Epilim (Sodium Valproate)

[WearProtection]

Hi,
I have recently been put on to Epilim (Sodium Valproate) 2 x 100mg per day, for the ever so beautiful (sarcasm), bipolar disorder. Anyhow I have noticed a reduction in my long term Tinnitus, that was caused from hearing loss. At times, it seems to be gone. The only other time it gets anywhere near as quiet for me is if I have a very very long nights sleep. Other things that affect my Tinnitus volume are caffeine and stress. I have been on and off anti depressants for 8 years and Tinnitus for 2. Hopefully this information will help someone with research.

 

[undecided]

Epilim is a typical sodium channel blocker, much like the vast majority of anti-seizure drugs (that is it's main use, treating bipolar was discovered sometime along the way).
And much like the vast majority of anti-seizure drugs, it may reduce tinnitus temporarily for some people - and actually cause tinnitus for some others. Plus, sodium valproate is an ancient drug, has a truckload of bad side effects.
One might be more inclined to use something like Oxcarbazepine, which does more or less (chemically) the same thing but has less side effects and less drug interactions (not that it's safe or anything, just a bit safer).

It's good that it's working for you though, maybe someone with the same cause/symptoms can find Epilim useful.

 

[Danny Boy]

Although the mechanism of action of valproate is not fully understood, traditionally, its anticonvulsant effect has been attributed to the blockade of voltage-dependent sodium channels and increased brain levels of gamma-aminobutyric acid (GABA). The GABAergic effect is also believed to contribute towards the anti-manic properties of valproate. In animals, sodium valproate raises cerebral and cerebellar levels of the inhibitory synaptic neurotransmitter, GABA, possibly by inhibiting GABA degradative enzymes, such as GABA transaminase, succinate-semialdehyde dehydrogenase and by inhibiting the re-uptake of GABA by neuronal cells.

Prevention of neurotransmitter-induced hyperexcitability of nerve cells, via Kv7.2 channel and AKAP5, may also contribute to its mechanism. Also, it has been shown to protect against a seizure-induced reduction in phosphatidylinositol (3,4,5)-trisphosphate (PIP3) as a potential therapeutic mechanism.

It also has histone deacetylase-inhibiting effects. The inhibition of histone deacetylase, by promoting more transcriptionally active chromatin structures, likely presents the epigenetic mechanism for regulation of many of the neuroprotective effects attributed to valproic acid. Intermediate molecules mediating these effects include VEGF, BDNF, and GDNF.

Valproic acid has been found to be an antagonist of the androgen and progesterone receptors, and hence as a non-steroidal antiandrogen and antiprogestogen, at concentrations much lower than therapeutic serum levels. In addition, the drug has been identified as a potent aromatase inhibitor, and suppresses estrogen concentrations. These actions are likely to be involved in the reproductive endocrine disturbances seen with valproic acid treatment.

Seizure-induced reduction in PIP3 levels contributes to seizure-activity and is rescued by valproic acid

 

[Vin]

Sodium Valproate For Tinnitus (Study)

In 1935 Barany serendipitously discovered the temporary relief of tinnitus after lignocaine injection of nasal turbinates. Since that time, other agents known to suppress the activity of excitable membranes have been tried, including antiarrhythmic and anti-convulsant drugs. Among such drugs, carbamazepine has the best documented efficacy in patients with a positive lignocaine test, but is generally unhelpful in unselected tinnitus populations and often discontinued due to adverse effects.

A 53 year old man with viral cardiomyopathy developed severe (60 dB) tinnitus after bilateral temporal lobe strokes. Various treatments including masking and diazepam were unhelpful. Carbamazepine (200 mg nightly) was effective, but was withdrawn due to progressive hyponatraemia (120 mM after two weeks of therapy), followed by the rapid recurrence of tinnitus. Sodium valproate (200 mg twice daily) was also promptly effective in suppressing tinnitus, and was well tolerated until his death due to cardiac arrhythmia one month later.

In part due to its diverse aetiology, pharmacotherapy of tinnitus has met with very limited success. Uncontrolled trials in the French and Japanese literature have indicated benefit from sodium valproate in selected patients, but its use seems not to have been described in English apart from a specialist monograph. Tinnitus loudness and sensorineural pathology but not lignocaine response seem to predict response. Valproate may also differ from carbamazepine in that it seems better tolerated in an unselected tinnitus population. Controlled studies of valproate for this common, often debilitating condition seem warranted.

https://jnnp.bmj.com/content/65/5/803.1

 

[Vin]

NOTE: Much like the majority of anti-seizure drugs, Sodium Valproate may reduce tinnitus for some people but actually cause tinnitus for some others. Tinnitus is actually listed as a rare side effect of Sodium Valproate.