A Delayed Acute Vestibular Syndrome and Diplopia in Ramsay Hunt Syndrome With Absent Facial Nerve Paralysis After Partially Treated Varicella-Zoster Virus (VZV) Oticus

Ramsay Hunt syndrome (herpes zoster oticus) is an uncommon neurological complication of varicella-zoster virus (VZV) reactivation caused by inflammation of the geniculate ganglion of cranial nerve VII. While Ramsay Hunt syndrome classically affects cranial nerve VII, concomitant involvement of cranial nerve VIII is well described. The classic triad includes unilateral lower motor neuron facial paralysis, otalgia, and vesicular rash in the auricle or auditory canal. Atypical presentations without these features are recognized and may delay diagnosis. We report an 82-year-old man with recent herpes zoster oticus who developed acute vestibular syndrome with gait instability, left-beating nystagmus, and vertical diplopia. He had left ear and temporal pain but no facial weakness. Contrast-enhanced MRI showed enhancement of cranial nerves VII and VIII in the cerebellopontine angle without clinical facial motor deficit. Following sequential antiviral therapy (intravenous acyclovir followed by oral valacyclovir) and corticosteroids, diplopia and nystagmus resolved within one week with substantial gait improvement by four weeks. This case highlights Ramsay Hunt syndrome presenting with predominant vestibulocochlear dysfunction despite radiographic facial nerve involvement. Prompt antiviral and corticosteroid therapy can prevent permanent sequelae such as sensorineural hearing loss or neurotrophic keratitis. Clinicians should maintain a high index of suspicion for VZV-related cranial polyneuropathy in older adults with acute vestibular syndrome after recent zoster, even in the complete absence of facial palsy.