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An experimental study on the perineurial window

神经周围窗的实验研究

基本信息

批准号：
10671383
负责人：
TAKAYAMA Shinichiro
金额：
$ 1.66万
依托单位：
Keio University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 1999
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10671383/
关键词：
perineurial window perineurium peripheral nerve needle entrapment neuropathy blood nerve barrier

项目摘要

To investigate the pathomechanism of perineurial development and nerve damage in the perineurial window, we designed the following two different sized models of perincurial windows using tibial nerves of Wistar rats : a 1 mm length window as a small perincurial window model and a 5 mm length window as a large window model. In the 1 mm model window group, marked herniation of the endoncurial contents was observed by 12 weeks, and the initial histological change was slight but it was sustained for a long time. In contrast, such herniation was not so prominent in the 5 mm model window group and although the initial nerve damage was severe, it recovered within 12 weeks. The regeneration of the perincurium and nerve fibers in the 1 mm model was slow compared with the 5 mm model. These results suggest that the main pathomechanism of nerve damage in the perineurial window is entrapment of nerve fibers at the window rather than disruption of endoneurial homeostasis. Herniation of endoneurial contents was observed and histological change was sustained by 24 weeks. This result suggests that the perineurial window might not heal naturally.To investigate the treatment of the perineurial window, we designed two different procedures, (1) sutured group : closing the window by suturing the perincurium, (2) releasied group : releasing the entrapment by clongating the window. The treatment of the perineurial window obtained a good result both in sutured group and released group. In clinical cases, which are usually chronic injuries, releasing the entrapment might be more useful.

为探讨神经束膜发育的病理机制及神经束膜窗内神经损伤的情况，本实验以Wistar大鼠胫神经为材料，设计了两种不同大小的神经束膜窗模型：1 mm长的神经束膜窗为小神经束膜窗模型，5 mm长的神经束膜窗为大神经束膜窗模型。在1 mm模型窗组中，12周时观察到明显的内膜内容物疝出，最初的组织学变化轻微，但持续时间较长。相比之下，在5 mm模型窗组中，这种疝并不那么突出，尽管最初的神经损伤很严重，但在12周内恢复。与5 mm模型相比，1 mm模型中的束膜和神经纤维的再生缓慢。这些结果表明，在神经束膜窗口的神经损伤的主要病理机制是在窗口的神经纤维卡压，而不是破坏神经内稳态。观察到神经内膜内容物疝出，组织学改变持续24周。为探讨神经束膜窗的治疗方法，我们设计了两种不同的手术方法：（1）缝合组：将神经束膜缝合关闭神经束膜窗;（2）松解组：将神经束膜松解。神经束膜窗的处理在缝合组和松解组均取得了良好的效果。在临床病例中，通常是慢性损伤，释放卡压可能更有用。