Fawkinchit

All solid points

Any chance of tracking that study down?

https://www.technologyreview.com/s/411201/detecting-subtle-brain-injuries/ pretty good article explaining the lack of precision for white matter damage in MRIs.

http://www.medfriendly.com/periventricular-white-matter.html here is a good site for anyone looking to understand the primary areas being referenced in the MRI results.

It’s possible that hallucinogens cause microangiopathy in the brain cutting of circulation to neurons and causing widespread neuronal loss.

Thanks for posting this! Seems like yours is the exact same outcome as mine. It seems others have had similar reports. White matter abnormalities associated with migraines. I think it is somewhat of a pattern enough to associate with HPPD. And yah obviously they didn’t list your symptoms properly lol.

Sound more like a side effect from the drug possibly. Give it some time to wear off maybe? Keep us updated

He’s obviously extremely busy. He sounds arrogant and ignorant, but he did say he would learn everything he could and admitted he doesn’t know everything. You probably need to leave him a note wth the secretary over the phone as he most likely just forgot.

I don’t see any reason for not monetizing it if it works. If he’s fortunate enough to discover a way to fix the disease he may as well profit from it. The question is, is it really a guide for true and complete recovery to point the brain was before the incident. Which personally I highly doubt.

DMT is why I am here. I had an amazing life with so much potential. It turned it all to complete hell, a flame of torment in my brains senses daily, sleeping was the only time I had peace for months, and waking was my nightmare. Based on that I think you can reason for yourself if it’s a good idea.

"In a survey of sixty five users of LSD, Holsten found fifty users who described post LSD disturbances eighteen months to four years later3." HPPD is wayyy more prevalent than people are estimating among LSD users. http://www.bjmp.org/content/25-years-hallucinogen-persisting-perception-disorder-diagnostic-challenge Its incredible to me that these findings arent more widely published. Hallucinogens are clearly neurotoxic. Holsten, F. (1976) Flashbacks: Clinical and social significance 1 ½-4 years after the first admission , Journal of Norwegian Medical Association; 96: 875-878

It could be possibly theorized, but its not a possibility to be honest because the symptoms would go away int he case of sensitivity. like I already said, receptors in the brain can be modified, by the brain. So your receptors have gone back to normal, you're brain however, clearly is not. This shows that its not caused by sensitivity. So Dr. Nichols is unfortunately inaccurate in his thoughts on what might be the cause of HPPD. No one knows whats causing the visuals right now. There is very little research on it and its unlikely that there will be much primarily because you're dealing with illegal substances. The hard answer of whats most probable is 5HT2A neurotoxicity(through glutamate modifications), so neuronal loss.

Just google it and you will find a couple. Most of them are from single users that report their disturbances to physicians and the physicians document the information/findings. Tbh I dont think there are going to be many due to governmental regulations on the scheduled substances known to lead to HPPD.

For now sedatives work just fine. Anything thats relaxing to the nervous system. GABA agonists of course, like benzos, or natural ones if you can find any. Lemon balm always helped my anxiety and I pretty much carry it with me everywhere I go. I've noticed that cowslip, which is good for sleeping, if I drink it at night the next day my anxiety is not so bad, but cowslip is hard to find so its not the best choice really. As for visuals I cant really comment because mine eventually went away and so did the DR/DP. Unless I drink A LOT of coffee then the DR/DP comes back slightly. I'm working on some other things but nothing that I will post on here as of yet. If I think of anything else I'll let you know.

“Danjoking, you're right. I apologize for my behavior” - TheMythos Yah post it if you want, it’s beneficial to compile all information we can. To be honest though I think everything is pretty much summed up and come to an end as far as the cause of HPPD. If you haven’t read the last couple pages, it’s gone over pretty thoroughly. Not that you’ll agree. Also please do not be rude to productive members like dayum_son.

No not really. For me personally though I don’t think the visual sector of my brain was affected as much as others. My anxiety was the worst by far and still is. I never got halos or drifters. Tbh I would trade you any day for the visual snow vs my anxiety, so be grateful lol. The visual snow also didn’t even set in for a couple weeks so idk, it could have even just been a symptom of rewiring. It also could have been from the scar formation process or the phagocytes cleaning up etc. who knows, but I haven t had any visual snow for years.

I'm just now seeing that. The 5ht2a receptor excitotoxicity is the most probable reason for this. Still its a guess. Its what I outline as the most probable case in my large thread if you haven't read it. The glutamate "acceleration" theory is definitely improbable if you mean it in terms of post drug use. If you mean during drug use you are basically rehashing exactly what I've said in my thread, so its already been covered. Glutamate levels after drugs use will stabilize, so its not a degenerative disease. Also glutamate "acceleration" and receptor sensitivity are not exactly comparable terms. If you mean specifically receptor sensitivity, its hardly likely that its caused by receptor sensitivity, as receptors will increase or decrease in time, or adjust. Its been four years so your glutamate receptors also have returned to normal. The only other alternative that they mention is GABA transmission disruption. Which I suppose could be a case but i dont exactly understand how it could be permanent. Unless like Dr. Abraham stated with GABA interneurons. Also, I think what you may not understand is that the excitotoxicity mentioned is cause for permanent neuronal loss, and it only occurs during the time of drug use.

If I understand this article right, it shows that hallucinogenic effects, are infact, just like I said directly linked to glutamate. Its super hard to understand though. 5-HT2A–mGluR2 Heteroreceptor Complexes Heteroreceptor complexes between 5-HT2A and mGlu2 receptors were demonstrated in cellular models and implicated in psychosis (Gonzalez-Maeso et al., 2008). mGlu2 receptors were also shown to form heterocomplexes with 5-HT2B but not with 5-HT2C receptors (Delille et al., 2012). Three residues at the intracellular end of transmembrane four (Ala-677(4.40), Ala-681(4.44), and Ala-685(4.48)) were essential for the 5-hydroxytryptamine 2A–metabotropic glutamate 2 (5-HT2A–mGlu2) receptor heteromerization and its psychoactive behavioral function (Moreno et al., 2012). Viral-mediated overexpression in the frontal cortex of wild-type mGlu2 receptor but not of a mutant mGlu2 receptor, which cannot heteromerize with 5-HT2A, rescued the behavioral actions of LSD and other related hallucinogenic drugs in mGlu2 knockout rodents (Moreno et al., 2011, 2012). An allosteric receptor–receptor interaction exists in this complex since mGlu2 receptor activation produces an increase in the affinity of hallucinogenic 5-HT2A agonists for the 5-HT2A protomer binding site (Gonzalez-Maeso et al., 2008). A bidirectional receptor–receptor interaction is present since 5-HT2A agonistsreduce the affinity of mGlu2 agonists for the mGlu2 protomer binding site. It is of substantial interest that the allosteric receptor–receptor interactions in these heteroreceptor complexes are dysregulated in postmortem brains from schizophrenia subjects (Moreno et al., 2012; Muguruza et al., 2013). Subsequent work from this group suggests that the 5-HT2A–mGluR2 heteroreceptor complexes make possible a Gq–Gi balance through signaling cross talk, which could be determined by using ion channels in oocytes from Xenopusas markers for Gi/o- and Gq/11-dependent signaling (Fribourg et al., 2011). A drug-induced pattern dominated by high Gi/o signaling predicts antipsychotic potential, while a pattern dominated by high Gq signaling predicts propsychotic potential. In a recent randomized phase II clinical trial (Patil et al., 2007), it was found that an mGlu2/3 agonist prodrug improved negative and positive symptoms of schizophrenia. However, this trial has so far not been confirmed. Selective 5-HT receptor antagonists also produce therapeutic effects, but they are rather weak in contrast to the therapeutic effects of atypical antipsychotic drugs that block 5-HT2A receptors with high potency (Meltzer, 2012, 2013; Meltzer et al., 1989, 2004). However, the biological relevance of the 5-HT2A–mGluR2 heteroreceptor complexes has been challenged since their formation inter alia does not always lead to effects on second messengers (Delille et al., 2012). Also in view of a limited colocation of 5-HT2A and mGlu2 receptors in the brain, interactions of the two signaling receptor systems through functional brain pathways independent of heteromerization probably play a significant role (Delille et al., 2013). Nevertheless, the molecular integration of the signaling in the 5-HT2A–mGluR2 heteroreceptor complexes via receptor–receptor interactions (Gonzalez-Maeso et al., 2008) remains one relevant mechanism for functional interactions according to the available evidence summarized earlier in the text. Future work will determine which of the two mechanisms operating at the molecular and network level, respectively, plays the leading role in mediating the integration of 5-HT2A and mGlu2 signaling of relevance for psychosis and its treatment.

My initial thought, is thats just some guys blog. I'm not saying that we should increase sensitivity, honestly I dont think 5ht2a receptors should be messed with at all. But if you wanted to counter balance serotonin neuronal loss specifically linked to 5ht2a receptors you would want to mildly increase sensitivity to attempt to make up for it, theoretically. I do not however think this would accomplish much. Although.... Ashwaganda might actually be a good choice for anti anxiety. I have no idea if it would work though. Also I believe that antipsychotic drugs tend towards antagonist of 5ht2a. But this is different than increasing or decreasing receptors. Also I think that Dr. Abraham's thoughts on interneuronal loss(I think he just states they're modified or something though) associated with GABA production is accurate as well. So increasing GABA mildly would be a good idea as well.

I could be wrong but I think you would want increased sensitivity. In the case that I make, which could eventually turn out to be wrong but I’m sticking with it from here on out, the Axons simply are just gone, so I honestly don’t see modulating 5ht2a receptors helping very much either way. You could try it but if the axons aren’t there it will do nothing lol. Basically you’ll need neurogenesis, and even that may have limitations.

5-HT2A receptors are found postsynaptically to serotonergic neurons, and are particularly concentrated in the frontal cortex. 5-HT2Areceptors are also found in high density in the claustrum, a region that is connected to the visual cortex, in parts of the limbic system (i.e., amygdala and hippocampus), and in the basal ganglia (Table 15-2). In the cortex, the 5-HT2Areceptor is located on local GABAergic interneurons, as well as on pyramidal projection neurons, which are known to be glutamatergic. The amygdala is probably the area effected causing severe anxiety. The claustrum maybe is the area effected causing visual symptoms?

I can add too that in the case of Risperodone, a 5ht2a inverse agonist, and other anti convulsion medications which are 5ht2a antagonists there is a correlation with palinopsia. Palinopsia being obviously common with HPPD, the most probable reason being, that the 5ht2a specific neurons that underwent glutamate excitotoxic apoptosis, are now gone, and therein laying a lack of 5ht2a input, which would be similar to that of these drugs, being inverse agonists and antagonists. So this gives even more credence that HPPD is caused by 5ht2a induced glutamate excitotoxic apoptosis.

HPPD is definitely not a degenerative disease. Unless you continue drug use. As long as you aren't doing drugs still your glutamate levels have normalized. Also Im not seeing anything on the wiki about palinopsia being directly related to 5ht2a receptors.

You've been posting this for weeks now. Why not just post it when you post it.....

Sounds like pretty much the best information he could have gave you for this condition. Theres really not anything else they have to offer. I dont completely agree with his stance on benzos if people feel their anxiety is bad enough that they need them. But there are alternatives in herbal medicine that would work as well. Hes right about alcohol too, but if you dont want to consume it thats not bad either. If you are trying to limit even minute amounts though that are in other foods its a bit unnecessary, as you should know, your body produces some ethyl alcohol in its own metabolism.