Exploration of possible mechanisms which produce tinnitus

[Working_Class]

I've been experimenting with psychedelics and nootropics for quite some time now, and I have been finding a trend during which substances such as base triptamimes produce tinnitus for and non-specific duration after administration, and some nootropics also produce this effect for an undetermined amount of time after administration.

Looking into the matter has illuminated some possible mechanisms by which this mysterious phenomenon manifests.

Below is an article which examines the relationship between excitatory and inhibitory neurotransmitters and the development of, or rather just one of the postulated mechanisms by which this condition develops.

Current view of neurotransmitter changes underlying tinnitus - PMC

www.ncbi.nlm.nih.gov

Anecdotally I believe it is significant because a number of the drugs that I had been experimenting with increase the expression of glutamate, and possibly cause downregulation of inhibbitory neurotransmitters / receptors, and or upregulation of excitatory neurotransmitters / receptors.

Some drugs that and possible items I've found that cause tinnitus are;

9-methyl-β-carboline
Bromantane
Electronic adaptors
Many electronic devices in general

Some drugs that I've found cause tinnitus and HPPD are;

Methylallyltryptamine
Dipropyltriptamine
LSD / analogues

This isn't something that really is causing me too much distress or anything. It's just an interesting thing to consider when experimenting. I know a lot of people experience similar side effects and this could possibly be bringing science one step closer to understanding just one of the possible mechanisms by which this condition might manifest. Which may also help produce hypothesis about how to treat the condition.

9-methyl-β-carboline is said to produce an increase in dendritic spine numbers / complexity, inhibbit GABA receptors, upregulate DA neuron expression ect ect. There is quite a body of evidence to suggest that various hallucagenic compounds have similarly complex actions which produce varying degrees of synaptogenesis, which may disrupt the balance of excitation / inhibbition in the brain. This may also help elucidate as to some of the "why / how" these drugs possibly affect cognitive processes for such a duration after administration. Personally, I feel like a more complete person with all the changes that have occured in my personal neurochemistry. I have a sharper memory, I notice things I wouldn't have otherwise noticed, I can read for pleasure for one of the first times in my life, and I enjoy math and have a much shorter attention span for things like videogames. Part of it I'm sure is just getting older and seeking to use time productively, and knowing we only have so much time to experience novelties more than one time in our life. This realization has made learning much more of a priority on my horizon. But back on topic..

For science, I feel like this consideration is worth exploring from a laboratory setting, but also in terms of personal anecdotes of other researchers in the community. More corroboration leads to better understanding when information is compiled over time, although I have no expectation that this post will be taken very seriously, these are still interesting things to consider when connecting neurochemical dots in experimentation, pathology, and pure intrigue. Scientific discoveries employ information and experiences from many corners of the world, in this corner we have anecdotes. Nothing more

I suppose as a side note, another type of disruption in neurotransmitter concentration could be illustrated by the abuse of benzodiazepines and the cessation of there after producing brain zaps and seizures. It's just another system in dissarray after pharmacological disruption. The higher the dose and frequency of the disruption, I'm fairly certan we can suggest the more adverse and far reaching the side effects / consequences might be.

Yet another solid example can be the withdrawal of an opioid after extended use. Writhing in pain in withdrawl is no mystery to me, especially going through fentanyl withdrawal after not bringing enough to a regional strongman competition and finishing the show. The drive back to my province was extremely uncomfortable. I've experienced all of these imbalances and they all have a slightly similar, yet unequivocal uniqueness to each of them.

Again, even the disruption in HTPA axis after cessation of testosterone and or other AAS.

I believe there is an obvious pattern forming from this extensive process of self destruction and experimentation. Although the process has been somewhat enjoyable.

TLDR;

With every high, there comes a low. For every to, there is a fro.

 

[Blowmonkey]

I was researching this years ago when I first got it, instead of drugs that caused it I searched for drugs that helped against it. I was so fucking bummed out I wasn't able to buy memantine easily back then without a lot of trouble, it was just in trial and approved for tinnitus around that time in france or something. It kinda helps, lot's of things kinda help, nothing will really cure it.

The underlying mechanims behind it are extremely complex (what isn't when it involves the brain), but downregulated dopamine systems and overexcitability from glutamate was what I was pretty sure of 10 years ago. I really don't like researching it further, I kinda glanced over this article, lol sorry, because there's nothing you can really do about it anyways.

I posted about this in another topic pretty recently, but if I notice mine getting worse I always take a magnesium tablet, some alpha-lipoic acid and a multivitamin (with at least enough A, C and E) apparently that helps, according to studies (if you want me to look for them I'll do so, not now though).

I went through some experimental treatment with a blood thinner (god knows which one, I can't recall) and high dose iv prednisone a week or so after I got it, because I wasn't taking it no longer, help in this country is non-existant regarding this, some quack in germany thought it could help, it also kinda did. Wether that was placebo or not, I don't care, it took care of some the intensity, decibels went down and instead of an extremely high pitched screeching beep, it went to an old constant television beep mixed with a pulsating metallic hiss, the kind of noise when you hit a cymbal, so annoying.

I mean, you explain it. Why is amitryptaline the only thing that really stops it all-together? Believe me, I've tried a lot.

The link between tinnitus and hppd/visual snow also is interesting btw, I stumbled upon this not all too recently, some guy doing a tedtalk for a class


Basically just eye tinnitus. Anyways, lol, I don't think my post was really helpful, but not quite sure what you're trying to get at here either.

 

[Working_Class]

This is interesting corroboration. I had just gone on a recent DXM trip that silenced it for the duration of the trip.

It doesn't bother me, but the way the visual snow, or ringing manifests itself is somewhat interesting to consider. And that memantine helps would also make some sense, as dissociative drugs cause a sort of synthetic discord in the brain, by inhibbition of NMDA / AMPA receptors, which could help quiet down overexcited systems that have been upregulated to compensate for a pharmacological disruption which regularly occurs.

The auditory pathway passes from the vestibulcochlear nerves to the medulla, then into structures in the midbrain before passing on to the thalamus, then axons extend into the auditory association areas of both hemispheres of the brain. The brain stem, if I remember correctly is where the NMDA receptors are abundant. This would connect some dots for sure. But it's still just purely playful speculation on my end.

I wonder if anyone has any experience using dissos to help ease the symptoms of benzo withdrawal? Not that I encourage that as a particular experiment to undertake.

Also, as another anecdote, I was using etizolam pretty much 5 days a week for probably around 5 months (with a few 7 day breaks inbetween just to make sure I could still sleep without it) to help me sleep and ran out while waiting for more. During the first 7 days off, on about the 7th day I engaged in the first LSD trip my girlfriend and I had ever gone on together. It was her first time, and we had a lot of fun.

But for a week afterward I had a headache seemingly around the central sulcus area of my brain, and I experienced some post trip brain fog that left me wondering if perhaps a simultaneous withdrawal from etizolam coupled with a 150 mcg LSD trip was maybe not the smartest thing to engage in. But, we had planned the trip for some time and I wasn't backing out.

Possible causes being, abruptly withdrawing a drug which produces an inhibitory effect on the CNS while simultaneously introducing a strong psychoactive stimulant could have caused some excitotoxicity.

It's possible that conflicting situations of upregulation trying to correct itself Via upregulation of glutamate because of regular dosing 1 - 1.5 mg etizolam, and concurrent withdrawl (slept shitty for a few days, nothing crazy). Then introducing LSD, which is known to cause an increse / flood of excitatory neurotransmitters which cause the cross talk of various regions of the brain, caused some sort of damage. Who knows.

I'm not really getting at anything really. Just making some vague observations based on personal experiences. And I do appreciate the input from others, as it does add some different takes on the same sort of situations.

I have planned a microdose LSD / DXM day some time in the next 10 days. Dunno where that fits into this conversation, but I'll definitely have this stuff on my mind as I go into it. It's just fascinating to consider all these interesting systems trying to sort themselves out, and the interplay they have with one another amidst our continuous xenobiotic augmentation of them.