Talk:Hallucinogen persisting perception disorder

Treatment section needs an an entire rewrite or removal
Entire section seems to be based off one person's opinion, there is no scientific evidence that fasting from water, supplements or sunglasses can cure or treat HPPD in any form besides placebo. Adding "Some sufferers reported" at the start of a sentence with no citation or evidenced reference doesn't make it any more truthful either. I believe the section should be rewritten to only include the fact there is no good evidence to support any treatment for the condition besides abstaining from psychoactive substance use. Any reference to add would be good. Christiaanp (talk) 14:32, 11 May 2021 (UTC)


 * Did. I only could find many studies on how Lamotrigine is used to treat HPPD and one small study for Clonidine. Big Brain Zero Time (talk) 16:33, 6 January 2022 (UTC)

Flashbacks
I think I'm just going to remove the " often reffered to as flashbacks" because there is a distinct difference, HPPD constant, it's damaged vision, flashbacks are just vivid memory of being on the whatever hallucinogen was taken.


 * Is it always damage? After a fairly long stint (years) of LSD and Ecstasy use, I noticed that I had permanently enhanced colour sensitivity. Once I was able to actually point out to a graphic artist that some fonts on one page were different colours, when no one else could see it - we tested the RGB values and I was proved correct. For me the differences were not only clear but striking. One set of characters was a radiant purple and the others a shadowy charcoal. The others in the room were simply unable to see the difference. I know it's anecdotal, but there you go. No other negative effects - no trails, nothing. Perhaps an unhealthy interest in philosophy of mind and other such wastes of time. —Preceding unsigned comment added by 83.208.165.249 (talk) 21:45, 28 March 2011 (UTC)

Here is pretty good page that covers that fact: http://www.erowid.org/psychoactives/health/hppd/hppd_faq.shtml#flashback Iameatingjam 00:27, 28 April 2007 (UTC)


 * My hypothesis is that the red and blue cone cells in your eye have either become more numerous and/or better connected. The shade of purple you see are due to your red and blue cones picking up on shades that their photo receptors interpret as black due to their red and blue not firing. You have an advantageous mutation. You were either born with it, or The hallucinogens have enhanced your vision the way stoned ape theorists believe early human ancestors developed enhanced vision through small amounts of psilocybin-containing mushrooms. Perhaps the visual snow is an unwanted neutral mutation. — Preceding unsigned comment added by 68.12.152.123 (talk) 05:31, 12 November 2015 (UTC)

Cognitive
I'm interested in higher cognition, but my experiences with HPPD make me want to know more about the mechanism involved with simple persistent perceptual distortions, e.g., "trails." I conjecture that HPPD is analogous to having learned to discriminate the morphemes of a foreign language. The effect is persistent because a percept's constituent sensations are "repacked" as a new (often salient) percept which is experienced and memorized. As learning a new language can degrade the cradle tongue temporarily and superficially, so HPPD can interfere with environmentally adapted perception. But these effects can be overcome in time by re-training the discriminations that created these categories of perception in the first place. In practice, this means concentrating on adaptive perceptions and ignoring any unwanted hallucinatory perceptions. Long periods of disuse will reduce HPPD hallucinations, until eventually, they should become difficult or even impossible to produce.

I have never heard of anyone being disabled because of HPPD per se, although HPPD can be unsettling if severe, or worrisome if the sufferer believes he or she has become permanently deranged. Although hallucinations are maladaptive in the natural environment, I wonder if there may be some benefit from controlled altered perception to global functioning, e.g., in adaptability, imagination, etc.

Concerning the discussion of Depersonalization disorder below, it seems, if true, that this transient and superficial dissociation ties in with self-awareness as a perception or perhaps a sensation, in this case slightly blocked, distorted or misplaced.

70.95.168.25 10:44, 14 January 2007 (UTC)


 * "The effect is persistent because a percept's constituent sensations are "repacked" as a new (often salient) percept which is experienced and memorized." 


 * This is not meant as an argument: I am seriously wondering what lead you to believe that this is the case (be it research, be it intuitiveness, etc.). --67.42.158.160 (talk) 04:34, 9 July 2008 (UTC)

Research
I wanted to note the research protocols designed by me (DSK) will be made available, along with a comprehensive series of papers on this syndrome, after publication, and currently in preparation with expected completion in May 2011. I would like to clarify I am not currently affiliated with any other research listed in this section. David Kozin (talk) 22:29, 17 January 2011 (UTC)

It would be interesting to see some unbiased research into this topic. Dr. Henry Abraham has done some initial research, but his obvious bias may taint his research. For instance are people who are prone to perceptual distortions and weak colour discrimination drawn to hallucinogenic drugs? Do they naturally have a different flicker threshold and persistence of vision?

How many people experience visual changes? What about other senses? How many users actually consider this a positive change?

This isn't necessarily always or even mostly a negative change.

Reply. As a self-diagnosed sufferer of HPPD I find it pretty harmless but overall annoying. before it had started i had smoked cannabis daily for over a year and had taken magic mushrooms, salvia and ecstacy several times. Whenever I concentrate on an object it usually seems to move around a few inches and whenever I am in a dark room, or close my eyes, I see mind blowing patterns all over the wall. A friend of similar age (17) has these too, they are usually spinning abstract shapes that collide into each other and form another, bigger shape that in turn spins and splits etc. etc. My friend and I do not find these threatening any more, as we know they are not real and a probably result of drug abuse, instead they make night time lying in bed a lot more interesting. It should probably be mentioned that my friend has only ever has salvia and cannabis, perhaps hinting at a relationship between salvia and this disorder? The other senses seem to be normal and perception of colour is always spot on with him, but they do blur after a while for me.


 * Well I am guessing salvia has a relationship to this disorder considering the name of it is Hallucinogen Persisting Perception Disorder, and Salvia is a hallucinogen. I disagree and don't think any of this should be mentioned considering it hasn't been studied enough to find the amount of people and those questions are just unimportant. If you would like to seek these answers view the official message board that Dr. Heny Abraham monitors. hppdonline.com Dcs937

Reply. I'm new to wikipedia so I hope I"m following etiquitee properly. In response to the suggestion that Dr. Abraham's work is biased, could the problem instead be that the person who wrote the article innacurately represented Dr. Abraham's work. I think the author of this wiki paraphrased an article by Dr. Abraham and may have omitted the actual reasoning that Dr. Abraham gives of why he can draw his particular conclusion from that experiment. I'm thinking that Dr. Abraham had a hypothesis about hppd which would be proven if the flicker sensitivity of individuals with hppd was decreased which the author neglected to include. Really, why would Dr. Abraham chose this particular experiment Vigual?


 * A reason to study flicker sensitivity is that visual information is split into separate channels and one of the channels can detect faster changes than the other. By measuring perception of flicker you can separately test that one channel.  With enough different tests, you can figure out the cause.  There definately does need to be more research on HPPD to figure out what its causes are and how to best treat it.  A group at the University of California @ Berkeley is collaborating with erowid.org to study HPPD in an unbiased fashion.
 * --67.101.147.33 (talk) 15:57, 9 May 2008 (UTC)

I have added a reference to another Dr. Henry Abrahams research paper. I made sure to include that it is just one study, and not completely conclusive. I believe it is constructive information and added the reference. Please edit as appropriate. We may not know the cause, but even preliminary findings are useful on a page with such little information on causes and possible cures. Please advise. Lasthurrah (talk) 13:47, 24 April 2010 (UTC)

Update: The reference has already been removed. Here is the abstract I got the information from, and that got deleted for some reason (I realize this must have to do with the fact I only registered yesterday): http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6TBW-3W258TB-2&_user=10&_coverDate=10%2F07%2F1996&_rdoc=1&_fmt=high&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=9bdaac82bb69bf6f199c93183945d7a1 Lasthurrah (talk) 14:19, 24 April 2010 (UTC)

'''Genetic Modifications to Specific Neuronal Protein Producing Genes. A cause for the change in neuronal circuitry that causes observable dysfunctional manifestations in the visual cortex after external stimuli exposure on quantitative EEG testing?' (Not a self-proclaimed title for an article, just distinguishing the title for this little proposition i'm about to type out'')

Although there is no legitamate and archived clinical testing to show this idea as to why some people develop a condition in which normal visual processing is altered to the extent of producing permanent, static changes in how an HPPD patients visual response to external stimuli is changed to the level of producing stress, psychological mood impairments, prolonged (sometimes permanent) dissociative mental states, and agitation. I believe, solely through my own reading and experiences with the condition (yes i am diagnosed with HPPD), that HPPD is a physiological change to the chromatin structure (which is defined as the 8 histone proteins that surround the DNA double helix and, for lack of a better descriptive word, protect the gene loci from activation.) inside neuronal nuclei. This series of events would be termed acetylation in the study of epigenetics. It is caused by chemical initiation of a remodeling chain of events that literally can turn on genes that code for proteins.

This can happen to any type of cell in your body, but i'm discussing changes in neuronal Transcription (genetics). Histone acetylation to neuronal chromatin would loosen the chromatin proteins that are compacted around certain genes on the dna helix and activate genes that would, in my opinion, essentially protect a neuron from excitotoxicity by upregulating genes that code for neuronal proteins and messenger RNA's for ion and neurotransmitter channels to keep a steady state between inhibitory and excitatory membrane potentials. This process would begin if an individual ingests enough of a chemical that has the ability to produce vast changes in brain activity, thereby greatly changing the steady state of the rest of the body.

Acetylation is initiated by a "penetration", in sense, by calcium ions, through glutamate receptors and calcium channels, into the nuclear envelope. From there, a series of post-synaptic density proteins, for example (PDZ domain) as well as secondary signalling cascade proteins (for example CREB) are drawn to the nucleus of the neuron and begin to immediately upregulate what i would refer to as "emergency" genes to begin the production of additional or new proteins to reconstruct and add to parts of the cellular membrane for the purpose of keeping a normalized temperature, excitatory/inhibitory balance, or a prevention of cellular apoptosis. After the drug has made its way out of the body, these genetic changes linger. In the cases of HPPD, they would linger for a very long time, perhaps permanently.

The proposed series of events above would leave a genetically susceptible person's brain in a state of over drive. What i mean by over drive is that a large number of post-synaptic relay neurons, perhaps mainly inhibitory, in certain layers of the visual cortex (layers II/III i believe), and also neurons in the thalamocortical region responsible for relay of external stimuli information, have been physiologically altered to the point of what would appear to be a dysfunctioning problem of the visual cortex, when looked at carefully in a qEEG test. The proposed effected areas i've mentioned above could be the reason why a regular EEG, aka Electroencephalography test wouldn't show abnormal activity since those layers lay considerably deeper in the brain than what the EEG electrodes pick up on the scalp. A few members from HPPDonline.com have had this slightly altered test done, and their results have shown, according to statements by thier licensed doctors, abnormal responses in the inhibitory tone of the visual area of the brain when exposed to light.

I'm certainly not claiming that this is the for sure cause of HPPD, but it definitely deserves more attention in the research area as possible mechanisms of action for causation. —Preceding [[User:Shaolinbomber|Shaolinbomber (talk) 08:29, 17 June 2010 (UTC)]] comment added by Shaolinbomber (talk • contribs) 08:16, 17 June 2010 (UTC)

Flashbacks
This article needs some discussion of HPPD in the context of "flashbacks" of a psychedelic experience. I've heard HPPD described as a medical diagnosis of what is colloquially called a "flashback", but I've also heard of "flashbacks" covering a wider range of phenomena, and that HPPD is the most extreme manifestation of HPPD.

Also, this article is somewhat POV - the extent and seriousness of HPPD and "flashback" phenomena are questioned by many, and these questions should be addressed in this article. Peter G Werner 18:38, 5 April 2006 (UTC)


 * Agreed. The LSD article mentions several theories as to the causes of HPPD, only 1 of which is mentioned here. Adding the POV tag for now, until someone with more knowledge of the subject matter looks into it. Mzyxptlk 19:37, 8 December 2006 (UTC)


 * Disagreed. HPPD stands for Hallucinogen Persisting Perception Disorder. Flashbacks is a common misinterperit that doctors seem to think it is. Or simply just a term. Dcs937

I have removed my discussion here for the moment. I will be adding additional information, but this must be cleared prior to publication. David S. Kozin 23:17, 28 September 2009 (UTC)


 * : : Since someone more knowledgeable (David) has looked into it, I am removing the POV tag. --Generalmiaow 21:56, 19 January 2007 (UTC)

Help needed
I would like to mention on this page that HPPD is very often comorbid with Depersonalisation Disorder which it is (a quick survey of dpselfhelp.com or hppdonline.com would show that about a third of HPPDers have Depersonalisation) However there is no serious academic article that says there is (apart from the forthcoming NODID study with has not been published yet). What should I do? Say that it's based on a web forum? There is so little about HPPD out there, but this is definitely true, just not backed up by research yet... Generalmiaow 23:28, 8 May 2006 (UTC)

I have deleted much of my talk from a previous series of entries. The updates for HPPD and the DPD - HPPD relationship are as follows:

The research on DPD is completed and published. The results are available in the Abstract or full articles:

Simeon, D., Kozin, D. S., Segal, K., & Lerch, B. (2009). Is depersonalization disorder initiated by illicit drug use any different? a survey of 394 adults. The Journal of Clinical Psychiatry,2009;70(10):1358–1364 doi:10.4088/JCP.08m04370

Simeon, D., Kozin, D. S., Segal, K., Lerch, B., Dujour, R., & Giesbrecht, T. (2008). De-constructing depersonalization: further evidence for symptom clusters. Psychiatry Research, 157(1-3), 303-306. doi:10.1016/j.psychres.2007.07.007

These articles do not answer you question regarding the comorbidity of DPD with the HPPD diagnosis. --David Kozin (talk) 08:58, 8 January 2010 (UTC)

I updated the research section of the page.--David Kozin (talk) 08:58, 8 January 2010 (UTC)

Some references need to be added to the front page. Here is a comprehensive list:

Abraham, H.D., 1980. A chronic impairment of colour vision in users of LSD. Br. J. Psychiatry 140, 518—520. Abraham, H.D., 1983. Visual phenomenology of the LSD flashback. Arch. Gen. Psychiatry 40, 884—889. Abraham, H.D., 1984. LSD flashbacks (Letters to the Editor – In Reply). Arch. Gen. Psychiatry 41, 632. Abraham, H.D., Aldridge, A.M., 1993. Adverse consequences of lysergic acid diethylamide. Addiction 88, 1327—1334. Abraham, H.D., Duffy, F.H., 1996. Stable quantitative EEG difference in post-LSD visual disorder by split-half analysis: evidence for disinhibition. Psych. Res. Neuroimaging 67, 173—187. Abraham, H.D., Duffy, F.H., 2001. EEG coherence in post-LSD visual hallucinations. Psych. Res. Neuroimaging 107, 151—163. Abraham, H.D., Mamen, A., 1996. LSD-like panic from risperidone in post-LSD visual disorder. J. Clin. Psychopharmacol. 16, 228—231. Abraham, H.D., Wolf, E., 1988. Visual function in past users of LSD: psychophysical findings. J. Abnorm. Psychol. 97, 443—447. Abraham, H.D., Aldridge, A.M., Gogia, P., 1996. The psychopharmacology of hallucinogens. Neuropsychopharmacology 14, 286—298. Alarcon, R.D., Dickinson, W.A., Dohn, H.H., 1982. Flashback phenomena: clinical and diagnostic dilemmas. J. Nerv. Ment. Dis. 170, 217—223. Aldurra, G., Crayton, J.W., 2001. Improvement of hallucinogen persisting perception disorder by treatment with a combination of fluoxetine and olanzapine: case report. J. Clin. Psychopharmacol. 2, 343—344. American Psychiatric Association, 1994. Diagnostic and Statistical Manual of Mental Disorders, IV. American Psychiatric Press, Inc., Washington, D.C. Anderson, W., O’Malley, J., 1972. Trifluoperazine for the trailing phenomenon. J. Am. Med. Assoc. 220, 1244—1245. Annis, N.M., Smart, R.G., 1973. Adverse reactions and recurrence from marijuana use. Br. J. Addict. 68, 315—319. Apter, J.T., Pfeiffer, C.C., 1957. The effect of the hallucinogenic drugs LSD-25 and mescaline on the electroretinogram. Ann. N.Y. Acad. 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Mescal: a new artificial paradise. Contemporary Review 73:130—141 (reprinted in The Smithsonian Institution Annual Report 1898, pp. 537—548). Favazza, A.R., Domino, E.F., 1969. Recurrent LSD experience (flashbacks) triggered by marijuana. Univ. Mich. Med. Cent. J. 35, 214—216. Fischer, R., 1971. The ‘flashback’: arousal-statebound recall of experience. J. Psychedelic Drugs 3, 31—39. Fischer, R., 1977. On flashback and hypnotic recall. Int. J. Clin. Exp. Hypn. XXV, 217—235. Fischer, R., Hill, R.M., Worshay, D., 1969. Effects of the psychedysleptic drug psilocybin on visual persception. Experientia 25, 166— 167. Frosch, W.A., Robbins, E.S., Stern, M., 1965. Untoward reactions to lysergic acid diethylamide (LSD) resulting in hospitalization. N. Engl. J. Med. 273, 1235—1239. Gastaut, H., Ferrer, S., Castells, C., 1953. Action de la die´thylamide de l’acide d-lysergique (LSD-25) sur les functions psychiques et l’e´lectroence´phalogramme. Confina Neurol. 13, 102—120. Genova, P., 2000. The Thaw: 24 Essays in Psychotherapy. Dorrance Publishing, Pittsburgh, pp. 17—19. Halpern, J.H., Pope, H.G., Jr, Sherwood, A., Hudson, J.I., Yurgelun- Todd, D., 2001. Neuropsychological effects of long-term hallucinogen use in Native Americans (abstract). Drug Alcohol Depend. 63 (S1), S62. Harley-Mason, J., Laird, A.H., Smythies, J.R., 1958. The metabolism of mescaline in the human. Confina Neurol. 18, 152—155. Heaton, H.K., 1975. Subject expectancy and environmental factors as determinants of psychedelic flashback experiences. J. Nerv. Ment. J.H. Halpern, H.G. Pope, Jr / Drug and Alcohol Dependence 69 (2003) 109—119 117 Heaton, H.K., Victor, R.G., 1976. Personality characteristics associated with psychedelic flashbacks in natural and experimental settings. J. Abnorm. Psychol. 85, 83—90. Hemsley, D.R., Ward, E.S., 1985. Individual differences in reaction to the abuse of LSD. Person. Individ. Diff. 6, 515—517. Holiday, A.R., Hall, F.M., Sharpley, R.P., 1965. 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Ophthalmol. 64, 724—733. Landis, C., Clausen, J., 1954. Certain effects on mescaline and lysergic acid on psychological functions. J. Psychol. 38, 211—221. Lerner, A.G., Oyffe, I., Issacs, G., Mircea, M., 1997. Naltrexone treatment of hallucinogen persisting perception disorder. Am. J. Psychiatry 154, 437. Lerner, A.G., Finkel, B., Oyffe, I., Merenzon, I., Sigal, M., 1998. Clonidine treatment for hallucinogen persisting perception disorder. Am. J. Psychiatry. 155, 1460. Lerner, A.G., Gelkopf, M., Oyffe, I., Finkel, B., Katz, S., Sigal, M., Weizman, A., 2000. LSD-induced hallucinogen persisting perception disorder treatment with clonidine: an open pilot study. Int. Clin. Psychopharmacol. 15, 35—37. Lerner, A.G., Skladman, I., Kodesh, A., Sigal, M., Shufman, E., 2001. LSD-induced hallucinogen persisting perception disorder treatedwith clonazepam: two case reports. Isr. J. Psychiatry Relat. Sci. 38, 133—136. Lowry, J.V., 1969. Mental health services for misusers of drugs in California. 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Flashbacks and memory phenomena: a comment on ‘‘Flashback phenomena*/Clinical and diagnostic dilemmas’’. J.Nerv. Ment. Dis. 172, 273—278. McGlothlin, W.H., Arnold, D.O., 1971. LSD revisited: a ten-year follow-up of medical LSD use. Arch. Gen. Psychiatry 24, 35—49. McGuire, P.K., Cope, H., Fahy, T.A., 1994. Diversity of sychopathology associated with use of 3,4-methylenedioxymethamphetamine.(‘Ecstasy’). Br. J. Psychiatry 165, 391—395. Morehead, D.B., 1997. Exacerbation of hallucinogen-persisting perception disorder with risperidone. J. Clin. Psychopharmacol. 17, 327—328. Moskowitz, D., 1971. Use of haloperidol to reduce LSD flashbacks. Mil. Med. 136, 754—756. Naditch, M.P., 1974. Acute adverse reactions to psychoactive drugs, drug usage, and psychopathology. J. Abnorm. Psychol. 83, 394— 403. Naditch, M.P., Fenwick, S., 1977. LSD flashbacks and ego functioning. J. Abnorm. Psychol. 86, 352—359. Nichols, C.D., Sanders-Bush, E., 2002. 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Visual disturbances experienced by hallucinogenic drug abusers while driving. Am. J. Psychiatry 127, 683—686. Worarz, N., 1993. ‘Ecstasy’-induced psychotic depersonalization syndrome. Nervenarzt 64, 478—480. Yager, J., Crumpton, E., Rubenstein, R., 1983. Flashbacks among soldiers discharged as unfit who abused more than one drug. Am. J. Psychiatry 140, 857—861. Young, C.R., 1997. Sertraline treatment of hallucinogen persisting perception disorder. J. Clin. Psychiatry 58, 85. Zeidenberg, P., 1973. Flashbacks. Psychiatr. Ann. 3, 14—19. —Preceding unsigned comment added by 75.3.118.216 (talk) 02:57, 24 October 2007 (UTC)

Hippo rubbish...
Someone has sabotaged this page with some rubbish about hippos... Please can someone with the relevant knowledge correct it...

Thanks —Preceding unsigned comment added by 222.123.153.94 (talk) 22:26, 9 June 2008 (UTC)

Cannabis
I have never heard anything about HPPD being caused by Cannabis, ever, could somebody check the references for this fact? 24.65.42.159 (talk) 04:02, 2 July 2008 (UTC)
 * I just checked the laffey reference out, it doesn't even mention anything about hppd. but this does not mean we can rule out cannabis as a cause or not for hppd. When we come to a problem like this i think it is best we leave out that strong fact that it does not cause HPPD, and just not put anything in. 24.34.208.193 (talk) 00:22, 20 September 2009 (UTC)
 * Hello. I know that stories of the kind of "in my case" are not a reliabel ressource, but yet I have to tell it. In my personal case I am pretty sure that my HPPD (not very strong and I do not have suffering due to it) was caused by Cannabis, or at least Cannabis helped building it.
 * But I have to add that I am not really happy with the name of the diagnoses. It is not really a disorder of perception it is more like an additional perception to normal perception, which might cause in some cases secondary feelings of anxiety or similar feeling due to negative associations. I once met somebody who even did not now that there is a name for his "dancing points". In my opinion the best treatment is to calm people down.
 * Sorry for going a bit off-topic, yet I thought that it is important to report my point of view as somebody who has this rare symptom.--178.83.159.75 (talk) 22:20, 26 March 2014 (UTC)

Synthesis?
A lot of references seem to be research into symptoms that are similar to the effects described as "HPPD", but are not specifically about it. Some are merely research into "flashbacks", "depersonalization" and the effects drugs have on schizophrenics.Yonskii (talk) 01:38, 4 September 2011 (UTC)

Floaters
Article mentioned higher awareness to floaters. But cant these be also CREATED by drugs that rise ocular pressure? 83.28.218.133 (talk) 08:58, 10 September 2014 (UTC)

Interesting, People also have heightened awareness to floaters after cataract or eye-laser surgery. Many people have heightened awareness to floaters when the ambient light is brighter than usual. 24.138.60.176 (talk) 04:38, 30 May 2018 (UTC)

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Visual Snow Syndrome similitudes
I added a paragraph on the exact similitudes regarding both pathologies and why it's important to differentiate HPPD symptomatology from the actual "flashback" pop culture urban myth   -- Thanks for removing my insertion but the definition here is really wrong and should be updated. flashbacks have nothing to do with HPPD and is not the main symptom of it.

— Preceding unsigned comment added by 217.128.155.105 (talk) 10:47, 30 May 2019 (UTC)

HPPD is a niche of the Visual Snow Syndrome.

Establishing this officially in the medical community ( on wikipedia and all mainstream online documentation ), will also bring patients into the right health care process with real chances of social recovery, while actually, most of the recent patients will be mislead into psychiatric therapy ( real shame ).

Also, VSS searcher can benefit a lot from our experience, and our condition can definitely help understand how this symptomatology is acquired — Preceding unsigned comment added by 178.208.8.157 (talk) 08:34, 10 July 2019 (UTC)

Source for Antibiotic's Affect
The source for antibiotics causing HPPD is based on a forum post (Source 4). It should either be replaced with something more official or removed. I don’t think it’s a good idea to give unverified information that would make people avoid using antibiotics. 2603:9001:7C00:1123:E0BB:F4AE:7C2B:72B2 (talk) 16:33, 11 December 2022 (UTC)