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Objective: To evaluate vestibular restoration and the evolution of the compensatory saccades in acute severe inflammatory vestibular nerve paralysis, including vestibular neuritis and Ramsay Hunt syndrome with vertigo., Study Design: Prospective., Setting: Tertiary referral center., Patients: Vestibular neuritis (n = 18) and Ramsay Hunt syndrome patients with vertigo (n = 13) were enrolled., Intervention: After treatment with oral corticosteroids, patients were followed up for 6 months., Main Outcome Measures: Functional recovery of the facial nerve was scored according to the House-Brackman grading system. Caloric and video head impulse tests were performed in every patient at the time of enrolment. Subsequently, successive video head impulse test (vHIT) exploration was performed at the 1, 3, and 6-month follow-up., Results: Eighteen patients with vestibular neuritis and 13 with Ramsay Hunt syndrome and associated vertigo were included. Vestibular function was significantly worse in patients with Ramsay Hunt syndrome than in those with vestibular neuritis. Similar compensatory saccades velocity and latency values were observed in both groups, in both the caloric and initial vHIT tests. Successive vHIT results showed a significantly higher vestibulo-ocular reflex gain recovery in vestibular neuritis patients than in Ramsay Hunt syndrome patients. A significantly faster reduction in the latency, velocity, and organization of the compensatory saccades was observed in neuritis than in Ramsay Hunt syndrome patients., Conclusions: In addition to the recovery of the vestibulo-ocular reflex, the reduction of latency, velocity and the organization of compensatory saccades play a role in vestibular compensation.

Patients with herpes zoster oticus (HZO) may exhibit diverse symptoms regarding cochleovestibular dysfunction. This study investigated the clinical manifestations of HZO by comparing symptoms associated with dysfunctions of the 7th and 8th cranial nerves (CN VII and VIII, respectively). This study is a retrospective case series. Eighty-one patients with HZO who had dysfunction of CN VII or VIII were included in this study. Electroneuronography (ENoG) values were compared among patient groups with facial weakness. Patients with ipsilateral facial weakness (62 of 81) were more common than those without. Among 81 patients, those with facial weakness, hearing loss, and vertigo were most common, and only 1 patient had vertigo without hearing loss or facial weakness. Most patients with vertigo also had hearing loss (28 of 30), and patients without hearing loss did not have vertigo (19 of 21). While patients with vertigo had worse ENoG values than those without vertigo, ENoG values were not significantly different between patients with and without hearing loss. In conclusion, various clinical manifestations of CN VII and VIII dysfunction are possible in patients with HZO. Patients with vertigo had worse ENoG values than those without, which may indicate that vertigo reflects more severe facial nerve degeneration in HZO patients with facial weakness.

We herein present a case of 6-year-old female demonstrating atypical Ramsay-Hunt syndrome. She presented with an earache, severe vertigo, and vomiting at onset, and thereafter, herpes zoster oticus appeared. No facial nerve palsy was seen. She was vaccinated for varicella and had no past history of apparent varicella infection. The patient showed positive IgG and negative IgM serum antibodies for varicella-zoster virus (VZV). An analysis of VZV-DNA from the patient's ear lesion using alleric discrimination real-time PCR identified a wild-type strain of VZV. We diagnosed her to have atypical Ramsay-Hunt syndrome caused by reactivation of the VZV. Aciclovir and prednisolone were administered, and she recovered completely. This case indicates that Ramsay-Hunt syndrome could be caused by a VZV infection after vaccination, even though its frequency is low. Ramsay-Hunt syndrome may thus be considered as one of causes of sudden onset vertigo in children.

Objective: To research the frequency characteristics of the semicircular canals lesion in Hunt syndrome with vertigo and the clinical value of the video head impulse test (vHIT) for vestibular function evaluated in this disease., Methods: Thirty normal persons (control group) accepted the vHIT, 26 patients with Hunt syndrome with vertigo (study group) accepted low, mid and high frequency vestibular function tests, including caloric test (CT), head shaking test (HST) and vHIT. The parameters of the unilateral weakness (UW), head shaking nystagmus (HSN) and video head impulse test gain (vHIT-G) were observed. The correlations and characteristics of the results of the three tests in Hunt syndrome with vertigo deal were analyzed with SPSS 16.0 software., Results: The values of vHIT-G of the six groups semicircular canal in the control group were normal distribution without statistical significance (F = 0.005, P < 0.01), two sides anterior, horizontal and posterior semicircular canals vHIT-G average (x ± s) were (16.80 ± 9.80)%, (16.57 ± 10.30)%, (16.52 ± 11.12)% respectively; in the study group the separately vHIT-G of the three canals of the affected side were (46.96 ± 34.54)%, (75.35 ± 35.29)% and (41.65 ± 32.87)%, in which statistical significance comparing with the control group was detected (all P < 0.01); the positive one of the three tests vHIT, HSN and CT were 23 cases (88.46%), 22 cases (84.61%) and 24 cases (92.31%), bilateral exact probability χ² test all the P > 0.05;there were Positive correlation between UW and the vHIT-G of lateral semicircular canal (r = 0.692, P < 0.01)., Conclusions: The vestibular lesion of Hunt syndrome with vertigo is almost complete or multiple-frequency, which is characterized by the reduced or even aborted nerve conduction. Therefore, vHIT can be ultimately used for the screening test evaluating due to the vestibular function in Hunt syndrome with vertigo.

A 60-yr-old man presented with chronic vestibulopathy induced by Ramsay Hunt syndrome for 1 yr. Prolonged dizziness and postural imbalance affected his quality-of-life. He was treated using a 2-mo protocol of customized vestibular rehabilitation therapy consisting of 16 treatment sessions in a rehabilitation clinic and daily home exercises. Significant improvements in the subjective perception of dizziness and objective balance function were found. The results suggest that vestibular rehabilitation therapy may be an effective therapeutic method for chronic vestibulopathy of Ramsay Hunt syndrome.

Objectives: The mechanism by which varicella-zoster virus (VZV) reactivation causes cochleovestibular symptoms (CVSs) in patients with Ramsay Hunt syndrome (RHS) remains to be elucidated. The present study analyzed the relationship between VZV load and the onset of CVSs in RHS., Methods: The subjects consisted of 56 patients with RHS; 29 exhibited CVSs and facial paralysis (FP; group 1), and 27 exhibited FP without CVSs (group 2). The VZV DNA copy number in the saliva was measured with a quantitative polymerase chain reaction. Anti-VZV antibodies were assayed by an enzyme-linked immunosorbent assay with paired sera., Results: There was no significant difference in maximum viral copy number between the two groups. In group 1, CVSs occurred at various times between the early phase and the regression phase of VZV reactivation. In some patients, CVSs occurred in the early phase of VZV reactivation, before the onset of zoster lesions and FP., Conclusions: There are various different patterns in the development of eighth cranial nerve dysfunction, which is caused by progression of neuritis or labyrinthitis following VZV reactivation. Our data suggest that CVSs in RHS may also be caused by reactivation of VZV in the spiral and/or vestibular ganglia.

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.