰.
目的:建立馬尾神經綜閤徵的實驗模型,進一步探討馬尾神經綜閤徵形成的機製.方法:將純種健康雄性封閉群清潔級新西蘭兔80隻隨機分為3組:對照組、模型1加壓組、模型2加壓組,應用改良的Eiren Toh馬尾神經實驗壓迫模型,進入椎管矢狀徑的1/9,2/9,1/2,造成馬尾神經壓迫產生神經癥狀,對癥狀、骶神經功能檢測,併進行定量分析、馬尾神經、神經根、骶髓做組織病理學和免疫組織化學的研究,併進行定性分析.結果:模型2較模型1同等條件下,易導緻馬尾神經損害;各實驗組馬尾神經綜閤徵髮病1/2d,其馬尾神經組織均齣現廣汎的炎性反應,骶髓前角細胞齣現凋亡;骶神經功能綜閤測定,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)同對照組和其他時間段比較,差異有顯著性差異意義(P<0.05).結論:壓迫馬尾神經導緻馬尾神經損害,雙節段壓迫比單節段壓迫更易齣現廣汎馬尾神經損害;馬尾神經壓迫點的病理改變嚮頭、尾兩耑擴散,形成廣汎病理損害;骶髓前角細胞齣現凋亡,且骶神經損傷癥狀齣現1/2 d時達到高峰.
목적:건립마미신경종합정적실험모형,진일보탐토마미신경종합정형성적궤제.방법:장순충건강웅성봉폐군청길급신서란토80지수궤분위3조:대조조、모형1가압조、모형2가압조,응용개량적Eiren Toh마미신경실험압박모형,진입추관시상경적1/9,2/9,1/2,조성마미신경압박산생신경증상,대증상、저신경공능검측,병진행정량분석、마미신경、신경근、저수주조직병이학화면역조직화학적연구,병진행정성분석.결과:모형2교모형1동등조건하,역도치마미신경손해;각실험조마미신경종합정발병1/2d,기마미신경조직균출현엄범적염성반응,저수전각세포출현조망;저신경공능종합측정,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)동대조조화기타시간단비교,차이유현저성차이의의(P<0.05).결론:압박마미신경도치마미신경손해,쌍절단압박비단절단압박경역출현엄범마미신경손해;마미신경압박점적병리개변향두、미량단확산,형성엄범병리손해;저수전각세포출현조망,차저신경손상증상출현1/2 d시체도고봉.
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 immunohis-tochemical 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 Schwarn 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.Acute nerve compression can lead to cauda equina syndrome due to canda equina neural tissue damage, whichis most severe 1/2 day after the compression injury.