Ramsey Hunt causes more widespread vestibular dysfunction that other causes of acute peripheral vestibulopathy
Reviewed by Victor Osei-Lah

The extent of semicircular canal dysfunction in different conditions causing acute vestibular syndrome (AS) has not been widely studied. The authors share their findings in a retrospective study of patients presenting with AVS in three conditions: Ramsay Hunt syndrome (RHSD), vestibular neuritis (VN) and sudden sensorineural hearing loss with vertigo (SHLV). Using strict inclusion criteria, 23 patients with RHSD, 44 patients with VN and 70 patients with SHLV were enrolled in a study spanning three years at a single centre. The outcome measure was the extent of semicircular canal (SSC) impairment using the video head impulse test (vHIT). Although there were no significant differences in the rate of caloric abnormalities between groups, the degree of canal paresis was significantly higher in the RSHD and VN than the hearing loss group. In cluster analysis, the authors identified seven groups of vHIT impairment (low VOR gain and presence of corrective saccades) involving either single or multiple canals. The most common impairment in VN was horizontal semicircular canal (HSCC) followed by a combination of HSCC and anterior semicircular canal (ASCC). In Ramsey Hunt, the most common impairment pattern was ASCC, HSCC and posterior semicircular canal (PSCC) whereas in the hearing loss group, the most common was PSCC only. One explanation for the extensive multi-canal impairment in Ramsey Hunt in particular, and VN in general, was the viral aetiology as opposed to a vascular theory for sudden hearing loss. The latter is supplied by the common cochlear artery which also supplies the PSCC, the most common canal affected in the hearing loss group. Furthermore, the immune response to the viral insult was used to explain the severity of impairment in RSHD vs. VN: for the former, the immune response to varicella zoster is driven by CD4 + T cells, whereas for VN, the response to HSV-1 is noncytolytic response driven by CD8 + T cells. It is worth noting that both vestibular nerves – superior and inferior – were affected in Ramsey Hunt whereas in VN and SHLV, the superior and inferior vestibular nerves respectively were solely involved. The authors admitted that the absence of otolith organ evaluation with vestibular evoked myogenic potentials (VEMPs) was a limitation. The main conclusion was obvious: Ramsey Hunt causes more severe and extensive canal impairment than VN and SHLV. Would that explain why recovery from vestibular dysfunction in Ramsey Hunt appears to be more protracted than other peripheral vestibular pathology?

Comparison of vHIT deficits with Ramsay Hunt syndrome with dizziness, vestibular neuritis, and idiopathic sudden sensorineural hearing loss with vertigo.
Liu Y, Chen X, Shen X, et al.
J VESTIB RES
2025;35(3):121–31.