After benign paroxysmal positional ...

After benign paroxysmal positional vertigo, vestibular neuritis is the nearest most common cause of peripheral vestibular vertigo. The typical presentation is an acute attack 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. force inflammation or ischemia has been postulated as an etiology for vestibular neuritis, if it were not that more recent studies have refer toed that reactivation of herpes simplex virus may be the causative factor. Strupp and co-investigators designed a trial of steroid (methylprednisolone), antiviral agent (vala-cyclovir), and combination treatment for vestibular neuritis.

consideration participants were recruited from the necessity departments of two hospitals with specialized vertigo center Adult patients presenting with an acute attack of severe vertigo within the previous three days were riddleed for enrollment. Exclusion criteria included any prior history of vestibular dysfunction, tinnitus, hearing los or any central vestibular or oculomotor dysfunction.

Of the initial 157 patients who were protectioned 141 remained for randomization after exclusion criteria were applied. All contemplation subjects had an otherwise normal out and out neurologic examination, provocative testing that confirmed vestibular neuritis and a normal magnetic resonance scan of the brain. The four randomized clusters were treated with (1) placebo, (2) methylprednisolone taper (100 mg one time per day starting dose, decreasing by the agency of 20 mg every three days until day 16 [10 mg] for a total course of 22 days), (3) valacyclovir (1000 mg three times daily for seven days), or (4) a combination of one as well as the other the steroid and the antiviral medication.

The step of vestibular loss was measured at presentation and at 12-month follow-up by the agency of 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 lay open unilateral peripheral vestibular loss. Of the 141 randomized enthralls 27 (19 percent) were not available for final analysis because they dropp abroad of the study, were noncom-pliant with the medications, or were not to be found to follow-up. Similar numbers of patients were dissipated from each of the four treatment arms of the study

The average value for vestibular paresis among the application of mind subjects was 78 percent before treatment. Repeat examination 12 month 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 clump Complete or almost complete redemption of vestibular function occurred in 76 percent of exposes whose treatment assignment included meth-ylprednisolone, compared with 27 percent of subdues who used placebo.

The authors judge that treatment of vestibular neuritis within three days of assault with methylprednisolone improves vestibular function at 12 month of follow-up nevertheless treatment with valacyclovir does not improve function.

Strupp M et al. Methylprednisolone, valacyclovir, or the combination for vestibular neuritis. strange Engl J Med July 22 2004;351:354-61

COPYRIGHT 2005 American Academy of Family Physicians

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