Corticosteroids effective in idiopathic facial nerve palsy (Bell's Palsy) but not necessarily in idiopathic acute vestibular dysfunction (Vestibular Neuritis)

Most authorities would now agree that there is good evidence that corticosteroids are effective in the management of patients with acute idiopathic facial nerve palsy (Bell’s palsy) if given early in the condition. The mechanism of action in such settings is believed to be related to their potent anti-inflammatory properties, resulting in decompression of the facial nerve within the temporal bone. What has not been clear up until recently is whether corticosteroids would be equally effective in the management of patients with acute idiopathic vestibulopathy (vestibular neuritis). It has been argued that vestibular neuritis results from compression of the vestibular nerve within the temporal bone secondary to inflammation. Given the similarities in proposed etiology between this and Bell’s palsy, one might assume therefore that corticosteroids should be equally effective in the management of patients with vestibular neuritis. This formed the basis of a hypothesis which has recently been tested. Several randomized controlled trials have assessed the effectiveness of corticosteroids in patients with vestibular neuritis, which warranted a Cochrane systematic review and meta-analysis of the subject that has recently been completed. Although a beneficial effect of corticosteroids is seen on caloric testing at 1 month (risk ratio[RR]: 2.81; 95% confidence interval [CI]: 1.32-6.00, P 1⁄4 .007), this effect was not sustained, and there was no significant difference seen at 12 months (RR: 1.58; 95% CI: 0.45-5.62, P 1⁄4 .48). In addition, there was no significant difference between corticosteroids and placebo medication in the symptomatic recovery of vestibular function following vestibular neuritis with respect to vertigo at 24 hours (RR: 0.39; 95% CI: 0.04-3.57, P 1⁄4 .40) and use of the Dizziness Handicap Inventory score at 1, 3, 6, and 12 months. The learning points that can concluded from the above observations are several-fold (Table I). First, until we fully understand the exact etiologies of such conditions (and how their treatments act), it is difficult to predict with certainty which treatments will be effective and under what circumstances. Currently, the most popular theory of the pathogenesis of vestibular neuritis is based on viral infection (viral hypothesis). Clinical supporting evidence that viral agents are responsible for this condition (viral hypothesis) is based on epidemiological evidence of an increased incidence of this vestibular condition during an epidemic of viral infections, and clinical evidence that an upper respiratory viral disorder