Discussions that mention acyclovir

Inner Ear Disorders board

Hi John,

Welcome to the board!! After reading your story I was wondering if it is in fact just a nasty case of VN. It has been hypothesised that, in some, VN may be caused by the herpes virus. In your case this might explain the recurrent attacks and the viral feeling you have before the attacks. I'm a herpes sufferer too and know the feeling although I don't get full blown attacks like you describe, although I do feel much worse when an attack is on in terms of disequilibrium and mild depression.

If this is the case, I'm wondering if a daily antiviral med might work for you such as acyclovir. Or apparently St John's Wort also reduces herpes attacks.

[QUOTE]Curr Opin Neurol 2002 Feb;15(1):5-10
Magnusson M; Karlberg M
Dept of Otorhinolaryngology, Lund University, Sweden

Peripheral vestibular disorders with acute onset of vertigo

Disorders of the vestibular nerve and end organs are the most common causes of vertigo. In acute vestibulopathy, suspicions of the activation of herpes virus infections as a causative agent are increasing, but no reports on the treatment of such infections are yet available.

or this....

Enhancement of the eighth cranial nerve and labyrinth on MR imaging in sudden sensorineural hearing loss associated with human herpesvirus 1 infection: case report

AJNR Am J Neuroradiol 2001 Aug;22(7):1380-2
Lavi ES; Sklar EM

The case of a 61-year-old woman who presented with herpes labialis, subclinical meningitis, and sudden onset of bilateral sensorineural hearing loss is presented. Contrast-enhanced MR imaging showed marked bilateral enhancement of the intracanalicular portion of the eighth cranial nerve, right cochlea, and left vestibule. Polymerase chain reaction was positive for human herpesvirus 1 obtained from the cerebral spinal fluid, which suggested the diagnosis of viral neuritis.
Hi John,

Yes, it might be worth a try to have a daily acyclovir just as a trial to see if the attacks stop. A good time to experiment given the frequency of your attacks. Can you correlate attacks with stress at all? Stress of course, can trigger a herpes attack. Another thing might be to take acyclovir or famvir when you feel an attack coming on to see if it stops the attack or possibly reduces the fallout.

All the best....Scott
Hey again John,

I just checked out the link you gave to the NEJM article. It is an excellent paper and very current! I missed this one. Very strong study too as it was a prospective, randomized, double-blind trial. I basically gave you info above that you might have already seen in this paper as it also addresses herpes as a cause - DOH! Thought I'd write down some of the highlights for others to see of these findings as it is the most up-to-date info on VN treatment so far.

[QUOTE]Methylprednisolone, Valacyclovir, or the Combination for Vestibular Neuritis
M Strupp et al
N Engl J Med, Jul 22 2004, 351(4) p354-61

Background: Vestibular neuritis is the second most common cause of peripheral vestibular vertigo. Its assumed cause is a reactivation of herpes simplex virus type 1 infection. [It] has an incidence of about 3.5 per 100,000 population. Currently, a viral cause is favoured. The evidence, however, remains circumstantial. Indications are that the vestibular ganglia are latently infected by HSV-1, as are other cranial-nerve ganglia. Recovery after vestibular neuritis is usually incomplete....in one study, caloric responses normalized in only 42 percent in a study of 60 patients. Despite the assumed viral cause of vestibular neuritis, the effects of corticosteroids, antiviral agents, or the two in combination are uncertain.

Results: Of the 141 patients, 38 were randomly assigned to the placebo group, 35 to the methylprednisolone group, 33 to the valacyclovir group, and 35 to the methylprednisolone-plus-valacyclovir group. The number of patients who had complete or partial recovery was 8 of 30 in the placebo group, 22 of 29 in the methylprednisolone group, 10 of 27 in the valacyclovir group, and 22 of 28 in the methylprednisolone- plus-valacyclovir group.

Conclusion: Treatment with methylprednisolone alone significantly improved the long-term outcome of peripheral vestibular function among patients with vestibular neuritis, whereas treatment with the antiviral agent valacyclovir did not improve the outcome. The combination of these drugs was no more effective than methylprednisolone alone. Replication of HSV-1 in the vestibular ganglia may conceivably have already occurred by the time the antiviral drug was initiated (thus it was not effective in this study). 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 temporal bone, which is also assumed in Bell’s palsy. The anti-inflammatory effect, which results in reduced swelling, may explain why treatment with corticosteroids results in improvement in both disorders.

There was something written in this paper that I didn't like reading however. It said the following: "On the basis of the incidence of this condition, a substantial and permanent unilateral dynamic deficit of the vestibuloocular reflex, which cannot be compensated for by other mechanisms, develops in approximately 4000 people per year in the United States alone." I followed up the reference for this comment which said the following in its abstract (I can't get the full article yet unfortunately):

[QUOTE]Vestibular compensation: a review of the oculomotor, neural, and clinical consequences of unilateral vestibular loss.
J Vestib Res 1995 Mar-Apr;5(2):67-107
Curthoys IS; Halmagyi GM - University of Sydney (my university!!)

Vestibular sensory input is just one sensory input involved in the control of functions such as gaze and posture. The recovery of gaze and posture control after partial or complete unilateral loss of vestibular input is reviewed. The relatively rapid and apparently complete behavioral recovery after unilateral vestibular loss was once regarded as justifying vestibular compensation being used as a text-book example of plasticity in the CNS. This review emphasizes how false that impression is: Detailed examination shows that vestibular compensation is not a single process that recovers completely at a rapid rate but is made up of a number of subprocesses that recover to different levels and at different rates. In some subprocesses there is very modest recovery; in other subprocesses there is probably substitution of other sensory input for the affected vestibular input. It also seems that in some instances new behavioral strategies appear to be learned to allow gaze and posture control to operate as if normal. Recent evidence concerning the physiological and pharmacological mechanisms underlying vestibular compensation is reviewed.

Hmmmm....can't see anything in there that says total compensation is unlikely but rather it is obviously not a simple and linear process at all, and don't we know it!!

Sorry this has been a such long post but it's info we all need to know about. Crazy Labyrinth, maybe you can ask London about the methylprednisolone treatment.

Scott :cool: