Antidepressants (SSRIs, SNRIs, MAOs, TCAs, TeCAs)

50% reduction. I have no idea if it's permanent, as I don't have a placebo clone of myself.

Why was his video distressing? Was it the 25-minute one where he discusses the three pathways?

 

I apologize for making you repeat yourself, @Nick47. I'm sure you've been asked before, but what was the breakdown of the cocktail?

 

Yeah, it was the 25-minute one.

It was distressing for two specific reasons:

I already knew beforehand it was a network disorder. Still, Dr. Dirk De Ridder says if you attack it with a selective drug and hit one part of the network, the signal travels around and finds other ways to transmit itself, so it is still perceived by your brain after a while. That's why a cocktail is recommended to abolish the entire network. Perhaps this is also why Retigabine lost effectiveness in many users after a while.

The second reason is specific to the kind of tinnitus I have; he mentions neuroinflammation, the neurological changes it brings, and specific epigenetic changes brought on by drugs or other stuff, and details potential treatments like taking antioxidants. The same things are discussed on withdrawal and visual snow syndrome forums. Hence, I'm not a stranger to these concepts, but with visual snow syndrome and tinnitus, those suggested treatments have limited to no efficacy based on the users who tried them.

There's much more I could say on this subject alone, but I don't want to hijack the thread.

Pretty sure that the HCN2 drug won't be for me because it does not cross the blood-brain barrier, and the Kv7 drug (my last hope...) will have limited efficacy, if it has any.

My tinnitus these days is heavily somatic and can be influenced by jaw and neck movements. It gets loud when I press on my chin, but it is not tonal at all. It sounds like an electrical hiss and feels like it is coming from the back of my neck. It is close to the left ear but can be heard in both ears. It likes to travel around depending on which ear I sleep on.

The way our brains work has been altered. Nothing is coming out to reverse these changes, and the upcoming drugs will have limited efficacy (perhaps none), which is why I'm distressed.

 

My taken-as-needed cocktail:

• 1 Deanxit or 5 mg Prochlorperazine
• 300 mg Gabapentin
• 0.75 mg Clonazepam
• 8 mg Betahistine

My daily cocktail:

• 22.5 mg Mirtazapine
• 300-600 mg Gabapentin
• 600 mg Alpha-Lipoic Acid

Dr. Dirk De Ridder's daily cocktail:

• 0.5 mg-1 mg Clonazepam
• 1 Deanxit
• 2 mg Aripiprazole
• +/- Cyclobenzaprine
• +/- 5 mg LDN

The above for 2-3 months, then every 2 days, then every 3 days, then the lowest maintenance dose, along with some sort of electrical stimulation + CBT.

Dr. Hamid Djalilian's daily cocktail:

• 10 mg - 50 mg Nortriptyline
• Topiramate
• 400 mg Magnesium BID
• Vitamin B2
• +/- Gabapentin
• CBT + Sound Therapy

Dr. Abraham Shulman's daily cocktail:

• Clonazepam
• Gabapentin

Have hope. Retigabine probably worked for some because it was a cocktail in itself. This is part of why I think selective Kv7.2/3 channel openers will fall flat. I know some people have tried them to no effect and had the same side effects as Retigabine.

Flupentixol is the most important part of Deanxit. Dopamine is involved in perception, and Prof. Rauschecker says it is involved in the gating.

I think future drug treatments will involve a cocktail anyway, like for many diseases, unless HCN2 drugs are highly effective.

In fact, most diseases are treated with several interventions anyway.

 

I'd take it with a pinch of salt. He makes unfounded comments about Dr. Shore's device that aren't accurate or fair, in my opinion, and almost dismisses her idea of bi-modal stimulation as a treatment. Yet he and his buddy from another university are putting together something that looks like it was made for a sixth form electronics project based on the same principle.

I wouldn't even call the War on Tinnitus a mind map of ideas, more a brain fart.

Aripiprazole is a dopamine antagonist, and Prof. Rauschecker stated that dopamine is responsible for gating. So, is it the case of too much dopamine, then? Or is it a case-by-case experiment trying both agonists and antagonists to see what happens? Mucuna is a proven natural supplement (studies done) for increasing dopamine.

 

Did they get any of the visual symptoms? Was the product official or compounded?

I can't do cocktails that act on the serotonin, dopamine or noradrenaline. I'm kindled. I get paradoxical rections on most drugs now.

I was banking on the NKCC1 and Kv7 stuff, but the later papers and developments suggest they are dead ducks.

It seems like there is no way out for me.

 

Update on the Amitriptyline 10 mg per day:

After five days, I can report no change in tinnitus; side effects appear to be a disrupted gut and a left-sided headache with some minor irritation in my left ear, similar to after receiving the COVID-19 vaccine. Hopefully, it is a good sign that there is irritation, which will lead to healing.

 

Do you think there are risks in taking Deanxit alone without Clonazepam? I also got it prescribed by Dr. De Ridder but I am a bit scared about the drug given the number of countries that have decided not to market it. What do you think helps you the most between the two?

 

Most people are fine on Deanxit alone. The cocktail just works better, I guess. Many diseases have a combination treatment. Dr. De Ridder prescribed Aripiprazole, too, but I don't have any of that. It was the lowest dose, like 2 mg. Try it for a month and see.

You could take 0.25 mg of Clonazepam at night if you are worried about side effects.