Fawkinchit

If per say that the neurons are not lost, then the mitochondria can repair and replenish. Unfortunately its just not known whether or not we have lost neurons.

https://translate.google.com/ Just type it in to here.

a single lesion, or microlesions? Can you possibly post the actual results?

Ok, yah, that's pretty consistent with some form of HPPD then.

I'm guessing you have already done physical exams to rule out completely all physical problems with the eyes that can cause these symptoms correct? I could see these issues making it difficult to play Modern Warfare lol.

Best I could do honestly is I would have to see the MRI, or MRI report to evaluate what was said. "Found something not organic" is extremely vague and could be so many things on an MRI. If you have past drug use, have HPPD like symptoms, you likely have HPPD. If you have micro hyperintensities on your MRI finding that is typically found in about 25% of HPPD patients.

Best suggestion is to just explain that most research shows benzodiazepines as the only safe treatment for HPPD. And yes personally I wouldn’t try the Hydroxyzine. If the doctor still won’t prescribe benzos just move on to one that is more understanding.

I completely agree 100% with what Jay is saying. Especially with the Adderall, if you feel you have HPPD you should definitely remove at the very least that, as I would most likely assume it would exasperate symptoms. The Vistaril is an antihistamine, I'm assuming he prescribed it cause sometimes it used for anxiety?? But its a pretty poor choice. Drug manufacturers love having multiple reason for prescription of their drugs so they try and get it approved for any condition they can, regardless of whether it works significantly or not. For example metformin for "weight loss" lmao. Main one to stick to on that list if your symptoms are really bad is the klonopin/benzodiazepine Also stop all drug usage.

Damn bro, sorry about your condition. I think what you have just described might actually be the most extent symptoms I have come across. You have my deepest sympathies, I wish humans were more understanding, but they are not. I hope you stick around and post here more. We're all trying to find a better solution to all this.

Probably one of the fastest, easiest, and efficient ways is simply vitamin e, add in something like rose hip tea for flavonoids and vitamin c. eat fruits and veggies. wheat germ oil. etc etc. Theres all kinds of things. you can even just take grape seed extract.

Its probably HPPD, if you had pretty near immediate symptoms following drug use. Sometimes it can get worse for a while after, and then usually halts at some point. If its getting worse still try to up your antioxidant profiles. Its normal for HPPD patients to have no noticeable physiological defects, as far as scans are able to tell thus far.

To explain simply, antioxidant profiles in people who get HPPD are probably lower, that's essentially my theory. Glutathione appears to be specific in this case according to the studies. In the studies listed, supplementing antioxidants reduced neuronal loss. So basically, neuronal loss is going to be dependent on dose, duration, and antioxidant levels. Its possible for people to have deficiencies in antioxidants, its actually the cause of scurvy, they lack vitamin c. Basically it appears to be a possibility that people who get HPPD, could possibly have lower or maybe even severely deficient levels of antioxidant profiles. Hence the reason that some get HPPD, and others appear not to get it. However, in both cases they both will have neuronal loss, however in the low antioxidant people, the neuronal loss will be more profuse. If that makes sense. It also will depend on dose and duration of use. Once the damage is done, its not something that the antioxidants can repair as far as I know in medical literature. They're not a treatment, but rather a preventative measure.

Yah absolutely, however, as intricate as the brain is, I would assume there may be challenges at getting near the same architecture, or it may even be impossible to get the same architecture, especially if long distance neurons are affected. Basically, there can likely be a significant degree of recovery, but if the architecture doesn't return to complete normal, there will likely still be residual symptoms that are mild and light, or even be scarcely noticeable until say, drinking a lot of coffee. Ultimate goal is to find a way to recover to exact architecture. Neurogenesis in my opinion is the easy part.

Je pensais que tu faisais une FMRI

Ok, so it would appear that its quite likely that the glutamate release is activated by 5ht2a/5ht receptors, and would pretty much solidify the neurotoxicity or any 5ht2a agonist, specific to interneurons. Here is the study that basically shows the link between glutamate and 5ht2a. https://www.nature.com/articles/1395430 So, I think everything really came around and connected everything together finally. 5ht2a agonism increases glutamate, we know already glutamate storms are neurotoxic. The neurotoxicity is mediated through reactive oxygen species leading to mitochondrial DNA damage/failure, which is going to cause them to signal apoptosis, leading to intraneuronal loss. Interneurons are regulatory neurons and without their involvement excitatory neurons will act unregulated giving the symptoms of HPPD. The only thing that can show otherwise at this point is if say classical hallucinogens like LSD or DMT etc do not show the same release of glutamate. But based on the study posted here I think its likely it will be the same. What some people may be wondering then is why do some not appear to get HPPD and others do, but in this case the answer is simple. Because eventual neuronal loss is caused by reactive oxygen species its going to be mediated through various antioxidant profiles and according to one of the studies it looks to be glutathione, people who do not appear to get HPPD realistically are still probably losing neurons, however in the case of people with HPPD they likely have altered glutathione levels, which can occur for various reasons. Well I'll try and add some positivity for anyone reading this, cause even after studying this for 10 years now this is a pretty hard read. The positive side is, that interneurons as far as I understand are specifically close proximity neurons and have short connections, so recovery under stimulation of neurogenesis is likely to be higher than say if long distance axons were damaged/lost. To say that other neurons in the surrounding areas are not affected, I'm not sure, but when I have time I will look in to the possibility. I think though this most likely explains the cause and etiology of HPPD. Maybe we can get the information stickied so that people understand what it is that these compounds do, and will help to prevent the future use of them. It explains as well why benzodiazepines assist the best in the condition but do not mute the symptoms entirely, is that there are no receptors/synapses/neurons to exhibit GABA for excitatory neurons, and it is probably acting on downstream neurons that still have their interneuron connections. Big thanks to @MentholFlavoring for find those studies.

It seems as though it still may not be the case as the actual neurotoxicity is still via glutamate, but the glutamate release requires the serotonin receptors. So still not solid. normal hallucinogens as far as my understanding goes do not cause increases in glutamate. https://pubmed.ncbi.nlm.nih.gov/25936514/

Damn dude, that's probably it. I mean, its true, they don't state the dose, its pretty important information. I will see if I can contact any of them to find out. Thing is though it shows that over stimulation of the 5ht2a receptor is the specific cause of the neuronal loss, via free radical production. "Cortical neurons can be broadly divided into two classes: interneurons and projection neurons. The interneurons are a varied subgroup of cells, which occupy many different cortical layers and largely utilize GABA as a neurotransmitter." So that's probably it, see there was a study that I found once that showed DMT had no notable neurotoxicity on neurons in vitro, but they were normal neurons if I remember correctly. Maybe I will have to find the study again. But these are specifically cortical, and I bet that's not what they used in the other study. I will try and find it.

It appears its possible https://www.frontiersin.org/articles/10.3389/fncel.2017.00423/full https://www.frontiersin.org/articles/10.3389/fncel.2022.827628/full Also more info on interneurons https://www.sciencedirect.com/topics/neuroscience/5-ht2a-receptor https://elifesciences.org/articles/66960

If I can find a way to culture Interneurons it would be simple to test the potential for toxicity of hallucinogenic compounds. And also test for potential neurogenesis. I already have the equipment I would need I will just have to figure out a way to culture them.

Wow thank you for posting this, this is a great find! I was trying to get around to making a post and some of it was going to be in regards to interneurons and the subtypes, and on how hallucinogens cause depolarization of these neurons. I was going to explain that I think Dr. Abraham may very well be right in his hypothesis of interneuron loss. So much so that I wonder if he knows that it is, and just doesn't want to say due to the overwhelming emotions it can cause patients with this condition. Anyways I think this link may very well be the answer we have been looking for. Great job man! And thank you. The one thing that I see is that it does say its mediated through 5HT2A, I'll have to look up whether or not MDMA acts as a 5HT2A agonist like hallucinogens, in which case I suppose its likely the end of this research. The other article I posted is just some interneuron regeneration stem cell therapy. I can't remember at this exact moment why I have it saved with the other link, but thought it may be encouraging to post. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2855184/ https://stemcellsjournals.onlinelibrary.wiley.com/doi/full/10.1002/stem.3252 Edit: I reviewed the article a little and it states "Recently, it was shown that MDMA increases extracellular glutamate concentrations in the dorsal hippocampus, which is dependent on serotonin release and 5HT2A/2C receptor activation. The increased extracellular glutamate concentration coincides with a loss of parvalbumin-immunoreactive (PV-IR) interneurons of the dentate gyrus region." It looks like its primarily the glutamate that causes the parvalbumin interneuron loss, and that it somehow is dependent on 5HT2A. So it still doesn't exactly show that hallucinogens cause interneuron loss through 5HT2A receptor agonism. 5HT2A receptor agonists(Hallucinogens) method of action is the depolarization of these interneurons as it might appear, allowing for other sensory neurons to become overexcited. As far as I understand it at least. So I would have to say its still not definitively neuronal loss yet. But I think that interneurons are a avenue to go down, to further understand the methodology of the compounds and their effects on the central nervous system.

Its been almost 2 years since he posted lol.

You could most absolutely make your current condition worse. Its astonishing to me that you are still using drugs. Please stop smoking weed or doing any other drugs. I know a guy that had light or mild HPPD, very mild, and tried a drug only once, and now he has terrible HPPD.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4208100/ just posting this here for a future post so I dont lose it.

Thanks man! Means a lot to me

I forgot all about this thread, I apologize to anyone I may have offended, my attitude was rude and uncalled for, I should have been more polite.