Ying-Chih Lu1, Yi-Ho Young. 1. Department of Otolaryngology, National Taiwan University Hospital, Taipei, Taiwan.
Abstract
OBJECTIVE/HYPOTHESIS: This study aims to analyze which division of vestibular nerve in the internal auditory canal is responsible for inducing vertigo in patients with herpes zoster oticus (HZO). METHODS: Eight patients (three men and five women) suffered from auricular vesicles, otalgia, and facial palsy, and five of them also had vertigo. Each patient received a battery of tests, including neurological examination, blood examination, audiometry, caloric test, electronystagmography, and vestibular evoked myogenic potential (VEMP) test. RESULTS: All five HZO patients with vertigo had facial palsy on the lesioned side and spontaneous nystagmus beating toward the healthy side. Absent VEMPs were noted in five patients, absent caloric response was noted in four, and sensorineural HL was noted in three. Compared to another three HZO patients without vertigo, all revealed normal responses in both the caloric test and the VEMP test. On MRI scan, two out of four had abnormal gadolinium enhancement along the nerve segments within the internal auditory canal. Six months after treatment, a follow-up caloric test and VEMP test in these eight patients did not alter the results compared with before treatment. CONCLUSION: The nerve trunks within the internal auditory canal are widely affected in HZO patients with vertigo. Both superior division and inferior division of the vestibular nerve attribute to the vertiginous attack. Further, large numbers of HZO patients undergoing caloric testing and VEMP testing are required to support this tentative conclusion.
OBJECTIVE/HYPOTHESIS: This study aims to analyze which division of vestibular nerve in the internal auditory canal is responsible for inducing vertigo in patients with herpes zoster oticus (HZO). METHODS: Eight patients (three men and five women) suffered from auricular vesicles, otalgia, and facial palsy, and five of them also had vertigo. Each patient received a battery of tests, including neurological examination, blood examination, audiometry, caloric test, electronystagmography, and vestibular evoked myogenic potential (VEMP) test. RESULTS: All five HZO patients with vertigo had facial palsy on the lesioned side and spontaneous nystagmus beating toward the healthy side. Absent VEMPs were noted in five patients, absent caloric response was noted in four, and sensorineural HL was noted in three. Compared to another three HZO patients without vertigo, all revealed normal responses in both the caloric test and the VEMP test. On MRI scan, two out of four had abnormal gadolinium enhancement along the nerve segments within the internal auditory canal. Six months after treatment, a follow-up caloric test and VEMP test in these eight patients did not alter the results compared with before treatment. CONCLUSION: The nerve trunks within the internal auditory canal are widely affected in HZO patients with vertigo. Both superior division and inferior division of the vestibular nerve attribute to the vertiginous attack. Further, large numbers of HZO patients undergoing caloric testing and VEMP testing are required to support this tentative conclusion.