Acute Vertigo Caused by Herpes Zoster Oticus

By Louise M. Klebanoff, MD

Assistant Professor of Clinical Neurology, Weill Cornell Medical College

SYNOPSIS: Herpes zoster oticus (HZO) and vestibular neuritis (VN) can be difficult to distinguish, but treatments may be different. Magnetic resonance imaging may help by showing inflammatory lesions in the vestibular nuclei or the proximal portions of the eighth nerves in HZO, but not VN.

SOURCE: Yacovino DA, Perez Akly MS, Ibanez T, Cherchi M. Vestibular nucleus involvement in patients with acute vertigo due to herpes zoster oticus or vestibular neuritis. Neurology 2023;101:e1461-e1465.

Herpes zoster oticus (HZO) and vestibular neuritis (VN) both can cause acute vestibular dysfunction. HZO is characterized by a painful, blistering rash in the auricular and external auditory canal accompanied by audiovestibular dysfunction. When there is concomitant facial palsy, the syndrome is termed Ramsay Hunt syndrome. HZO is thought to be caused by reactivation of latent varicella zoster virus (VZV) in the geniculate ganglion. In addition to involvement of the trunks of the nerves in the internal auditory canal, additional neurological complications of VZV, including meningoencephalitis, neuromyelitis, cerebellitis, vasculitis, and cranial neuritis can occur. The vestibular dysfunction can be disabling. On post-mortem examinations and on magnetic resonance imaging (MRI) studies, evidence of inflammation has been seen in the vestibular and auditory nerves and the labyrinth. Vestibular dysfunction associated with HZO is more severe and has a poorer outcome than that associated with VN. To distinguish these two diagnostic entities, the authors did a retrospective case-controlled study to investigate radiological changes in the vestibular nuclei of the brain as seen on MRI in patients with acute vertigo caused by HZO vs. VN.

The authors conducted a retrospective review of patients with a diagnosis of HZO and VN from a database of dizzy patients seen from 2012 to 2022. The diagnosis of VN was made on the basis of spontaneously occurring acute vestibular syndrome lasting more than 24 hours within the past 15 days, physical examination showing nystagmus consistent with peripheral vestibular dysfunction, 6-axis video head impulse testing compatible with unilateral vestibular dysfunction, MRI performed after 72 hours but before 15 days from the onset of symptoms showing no lesions in the posterior fossa, audiogram showing no synchronic hearing loss ipsilateral to the side of the vestibular weakness and no subjective complaints of hearing loss, and no evidence of a more convincing diagnosis.

The diagnosis of HZO with vertigo was made on the basis of herpetic eruption on the auricle and external ear canal ipsilateral to the vestibular loss, with or without ipsilateral facial palsy and hearing loss, acute vertigo and nystagmus with the same clinical characteristics of the VN group, and brain MRI obtained between 48 hours and 15 days of onset of symptoms. All MRI images were reviewed by a trained neuroradiologist and neurotologist, looking specifically for lesions of the vestibular nuclei complex in the pontomedullary region.

The authors retrospectively reviewed the MRIs of 35 patients with acute VN and 10 with acute HZO. In all patients with HZO, there was contrast-enhancement or thickening of the vestibular cochlear nerve in the cerebellopontine cistern or in the internal acoustic canal (IAC) fundus. Five of the 10 patients with HZO also had fluid-attenuated inversion recovery (FLAIR) sequence signal abnormalities involving the vestibular nuclei; the diffusion-weighted imaging (DWI) was negative in all five cases, arguing against an ischemic etiology for the vestibular dysfunction. None of the 35 patients with VN were found to have brainstem lesions on MRI.

Half of the patients with HZO in this study were found to have brainstem lesions involving the vestibular nuclei, whereas none of the 35 patients with VN had similar brainstem lesions. This brainstem involvement was more likely to be caused by vestibular nucleitis as the result of retrograde viral infection and inflammation; the lesions involved more than one vascular territory, and the DWI images were negative for ischemia.

COMMENTARY

This small, retrospective study looking at MRI findings in patients with acute vestibular dysfunction caused by HZO vs. VN found that half of the patients with HZO had corresponding brainstem lesions on MRI whereas none of the patients with VN had similar lesions. This difference raises the possibility of using MRI to distinguish HZO vs. VN in the acute setting. Corticosteroid therapy is indicated in the acute treatment of HZO but has not been shown to be of benefit in VN; therefore, the ability to rapidly and easily differentiate between these two diagnoses in the acute setting may have treatment implications. A larger, prospective study would be helpful to confirm these findings and provide treatment guidelines.