Sugita T, Murakami S, Yanagihara N, Fujiwara Y, Hirata Y, Kurata T
Department of Otolaryngology, Ehime University School of Medicine, Japan.
Ann Otol Rhinol Laryngol. 1995 Jul;104(7):574-81. doi: 10.1177/000348949510400713.
We have been the first to succeed in producing an acute and transient facial paralysis simulating Bell's palsy, by inoculating herpes simplex virus into the auricles or tongues of mice. The KOS strain of the virus was injected into the auricle of 104 mice and the anterior two thirds of the tongue in 30 mice. Facial paralysis developed between 6 and 9 days after virus inoculation, continued for 3 to 7 days, and then recovered spontaneously. The animals were painlessly sacrificed between 6 and 20 days after inoculation for histopathologic and immunocytochemical study. Histopathologically, severe nerve swelling, inflammatory cell infiltration, and vacuolar degeneration were manifested in the affected facial nerve and nuclei. Herpes simplex virus antigens were also detected in the facial nerve, geniculate ganglion, and facial nerve nucleus. The pathophysiologic mechanisms of the facial paralysis are discussed in light of the histopathologic findings, in association with the causation of Bell's palsy.
我们首次成功地通过将单纯疱疹病毒接种到小鼠的耳廓或舌头，制造出一种模拟贝尔氏面瘫的急性短暂性面瘫。将该病毒的KOS株注入104只小鼠的耳廓以及30只小鼠舌头的前三分之二部位。面瘫在病毒接种后6至9天出现，持续3至7天，然后自行恢复。在接种后6至20天对动物实施无痛处死，以进行组织病理学和免疫细胞化学研究。组织病理学上，受影响的面神经和神经核表现出严重的神经肿胀、炎性细胞浸润和空泡变性。在面神经、膝状神经节和面神经核中也检测到单纯疱疹病毒抗原。结合贝尔氏面瘫的病因，根据组织病理学发现对面瘫的病理生理机制进行了讨论。
