case study of a similarly positive reaction to anti-virals
Interesting … but not a controlled study and it followed only one patient?
well, it is a case report… after this people start experimenting
Interesting, when I had sudden hearing loss in 2010 I was put on Valtrex for a while as one possible theory was HSV. I wonder if it would be a reasonable thing to try again at some point if my progress slows. I don’t recall any side effects.
May I ask, Erik, if your hearing loss reversed either with the meds or spontaneously…or not. I’m interested because in March I lost hearing in the previously ‘good’ ear and was prescribed an anti-viral and prednisone which did nothing to relieve the hearing, pressure or loud tinnitus. It did however resolve just as suddenly 6 months later. I have long standing Meniere’s.
Sure, yes, it never reversed. It went out one afternoon in a matter of 1-2 hours and its been like that for 8 years, despite lots of health experimentation on my part. I also had Prednisone injected through the ear drum within 2 days of the initial attack. I have some low frequency hearing left so I can pick out some speech, but above 2kHz it falls off pretty quick. My best guess is a migraine-related vasospasm that cut off blood supply to part of the cochlea. Back then I never had dizziness or ear pressure or bubbling/fluid sensations in the ear and my tinitius/hearing has never changed, so was never diagnosed with meneirs. The virus theory never really made sense to me, why would it kill only high frequency hair cells? But if the virus was causing the migraine, I guess that could make sense.
My doctor says that in order that antivirals work you need to have a high dose for 2-3 months to start in order for them to pass to the nerves on the brain and also to fight the dormant virus and then continue a low dose for very long period to prevent them to come back, mine were coming back with stressful events.
Since these vestibular syndromes are a manifestation of viral neuropathy, the use of anti- viral 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
DOI: 10.1159/000348710 © 2013 S. Karger AG, Basel
Gacek: A Perspective on Recurrent Vertigo
vertigo not controlled with conservative measures (diuretics, low-salt diet, meclizine and valium). This represents an extension of a series of patients reported earlier . 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. Valacyclovir (Valtrex) has better bioavailability but is much more expensive and may not be covered by most insurance plans. All of these patients had failed standard medical treatment for recurrent vertigo (meclizine, valium, diuretics and low-salt diet) for periods ranging from 6 months to years. They were considered refractory to the standard treatment of vestibulopathy.
Attempts to construct a control group of patients undergoing antiviral treatment were unsuccessful. Having failed traditional treatments, these patients with significant vertigo were referred because they desperately sought relief. Therefore, these results can be viewed as uncontrolled. However, there is support for a practice-based approach [64, 65] to determine the effectiveness of new treatments for disorders of unknown etiology.
The antiviral treatment protocol for patients with recurrent vertigo is as indicated below.
Discontinue all previous medical treatments; ensure that patients are cleared for normal renal and liver function; use acyclovir tabs 800 mg t.i.d. for 3 weeks and reexamine. If there is significant relief of vertigo, decrease to 800 mg b.i.d. for 3 weeks, then to 800 mg daily as a maintenance dose. If valacyclovir is selected (in those who fail to respond to acyclovir), use 1 g t.i.d. for 3 weeks with taper to b.i.d. for a further 3 weeks and then 1 g daily as a mainte- nance dose. The starting dose of acyclovir was given for a longer period (3 weeks) than that used for zoster because it was felt necessary to cross the blood-brain barrier to reach ganglion and satellite cells with virus. Most patients experienced relief from vertigo in the first 2 weeks but some required a longer period. The gradual lowering dose was then used to find the lowest level maintenance dose for a given patient. Most were controlled on a single dose daily but occasionally a patient required an adjustment to 1,200 mg of acyclovir or 1,500 mg of valacyclovir.
These dosages may require adjustment in patients with impaired kidney or liver function. The follow-up period was as short as 3 years in the most recent patients and 8 years in the earliest patients in the series. 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. Between the use of antivirals and repositioning maneuvers (physical therapy), the number of chronically disabled patients who were candidates for ablation of posterior semicircular canal function (canal occlusion or singular neurectomy) was reduced significantly.
As a result of these morphological and clinical observations, our approach to the patient with recurrent vertigo has been simplified. It goes without saying that the patient without recurrent balance symptoms needs no further treatment after a hearing test and MRI of the brain (assuming that these are normal). A Hallpike maneuver is included in the initial exami- nation. Those patients with recurrent vertigo are offered a trial of oral acyclovir (or Valtrex) for 3 weeks.
Examination at the 3-week period will determine the sensitivity of the particular NT virus to the antiviral. If there is no relief of vertigo with acyclovir or valacyclovir, treatment is followed by vestibular tests (videonystagmography and vestibular-evoked myogenic potential) to determine the responsible ear. If these results are abnormal chemical labyrin- thotomy is offered. The patient is offered a choice between dexamethasone (12 mg/ml) or gentamycin (80 mg/2 ml), considering the risk of hearing loss (dexamethasone 0%; genta- mycin usually negligible if used in a single small dose).
ORL 2013;75:91–107 DOI: 10.1159/000348710
Gacek: A Perspective on Recurrent Vertigo
© 2013 S. Karger AG, Basel www.karger.com/orl
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 trans- mission 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 . Usually this recovery is effective leaving no detectable clinical deficit. However, if there is degener- ation of a sense organ (otolith) which normally has an interrelationship with another sense organ (crista ampullaris), the syndrome of benign paroxysmal positional vertigo may appear. Since similar histopathological changes are found in the contralateral TB of patients with these vestibulopathies [27, 47], antiviral treatment may have a role in the prevention of bilateral symptoms.
The use of this class of antivirals in the management of recurrent vertigo contrasts with the disappointing results observed when they were used to treat other viral insults to the labyrinth. The localization of the pathological lesion (sense organ) in sudden sensorineural hearing loss indicates viral entry via the vascular or cerebrospinal pathway rather than intra- neural entry. Therefore, it is likely that the virus has left the labyrinth with the clinical presen- tation of hearing loss, and the goal is to limit or reverse the pathological lesion using steroids.
Finally, since the efferent neural system to both the auditory and vestibular sense organs travels through the vestibular ganglion , associated symptoms may be relieved with anti- viral therapy. Tinnitus associated with enhanced otoacoustic emissions due to loss of efferent olivocochlear neural activity [67–69] may be relieved with antiviral therapy. Failure to improve hearing loss or relieve tinnitus is dependent on the degeneration of spiral ganglion cells or the efferent bundle. Symptoms caused by loss of efferent vestibular system function are not known since the function of this component is unknown .
I’m not convinced a significant amount of vertigo is viral: a lot of vertigo is experienced as positional vertigo or triggered by position, e.g. lying down. That’s not a virus in those cases, surely?. Imho the issue there is due to blood pressure on the ears exacerbated when you lie down or turn over. You can even sometimes turn positional vertigo on and off like a tap.
First they check if you don’t have posititional vertigo, fix it if possible if not the second step was this for me.
That makes sense
Thank you for replying! Sorry that yours has not reversed. After the meds failed to improve anything, I was told that it was progression of the Meniere’s to bi-lateral, the hearing would fluctuate due to the cillie (sp?) dying and eventually go altogether. It did a lot of fluctuating - but remained way below normal (with one tiny spike still functioning in the high range!) to totally gone! And then I woke up one morning and it was back to my previous level - which is not good (I am, after all 70 and have had Meniere’s since I was 20) - but I can cope fine - and have a hearing aid, which I try to remember to wear when I leave the house!! I still have no idea what caused it (like so much about this ‘disease’), but am just hoping that it stays away now.