Causes of Vestibular Neuritis
Vestibular neuritis is most likely caused by reactivation of latent herpes simplex virus type 1 (HSV-1) infection within the vestibular ganglion, though the exact etiology remains incompletely understood. 1, 2
Primary Etiologic Theory: Viral Reactivation
HSV-1 reactivation in the vestibular ganglion represents the leading etiologic hypothesis, supported by detection of HSV-1 DNA and RNA in human vestibular ganglia at autopsy. 2
HSV-1 DNA has been identified in 48% of human vestibular labyrinths and 62% of vestibular ganglia in temporal bone studies, demonstrating widespread viral presence in the vestibular apparatus. 3
Experimental evidence confirms that vestibular ganglion neurons can harbor latent HSV-1 infection and undergo reactivation when exposed to histone deacetylase inhibitors in cell culture models, establishing biological plausibility for viral reactivation as the disease mechanism. 4
The inflammatory process involves demyelination and degeneration of the superior vestibular nerve, documented in histopathological studies of patients who died from unrelated causes after experiencing vestibular neuritis. 5, 6
Supporting Evidence for Inflammatory Pathogenesis
Elevated plasma fibrinogen and C-reactive protein levels during the acute phase, prolonged brainstem auditory evoked response latencies, and increased gadolinium uptake in the vestibular nerve and Scarpa's ganglion on MRI all confirm the inflammatory nature of the condition. 6
Animal models using retroauricular inoculation of herpes simplex virus in mice successfully reproduce vestibular neuritis, providing experimental support for viral causation. 6
Alternative Proposed Mechanisms (Less Supported)
Vascular occlusion has been proposed but lacks strong supporting evidence and does not explain the characteristic pattern of superior vestibular nerve involvement. 5
Immune-mediated mechanisms have been suggested, though whether this represents primary autoimmunity or secondary immune response to viral infection remains unclear. 5
Bacterial and protozoal infections, as well as allergic causes, have been proposed historically but are not supported by current evidence. 6
Clinical Context and Epidemiology
Vestibular neuritis is the second most common cause of peripheral vestibular vertigo (after BPPV), with an annual incidence of 3.5 per 100,000 population and accounting for 7% of patients at specialized vertigo clinics. 2
The condition affects both sexes equally, with peak incidence at 40-50 years of age. 6
The characteristic presentation includes sudden onset of severe rotatory vertigo lasting more than 24 hours (typically 12-36 hours of peak intensity), with severe nausea and vomiting, but crucially without auditory symptoms such as hearing loss, tinnitus, or aural fullness. 1
Critical Diagnostic Caveat
Always exclude brainstem or cerebellar stroke in patients with significant vascular risk factors, even when the presentation appears consistent with vestibular neuritis, as posterior circulation stroke can present identically and carries life-threatening implications. 1
The absence of hearing loss distinguishes vestibular neuritis from labyrinthitis, though HSV-1 presence in the labyrinth itself suggests inflammation may extend beyond the nerve in some cases. 3
Therapeutic Implications of Viral Etiology
Despite viral causation being the leading theory, antiviral agents (such as acyclovir) have not been shown to improve outcomes in clinical trials, whereas corticosteroids achieve 62% recovery of labyrinthine function within 12 months. 5, 2
This paradox suggests that either the inflammatory cascade becomes self-sustaining after viral reactivation, or that treatment timing relative to viral replication is critical but difficult to achieve clinically. 5