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  • Updated 05.15.2024
  • Released 05.26.2023
  • Expires For CME 05.15.2027

Viral labyrinthitis and vestibular neuritis

Introduction

Overview

This article discusses viral infections of the membranous labyrinth or eighth nerve acquired after birth and without associated neurologic symptoms or signs: vestibular neuritis (ie, vestibular loss alone) and viral labyrinthitis (ie, cochleovestibular loss). Viral labyrinthitis can occur as part of a systemic viral illness, or it may occur with localized involvement of the labyrinth or eighth nerve without apparent systemic involvement. Multiple viruses have been implicated with viral labyrinthitis, but the evidence supporting a viral etiology is often circumstantial. Nevertheless, viral reactivation (eg, latent herpes simplex type 1) in vestibular ganglia is a suspected cause of vestibular neuritis. Diagnostic criteria for these disorders are summarized. The management of the acute phase of vestibular neuritis or viral labyrinthitis is primarily medical, whereas long-term treatment is designed to improve vestibular compensation. Symptomatic medication is indicated during the acute phase to relieve the vertigo and nausea/vomiting. Antihistamines, anticholinergic agents, antidopaminergic agents, and GABAergic agents are useful in acutely suppressing vertiginous symptoms. Corticosteroids are beneficial, but the available evidence does not support the use of antiviral agents.

Key points

• Vestibular neuritis (ie, vestibular loss alone) and viral labyrinthitis (ie, cochleovestibular loss) may both be caused by viral infections.

• Viral labyrinthitis can occur as part of a systemic viral illness, or it may occur with localized involvement of the labyrinth or eighth nerve without apparent systemic involvement.

• Multiple viruses have been implicated with viral labyrinthitis, but the evidence supporting a viral etiology is often circumstantial.

• Viral reactivation of latent herpes simplex type 1 in vestibular ganglia is a suspected cause of vestibular neuritis.

• Inclusion criteria for “acute unilateral vestibulopathy” (vestibular neuritis) are (1) acute or subacute onset of sustained vertigo (acute vestibular syndrome) of moderate to severe intensity that is symptomatic for at least 24 hours; (2) spontaneous peripheral vestibular nystagmus; and (3) reduced vestibulo-ocular reflex (VOR) function on the affected side.

• Exclusions to a diagnosis of “acute unilateral vestibulopathy” (vestibular neuritis) include (1) acute central neurologic symptoms, audiological symptoms, or otologic symptoms; (2) acute central neurologic signs (eg, skew deviation or gaze-evoked nystagmus); (3) acute audiological signs; and (4) the condition is better accounted for by another disease or disorder.

• The management of the acute phase of vestibular neuritis is primarily medical, whereas long-term treatment is designed to improve vestibular compensation.

• Symptomatic medication is indicated during the acute phase to relieve the vertigo and nausea/vomiting.

• Antihistamines, anticholinergic agents, antidopaminergic agents, and GABAergic agents are useful in acutely suppressing vertiginous symptoms.

• Corticosteroids are beneficial, but the available evidence does not support the use of antiviral agents.

Historical note and terminology

This article considers viral infections of the membranous labyrinth or eighth nerve acquired after birth and without associated neurologic symptoms or signs. Thus, involvement of the membranous labyrinth or eighth nerve due to congenital (in utero) viral infections, herpes zoster oticus (ie, Hunt syndrome or Ramsay Hunt syndrome with facial paresis), and bacterial or carcinomatous meningitis are outside the scope of this article. Virus-mediated sudden deafness without vestibular involvement is also outside the scope of this article.

Vestibular neuritis was first reported in 1949 and was described more fully in 1952 by British neuro-otologists Margaret Ruth Dix (1902–1991) and Charles Skinner Hallpike (1900–1979) (17; 18). Dix and Hallpike, working at the National Hospital, Queen Square, London, had first recognized the disorder in 1946, just after World War II. They argued that it was "some form of organic disease confined to the vestibular apparatus and localized, in all probability, to its peripheral nervous pathways up to and including the vestibular nuclei in the brain stem." They also noted that "[i]n a fairly high proportion of the subjects the onset of the symptoms is associated with some kind of febrile illness, or with evidence of infection of the ears, nose and throat..."

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