Labyrinthitis and Vestibular Neuritis

Viral labyrinthitis and vestibular neuritis represent a spectrum of acute peripheral vestibulopathy. HSV-1 reactivation in the vestibular ganglion (Scarpa's ganglion) is the proposed mechanism for vestibular neuritis, supported by autopsy studies demonstrating HSV-1 DNA in vestibular ganglia and histological evidence of inflammatory neuronal degeneration. In labyrinthitis, inflammation extends to the cochlea. The acute vestibular loss creates a tonic firing imbalance between vestibular nuclei, generating sustained vertigo and spontaneous nystagmus. Recovery depends on central vestibular compensation — neuroplastic reorganization in the vestibular nuclei, cerebellum, and cortex that recalibrates the vestibular system. Bacterial labyrinthitis occurs via tympanogenic (round window, oval window, or fistula from cholesteatoma) or meningogenic (via cochlear aqueduct or internal auditory canal) routes and carries significant risk of permanent deafness and intracranial complications. The clinician must differentiate acute vestibular syndrome from posterior circulation stroke (AICA, PICA territory), vestibular migraine, Meniere's disease, and autoimmune inner ear disease, and initiate appropriate pharmacotherapy including corticosteroids, antivirals, and antibiotics.