Clinical Drug Experience Knowledgebase

Vestibular neuronitis is the second most common cause of peripheral vestibulopathy (the first being benign paroxysmal positional vertigo) with incidence of about 3.5/100000. Currently vestibular neuronitis is explained by a viral pathogenesis.

Vestibular neuronitis is considered to have a benign course. The static rotatory vertigo and disequilibrium, present even when the patient is completely at rest, subside in most cases within a few days, and a gradual return to daily activities is the rule. However, it has been shown that there is generally incomplete restoration of peripheral function, and clinical recovery is achieved by proprioceptive and visual substitution for the unilateral vestibular deficit, combined with central vestibular compensation of the imbalance in vestibular tone. Although vestibular neuronitis is usually restricted to one attack, several studies have reported continuous or episodic vertigo or unsteadiness in 43% -53% of patients. The main residua include impaired vision and disequilibrium during walking and especially during head movement toward the affected ear. The rate of positive finding on vestibular evaluation may reach 60%. However, vestibular impairment as reflected by positive bedside testing and vestibular laboratory evaluation is not necessarily accompanied by subjective complaints and does not always reflect the level of incapacity.

The assumed HSV-1 etiology of vestibular neuronitis and the reported benefit of the combination of steroids and acyclovir in Bell's palsy suggest similar advantage in the treatment of vestibular neuronitis. Also, glucocorticoid receptors activation was reported to enhance vestibular compensation after acute peripheral vestibular insults in various animal models. A recent study investigated the effect of prednisolone versus valacyclovir and placebo on canal paresis in vestibular neuronitis patients. It was found that steroid treatment significantly improved peripheral vestibular function to the extent reflected by the caloric testing. However, bedside findings, patients' complaints and daily handicap were not evaluated. The relevance of the EOG caloric test results to clinical improvement could be argued in light of a previous report showing no correlation between EOG findings and residual symptoms in a long-term follow-up of vestibular neuronitis patients, and the finding that corticosteroid therapy had no effect on symptoms despite significant recovery of the caloric-test results.

The purpose of the study:

Prospective controlled longitudinal 12-month evaluation of the value of steroids in the treatment of vestibular neuronitis. The potential benefits of steroid therapy would be analyzed by the clinical response, self-perceived handicap and EOG laboratory parameters.