Etiopathology and eary diagnosis of Bell's palsy

在小鼠模型系统中对单纯疱疹病毒I型(HSV-1)感染所致面神经麻痹的免疫学方面进行了研究。抗HSV-I抗体或HSV-1免疫的脾T细胞在HSV-1接种后3小时被动转移到4周龄小鼠体内可防止面神经麻痹和死亡，而在HSV-I接种48小时或96小时后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T细胞功能被抗CD3抗体抑制的6周龄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这种动物模型中面神经瘫痪的原因。Ramsay Hunt综合征通常被诊断为面瘫、耳廓小泡和/或前庭耳蜗功能障碍。然而，首次就诊时无病因性水泡的带状疱疹和Ramsay Hunt综合征患者被误诊为贝尔麻痹。应用聚合酶链式反应发现，在水泡出现之前，正弦带状带状疱疹或Ramsay Hunt综合征患者的耳廓渗出液中经常可检测到VZV基因组。在Ramsay Hunt综合征患者的面神经鞘、中耳粘膜和脑脊液中也检测到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中。

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.