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Year : 2017  |  Volume : 23  |  Issue : 4  |  Page : 233-236

Role of antivirals in treatment of vertigo due to vestibulopathies

Department of Otorhinolaryngology and Head Neck Surgery, Government Medical College, Srinagar, Jammu and Kashmir, India

Date of Web Publication2-May-2018

Correspondence Address:
Dr. Zafarullah Beigh
Marouf Colony 90 Feet Road Bachapora, Srinagar - 190 020, Jammu and Kashmir
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/indianjotol.INDIANJOTOL_47_17

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Objective: The objective of this study is to study the role of antiviral medication on treatment of recurrent vertigo due to various vestibulopathies. Materials and Methods: Sixty-six adult patients of vestibular neuronitis (VN), Meniere's disease (MD), and benign paroxysmal positional vertigo were enrolled in this study, patients in each disorder where distributed randomly in two groups, Group A (antiviral) and Group B (nonantiviral). All Patients were assessed on the basis of reduction in dose of vestibular sedative drugs needed for control of vertigo on 1st, 3rd, and 5th day of treatment. Results: Statistically significant reduction in dose of labyrinthine sedatives was found to control vertigo in Group A patients as compared to Group B patients in both VN and MD. This reduction in dose of labyrinthine sedatives was seen on day 3 as well as on day 5 of treatment. Conclusion: This study shows that use of antiviral drugs significantly reduces the dose of vestibular sedatives needed for control of vertigo in MD and VN and hence should be used on a regular basis to treat these ailments.

Keywords: Benign paroxysmal positional vertigo, Famciclovir, Meniere's, vestibular neuronitis

How to cite this article:
Beigh Z, Maqbool T, Ahmad R. Role of antivirals in treatment of vertigo due to vestibulopathies. Indian J Otol 2017;23:233-6

How to cite this URL:
Beigh Z, Maqbool T, Ahmad R. Role of antivirals in treatment of vertigo due to vestibulopathies. Indian J Otol [serial online] 2017 [cited 2023 Mar 21];23:233-6. Available from: https://www.indianjotol.org/text.asp?2017/23/4/233/231644

  Introduction Top

Recurrent vertigo represents a significant disability with serious economic and social implications.[1] The most common vestibular syndromes seen in clinical practice are vestibular neuronitis (VN), Meniere's disease (MD), and benign paroxysmal positional vertigo (BPPV). While VN has been commonly regarded as an inflammatory neuropathy,[2],[3] MD and BPPV are thought to be vastly different pathological entities. MD has been regarded as a disturbance in endolymph homeostasis producing endolymphatic hydrops.[4] This has given rise to medical and surgical treatments aimed at reducing the volume of endolymph in the responsible ear. The pathophysiology responsible for BPPV has been assumed to be dislodged gravity-sensitive otoconia from an otolith receptor in the labyrinth which can transform a semicircular canal receptor (usually the posterior semicircular canal) into a gravity-sensitive sense organ.[5],[6] However, normal adult [7] and pediatric [8] temporal bones (TBs) show similar free-floating and cupular fixed deposits in the vestibular labyrinth. Many TB from patients with BPPV do not show otoconial debris in the endolymph,[9] and Parnes [6] has reported particles in only one-third of the patients with severe BPPV who did not respond to repositioning maneuvers. Nevertheless, on this basis repositioning of the loose otoconia by physical maneuvers has gained popular support as conservative management of symptoms. As well the conservative measures used to relieve vertigo in MD [10] and BPPV [11],[12],[13] have yielded equivocal results when evaluated in controlled studies. Only ablation of the responsible sense organ has yielded a significant level of relief.[14] Therefore, the pathological mechanism in these common vestibulopathies needs reconsideration.

Certain features are shared by VN, MD, and BPPV.

  1. They commence frequently in adults as a spontaneous event, occasionally as a result of head trauma [4],[7]
  2. They typically undergo spontaneous remission and become recurrent [4]
  3. They usually involve one ear with a 15%–20% incidence of bilaterality [15]
  4. They may coexist in the same ear, i.e., VN + BPPV or MD + BPPV [16]
  5. There is a significant loss of vestibular neurons and degenerated facial nerve sensory ganglion cells in all three vestibulopathies [17]
  6. There is a tendency for these syndromes to affect other members of the same family. They frequently follow a period of extreme physical or nonphysical stress in the patient's life.[18]

The many shared features of these three syndromes support the concept of a common etiology. The incidence of elevated HSV-I antibody levels (60% in the population worldwide by the age of 25 and 90% by the age of 60) raises the question of a role of neurotropic (NT) viruses (alpha herpes virinae subfamily) in these vestibulopathies. This group of viruses has a propensity for invading sensory neurons, establishing latency within the nucleus of the ganglion cell, and becoming reactivated at a later (years) date during a period of extreme stress. The best-known members of this group of viruses are herpes simplex HSV Types 1 and 2 and herpes zoster (varicella) virus.[19] Other members of this family of NT viruses are cytomegalo inclusion virus, pseudorabies, and Epstein–Barr virus.

Other studies have demonstrated the presence of HSV antibodies or DNA investibular nerves and nuclei from patients with VN and MD and in the perilymph of patients with MD. Furthermore, MRI imaging has demonstrated enhanced vestibular nerve ganglia in patients with VN and MD, suggesting an inflammatory process in the vestibular nerve. The chemicals elevated in the stress response (cortisol and adrenaline) are capable of allowing the virus to reactivate and cause symptoms by destroying groups (clusters) of ganglion cells. Reactivation of latent HSV-1 has been confirmed in animal-cultured (rat) vestibular ganglion cells.[19] Despite the assumed viral cause of vestibular neuritis, the effects of corticosteroids, antiviral agents, or the two in combination are uncertain.

This clinical study was done to study the efficacy of antiviral drugs on patients suffering from VN, MD, and BPPV.

  Materials and Methods Top

A total of 66 adult patients of VN, MD and BPPV were enrolled in this study. Patients in each disorder were distributed randomly in two groups, Group A (antiviral) and Group B (nonantiviral). In each disorder, patients in Group A were treated with antiviral drugs (tablet Famciclovir 500 mg BD for 10 days) in addition to routine medications. In Group B of each disorder, patients were treated with routine medications (labyrinthine sedatives, corticosteroids and proton-pump inhibitors + diuretics MD and Epleys maneuver BPPV without antivirals.

Patients were assessed on the basis of reduction in dose of vestibular sedative (dimenhydrinate) needed for control of vertigo on 1st, 3rd, and 5th day of treatment.

  Results Top

Results are given in [Table 1], [Table 2], [Table 3], [Table 4].
Table 1: Distribution of vertigo patients in various vestibulopathies

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Table 2: Dose of dimenhydrinate needed for control of vertigo in acute attack of Meniere's disease

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Table 3: Dose of dimenhydrinate needed for control of vertigo in vestibular neuritis patients

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Table 4: Dose of dimenhydrinate needed for control of vertigo in benign paroxysmal positional vertigo patients

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  Disscussion Top

The concept that recurrent vertigo is caused by reactivation of an NT virus (Herpes family) is based on TB changes in the meatal ganglion of the facial nerve as well as in the adjacent vestibular ganglion. These light microscopy observations are supported by transmission electron microscopy, which demonstrated fully formed viral particles in vestibular ganglion cells excised from patients with VN and MD. Treatment with acyclovir has the advantage of preserving the vestibular neural network, allowing compensation of the deficits caused by vestibular ganglion cell degeneration resulting from virus reactivation.[20]

Over 50 years ago, Lempert et al. suggested that MD was caused in the majority of ears by a herpes virus.[21] The herpes family of viruses consists of at least eight members including HSV1 (causes cold sores), HSV2 (causes genital herpes), VCV (causes chicken pox and shingles), EBV (causes glandular fever), and CMV (causes birth defects). The herpes virus has been found in autopsy specimens obtained from MD sufferers in both the endolymphatic sac and in the ganglion of the vestibular and cochlear nerves. However, ears from non-MD sufferers often also contain the virus. The idea of a herpes virus causing the initial inflammatory response in the inner ear is compelling. For example, herpes simplex virus causes cold sores which erupt on the lip and then the virus lies latent or hides in the nerve for a while and then can erupt again causing more cold sores. It is postulated that a similar virus causes an initial inflammatory response in the ear and results in inflammation which causes excess endolymphatic fluid (endolymphatic hydrops). As the virus lies latent within the ear, it can erupt again causing another cluster of attacks.

The most convincing evidence of the viral cause of VN is the TB studies of Schuknecht and Kimura. Isolated atrophy of the vestibular nerve in four patients who reported prolonged vertigo attack suggestive of VN. Besides the atrophy of vestibular nerve, there was also additional atrophy in the vestibular end-organ. The atrophy of the end-organs and nerves were similar to patients with vertigo who had well documented viral disorders such as mumps and measles.[22] Another suspected cause of VN is reactivation of herpes simplex virus Type 1 in the vestibular ganglion, but this has never been demonstrated. Adenovirus infection was also reported as a cause of VN. An infective etiology in the development of VN has long been hypothesized because of its association with infections and its frequent occurrence.

Shimizu et al. evaluated 57 cases of VN for viral infection by means of serum antibody titer.[23] The viruses tested were HSV, VZV, CMV, EBV, adenovirus, influenza virus A, influenza virus B, parainfluenza virus 3, mumps virus, rubella virus, and measles virus. They found a significant change in 26 cases in viral antibody titer and only one case showed high HSV 1 IgM antibody level by ELISA method. Thus, VN in this case was assumed to have a close relation to viral infection. In another study, Hirata et al. evaluated 44 patients and 17 out of 36 patients showed a significant change in serum antibody titers. These viruses were HSV, two cases, CMV, one case, EBV, seven cases, rubella, two cases, adenovirus, two cases, influenza A, one case, influenza B, and two cases. In these cases, infection caused by these detected viruses were assumed to play an important role in the onset of vertigo in each case.[24]

Since these vestibular syndromes are a manifestation of viral neuropathy, the use of antiviral drugs should provide clinical evidence of the viral cause. A clinical series of patients with a diagnosis of MD, VN, or BPPV were treated orally with acyclovir or valacyclovir to relieve vertigo not controlled with conservative measures (diuretics, low-salt diet, meclizine, and valium). This represents an extension of a series of patients reported earlier.[25] These 211 patients include 140 females and 71 males (aged 23–88 years) who were treated from April 2004 to March 2009. The choice of acyclovir as antiviral medication was based primarily on cost. Of 106 patients with VN (the earliest patients evaluated up to 8 years), 93 (88%) had complete relief of symptoms with oral acyclovir, 54 of 60 patients (90%) with MD were relieved of vertigo, and 27 of 45 patients (60%) with posterior canal BPPV were relieved of symptoms.

Strupp et al.2006[26] conducted a prospective, randomized trial of corticosteroids, and antivirals alone with combinations of these treatments in patients with vestibular neuritis. They assessed vestibular function at baseline and the change after 12 months. The antiviral drug did not improve the outcome in patients with vestibular neuritis, despite the assumed viral cause. Replication of HSV-1in the vestibular ganglia may conceivably have already occurred by the time the antiviral drug was initiated that is, within 3 days after the onset of symptoms.

Furthermore, there is good evidence that the major damage in vestibular neuritis is caused by the swelling and mechanical compression of the vestibular nerve within the TB. The anti-inflammatory effect, which results in reduced swelling, may explain why treatment with corticosteroids results in improvement in this disorder.

In our study, statistically significant reduction in dose of labyrinthine sedatives was found to control vertigo in Group A patients as compared to Group B patients in both VN and Meneiers disease patients. This reduction in dose of labyrinthine sedatives was seen on day 3 as well as on day 5 of treatment. Although reduction in dose of labyrinthine sedative was found in Group A patients of BPPV also but that reduction was not statistically significant.

  Conclusion Top

Large randomized controlled trials are needed to confirm the role of antivirals on control of vertigo due to various vestibulopathies; however, this study shows that use of antivirals significantly reduces the dose of vestibular sedatives needed to control vertigo in Meniere's disease and VN and hence should be used on a regular basis to treat these ailments.

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Conflicts of interest

There are no conflicts of interest.

  References Top

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  [Table 1], [Table 2], [Table 3], [Table 4]

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