Vestibular Neuritis and Bell’s Palsy: Same Cause? Same Treatment?

Abstracts & Commentary

Synopsis: Methylprednisolone significantly improves the recovery of peripheral vestibular function in patients with vestibular neuritis, whereas valacyclovir does not.

Sources: Strupp M, et al. Methylprednisolone, Valacyclovir, or the Combination For Vestibular Neuritis. N Engl J Med. 2004;351:354-361; Johnson RT. Vestibular Neuritis, or Driving Dizzily Through Donegal. N Engl J Med. 2004;351:322-323; Gilden DH. Bell’s Palsy. N Engl J Med. 2004; 351:1323-1331.

The syndrome of vertigo without auditory symptoms, vestibular neuritis, is thought to result from inflammation of the vestibular nerve from a viral cause. Two different modes of viral injury have been proposed: either primary infection by a variety of viruses, or activation of herpes simplex virus type 1 (HSV1), latent in vestibular ganglia. According to the latter theory, vestibular neuritis and Bell’s palsy share the same pathogenesis. Therefore, Strupp and colleagues reasoned that corticosteroids, antiviral agents, or a combination of both might improve the outcome in patients with vestibular neuritis.

In a randomized trial, they assigned 141 patients with vestibular neuritis to treatment with placebo (n = 38), Methylprednisolone (35), Valacyclovir (33), and Methylprednisolone plus Valacyclovir (35). Vestibular function was determined by caloric irrigation within 3 days of onset of symptoms, and again 12 months later. The mean (+SD) improvement in peripheral vestibular function at 1-year follow-up was 40 ± 28 percentage points in the placebo group, and 62 ± 17 percentage points in the Methylprednisolone group. Analysis of variance showed a significant effect of Methylprednisolone (P < 0.001), but not of Valacyclovir. The combination of Methylprednisolone and Valacyclovir was not superior to corticosteroid monotherapy.

Strupp et al compared their results with meta-analyses of studies of treatment for Bell’s palsy and the statement of The Quality Standards Subcommittee of the American Academy of Neurology that early treatment with oral corticosteroids is probably effective in improving facial function outcomes in Bell’s palsy, but that the addition of acyclovir to prednisone is only possibly effective.1

Gilden reviewed the evidence in support of medical and surgical treatments of Bell’s palsy and has updated recommendations for treatment of patients within 2 to 14 days after onset of symptoms: oral prednisone 1 mg./kg combined with oral Valacyclovir (1g b.i.d.) or famcyclovir (750 mg. t.i.d.) for 7 days.


Although Strupp et al assumed that Bell’s palsy and vestibular neuronitis share the same pathogenesis, activation of HSV 1 at the time of disease has not been documented in vestibular neuritis as it has in Bell’s palsy. Furthermore, Strupp et al found that antiviral treatment alone was not better than placebo. Nevertheless, as noted by Johnson in his editorial comments, it may be that HSV 1 is not involved, or is only 1 of many causes of vestibular neuritis, so that any beneficial effects of Valacyclovir were so diluted as to be undetectable.

By documenting that treatment with corticosteroids during the acute phase of vestibular neuritis improved caloric responses 1 year later, Strupp et al have, at a stroke, changed clinical practice. Corticosteroids should and will become part of the standard treatment for vestibular neuritis. The place, if any, for antiviral drugs in acute vertigo remains uncertain, and should be the subject of further studies. —John J. Caronna


1. Grogan PM, et al. Neurology. 2001;56:830-836.

John J. Caronna, MD Vice-Chairman, Department of Neurology, Cornell University Medical Center; Professor of Clinical Neurology, New York Hospital is Associate Editor of Neurology Alert.