Etiopathology and eary diagnosis of Bell's palsy

在小鼠模型系统中研究了单纯疱疹病毒1型（HSV-1）感染引起面神经麻痹的免疫学方面。在接种HSV- 1后3小时，将抗HSV- 1抗体或HSV- 1免疫的脾T细胞被动转移到4周龄小鼠体内，可防止面神经麻痹的发生和死亡，而在接种HSV- 1后48小时或96小时，这种转移不能预防或加重面神经麻痹。这些结果表明，小鼠的免疫效力与面神经麻痹的发病机制密切相关。即使在6周大的t细胞功能被抗cd3抗体抑制的小鼠中也发生了面神经麻痹，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·亨特综合征通常通过面瘫、耳泡和/或前庭耳蜗功能障碍来诊断。然而，患有带状疱疹和拉姆齐亨特综合征的患者在初次就诊时没有病状囊泡，被误诊为贝尔麻痹。通过聚合酶链反应，我们发现在带状疱疹或拉姆齐亨特综合征患者的耳部皮肤分泌物中经常检测到VZV基因组，然后出现囊泡。在拉姆齐·亨特综合征患者耳廓、口腔囊泡、面神经鞘、中耳黏膜和脑脊液中均检测到VZV基因组。结果表明，VZV广泛分布于神经成分、皮肤粘膜组织和脑脊液。

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.