After benign paroxysmal positional vertigo, vestibular neuritis is the next most common cause of peripheral vestibular vertigo. The typical presentation is an acute onset of sustained rotatory vertigo. Examination reveals horizontal nystagmus toward the unaffected ear and hyporesponsiveness to provocative testing with warm- and cold-water irrigation of the ear. Nerve inflammation or ischemia has been postulated as an etiology for vestibular neuritis, but more recent studies have suggested that reactivation of herpes simplex virus may be the causative factor. Strupp and co-investigators designed a trial of steroid (methylprednisolone), antiviral agent (valacyclovir), and combination treatment for vestibular neuritis.

Study participants were recruited from the emergency departments of two hospitals with specialized vertigo centers. Adult patients presenting with an acute onset of severe vertigo within the previous three days were screened for enrollment. Exclusion criteria included any prior history of vestibular dysfunction, tinnitus, hearing loss, or any central vestibular or oculomotor dysfunction.

Of the intial 157 patients who were screened, 141 remained for randomization after exclusion criteria were applied. All study subjects had an otherwise normal complete neurologic examination, provocative testing that confirmed vestibular neuritis and a normal magnetic resonance scan of the brain. The four randomized groups were treated with (1) placebo, (2) methylprednisolone taper (100 mg once per day starting dose, decreasing by 20 mg every three days until day 16 [10 mg], for a total course of 22 days), (3) valacyclovir (1,000 mg three times daily for seven days), or (4) a combination of both the steroid and the antiviral medication.

The degree of vestibular loss was measured at presentation and at 12-month follow-up by provocative testing with caloric irrigation. Because of the inherent variability in nystagmus with caloric testing, the authors used a previously validated “vestibular paresis formula” that had been shown to reliably detect unilateral peripheral vestibular loss. Of the 141 randomized subjects, 27 (19 percent) were not available for final analysis because they dropped out of the study, were noncompliant with the medications, or were lost to follow-up. Similar numbers of patients were lost from each of the four treatment arms of the study.

The average value for vestibular paresis among the study subjects was 78 percent before treatment. Repeat examination 12 months after assigned treatment showed that the mean improvement in vestibular paresis was 40 percent in those who received placebo, 62 percent after treatment with methylprednisolone, 36 percent in those who took valacyclovir, and 59 percent in the combination treatment group. Complete or almost complete recovery of vestibular function occurred in 76 percent of subjects whose treatment assignment included methylprednisolone, compared with 27 percent of subjects who used placebo.

The authors conclude that treatment of vestibular neuritis within three days of onset with methylprednisolone improves vestibular function at 12 months of follow-up, but treatment with valacyclovir does not improve function.