Evidence for a Viral Neuropathy in Recurrent VertigoGacek R.R.
Department of Otolaryngology-Head and Neck Surgery, University of Massachusetts Medical School, Worcester, Mass., USA
The concept that reactivation of latent neurotropic viruses (i.e. Herpesviridae group) in the vestibular ganglion is responsible for recurrent vestibulopathies is presented. A similar histopathologic degeneration of vestibular ganglion cells in vestibular neuronitis (VN), Ménière’s disease and benign paroxysmal positional vertigo is presented to support this concept. The clinical response (relief of vertigo) to the administration of antiviral medication in these syndromes provides practical evidence of a viral neuropathy in patients with recurrent vertigo. Relief of vertigo after this treatment was 90% in VN, Ménière’s disease and VN. The relief of positional vertigo (benign paroxysmal positional vertigo) was 66%.
© 2008 S. Karger AG, Basel
J.R. García-Berrocal: The author addresses the role of viral infection in diverse manifestations of recurrent vertigo such as VN, MD and BPPV. As a result of TB studies, focal axonal degeneration and vestibular ganglion cell loss are mainly observed in such conditions. Particularly, regarding BPPV a new concept (neural) has been proposed which contrasts the long-held mechanical concept. We totally agree with Dr. Gacek in this respect. Nevertheless, the clinical study proposed to support a viral etiology for these vestibulopathies lacks a control group for comparison. The outcome of antiviral treatments needs a control group since positive results of the treatment are not sufficient to prove the validity of the hypothesis. This interesting approach of recurrent vertigo encourages us to consider the use of antiviral drugs for controlling one of the most disabling symptoms in clinical practice. The design of noninvasive molecular analysis of the inner ear would be highly beneficial for understanding the crucial mechanisms involved in recurrent vestibulopathies as well as for comparing the findings in different episodes presented in the clinical course.
T. Linder: As presented in our study in this issue of ORL [Gärtner et al., pp. 28–31], we were not able to confirm the herpes 1 or 2 viral presence in Scarpa’s ganglion of patients with disabling MD. Our personal experience with patients undergoing transtemporal-supralabyrinthine vestibular neurectomy for incapacitating vertigo is very favorable, with over 90% permanent relief of their dizzy symptoms within a few days following the neurectomy. These results have also been confirmed by many other surgical publications. A central propagation of the virus with persistence of clinical symptoms is highly unlikely to be the reason for the very few failures following surgical treatment. Since most patients with unilateral cochleovestibular symptoms at some point do get an MRI scan, we were not able to confirm a pathologic enhancement of the vestibular ganglion in these patients. In contrast, patients with Bell’s palsy consistently present with pathologic gadolinium enhancement within the internal auditory canal, labyrinthine segment and geniculate ganglion, and patients with herpes zoster oticus and facial palsy often present with radiologic signs of polyneuritis within the internal auditory canal, affecting also the vestibular nerves. One is therefore skeptical to apply the viral theory to the most frequent pathologies of vestibular disorders such as MD, VN and BPPV. The arguments that only certain patients harbor the viral receptor enabling the invasion of sensorineural cells and that different virus types and strains may be responsible for a wide variety of clinical presentations of the disease are quite hypothetical and are not supported by enough facts. The success rate presented in the paper by oral intake of 3 times 800 mg acyclovir is quite unique. The dosage to kill HSV is, however, quite low and for VZV virus it is definitely too low. An important study from Munich  should also be cited: the authors performed a prospective, randomized, double-blind, two-by-two factorial trial in which 141 patients with acute vestibular neuritis were randomly assigned to treatment with placebo, methylprednisolone, valacyclovir, or methylprednisolone plus valacyclovir. Methylprednisolone significantly improved the recovery of peripheral vestibular function in patients with vestibular neuritis, whereas valacyclovir did not (1-year follow-up).
As long as there is no definitive confirmation on the viral etiology of VN, MD and BPPV, prolonged use of antiviral drugs may actually rise the costs for (unnecessary) treatment.
1 Strupp M, Zingler VC, Arbusow V, et al: Methylprednisolone, valacyclovir, or the combination for vestibular neuritis. N Engl J Med 2004;351:354–361.
R. Maire: My criticism of this ‘all viral’ theory for labyrinthine diseases is that the postulate is mainly based on histopathologic observations. Indeed, the prevalence of herpes virus infection in the population is very high worldwide and approximately 90% of adults are seropositive for different groups of the herpes virus family. If reactivation of latent virus actually explains recurrent cranial neuropathies, recurrent facial and vocal cord palsy, trigeminal and glossopharyngeal symptoms should also be observed in the population. Epidemiological evidence does not confirm this fact. The author yields no critical view why reactivation of latent neurotropic viruses would be so frequent in the inner ear and not in other cranial nerves.
On the other hand, the author observed that antiviral therapy was effective to relieve vertigo in patients suffering from VN, MD and BPPV, supporting the viral basis for recurrent inner ear disorders. However, the patients evaluated in his study were not included in a randomized, placebo-controlled clinical trial. The following remarks weaken the positive results obtained in this study: (1) BPPV spontaneously resolves in most cases; (2) symptoms of VN usually disappear with either central compensation or recovery of peripheral vestibular function; (3) MD patients were not compared with a control group.
C.A. Oliveira: The histopathologic evidence presented is interesting. However, because exposure to the HSV is so common, a study of the incidence of these changes in the nonvertiginous population is in order. It is crucial to prove that the incidences of these changes are statistically significantly different when vertiginous and nonvertiginous populations are compared. The same apply regarding treatment with antiviral drugs. A control group is absolutely necessary in order to validate this treatment. The whole concept remains therefore an alternative hypothesis.
I. Pyykkö: The evidence based on histological evaluation of the TB has some drawbacks such as the latency between TB evaluation and the existence of the symptoms. However, the paper convincingly indicates that there are cases in which viral infection plays a role and may contribute to the vestibular and cochlear symptoms. The treatment effect, although beneficial, may depend on other effects not linked to acyclovir, as placebo treatment was not included. Furthermore, a reliance on antiviral treatment as a proof of viral etiology may be irrational as the immune response is most often making the structural damages that cannot be prevented by antiviral agents.