Fawkinchit

He definitely has developed a form of HPPD. Please tell him to stop using drugs.

It will definitely improve. The fact that your episode was induced by Cannabis would lead me to believe that you will probably recover better since its not such a hard hitting compound neurologically speaking. To say how much youll improve no one here will be able to tell you. You will have to wait that out and see. Definitely do not try and smoke weed or any other drugs even if it improves.

Had it for 6-7 years now. Definitely isn't as bad as it used to be. It definitely improves. My visual snow even went away. Does it still affect me daily? Yes, absolutely. Definitely not the same person that I used to be.

I'd like to add briefly that if anyone would like to continue the research. Basically at this point finding a way to repair axonal tracts is the biggest impediment. Also finding information on axonal tract formations. Growth cones. Etc...

Basically if you go through this study it vigorously goes through the steps of showing how MDMA and other amphetamines cause not only axonal damage specifically related to serotonin receptors, but also axonal degeneration(loss). So at this point I'm going to stand my ground and say that HPPD is definitely and unarguably a disease/disorder caused by excitotoxic axonal and potential neuronal degradation. The losses are not seen in MRIs because the damage and losses are selective/scattered. The losses are not recoverable involving axonal degeneration and neuronal death. When I get a chance I'll try to elaborate on things more proficiently, but at this point I'm pretty much done with my research. Ill try and go over the areas that are effected, how, why, and why even with neurogenesis its an incurable disorder, though might be slightly improvable. Also I hope that we can get a sticky filled with proper information warning people of the dangers of using hallucinogens and other drugs. There are a lot of people that will argue that these compounds do not cause neuronal damage, and they are very entirely wrong, I believe everyone has the right to accurate information on this matter and hope to help them not make the same terrible decision that I did.

I've taken them before and haven't had any adverse effects. Its not guaranteed to effect you the same. Basically though codeine breaks down in the liver to morphine(heroin). Only thing it does to me is seems to infer depression, so personally I dont like it.

Selective neuronal loss, as in one of the studies that I have posted in my very large thread clearly shows that now all neuronal loss is shown on MRIs. So basically more plainly, scattered specific neuronal loss doesn't show on MRIs. So just because an MRI is normal, doesn't mean our brains are. Thanks for posting your results though.

Looking pretty bad guys. http://www.cell.com/neuron/pdf/S0896-6273(16)30409-3.pdf ill elaborate on this study later.

Heres some pretty interesting information on axon guidance https://en.wikipedia.org/wiki/Axon_guidance

http://medind.nic.in/iaw/t03/i1/iawt03i1p1.pdf Super good read on serotonin receptors.

Cool thing to note here as well is that glutamate, acting directly on the neuronal bodies, causes neuropathic toxicity, where as chemicals acting on the axons, generally cause axonopathic toxicity, and generally aside from extreme cases, leaves the neurons intact, localizing damage specifically to the axons. 5 HT for as far as I can find act specifically on the synapses. This leads to higher potential for axonopathic toxicity. Granted, 5 HT receptors do regulate glutamate, so glutamate still could be the end product of an excitotoxicity cascade.

This is on selective neuronal loss and not showing up on MRIs https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3887360/ So even though MRIs are fine, its not proof of neuronal loss. Honestly at this point, again, even after the MRI information. Its looking like probably neuronal loss.

Pretty intense read https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2677829/ mentions potential for scattered neuronal necrosis. Fine diameter axonal loss. And other potential aspects like transport factors etc.

It would be a far better idea to convince your brother to tell them. If he refuses and continues with the idea to use hallucinogens in the future I would highly recommend informing your parents that they can prevent him from doing so and further ruining his future. Also please help him to educate himself on this condition. Its a completely insufferable disease.

It would be extremely unfortunate. Normally in that instance it would be most notable of their inability to reconnect in axonal tracts, which are long and throughout the brain. The best way we have to measure or detect neuronal loss in a living subject is an MRI. Which apparently for the most part, most peoples HPPD related MRIs come back normal. In the case of neurogenesis which does not happen naturally in the human brain on a large scale, it would most likely take 3 months to get a decent amount of new neurons, and I would assume 1 to 2 years for the most regrowth that you will get. Granted even in neurogenesis its unlikely that there will be 100% recovery. Even the liver when resected though it regenerates usually will only account for 90% of the size it originally had. If there is neuronal loss in the gray matter, there are no axonal tracts there, and the neurons are much more densely populated with short axons, regeneration of these areas would be much more notable for functional recovery. There are also potentials for axonopathic toxicity, where only the axons would be damaged for the most part and suffer extreme demyelination, in this case everything in my opinion would be mostly recoverable. Some toxins act mostly on the axons, others, like glutamate, directly on the neuronal bodies. I dont know what 5 HT receptors act directly on yet, but I do know they alter glutamate production, which leads for potential in neuropathic toxicity. I do not know yet if neurons over produce glutamate under influence of hallucinogens. If anyone can find answers to those questions it would be extremely appreciated.

Absolutely you have caused the HPPD symptoms with DMT. Theres literally no doubt in my mind. No, unfortunately no one experiences what you are unless they have some psychological disorder. Im not trying to freak you out, your symptoms will improve, but please do not do any hallucinogens anymore. Give it some months time and you will notice improvement. DMT is a very strong hallucinogen and what I used, I developed HPPD from one single use of it, its the reason Im here. Symptoms may improve even a year in.

Yup, totally agree, its the anxiety, like some crushing feeling of internal doom. Absolute worst

I honestly disagree(to a degree) with the responses here, anxiety months following hallucinogen use definitely could signify potential neuropathic alterations. They may not be distinguished in the the most classical sense of HPPD, but it doesn't mean that changes haven't occurred. I would above what most are saying in this thread advise you to definitely NOT use any hallucinogens again. You could very well be breaching in to the realm of HPPD, and trust me, you dont want to be here. I do find it very weird that alcohol is giving you anxiety, especially if it has never done that before. Do try to relax though and give it some time. Sounds like you're getting off pretty easy.

Damn his symptoms sound exactly what I went through. The anxiety was so bad I remember looking down at the shower floor and there was hair everywhere. Freaked me out.

So recently K. B. Fante brought to my attention the possibilities of the parasympathetic and sympathetic nervous system being involved. And after some discussion, thought, and contacting Dr. Abraham, its pretty clear that Dr. Abraham must not have meant the interneurons in the brain, but rather the interneurons of the spinal column. I dont have the initial report from Dr. Abraham's commentary that I had found in a book involving toxicological pathologies, but ill try to find it. He basically expressed that the interneurons are believed to play a critical role, a lot being that they are highly involved in GABA and glutamate release. This would have a direct modulation on the parasympathetic and sympathetic nervous system, nay, it seems to be one of the primary regulating components. From Wiki, spinal interneurons https://en.wikipedia.org/wiki/Spinal_interneuron Neurotransmitter The sensory information that is transmitted to the spinal cord is modulated by a complex network of excitatory and ihibitoryinterneurons. Different neurotransmitters are released from different interneurons, but the two most common neurotransmitters are GABA, the primary inhibitory neurotransmitter and glutamate, the primary excitatoryneurotransmitter.[9][10] Acetylcholine is a neurotransmitter that often activates interneurons by binding to a receptor on the membrane.[11] One of the things that Dr. Abraham mentions is that this may be why GABA agonists(benzos) are beneficial. We might have our guys. The best part about this is they are located in the CNS spinal column, which means there will be no scar tissue, AND they are primarily grey matter neurons, which means short axons and densely populated neurons, giving room for possible regeneration. It would also explain the anxiety in HPPD, related to the sympathetic nervous system that K. B. Fante noted. And would explain why brain MRIs come back for the most part, normal. I dont know of anyone that has had spinal MRIs that have HPPD.... Also it lines up with the study that I think I posted, but did find that relates specifically to interneurons being excited by 5ht2a receptors, aka hallucinogenic use.

I emailed Dr. Abraham involving MRIs, I thought it to be appropriate to post here instead of my huge thread. Hes pretty vague. Maybe he doesn't know, or maybe he doesn't want to just give that information out.

Thanks for posting Danny! Definitely a move forward in understanding this. Mine showed "scattered nonspecific subcortical and centrum semiovale white matter hyperinstensities(lesions)" If more will post maybe we can find some pattern here.

This study gives some hope that the axon terminals are still intact and the the main route of damage is demyelination. Toxic Leukoencephalopathy Many toxic brain disorders preferentially affect the cerebral WM.145 A spectrum of severity has been described, ranging from mild, reversible confusion, to coma and death, with concomitant MRI and neuropathological WM changes.145 Cranial irradiation and cancer chemotherapeutic drugs, most notably methotrexate146,147 (Fig. 12), are leukotoxic, an effect that complicates the treatment of many malignancies. Figure 12 FLAIR MRI in the axial plane of a patient with cognitive decline after receiving methotrexate.2 Toluene leukoencephalopathy (TL) is an intriguing disorder that convincingly illustrates the ability of pure WM damage to produce dementia.148–152 Toluene (methylbenzene) is a common household and industrial solvent and is the major solvent in spray paint. It is abused by millions of people worldwide for its euphorigenic effect, an abuse that has a lifetime prevalence in the United States estimated at 18%.152 The intentional inhalation of toluene, often for years without respite, results in a dramatic syndrome of dementia, ataxia, and other neurologic signs.149,150 The effects are readily detectable on MRI and include diffuse cerebral and cerebellar WM hyperintensity (Fig. 13). The degree of cerebral involvement strongly correlates with the severity of dementia, which is the most prominent manifestation of the syndrome.148,150 Autopsy studies of TL reveal selective myelin loss that spares the cerebral cortex, neuronal cell bodies, and even axons in all but the most severe cases.151,152 TL thus ex-emplifies the toxic WM disorders and stands out as a convincing example of WM dementia (WMD).6,116,153 Figure 13 T2-weighted MRI appearance in the axial plane of toluene encephalopathy in two patients (A, B). Inhalation of heated heroin vapor (colloquially termed “chasing the dragon”) produces a devastating, progressive spongiform leukoencephalopathy. The MRI appearance154–156 is highly suggestive, if not pathognomonic (Fig. 14). Cocaine use may produce similar findings, including symmetric and widespread involvement of the posterior cerebral hemispheric WM, cerebellar WM, splenium of the CC, and brain stem (medial lemniscus and lateral brain stem), with sparing of the deep cerebellar nuclei. MRS in areas of parenchymal damage demonstrates elevated lactate and myoinositol, reduced NAA and creatine, normal to slightly decreased Ch, and normal lipid peak. Neuropathologically this is WM spongiform degeneration with relative sparing of U-fibers, whereas electron microscopy reveals intramyelinic vacuolation with splitting of intraperiod lines. Preservation of axons with no evidence of Wallerian degeneration, inflammatory cellular reaction, or demyelination is taken to indicate that axons may be relatively spared, consistent with the degree of recovery in some cases.154 Clinical manifestations include cerebellar motor findings of ataxia, dysmetria and dysarthria, bradykinesia, rigidity, and hypophonia, and the syndrome may progress over weeks to pseudobulbar palsy, akinetic mutism, decorticate posturing, and spastic quadriparesis. Death occurs in approximately 20% of cases. Clinical and MRI findings can progress after cessation of drug use, indicating that the toxic exposure precipitates an evolving injury. The lack of concordance between MRI perfusion and spectroscopy may reflect impaired energy metabolism at the cellular level. The lactate peak on MRS; mitochondrial swelling and distended endoplasmic reticulum in oligodendrocytes on autopsy; and apparent response to antioxidants and mitochondrial cofactors such as vitamin E, vitamin C, and coenzyme Q suggest mitochondrial dysfunction as a basis for this entity.154,155,157 Figure 14 MRI scans after heroin inhalation, known colloquially as “chasing the dragon.” FLAIR images in the axial plane (A–D). Corresponding 1H MRS imaging spectra in two of the images show characteristic lactate peak and decreased NAA. ... Other toxin-induced spongiform leukoencephalopathies with fluid accumulation restricted to myelin sheaths include those precipitated by cuprizone, ethidium bromide, actinomycin D, triethyl tin, hexachlorophene, isonicotinic acid, hydrazine, and cycloleucine.154,158

Its still a possibility that HPPD is brain damage. It sounds like you definitely have HPPD. I dont know if your eye is connected to the HPPD. You should have a second opinion done. Did you have scans done to make sure you dont have any growths behind the eye? It almost looks as though its bulging in the picture you uploaded. Dont do drugs anymore Lmao look at the picture he uploaded. Theres also no evidence to suggest that its not. And there is speculative evidence to suggest that it could be, mainly that the symptoms do not always completely resolve.

Please let me know exactly what the lab reports say. Not just whether or not the doctor said it was ok.