I am not sure what is and is not accepted on this forum. May I include random excerpts from an online article? If yes, here are some. If no, please let me know.
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Below are random (not in order) excerpts from this larger article:
http://www.tampabayhearing.com/vestibularneuritis.php
"Our clinical experience is that among those patients with chronic vestibular neuritis symptoms, a high percentage, as R Gacek suggests, improve and stay improved on long term antivirals." (more below)
Recurrences of acute viral vertigo had been thought to be uncommon, generally with an incidence rate in earlier publications of under 5% with follow up of under 10 years.
[33],[34] A more recent study found vestibular neuritis to have a nearly 11% recurrence risk by telephone interview and benign paroxysmal positioning vertigo, often a sequela of vestibular neuritis, had a greater than 15% recurrence risk.
[35] In the same study, recurrence of vertigo symptoms of any type was at a 26% incidence suggesting that some degree of recurrent symptoms is not rare at all and that fits with our clinical experience.
The cause of chronic,
recurring vestibular neuritis is thought to be viral and relatively recent postmortem pathology supports that notion.[42] Another study shows that the vestibular ganglion and vestibular nerve are commonly colonized by Herpes simplex.[43]
For chronic and recurring vestibular neuritis and its derivative disorders, Meniere’s disease and benign paroxysmal positioning vertigo (the latter has more than one etiopathogenic pathway), there is evidence that long term antivirals are effective but dosage is not specified.
[46],
[47] The notion that recurrent vestibular neuritis is Herpes-Simplex-associated is growing.[48] A literature search on PubMed with “vertigo herpes” found literally dozens of references, many of which conclude that neurotropic viruses like HSV likely play a role.
[49],
[50],
[51],
[52] Many other references argue for and against as would be expected.
Viral reactivation:
Newer studies are now elucidating a mechanism whereby re-activation of virus in cells colonized by HSV is controlled by a complex mechanism of CD8+ effector T cells with specific gamma interferon.
[53],
[54] Another study looked in detail at the glycoprotein antigens produced as HSV reactivates in neural tissue, antigens which are specifically recognized by CD8 T cells which influence these CD8 cells to participate in the inflammatory response to HSV reactivation.
[55] Evidence suggests that low level production of a specific HSV glycoprotein prior to viral DNA synthesis is what keeps HSV specific CD8 T cells in the infected tissue and activates them to respond, preventing viral reactivation.20,
[56] Stress-induced glucocorticoids appear to suppress these HSV specific CD8 T cells and may play a role in re-activation of latent HSV.
[57],
[58] In addition, experimental suppression of HSV specific CD8 T cells induces reactivation of HSV infection.
[59] It also appears that CD4 T cells are important in HSV clearance.
[60] However, the local control of HSV in neural ganglia appears mostly dependent on a local population of HSV specific CD8 T cells, apparently independent of blood circulating CD8 T cells.
[61] The latter implies that peripheral antibody titers are not likely to change with flare-ups, especially if not severe enough to cause major loss of neural tissue. Most interestingly, shingles, Herpes Zoster/Varicella related disease, appears to have a quite similar CD8 T cell relationship within the ganglia of affected nerves.
[62] Of course, shingles is a viral neuritis resulting from reactivation of a latent Herpes family virus as is postulated to occur from Herpes Simplex for both vestibular neuritis and Bell’s palsy. Our experience is that all patients who have vestibular neuritis whom we have checked have positive VZV IgG titers but not all have positive HSV IgG titers. An interesting question is whether the causative virus might sometimes or even often be VZV in at least some of the more severely affected persons. Indeed, some researchers do believe that a correlation between the influenza type B, Coxsackie B5, and VZV plays a role in vestibular neuritis.
[63]
Much more is known about how the Herpes family viruses interact with the immune system and neural tissue such as the vestibular nerve and other cranial nerve ganglia that cannot be reviewed, here.
Our clinical experience is that among those patients with chronic vestibular neuritis symptoms, a high percentage, as R Gacek suggests, improve and stay improved on long term antivirals.
Our clinical experience mirrors that of R Gacek and is that a high percentage of patients with chronic or recurring vestibular neuritis induce remission of symptoms on high dose valacyclovir; that fewer do so on long term acyclovir and as dose drops below 500 mg valacyclovir po TID, the recrudescence rate goes up. In our experience, about 30% of patients relapse within several months after stopping antiviral therapy. It is clear as well that some patients never attain suitable relief of symptoms, that many but not all of them have some degree of permanent documented vestibular impairment, and that psychological factors and motion intolerance are common in this group of patients.
