# Case Report: Ramsay Hunt syndrome with simultaneous bilateral vestibular dysfunction as the initial manifestation in a patient with a history of breast cancer

## TL;DR

A 60-year-old breast cancer patient presented with rare bilateral vestibular dysfunction as the first sign of Ramsay Hunt syndrome, highlighting an unusual clinical pattern.

## Contribution

This case report documents the rare occurrence of simultaneous bilateral vestibular dysfunction preceding Ramsay Hunt syndrome.

## Key findings

- The patient exhibited bilateral vestibular hypofunction confirmed by video head impulse and caloric testing.
- Facial nerve impairment and herpes zoster oticus were present, consistent with Ramsay Hunt syndrome.
- Bilateral vestibular dysfunction occurred before the typical facial palsy and otalgia, differing from classical RHS patterns.

## Abstract

Ramsay Hunt syndrome (RHS) typically presents with unilateral otalgia, herpes zoster oticus, ipsilateral peripheral facial palsy, and often ipsilateral vestibulocochlear involvement. Bilateral/contralateral vestibular dysfunction is extremely rare.

A 60-year-old female with a history of right breast cancer presented to our clinic with 1 week of vertigo, followed by 2 days of right-sided facial deviation and otalgia. Physical examination revealed vesicular eruptions around the right ear and external auditory canal, right-sided peripheral facial palsy, spontaneous horizontal-rotatory nystagmus (with a fast phase to the left), and postural instability. Further evaluation confirmed bilateral vestibular hypofunction: the video head impulse test showed reduced gains and/or saccades in all canals; bithermal caloric testing demonstrated bilateral vestibular weakness (sum of slow-phase velocity: 10.1°/s); and symptom assessments yielded a visual analog scale (VAS) score of 7/10 and a dizziness handicap inventory (DHI) total score of 52. Facial nerve electrophysiological testing indicated significant impairment of the right facial nerve, with an amplitude reduction exceeding 50%. The stapedial reflex, Hallpike-Dix test, Roll test, pure-tone audiometry, brain and cranial nerve MRI, and routine laboratory tests showed no significant abnormalities. A diagnosis of RHS with bilateral vestibular dysfunction was established, and treatment was administered per current guidelines, including antiviral therapy, oral corticosteroids, analgesics, anti-vertigo medications, acupuncture, and vestibular rehabilitation. After 2 weeks, symptoms (facial palsy, otalgia, herpes zoster, and dizziness) improved slightly, with crusting of the herpes lesions. At the 3-month follow-up, the herpes zoster had resolved without residual pain, though mild residual dizziness (VAS 2, DHI 20) and facial weakness persisted.

This case shows rare bilateral vestibular involvement and initial vestibular impairment preceding RHS (distinct from classical ipsilateral or rare post-RHS contralateral patterns). Elucidating the specific pathogenic mechanisms underlying this presentation holds significant clinical importance for understanding bilateral vestibular involvement.