Clinical analysis of primary facial nerve neuroma / 中华耳鼻咽喉头颈外科杂志

<p><b>OBJECTIVE</b>To analyze the clinical features of facial nerve neuroma about its diagnosis and management.</p><p><b>METHODS</b>Ten patients with facial nerve neuroma were analyzed retrospectively from February 1993 to August 2005. The period of follow-up varied from 1.5 years to 10 years (mean 5 years). Facial nerve function was evaluated with House-Brackmann grading system.</p><p><b>RESULTS</b>The patients complained of facial paralysis in 7 cases, otitis media in 1 case, a mass in parotid gland in 1 case and a mass on the side of the orbital on face in 1 case. Seven patients were undergone either CT scan or MRI or both. Image studies revealed mass located along the facial nerve course from the nerve endings to the intracranial parts. All the patients accepted the surgery. Intraoperative findings showed that the tumor location matched the image findings. Postoperative pathological diagnosis demonstrated 8 Schwannoma, 2 neurofibroma. There was partial tumor resection in 1 patient accepted and his nerve function was unchanged. Four patients were undergone facial nerve graft but 1 case failed while facial nerve function was improved in 3 other patients. Two patients underwent tumor resection while the continuity of facial nerve was preserved as result their facial nerve function improved respectively. No facial nerve reconstruction was done on other 2 patients.</p><p><b>CONCLUSIONS</b>Multiple origins of facial nerve neuroma were noted and the most common system was facial nerve palsy. The decision on how to treat these patients should be individualized and based on initial facial function, growth rate, surgical experience and informed patient consent. The more effective methods need being seeked for the management of facial nerve neuroma.</p>

Effects of CD4+ T cell transplantation on facial motoneuron survival in nude mice model with facial nerve axotomy / 中华耳鼻咽喉头颈外科杂志

<p><b>OBJECTIVE</b>To investigate the specific T cell subpopulation and the relationship with facial motoneuron in immune deficiency mouse model with facial nerve paralysis, so as to find information for new strategy of facial palsy treatment.</p><p><b>METHODS</b>Firstly, purifying the CD4+ T cell from wild type mouse and reestablishing the immune function of nude mouse by infusing the CD4+ T cell through the tail vein a week before the surgery. Then the all nude mouse (BALB/c background) and wild type mouse (BALB/c background) were subjected to a right facial nerve axotomy. Then the mouse was studied by application and assessment with fluorogold retro tracer at specific time. After collecting the slices of brain stem three days post the operation, the facial motoneurons was observed under fluorescence microscope, then analyzed and counted with the software Image Pro Plus5. 1.</p><p><b>RESULTS</b>The number of survival facial motoneuron in the group with CD4+ T cell transplantation and control group was (3444.5 +/- 84.2, x +/- s) and (3013.2 +/- 65.3) respectively. There was significant difference of the number of survival facial motoneurons between nude mouse transplanted with CD4+ T cell and PBS at three days post the operation (t = 5.52, P = 0.0003). But there was no significant difference of survival facial motoneurons between nude mouse transplanted with CD4+ T cell and wild type mouse three days post the operation (t = 0.49, P = 0.6347). It was the transplantation of CD4+ T cell that rescued the survival facial motoneuron to the level of wild type.</p><p><b>CONCLUSIONS</b>CD4+ T cell have the ability to rescue the injuring facial motoneuron from death. It may suggest that there is a critical role of the specific T cell subpopulation in facial nerve repair and regeneration.</p>

Bilateral facial nerve paralysis-diagnosis and treatment / 中华耳鼻咽喉头颈外科杂志

<p><b>OBJECTIVE</b>To observe the ways of diagnosis and treatment of bilateral facial nerve palsy.</p><p><b>METHODS</b>Seven cases of bilateral facial nerve paralysis in 1996 - 2003 were retrospectively reviewed, and then the ways of diagnosis and therapies of these cases were analyzed. There were 6 patients with doubtless diagnosis. They were diagnosed as acute leukaemia, Vogt-Koyanagi-Harada disease (VKH), Machado-Jesoph disease, bilateral mandible fractures, Guillain-Barré syndrome, and Bell's palsy. The last one was diagnosed as Herpes zoster virus infection or Lyme disease. In all these cases, there were 4 of 5 positive cerebrospinal fluids test, 1 of 6 positive lyme antibody test, 2 of 5 positive images test, 7 of 7 EMG and Br test showed that the paralysis was peripheral palsy. All the 7 cases were treated with steroid and vitamin.</p><p><b>RESULTS</b>House-Brackmann I was defined as complete recovery, after up to 2 months follow up, there were four cases got completely recovery while 2 cases incomplete recovery, and 1 case was not reacted to the therapy.</p><p><b>CONCLUSIONS</b>Bilateral facial nerve paralysis was rare, and it was difficult to diagnosis and differentiation, while diagnostic mistakes would be serious. More attention should be paid to it in clinic.</p>

Animal model of facial neuritis induced by herpes simplex virus / 中华耳鼻咽喉头颈外科杂志

<p><b>OBJECTIVE</b>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.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSIONS</b>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.</p>