Objectives. To review the current knowledge of the aetiology of vestibular neuritis including viral infections, vascular occlusion, and immunomediated mechanisms and to discuss the pathogenesis with relevance to pharmacotherapy. Systematic Review Methodology. Relevant publications on the aetiology and treatment of vestibular neuritis from 1909 to 2013 were analysed. Results and Conclusions. Vestibular neuritis is the second most common cause of peripheral vestibular vertigo and is due to a sudden unilateral loss of vestibular function. Vestibular neuronitis is a disorder thought to represent the vestibular-nerve equivalent of sudden sensorineural hearing loss. Histopathological studies of patients who died from unrelated clinical problems have demonstrated degeneration of the superior vestibular nerve. The characteristic signs and symptoms include sudden and prolonged vertigo, the absence of auditory symptoms, and the absence of other neurological symptoms. The aetiology and pathogenesis of the condition remain unknown. Proposed theories of causation include viral infections, vascular occlusion, and immunomediated mechanisms. The management of vestibular neuritis involves symptomatic treatment with antivertiginous drugs, causal treatment with corticosteroids, and physical therapy. Antiviral agents did not improve the outcomes. 1. Introduction Vestibular neuritis (VN) is the second most common cause of peripheral vestibular vertigo (the first being Benign Paroxysmal Positional Vertigo) and is a disorder thought to represent the vestibular-nerve equivalent of sudden sensorineural hearing loss. The first case of VN was reported by Ruttin in 1909 [1], and the term was coined by Hallpike in 1949 [2] and Dix and Hallpike in 1952 [3]. Synonyms for vestibular neuritis include acute labyrinthitis [4], acute unilateral vestibular paralysis [5], and epidemic vertigo [6]. Vestibular neuronitis is caused by a sudden unilateral loss of vestibular function. In the majority of cases, the functions of the organs that are innervated by the superior vestibular nerve (the superior and lateral semicircular canals and the utricle) are damaged, but the functions of the organs that are innervated by the inferior vestibular nerve (the posterior semicircular canal and the saccule) are spared [7]. Vestibular neuritis has an incidence of approximately 3.5 cases per 100,000 people [8]. The typical age of onset is between 30 and 60 years, and the age distribution plateau is between 40 and 50 years [8]. There is no significant gender difference, and 30% of all affected patients had
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