Etiopathology and eary diagnosis of Bell's palsy

贝尔麻痹的病因病理学和早期诊断

基本信息

批准号：
09671748
负责人：
MURAKAMI Shingo
金额：
$ 1.98万
依托单位：
Ehime University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1997
资助国家：
日本
起止时间：
1997 至 1998
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09671748/
关键词：
Bell's palsy Herpes simplex virus Animal model PCR Blood nerve barrier Zostes sine herpete eary diagnosis Ramsay Hunt症候群 HSV-1 顔面神経麻痺 PCR法 Zoster sine herpete 脱髄

项目摘要

The immunological aspects to facial nerve paralysis due to herpes simplex virus type I (HSV-1) infection were investigated in a mouse model system. Passive transfer of either anti-HSV- I antibody or HSV- 1 immunized splenic T cells into 4-week-old mice 3 hr after HSV- 1 inoculation prevented development of facial nerve paralysis and death, whereas such transfers 48 hr or 96 hr after HSV- I inoculation did not prevent or exacerbate facial nerve paralysis. These results demonstrated that the immunological potency of mice are closely related to the pathogenesis of facial nerve paralysis. Facial nerve paralysis developed even in 6-week-old mice whose T-cell function was suppressed with anti-CD3 antibody, suggesting virus induced cellular demyelination is unlikely as a cause of facial nerve paralysis in this animal model.Ramsay Hunt syndrome is usually diagnosed by facial palsy, auricular vesicles and/or vestibulocochlear dysfunction. However, patients with zoster sine herpete and Ramsay Hunt syndrome without pathognomonic vesicles at the initial visit are misdiagnosed with Bell's palsy. By use of polymerase chain reaction, we found that VZV genomes were frequently detectable in auricular skin exudate from patients with zoster sine herpete or those with Ramsay Hunt syndrome before the appearance of vesicles. VZV genomes were also detected not only in the vesicles on the auricles or oral cavity but also in the facial nerve sheath, middle ear mucosa and cerebrospinal fluid (CSF) from patients with Ramsay Hunt syndrome. The results indicated that VZV spreads widely in the neural components, mucocutaneous tissue and CSF.

在小鼠模型系统中研究了 I 型单纯疱疹病毒 (HSV-1) 感染引起的面神经麻痹的免疫学方面。在HSV-1接种后3小时将抗HSV-1抗体或HSV-1免疫的脾T细胞被动转移至4周龄小鼠体内可防止面神经麻痹和死亡的发展，而这种转移在接种HSV-1后48小时或96小时后进行HSV-I 接种不能预防或加剧面神经麻痹。这些结果表明，小鼠的免疫能力与面神经麻痹的发病机制密切相关。即使在用抗 CD3 抗体抑制 T 细胞功能的 6 周大小鼠中，也会出现面神经麻痹，这表明病毒诱导的细胞脱髓鞘不太可能是该动物模型中面神经麻痹的原因。拉姆齐亨特综合征通常被诊断为拉姆齐亨特综合征由面瘫、耳囊和/或前庭蜗功能障碍引起。然而，初次就诊时没有特征性水泡的带状疱疹和拉姆齐亨特综合征患者会被误诊为贝尔麻痹。通过使用聚合酶链反应，我们发现在水泡出现之前，在带状疱疹或拉姆齐亨特综合征患者的耳廓皮肤渗出液中经常可以检测到VZV基因组。不仅在耳廓或口腔的囊泡中检测到了 VZV 基因组，而且在拉姆齐亨特综合征患者的面神经鞘、中耳粘膜和脑脊液 (CSF) 中也检测到了 VZV 基因组。结果表明，VZV在神经成分、皮肤粘膜组织和脑脊液中广泛传播。