Experimental Monkey Model of Hemifacial Spasm and Electrophysiological Study of Mechanism Participating with Hemifaical Spasm

实验猴面肌痉挛模型及面肌痉挛参与机制的电生理研究

基本信息

批准号：
63570676
负责人：
NAGASEKI Yoshishige
金额：
$ 1.22万
依托单位：
Yamanashi Medical College
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1988
资助国家：
日本
起止时间：
1988 至 1989
项目状态：
已结题

项目摘要

As the management for essential trigeninal neuralgia (TN) and Hemifacial spasm (HFS), microvascular decompression (MVD) of the trigenianl nerve or facial nerve at their root entry zones was established by P. Jannetta since 1966. But the etiological mechanisms are controversial, because where the origin of the abnormal electrical activities are, is unclear. For example, it is speculated that the origins are in the cross-compressed lesion (the peripheral theory) or in the facial motonucleus (central theory). Therefore, we have been tried making experimental model of HFS in monkey two years ago for clarifying the mechanism. We thought that HFS appeared by making the nerve compression induced by silicon tube between the facial nerve and the skull base in the pathophysiologic status like HFS in human. We utilized 3 monkeys (weight of 3-4 Kg). Each monkey was seated in the monkey chair and microscopically operated by suboccipital craniectomy with Ketaral anesthesia (i.m) and 0.5% Xylocaine l … More ocal anesthesia. During the operation, the cerebellum was retracted by brain retractor and the facial nerve was exposed. Then we inserted a silicon tube (1mm diameter and 1cm length) in one monkey , rubber in the same size like the former in one monkey and a tube in the same size making of Gore-Tex surgical membrane in the residual monkey respectively, between the facial nerve and the skull base. After these manipulation we could recognized the fluctuation of the nerve with the brain stem. Furthermore, intraoperative face EMGs were monitored and face VTRs were recorded. We carefully observed the changes of facial status for seven months in one monkey, six months in one monkey and four months in the residual monkey. However, HFS have never been recognized in each monkey. The former two monkeys were died caused by other general diseases. Though we examined two brains and facial nerves stained for Nissl substance using cresyl violet, the degeneration and/or anatomical changes were riot confirmed. From now on, we will continue these trials developing the experimental methodology. Less

作为基本三子神经痛（TN）和下半径痉挛（HFS）的治疗，在其根部进入区域的三角形神经或面神经的微血管减压（MVD）是由P. Jannetta建立的，自1966年以来就建立了。例如，据推测起源在交叉压缩病变（外围理论）或面部摩托车（中心理论）中。因此，两年前，我们已尝试在猴子中制作HFS的实验模型，以阐明该机制。我们认为，HF通过使神经管与人类的HFS（如HFS）中的硅神经和颅底之间的硅管诱导的神经压缩而出现。我们利用了3只猴子（重量为3-4千克）。每只猴子都坐在猴子椅上，并通过枕下颅骨切除术和酮麻醉（I.M）和0.5％的Xylocaine l…进行显微镜操作。在手术过程中，小脑通过脑牵开器缩回，并暴露了面神经。然后，我们在一只猴子中插入了一只猴子中的硅管（直径为1mm和1厘米长），橡胶的大小相同，在一只猴子中分别插入了一个猴子的橡胶，并在残留的猴子中分别在面部神经和颅底之间以相同尺寸的戈尔 - Tex手术膜形成。经过这些操作后，我们可以识别出脑干的神经波动。此外，监测术中的面部EMG并记录脸部VTR。我们仔细地观察到一只猴子七个月的面部状况的变化，一只猴子六个月，在残留的猴子中四个月。但是，每只猴子从未得到过HFS的认可。前两只猴子死于其他普通疾病。尽管我们检查了使用甲三叶紫鼠对Nissl物质染色的两个大脑和面部神经，但证实了变性和/或解剖学变化。从现在开始，我们将继续这些试验开发实验方法。较少的