Liu Wen, Gao Zhi-Qiang, Shen Ping, Ni Dao-Feng, Quan Shi-Ming, Ni An-Ping, Zhang Yun
Department of Otorhinolaryngology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.
Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2006 Jan;41(1):17-21.
To study the role of herpes simplex virus type 1 ( HSV-1 ) in facial paralysis by developing an experimental animal model of viral facial paralysis.
Both sides of posterior auricular branch of facial nerve were anatomies and incised in 66 mice. The HSV-1 was inoculated into right ear branch and fetal bovine serum was inoculated into left ear branch as control. The symmetry of mouse face was observed and scored. The temporal bones were serially sectioned and stained with hematoxylin and eosin. The extratemporal facial nerves were stained with osmium tetroxide. HSV-1 DNA in bilateral facial nerve, brain stem, trigeminal ganglion and spinal cord was detected by the polymerase chain reaction.
Twenty-eight (42. 42%) mice developed right facial paralysis between 2 and 5 days after inoculation. Continuing 3-6 days, the facial paralysis recovered spontaneously. Thirty-eight mice had no signs of facial paralysis. Compared with the left, nerve swelling, inflammatory cell infiltration were manifested in right temporal facial nerve of paralyzed mice. The ratio of the cross-sectional area of the facial nerve to the facial canal ( FN/FC ) was significantly higher than that on the control side (P < 0.01). Demyelinated nerve fibers were seen in the right extratemporal facial nerve. Not only in paralyzed mice, but also in non-paralyzed mice, HSV DNA was detected in some nerve tissues.
Inoculating HSV-1 into posterior auricular branch of facial nerve can produce an acute and transient facial paralysis in mice. The possible pathophysiologic mechanism of the facial paralysis is viral invasion and transportation from distal branch to main trunk. Then the viral facial neuritis causes facial paralysis.
通过建立病毒性面瘫实验动物模型，研究单纯疱疹病毒1型（HSV-1）在面瘫中的作用。
解剖并切开66只小鼠面神经耳后支两侧。将HSV-1接种于右耳支，将胎牛血清接种于左耳支作为对照。观察并记录小鼠面部对称性并评分。对颞骨进行连续切片，苏木精-伊红染色。用四氧化锇对颞外面神经进行染色。采用聚合酶链反应检测双侧面神经、脑干、三叉神经节和脊髓中的HSV-1 DNA。
28只（42.42%）小鼠在接种后2至5天出现右侧面瘫。持续3至6天后，面瘫自发恢复。38只小鼠无面瘫迹象。与左侧相比，面瘫小鼠右侧颞面神经出现神经肿胀、炎性细胞浸润。面神经横截面积与面神经管横截面积之比（FN/FC）显著高于对照侧（P<0.01）。在右侧颞外面神经可见脱髓鞘神经纤维。不仅在面瘫小鼠，而且在未出现面瘫的小鼠的一些神经组织中也检测到HSV DNA。
将HSV-1接种于面神经耳后支可在小鼠中产生急性、短暂性面瘫。面瘫可能的病理生理机制是病毒从远端分支向主干侵袭和转运，进而引起病毒性面神经炎导致面瘫。
