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      This is the catch-all forum for posts. Discuss anything related to Hallucinogen Persisting Perception Disorder (HPPD) here.

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      A place to introduce yourself to the community and what you hope to seek out on this site. New members may share their experience and onset of HPPD and what drug(s) triggered it.

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      What are the symptoms? What do you feel encompasses HPPD?

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      The place to discuss pharmacological and other treatment options.

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    1. Research Articles, Publications and Studies

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    1. Community Open Space

      This is a location to talk about anything except your symptoms. Be respectful of other users, but any topic within the rules are open for discussion.

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  • Hallucinogen Persisting Perception Disorder (HPPD) support forum - HPPD, flashbacks, drug-induced visual snow syndrome and depersonalization/derealization.

    Common HPPD symptoms: visual snow, palinopsia (trails/afterimages), increased BFEP, increased floaters, ghosting, halos, starbursts, macropsia/micropsia, geometric hallucinations, closed-eye visuals, flashbacks, depersonalization/derealization, anxiety, depression, brain fog, cognitive dysfunction, tinnitus.

  • Recently Active Topics

  • Latest Posts

    • I have read that an increase in this acid has been observed in people with mental illness, and that a decrease in it improves cognitive performance in rats. Sorry for my English.
    • Nah, doesn't sound like HPPD at all. Maybe drug induced panic attacks with some DPDR.  Not sure SSRIs are a wise move though. As these are sporadic episodes, i would just ask for a fast acting anti anxiety med like Xanax for when they occur (just be very sensible with them).
    • Riboflavin Has Neuroprotective Potential: Focus on Parkinson’s Disease and Migraine Eyad T. Marashly* and Saeed A. Bohlega Department of Neurosciences, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia With the huge negative impact of neurological disorders on patient’s life and society resources, the discovery of neuroprotective agents is critical and cost-effective. Neuroprotective agents can prevent and/or modify the course of neurological disorders. Despite being underestimated, riboflavin offers neuroprotective mechanisms. Significant pathogenesis-related mechanisms are shared by, but not restricted to, Parkinson’s disease (PD) and migraine headache. Those pathogenesis-related mechanisms can be tackled through riboflavin proposed neuroprotective mechanisms. In fact, it has been found that riboflavin ameliorates oxidative stress, mitochondrial dysfunction, neuroinflammation, and glutamate excitotoxicity; all of which take part in the pathogenesis of PD, migraine headache, and other neurological disorders. In addition, riboflavin-dependent enzymes have essential roles in pyridoxine activation, tryptophan-kynurenine pathway, and homocysteine metabolism. Indeed, pyridoxal phosphate, the active form of pyridoxine, has been found to have independent neuroprotective potential. Also, the produced kynurenines influence glutamate receptors and its consequent excitotoxicity. In addition, methylenetetrahydrofolate reductase requires riboflavin to ensure normal folate cycle influencing the methylation cycle and consequently homocysteine levels which have its own negative neurovascular consequences if accumulated. In conclusion, riboflavin is a potential neuroprotective agent affecting a wide range of neurological disorders exemplified by PD, a disorder of neurodegeneration, and migraine headache, a disorder of pain. In this article, we will emphasize the role of riboflavin in neuroprotection elaborating on its proposed neuroprotective mechanisms in opposite to the pathogenesis-related mechanisms involved in two common neurological disorders, PD and migraine headache, as well as, we encourage the clinical evaluation of riboflavin in PD and migraine headache patients in the future.   Introduction With the huge burden of neurological diseases on patient’s life and society resources, the need of finding and having neuroprotective agents is critical and cost-effective. In fact, the advances in medical research have found up to date multiple agents having unique proposed neuroprotective mechanisms and influencing different neurologic disease processes. Riboflavin is one of those proposed neuroprotective agents; however, its neuroprotective abilities have been underestimated in comparison to other known neuroprotective agents. Our focus in this article is to shed light on riboflavin neuroprotective characteristics, encouraging more research to be done in the future in this regard. Riboflavin, a water-soluble vitamin, is part of the B complex vitamins, known as vitamin B-2. It is characterized by its unique bright yellow coloration of urine when taken in large amounts. Riboflavin plays a role in a wide range of metabolic pathways and processes, serving as a coenzyme for a variety of flavoprotein enzyme reactions. Riboflavin active forms are flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD). Importantly, 10–15% of global population have an inherited condition of limited riboflavin absorption and utilization; leading to a potential biochemical riboflavin deficiency worldwide (1). In fact, based on erythrocyte glutathione reductase activation coefficient test (EGRAC), 54% of British non-elderly adult population was at least having borderline riboflavin deficiency (1). Indeed, riboflavin deficiency across European countries ranges between 7 and 20% (2). As a matter of fact, neural tissue has a higher susceptibility to oxidative stress. Oxidative stress, a term refers to the injurious results in living organisms due to an imbalance favoring oxidants over antioxidants (3), has been implicated in multiple disease processes and aging. Oxidants are the normal results of in vivo interactions between oxygen and organic molecules. Concerning the brain, it forms 2% of total body weight with high levels of fatty acids, uses 20% of total body oxygen, and has lower antioxidant activity than other tissues. This gives the neural tissue a higher susceptibility to peroxidation (4) and oxidative damage in comparison to other tissues. In fact, oxidative stress has been implicated in multiple neurodegenerative disorder pathogenesis (4).   https://www.frontiersin.org/articles/10.3389/fneur.2017.00333/full
  • Recent Status Updates

    • jat  »  Onemorestep

      Hi  I have had hppd for 2 years and its been a dessent into hell.. It started very mild  then anti histamines celexa made it worse..then i tried for a year to make it better  clonapam was always my go to but was aware of dangers os treated with respect.. The next big spike was lions mane... gabapentin as working untill inclusion of lamotragine and then boom up another level.   im no longer ina space where i can just live with it.  intense snow visuals  flies buzing around  tactile bugs 247 makes my life unbearable..  gutted as two years ago i could barely see any snow let alone the rest... I decided as a last resort before ending things to move to a hot beach and see if the weather and see might rebalance my nervous system.. every spike i have had never came down  just pushed me up...
      Right now i started keppra 1000  take clonaspam every other day  and started risperadone for tactile ahllucinations (  i am aware of the risks but i have no choice)
      I have carbomazapine clpbazam topimerate and phenoarbital as back up. i am thinking antipeileptics are my best chance for relief...  
      Would appreciate any advice  i eat well relax  etc  but ignoring my visuals and ignoring the tactile sensations is not piossible..I need treatmentt I know some people used peptides.. Im basically trying to save my life...so any thoughts ?
      · 2 replies
    • SS1  »  Fawkinchit

      You look like your pretty active on here. Have you ever tried CBD or HEMP (100% THC free only kinds) for your symptoms? Or heard of anyone trying these? 
      · 1 reply
    • Sk1984  »  Alex79

      Hey Alex, how can we communicate in private? I really need some advice
      · 0 replies
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