Hallucinogen persisting perception disorder (HPPD) refers to the condition in which an individual, after the consumption of hallucinogens, experiences recurring sensory disturbances years afterwards that are reminiscent of those experienced during the intoxication of the hallucinogen. It is particularly associated with the consumption of lysergic acid diethylamide (LSD) ecstasy (MDMA) and other recreational and prescription medications.

This project is a collaboration of Macquarie University and ICAN, and is carried out by our highly specialised team of clinical researchers, Ophthalmologists and Psychiatrists who have been studying HPPD and its relevant visual symptoms for many years. The team is based in Australia with Dr Wei He (MQ/ICAN), Associate Professor Paul Sowman (MQ), Professor Harry McConnell (ICAN), Associate Professor Clare Fraser (MQ), Ms Anneliese McConnell (MQ/ICAN). We are also collaborating with Dr Steven Locke from Harvard and Dr Natalie Gukasyan from Johns Hopkins for the questionnaire part of this study.

Phase 1: The LimeSurvey Questionnaire

The questionnaire examines the nature of HPPD, the effect of hallucinogens on the condition and the changes in the brain processing of vision that may occur in patients with HPPD. The study involves an online survey to obtain information across basic demographics, drug use, HPPD symptoms and medical comorbidities. We are looking at the nature of symptoms, their medications and other conditions people may have.

Everyone is invited to participate in the questionnaire study. The questionnaire takes about 15 minutes - we will send you a link when you email us at hppd@mq.edu.au

**Please check your Spam or Junk mail box for the link once you have email us but not got the link.**

Phase 2: Neuroimaging Protocol (only for those who completed the questionnaire)

Patients in Australia who have completed the questionaries will also have the opportunity to participate in our functional Magnetic Resonance Imaging (fMRI) and Magnetoencephalography (MEG) studies to precisely measure the spatial and temporal activities of the visual pathways, which will be used to compare with control participants who are free from visual hallucinations.

If you are in Australia and are interested in participating the neuroimaging protocol once completed the questionnaire study, please fill in this Microsoft Form and we will contact you for more information.

We hope to be able to offer the neuroimaging protocol more widely, i.e., to non-Australian participants who completed the questionnaire study, in the future.

Note: This study was made possible through the generous support of several foundations, one of which is the Perception Restoration Foundation (PRF). If you'd like to find out more about the PRF you can do so here:

Intravenous ketamine, a dissociative anaesthetic, has been reported to alleviate major depression [1] and chronic pain [2] with minimal adverse effects [3,4], although perceptual disturbances are not uncommon [5]. Hallucinogen persisting perception disorder (HPPD)is an illness arising from the abuse of hallucinogens in which individuals suffer visual pseudohallucinations for months to years following exposure to LSD and similar drugs [6]. We now report a case of HPPD in a young man who received medically administered intravenous ketamine for treatment of a complex regional pain syndrome (CRPS).

Case Report

A 13 year old male piano student developed CRPS following a sacral injury. He had no history of substance use. At 15, chronic pain was treated with two continuous intravenous infusions of ketamine, each lasting a week, with maximal doses of 50 mg per hour. During each treatment he vomited and had visual and synesthetic hallucinations.Six months later he suffered the progressive onset of an array of visual pseudohallucinations and hypersensitivity to light and sound. Imagery included particles in the entire visual field seen in the air and on surfaces; large moving coloured blobs on surfaces; afterimages; trails of objects moving through his visual field, such as a tennis ball; objects changing their shape; and difficulty reading and playing the piano. He also suffered the incessant sensation of the euphoria he felt when given ketamine. These symptoms were reported as daily and constant on multiple follow-up visits over a three year period.A psychiatric evaluation found no evidence of psychosis or depression. The mental status examination confirmed a deficit in short term memory. The patient described continual visual disturbances during the examination. Reality testing was intact.There were no auditory hallucinations or delusions. Psychological testing confirmed a reading disorder. A quantitative EEG found evidence of an auditory processing disorder with irritability in the left temporal and occipital regions, including activation of the auditory system by visual stimuli, a putative marker for drug-induced synaesthesia.Medications including divalproex sodium, several SSRIs, gabapentin and pregabalin were unsuccessful. Lorazepam 2 mg twice daily reduced, but did not ablate, his symptoms for two months. In that time he returned to the piano and was admitted to a university music program. Relapse followed as the patient apparently developed tolerance to the treatment. A similar pattern followed use of diazepam10 mg a day. At the age of 18, he developed complex partial seizures which have been controlled with topiramate. However, the perceptual symptoms and ketamine euphoria have continued.

Discussion and Conclusion

Studies in subjects with HPPD suggest that the pathophysiology of the disorder involves either a slowly reversible or permanent disruption in the inhibition of visual information processing. This has been described from the use of LSD, MDMA, psychostimulants and a variety of botanical preparations of hallucinogens [7]. Evidence for visual disinhibition following LSD includes persisting after imagery [8],abnormal flicker fusion testing, impaired dark adaptation [9],electrophysiological measures of cortical disinhibition [10] and increased measures of cerebral coherence, a putative measure of increased cortical activation [11]. To the best of our knowledge this report is the first association between ketamine and HPPD.The mechanism by which ketamine antagonism of the NMDA receptor induces perceptual or psychotic symptoms is not known.Consistent in both animal and human studies, however, is the observation that ketamine increases activity of brain waves in the gamma (30 to 60 Hz) range. De la Salle et al. reported such an increase in gamma current density in the default mode network implicated ins chizophrenia, as well as activation of gamma frequencies across the cerebrum [12]. This finding supports a disinhibition model of HPPD.In addition, GABA-A agonists such as midazolam reduce HPPD symptoms [13].HPPD also appears to be associated with increased cerebral coherence, a measure of cortical connectivity [14]. Similarly, temporal lobe epilepsy involving the neocortex has been associated with increased coherence [15]. The role of ketamine in the generation or control of seizures is not known. But in our case, enhancement of cortical coherence with neurofeedback resulted in an exacerbation of HPPD.Ketamine, a schedule III drug which is an anaesthetic agent, can be prescribed by any physician. Enthusiasm for its use in treatment of refractory depression has yet to be tempered by a body of research establishing safety and efficacy [16]. The history of LSD in the 1960sfollowed such a course over time, in which a period of rising enthusiasm was followed by one of sober reconsideration as the risks and benefits were identified [17]. This report adds a note of caution to the process.

https://www.longdom.org/open-access/hallucinogen-persisting-perception-disorder-following-therapeuticketamine-a-case-report-2329-6488-1000281.pdf

hallucinogen-persisting-perception-disorder-following-therapeuticketamine-a-case-report-2329-6488-1000281.pdf

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2367001/

SUBJ: Faces of HPPD Survey/Research Published – RESULTS!

Dear HPPD Online Community:

As a mom with a grown son with HPPD, I was so fortunate to come across this forum several years ago for information and support. David Kozin, who runs this board, is an amazing man to have created and maintained this website and kept up his work/studies over the years – all the while suffering with HPPD. I would like to thank him for this platform, and well as thank those of you who participated in the survey that I launched four years ago to collect data about individuals who had received an official diagnosis of the disorder.

Fast forward…. Here it is June 2019. Long overdue for the published report, however, I lingered – always hoping to gain a larger sample of subjects.

I am fortunate to have a PhD in psychology, experience in research, and a heart to try to make a difference. Instead of publishing a book, it only made sense to get the results in the hands of the scientists and medical professionals through scientific writing. I am so happy to tell you… the peer-reviewed medical journal, Addictive Disorders & Their Treatment, published by Wolters Kluwer publishers, has reviewed and accepted my manuscript for publication in an upcoming issue. Last week the article completed rounds of publication editing and formatting. The article is posted at their website for advance release.

Lewis, DM, Faces of HPPD: Hallucinogen Persisting Perception Disorder Patient Survey Results and a Descriptive Analysis of Patient Demographics, Medical Background, Drug Use History, Symptoms, and Treatments. Addictive Disorders and their Treatments. Forthcoming 2019.

The link is here: https://journals.lww.com/addictiondisorders/Abstract/publishahead/FACES_OF_HPPD__Hallucinogen_Persisting_Perception.99733.aspx

(NOTE: This direct link will change probably in a month or two when the article is given a print-issue date – right now, it is advance copy, undated. In the future, you can search the article at https://journals.lww.com/addictiondisorders/ .

While the article is available for immediate download, many of you know that publishers charge money for copy downloads (this one is $49), and authors cannot give away their copy. This, I know, is not a good thing for some within the community who do not have the funds.

However (here’s the good news ), I contacted the publisher and obtained permission to publish a summary of the results (the important data!) and I created an infographic that provides you all the results. I am including it here as a .pdf file, attached. It’s reader-friendly, and I hope it provides insight.

I want to mention some findings that particularly concern me: the high rate of suicide ideation (among other co-morbid psychological/psychiatric symptoms reported), and the significant number of individuals who reported being unable to work due to HPPD. I feel strongly that HPPD needs recognition as potentially disabling – and I believe there are some individuals who may need government assistance (eg, Social Security Disability benefits). My future work leads me in the direction of carving a path for HPPD as a qualifying mental disorder for eligibility for assistance. I will keep you posted on that.

Again, thank you so very much for those who partook in the survey.

My best wishes to each of you for good health and peace of mind,

Doreen M. Lewis, PhD
https://www.facesofhppd.com
https://www.vellichorresearch.com

Faces of HPPD Infographic - LEWIS.pdf

I just published the article on my blog. It's very extensive, with each possible cause being discussed in detail.

I hope it doesn't have too many inaccuracies, and that it helps some people. Both with treating their HPPD and with advancing research in the future.

Thanks.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5608040/

I've lived for many years with HPPD although I have personality disorder as well.

Things became worse recently in terms of anxiety, visuals and muscle tensions.

I would like to convince my current psychiatrist(I am moving from place to place) that I suffer from HPPD and provide him trustworthy documentation

So my question is do you guys have some documents which I can show to my doc, can you provide it here?

Best Regards

Anyway, did anyone do that survey? They emailed everyone who had an account on this forum. Is the research ongoing? I never heard back about the survey and was really looking forward to it.

https://www.gofundme.com/visual-snow

'' Hello Eye on Vision Supporters!

I'm sorry that there was such a long delay in hearing from me, but I sustained an eye injury in Feb and am only recently returning to limited computer use.

I do have an update from London to share with you. Patients have begun to be qualified and scheduled for testing. Scans are scheduled for May and June at King's College. This is an important phase of research, because what is learned from these scans will determine how we enter into a treatment phase of research. Without this phase of research, we will not be able to proceed to medication testing. With that being said, I've been approached about funding for Dr. Puledda's salary for another year. Dr. Puledda works under Prof. Goadsby and is the primary doctor assigned to the Visual Snow research at King's college. As stated in previous updates we need approximately $70,000 USD per year to employ her. Currently we have only raised $20,000 USD which is a far off sum from what is actually needed to secure her.

Almost all of you reading this who have VS have likely undergone an MRI. You have likely seen the very high bill to your insurance, or you have paid out of pocket. It's not uncommon to see bills over $1000. We are very fortunate that King's College covers all of these costs towards VS research. We need to assist them though by being able to pay Dr. Puledda for her time and efforts on our behalf.

We would love for you to become a monthly donor and help us achieve our research funding goals. You can sign-up as a monthly donor here:
http://eyeonvision.org/donate-to-the-eye-on-vision-foundation.html

Thank you,
Jen Ambrose

Please everyone make donations!! I know you guys got visual snow syndrome from drugs ( just as the forum info section itself says : drug induced visual snow syndrome ) but the symptoms are the same . A cure could be on the horizon if we start making donations!!! I've posted links about few other rare diseases that have found cures( or are close to finding one) purely by making large donations and not giving up . This is what patient determination and donations can do :

https://www.hippocraticpost.com/innovation/gene-therapy-nervous-system-disorders/

https://www.technologyreview.com/s/603832/determined-parents-are-moving-the-needle-on-gene-therapy/

there are some other articles I came across a while back but I don't have the time to search for all of them again . However I hope that the above articles will inspire you to make donations for the visual snow syndrome research. It's the only option we all have left now !!!

https://www.google.com/amp/s/www.zmescience.com/science/news-science/lsd-stuck-brain-20022017/amp/

"Characterization, Frequency and Severity of Visual Phenomenology in Adults with Hallucinogen Persisting Perception Disorder"

Name and address of the principal investigator
David S. Kozin,

Site where the study will be performed: Online. The study will be carried out at the office of the principal investigator with 256-bit SSL encrypted server access.

Introduction

Hallucinogen Persisting Perception Disorder (HPPD) is a persisting, post-substance use disorder characterized by the diagnostic criterion of “the re-experiencing, following cessation of use of a hallucinogen, of one or more of the perceptual symptoms that were experienced while intoxicated with the hallucinogen (e.g., geometric hallucinations, false perceptions of movement in the peripheral visual fields, flashes of colors, intensified colors, trails of images of moving objects, positive afterimages, halos around objects, macropsia, and micropsia.” (DSM-5 (update definition)). Abraham (1993) completed the most complete characterization of symptoms Additionally, individuals reporting HPPD and anecdotal evidence from online support message boards suggest that a prominent portion of this population presents symptoms of depersonalization disorder and derealization without clinical memory or identity alterations typically present in other dissociative disorders (Simeon & Kozin et al, unpublished data). The course of HPPD with the most significant distress is typically chronic and continuous (Lerner et al. 2002 & online descriptions), however the DSM-5 (update definition) does not differentiate between the chronic and transient forms of perceptual disturbances as independent diagnostic entities (APA 2004).

HPPD often lasts for years and often individuals with significant symptom severity with have the disorder for over 30 years and likely will not end until the end of their lives. The triggering of the visual symptoms does not always occur immediately after the precipitant drug, but has been been reported to be associated either with trauma (self-reports) or a non-hallucinogenic drug is the precipitant, or increases symptoms (Alcántra, (1998), Favazza & Domino (1969), Lauterbach et al (2000) , Lerner et al (2002), Markel et al (1994), Morehead & Morehead (1997), Scott (1971), & Solhkhah (2000), unpublished online reports).

Dr. Roger Davis and David Kozin created a complete set of visual simulators for the symptoms described in Abraham’s 1983 symptom list. Davis and Kozin used images from individuals from an online HPPD community and completed a one week session where each visual simulator we presented to a live audience of individuals from the HPPD online community to constantly discuss with Davis and Kozin regarding the accuracy of each image. Ultimately, we need a catalogue of HPPD visual disturbances and these simulators are able to be included as tools within the survey. This could help develop an online catalogue where each "plate" in the represents a reference point through which patients can explain their vision to mental health professionals and other doctors. Unfortunately, at this point we we do not have a systematic and objective result from participants on their responses to these images. Eventually, the entire catalog of simulators could be distributed online for clinical consumption for doctors to help them understand HPPD perceptual disturbances, acquainting them with the disorder, and perhaps averting tragedies where, for example, HPPD patients are misdiagnosed with schizophrenia and given antipsychotic drugs that can worsen the disorder.

It is the goal of this survey to descriptively and systematically study in greater depth the frequency, duration, and severity of the visual symptoms of HPPD, the relationship between illicit and non-illicit drug use and HPPD-like symptoms, investigate other additional possible psychopathologies with valid instruments and/or self-report, and to investigate the differences between chronic and transient subtypes.

In light of the DSM-V’s goal of a dimensional approach to diagnosis, and also to not make the mistake of the DSM-III and IV to sacrifice validity over stability (personal communications with APA Task Force members during the ISSTD conference), a study that helps identify and improve diagnostic precision for these persisting drug-induced experiences, either transient or chronic, will help with choosing treatments and improving and clarifying research with improved definitions to match the variability in these disorders. This will improve the validity of the diagnosis, and lead to proper treatments associated with each subtype.

Mood, anxiety and personality disorders are often comorbid with HPPD, but none have been examined to predict symptom severity. The most common proximal precipitants of the disorder are hallucinogens (specifically HPPD), however non-hallucinogens have been reported to cause similar symptoms. These will be investigated by allowing non-hallucinogen users to participate if they match the visual symptom criteria and including a standard scale to measure mood and anxiety. Axis II disorders will unlikely be able to be examined within the time-frame anticipated for this study.

Reports from online forums for people with HPPD (such as the forum at http://www.hppdonline.com) and clinical experience suggests that: 1) The current DSM-5 (update definition) diagnosis for HPPD encompassed two disorders that have distinctly different etiologies and treatment responses, the clinical community lacks awareness of the complexity of this disorder (indicated by textbooks often referring only to the transient “flashback” type [examples are available]), and researchers reporting HPPD case studies often fail to mention chronic HPPD, and although treatments listed in the literature may be successful for flashback type, they are not proven to be successful in the chronic type – this could lead to unnecessary medication treatments for individuals with HPPD and increased cost of their health care. Potential subjects for this study, unsolicited and written in a public forum, often report on the message board or personal communication that the DSM-5 (update definition)’s inclusiveness of the phrase “flashbacks” in the name of the diagnosis as well as the often mis-use of the word in the literature has resulted in the clinician treating a chronic HPPD patient as one with temporary flashbacks resulting in the patient leaving therapy and not returning and feeling discouraged.

Research Objectives and Hypothesis

The purpose of this study is to investigate if the current definition of Hallucinogen Persisting Perception Disorder, excluding the criterion of the DSM-5 (update definition) requiring hallucinogen use, to produce multiple groups and to characterize the symptoms, comorbid disorders, and serve as the largest systematic study of HPPD participants to date. The study will gather accounts of people with vision problems not caused from hallucinogens and to investigate visual symptoms from drugs that have been reported in the literature. The hypothesis is that the current diagnosis truly encompasses two distinct sub types, and dimensional scales measuring the frequency, severity, and treatment responses will create two clusters within the current diagnosis.

Study Design and Research Methods

This survey will be posted on the internet, and we expect to recruit 200 participants over a 6-month period. Only individuals over the age of 18 will be eligible to take part. To expedite IRB review, one method would be to make the survey anonymous and protect the privacy of the participants by not inquiring about any identifying demographics, such as name, date of birth, address, or phone numbers, nor submission of e-mail addresses. However, including an initial phone interview, which could be done without recording personal data, could be set-up with the current survey software to have an initial interview over the phone and providing a unique “token” to an individual to ensure non-repeaters and help increase the potential that the participants do fit within our qualifications of having visual symptoms to those defined in HPPD. In this latter format, a participant will be able to take part in the study by contacting the laboratory by phone or e-mail, and afterwards the participant receive a token which will be activated after one day. When the 24 hours from the receipt of the token have elapsed, participants will be able to enter the survey page, enter their token information, and begin the survey. Upon completion of the survey, each token will no longer be useable and the participants will be debriefed.

Subjects will be recruited through HPPD related websites , other Internet forums related to drug-use, potentially advertised, and will require the participant to complete an online consent form.

Subjects will submit an online consent statement and questionnaire with questions on

1. Demographic information

2. A list of questions structured to diagnose HPPD based on DSM-5 (update definition) criteria

3. Drug History, past and current.

4. Using dimensional scales to rate frequency, duration, and severity of visual symptoms. questions will inquire about the disorder in-depth based on the information collected both in the literature and also using language collected from the community from the on-line support message board (Symptoms Descriptions and Stories from public forum are listed below).

6. Effects of treatments with self-reported measures of their effectiveness using the standard 7-point ical Global Impression – Improvement Scale (CGI-I)

8. The Sheehan Disability Scale will be administered. If the participant answers questions consistent with the DES, then they will be branched to take the Cambridge Depersonalization Scale.

7. Allow for a free-text description of symptoms and story for clinical narratives.

8. Include vision simulators and images for judging accuracy of these items.

Regarding the survey design and my discussions with Roger Davis, in terms of the psychometrics, we would consider using the Rasch
model to derive the scales with the goal of leading to uni-dimensional scales with a good distribution of item difficulties, this will be
necessary to quantify the disorder well at every point along its severity. We don't want to end up with scales that measure the disorder only at the more severe levels. Once we reach this point, we'll have a set of scales that could potentially be used in a next step for validation to be used by the individual clinician to assess an HPPD patient and be used by a researcher who wants to further investigate the syndrome (creating a uniform HPPD diagnosis versus the current variants of language in the literature where clinicians are using the same words to imply different syndromes). I believe this would be a reasonable first step, and also would produce a publication that allows for an updated review of HPPD. I realize that the DSM-III and IV sacrificed validity for reliability. In my opinion, moving back towards empirical research, it could be useful in discussing the possibility for suggesting (aligned with Lerner's publication and what we see online and in clinical settings) the consideration of lobbying for two subtypes of HPPD: transient flashbacks and continuous/chronic. Although I realize the knowledgeable clinician should consider this diagnosis correctly, we have seen in the literature the amount of flashback case studies, undifferentiated from chronic HPPD, eventually find homes in the pages of medical web sites and textbooks that characterize HPPD solely based on HPPD of the flashback variety. I have read many stories from HPPD'rs where this has caused considerable difficulty when trying to explain to the clinician the suffering caused from full-time perceptual disturbances and needing treatment to deal with their concern for its potential permanence; this often goes invalidated by the clinician because of the word "Flashbacks" associated with HPPD in the DSM-5.

The database of responses will be stored indefinitely in a locked filing cabinet. Data extracted will be stored in an SPSS data file, MySQL db, and Excel spreadsheet file saved on computers in the locked office of the principal investigator (same location).

Women and minorities will be included. Based on registration, members of online support message boards for HPPD are more often males, so we anticipate considerably greater participation among males (HPPDonline.com statistics). Subjects will not be audio- or videotaped. Subjects will not receive any payment for participation.

There are no potential risks to the subjects from participation in this study except for potential loss of confidentiality regarding their medical condition, which we minimize by keeping medical records in a locked filing cabinet in a locked office in a locked building. There are no direct benefits to the individual subject, nor is compensation provided for participation; however, the subject and society may benefit indirectly if this study leads to greater understanding of HPPD.

Descriptive statistics, two-sample comparisons between transient and chronic cases, and an exploratory factor analysis will be used to evaluate data collated from the survey. Dr. Roger Davis has agreed to help with question and study design and pilot testing the study with students in his graduate-level class on “Methodology of Psychometric Instrument Design”.

Anticipated Results and Potential Pitfalls

We expect the results will yield two psychometrically valid, clinically meaningful, and possibly conceptually discrete underlying dimensions of Hallucinogen Persisting Perception Disorder. Therefore, the derived frequency and symptom sets are well suited for a prospective field trial study using an adapted structured interview in an effort to derive clinically useful diagnostic criteria for HPPD for the DSM-V. We may also find evidence of positive and negative treatment self-reports dependent on subtype (for instance, greater efficacy of clonazepam for symptom reduction in chronic sub-type over periodic.) Pitfalls include that the survey precludes face-to-face diagnostics for Axis I disorders and is retrospective in nature,; however, methodological shortcomings are well recognized and characteristic of Internet-based surveys with self-referral. However, selection bias is minimized by including and advertising on targeted web sites to include individuals reporting to fit in the diagnosis and including questions designed to target individuals likely to be exaggerating symptoms, and possible inclusion of other validated scales. Additionally, using the initial phone inclusion method could help reduce common problems with online surveys. A prior online survey yielded strikingly similar results on standardized scales compared to those including diagnositics (Simeon & Kozin et al 2008 & Simeon & Kozin et al 2009)

Discussion of Next Steps

If acute and chronic types do form two distinct quantitatively valid subtypes, then two-sample comparisons between both groups and also between the hallucinogen-induced and non-hallucinogen induced groups will help will provide evidence for the difference between these groups and lead to an improved diagnosis that will follow in the spirit of the new DSM-V of designing diagnoses with the goal of ultimately benefiting the patient and lead to improved clarity of diagnosis for improved research. The study would score severity and frequency and seek a possible dimensional model for symptom descriptions, uncovering an effective HPPD symptom lexicon that should be shared with neurologists, ophthalmologists, and mental health professionals. Defining the perceptual disturbances with unified symptom descriptions within the disorder will improve the precision of the diagnosis and lead to improved treatment methods.

It is now firmly established that anomalies in the P300 response are associated with a wide variety of psychiatric conditions,
including substance abuse. It has repeatedly been shown that the offspring of alcoholics demonstrate P300 amplitude
reduction despite their lack of exposure to alcohol, thus suggesting that this anomaly is an endophenotype tapping the
underlying genetic risk for alcoholism.

Research with this putative endophenotype also is helping to explain patterns of psychiatric comorbidity often observed with
other substance use disorders. To the extent that amplitude reduction indexes underlying genetic risk, the pattern observed in
the figure is consistent with the hypothesis that the covariation among these disorders reflects shared genetic influences.
There is ample evidence to support this notion, including twin and family studies showing that shared genes account for most
of the covariance among these disorders.


Consistent with the notion that P300 provides a neurobiological representation of the underlying genetic risk, P300 amplitude
also covaries with these disinhibitory disorders, with shared genes accounting for the association.

Because ERPs are derived from the EEG, it is possible to use time frequency analysis to identify the constituent EEG waves,
which, because they are time locked to the stimulus presentation, compose the ERP waveform. This type of analysis makes it
possible to determine the amount of each EEG frequency present at each point in time elapsing from the onset of a stimulus
to the resolution of the associated ERP. These event-related oscillations (EROs) can be partitioned into the same frequency
bands identified for spontaneous EEG, but these stimulus-elicited rhythms are likely to be functionally different from the
frequency bands that compose resting EEG. With respect to P300, specific neural activity have different responses during
elicitation of P300.

Event-related oscillations also are beginning to provide insights regarding brain dynamics and psychopathology, especially
regarding the development of drug dependence. Reduced delta and theta EROs have been associated with risk for the
development of alcoholism over and above the risk associated with reduced P300 amplitude, suggesting that they add
important predictive information not tapped by measures of the P300 endophenotype.
These EROs have been linked to gene variants involved in cholinergic and GABAergic neurotransmitter systems, systems
that have been implicated in the neurochemical pathways involved in substance use and P300 generation. Collectively, this
line of ERP/ERO research highlights the evolving potential of electrophysiological correlates of human information
processing to identify those at genetic risk for the development of alcoholism and related comorbidities.

Gamma-aminobutyric acid-ergic deficits might increase the vulnerability to the psychotomimetic and perceptual altering effects of serotonergic agents. These data suggest that interactions between GABAA and 5-HT systems might contribute to the pathophysiology of psychosis and dissociative-like perceptual states.

This is a huge deal, you can really help the research big time, so please make use of this opprtunity!!! This research is no joke. There is real legitimate hope.

For more detailed info:

https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.3000307

https://www.sciencedirect.com/science/article/pii/S2352289516300509

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4903954/

In the very first keyword search on MAPS' database I came up with hundreds of articles about the dangers of psychedelics, including the following from an article titled "Ecstasy and Serotonin Neurotoxicity": http://www.maps.org/resources/psychedelic-bibliography

"The authors present evidence that the elicit recreational drug MDMA may cause persistent cognitive deficits and that these deficits are related to the extent of previous MDMA use... they conclude that MDMA causes neurotoxic injury to cortical serotonin axon terminals that may be reversible."

Again, out of literally hundreds of publications this is the very first article I clicked on, published in 2001, and basically confirms one of the most popular HPPD-including drugs as neurotoxic. And yet here we are 16 years later and nothing is being done about it. There's no public education, no desire to protect our youth from the dangers of these drugs, no follow-up studies or outreach to newspapers -- it's all just buried in some online vault virtually inaccessible to anyone outside of the most die-hard psychedelic enthusiasts in the world.

I guess what's so crazy about all this is that when I first got HPPD my understanding was that it was unbeknownst to doctors, scientists, educators, teachers, social workers and the public in general due to the fact nobody knew anything about this condition. Unfortunately what I'm discovering is that many powerful people have known about the dangers of psychedelics with regards to HPPD for decades, they've just chosen to stay silent.

I don't know how the hell this condition is ever gonna see the light of day and get the attention it deserves if the people who know most about it just chose to brush it under the rug.

This could help HPPD, or am I wrong?

Recently I received a mail from Brijder Jeugd (rehab center) where they tell about a new upcoming research by a neurological department from a medical center about visual snow sufferers, and they're looking for people that want to participe in the research. This could be another opportunity to shred some light on the visual snow and HPPD. The research is targeted for Dutch people but I wouldn't hesitate contacting them in English if you're interested in the research. You can reach them by sending an e-mail to the address below:

visualsnowonderzoek@lumc.nl

If you're interested about the medical center, you can visit their website with the link below:

Leiden University Medical Center
https://www.lumc.nl/?setlanguage=English

Thanks for your time

Note: I'm not related to the LUMC in any way

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3751336/
Efficacy of vitamin D supplementation in depression in adults: a systematic review protocol
"The efficacy of vitamin D supplementation in depression has raised lots of concern. Vitamin D is considered as a neurosteroid [56], and now it is attested that vitamin D metabolites can cross the blood–brain barrier [34]. Because of the widespread presence of vitamin D receptor in areas of the brain including the hippocampus which is associated with the development of depression [23], it could be speculated that there is a clinical effect of vitamin D on depression."

https://www.ncbi.nlm.nih.gov/pubmed/26680471
Vitamin D in anxiety and affective disorders.
"Reduced levels of vitamin or its metabolites have been reported in various psychiatric disorders. Insufficient levels of vitamin D in depressive patients have been confirmed by many authors. Significantly lower levels of calcidiol (vitamin D) were found in men and women with depression as well as in age matched patients with anxiety disorders.

https://www.ncbi.nlm.nih.gov/pubmed/25713056
Vitamin D and the omega-3 fatty acids control serotonin synthesis and action, part 2: relevance for ADHD, bipolar disorder, schizophrenia, and impulsive behavior.
"Serotonin regulates a wide variety of brain functions and behaviors. Here, we synthesize previous findings that serotonin regulates executive function, sensory gating, and social behavior and that attention deficit hyperactivity disorder, bipolar disorder, schizophrenia, and impulsive behavior all share in common defects in these functions. It has remained unclear why supplementation with omega-3 fatty acids and vitamin D improve cognitive function and behavior in these brain disorder"