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Hallucinogen Persisting Perception Disorder (HPPD) Support Forum

David S. Kozin

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David S. Kozin last won the day on August 19 2019

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About David S. Kozin

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  1. Mike, ACAD in Oct 2012 right? If you dont know, then ignore. But I think it was.
  2. Violet, you did list a few major qualifications that matches research and experiences: 1) I think Marijuana is a fine drug in general, but I never liked it. However, the first time I smoked it was a few weeks after my HPPD started -- I thought it would be a way to join the high my friends where having, but not take a hallucinogen --- I WAS WRONG. My symptoms shot to a 12 from what was probably a 6 just moments before a few hits. Then, symptoms gradually went down to the 10. Dr. Abraham goes so far as to say for someone with HPPD, he would avoid second hand smoke. It makes good sense. Honestly, why this happens is still a mystery. Generally, people who only use Marijuana very rarely get HPPD. However, people who have taken LSD and then smoke pot weeks, months and even longer, will have it feel like the pot was laced. Homes were bending like a cartoon. It seems that once the first time it jumps up that it doesnt have that same effect again. There are marijuana smoking HPPD people. How would it happen? LSD temporarily affects how certain brain cell's will produce different amounts of the receptors on a neuron. It takes a few days for this epigenetic action to stop working. Eventually, the way LSD changed the expression of those genes stop. This is why taking LSD for 7 days in a row eventually gets less effective until it has almost no effect. After a few days it begins to return to normal. If LSD & trauma together creates a specific state for these cells where nothing is noticeably wrong, but made the cells hyper sensitive to the effects of marijuana. That is a long way of saying, it makes sense what you are saying. The question is does it sound like HPPD? If you did not take any drugs for a month and told me not much has changed, it would sound like at least part of it is the syndrome we call HPPD. If you read some other first person descriptions you might find they click or they dont at all. As Robbie said, do you see what appears like TV static projected all over your vision? Hope that helps. Dk
  3. Essentially, the community does: 1: Introduce Themselves. 2: Comment and Share an Experience Relevant to an introduction. 3: Person asks questions (often repetitious, so it would be nice if suggested answers would be automatically included 4: People discuss mechanisms, medication and other topics that could be better and self organizing. 5: The board has lost 75% of activity in 2 years. My thought: 1) Have a verified user control that can't be spoofed for users that are verified. 2) Allow for creation of Questions like Quora, Topics Discussions, or Posting (like Facebook) 3) Users can be anonymous for some things. 4) Sign up with e-mail/etc or use social media login's like Twitter, etc if you choose. This is a free version of Tribe, and much of the extra features are not provided, but it seems like posts here just get lost into limbo, so why not have it make some sense and things that are hot topics stay that way, and things that are not go away, but can be searched. Also, MOBILE FRIENDLY! https://hppdonline.tribe.so/
  4. "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.
  5. HPPD STUDY IDEA: Prepulse Inhibition Study and Event-related Oscillations from Evoked Potentials: (P300 EEG, EMG & ERP) Mid-latency evoked responses are so designated to differentiate them from the earlier sensory potentials and later ERPs that are more affected by cognitive processing. The ERP measures that appear most important are the three most examined midlatency components in the auditory modality that are designated P50 (a positive component occurring between 35 and 80 ms after stimulus onset), N100 (a negative component occurring between 80 and 150 ms after stimulus onset), and P200 (a positive component occurring between 150 and 250 ms after stimulus onset). These components share the characteristic that their amplitude decreases with repetition (habituation or sensory gating). The P50 and N100 components have been studied extensively in psychiatric patients. Sensory gating of P50 is a potentially useful endophenotype of psychosis or latent psychosis. Evidence for an inhibitory abnormality (i.e., sensory gating deficit) in schizophrenic patients has been around for almost 25 years. The magnitude of the deficit is similar to the most robust findings reported in neuroimaging and neuropsychology in schizophrenia. The N100 electrode component has also been recently shown to exhibit a similar deficit in habituation in schizophrenic patients. 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.
  6. 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.
  7. DISCLAIMER: My ex-girlfriend was advised by her money manager not to put $25,000 into my suggestion to buy stock in the company that was testing this drug. It was October 2012, and it was $2.00. She didn't tell me she was going to buy some, she did it on her own in case it went down to $1.000 and she lost money. (Great Girlfriend, I know). Money Manager guy said it was not wise. She decided not to. I sent a facebook message to close family members. Nobody would listen, and I have given 2 stock suggestions in my life: Netflix, NVIDIA (in 2008, whenever it split twice in Feb). I explained why I was so certain it was going to pop. On my public Twitter account, I recommended it at 2.00. then at $4. $7. $9-11. All publicly, but I had no money and didn't realize how easy it would be to set up an investment account or I would have put at least 500 dollars in by selling everything I owned. The 25,000 would have bought 12,500 shares and two years later was worth $500,000‬. My family wishes they listened. So... I have been watching ACADIA since 2012, and although I had no money I recommended to wealthy family members and others to buy it at $2.00. I even publicly posted why. You can understand why it would appear on my radar right after finishing my degree and working on theoretical models and potential targets and I saw this. I have not stopped watching ACADIA, and later did own stock option calls and because of financial issues sold them. This is a very interesting drug. I knew it was going to get approved because the FDA needed a drug for Parkinson's, but I knew this was not the ultimate goal. The ultimate goal of a pharmaceutical company is to open up to a big market. Parkinsons as a target made it receive fast track status because no existing treatment for PD. Big institutional investors started getting in. Risperdal causes issues (theorized and along with Yale's Souza lab and others in similar human research) that unlike regular schizophrenia, where these atypical antipsychotics block 5-HT2A sites, which means that in the one system we often talk about that has 5-HT2A inputs to produce GABA inhibitory signals would mean LESS GABA inhibition, the drug addressed both this and new method for working on the DOPAMINE system where the COMT theories and other targets for HPPD were coming out. I designed a protocol study for HPPD using a pre-pulse inhibition design. I wrote out my theory for why this test would be useful and it ends there. I actually thought that it would be less helpful for pure HPPD visual symptoms, but most helpful for Depersonalization and Derealization symptoms. Maybe one day, we can get that study moving. But, I have been linked to this drug for a long time, and I would like to see something come out of it. Don't believe the CNN hype articles, they were manipulation stories that are part of biotech investments .
  8. It might make a useful post now. Unfinished. It can be your call. If you think helpful, then unhide it all and keep the conversation. One major step I worked to change is my ability to let go and trust others. Night!
  9. I was rambling on, and then wanted a break and to come back to it. It is perfectly fine to comment. ") it gives a good look into my brain I think. Also, if I am going to discuss something that may put me in a precarious situation, I just hide it and come back to it later. People with different learning styles or challenges in traditional classrooms or learning disorders are represented in a higher percentage than normal groups. This is Dr. Abraham's experience and I agreed. My qEEG and more specifically Dr. Frank Duffy's impression of my EEG back in 1999 is classic ADHD now. My front and central cortex has "astroundly high" amplitude for theta broadly across the region and even working on task, I am in this.high theta state. Of course, this is a state that monks are measured at achieving and people seek to reach this point with meditation. I can lucid dream almost at willner night if I thing about it for a few days. I can also see unusual connections in things and it has made what should have been an extremely lucrative stock trader. Howtoadhd in YouTube is a beautiful spirit with ADHD that has an wonderful channel she developed and has recently had other groups visiting on her channel. I'll post something about this soon enough, but it may be a video. Oh yes, my one point: more people with HPPD have these conditions, but do students feeling they are not working up to their own standards at school or life and are frustrated tend to take hallucinogens more than neurotypical and this is why the prevalence. I take Adderall for it, and it is a life changer. I was in tears at all the first. I finally graduated college in 2011 after starting in 1996 and having three publications in the interim. But in 2008 I read a book without skipping pages. I am celebrating that Inhave not missed a doctor or dental appointment in one year using my Bullet Journal, which I treat with every reverence. I would miss final exams and appointments routinely and it could be written on my hand. Ok, I have had trouble sleeping ever since I took a drop from 4 to 2mg of Klonopin recently and punctuated it with 7 days of klonopin free. I was in a safe space, so now I am trying 2mg and the day goes well, but sleep is not. This includes.that I have gabapentin to help. 20 years of benzos will definitely change expression of receptors, but I think we are much more resilient than we give ourselves credit for. - dk
  10. Mad Doc gives great advice. I can tell you that your choice of grammar for your post's subject already tells me -- I am recalling many years of people giving an introduction -- you said something that puts you in a group that has the best outlook. What is it? You used exclamation marks, but just to say Hi. Not like "My life is ending!!!" But "New Here!!" It may seem like a small observation, but if I have to make a judgement this is telling. It goes along with how well you are doing for your time frame and this is a great indicator. - dk
  11. Serotonin Syndrome is scary. I had a girlfriend get the onset of it, I checked her meds and the liver enzymes to break down an antibiotic potentates two other Serotonin active compounds and the first day she had trouble reading books, and she is an author. It required me taping her and playing it back to prove there was a problem. Had it gone one more day the toxicity would have been deadly. But, she claims lasting issues and not feeling as sharp as she once was. What you are trying to describe is difficult, but I think I relate. It is something a person in the early stages of their HPPD would experience. In my case, and MANY others, the initial stage of handling HPPD is a process where it affects almost every part of a person's life. A week earlier, you may have loved going to sports games, and suddenly it seems that you are disconnected from that person. Often, the fight to get back to that person and/or the worry you wont be that person again is precisely a major factor in not feeling that you are that person. It doesnt help if other parts of your life are changing also, and that feeling of neurological challenges can be very real, and at the same time he caused by additional stress or anxiety. The real biochemical mechanism is there just as someone that may have PTSD and suddenly shut find certain experiences challenging and risk taking or free flowing words dont feel there. One good test is if you have people close to you bring up your changes and they can see or hear it. Anxiety can do the same, and I know that as I work through the benzo tapering that my personality and my inner panic and feeling of relatedness to my body go through what feels like epic battles (usually while I am sitting on the toliet) where I am over thinking things. Even feeling constipated can effect mood significantly and I would say we are a group of people extra sensitive to these types of changes. However, just as the Doc described, there is a point where I often get an email from a person who would claim I didnt know what I was talking about and their life will never be the same, and then they wanted to tell me they havent been on the message board for the last 5 months because they could get back to enjoying life and apoligize for saying their HPPD must be worse than mine. My goal is that nobody would would visit this site and everybody had no complications, but I know it is a naive belief. Gabapentin is a strange one, but there is also a reason why people who "dont do drugs" liked to get it from bewildered dealers of cocaine and other serious drugs. I can day that I know a dealer that would actually trade a 1:1 pill of MDMA powder for an 800mg gabapentin. Admittedly, his source was good and in kilograms, but gabapentin helped his symptoms of taking daily doses of MDMA (I know, but it is possible and it isn't pretty) but Gabapentin helped that severe case. If anything works, or you have any other thoughts please post them and also email me at hppd@protonmail.ch . It is my most protective email and also doesnt have 10000 unread messages. Best of luck.
  12. Hi Thomz, I wish I could give you a great answer, but I can try and be reassuring and if you can tell more than it could help, but ultimately it will be you and a doctor that makes that decision. 1) Yes, the symptoms of HPPD may not appear until later in life, but typically it is much sooner than later. Also, research and personal experiences are pretty clear that alcohol is not a common if almost never a drug that starts HPPD after hallucinogen use. 2) Visual Disorders that share very similar symptoms, but the individuals have never taken a hallucinogen inside Visual Snow (this name is misleading, as the symptoms can include much more than the static snow symptom). Other disorders are best rule out by a Neurologist, but just to be complete with my answer I will mention Temporal Lobe Epilepsy. 3) Most people with HPPD will not question whether they have it or not after they have read the list of symptoms. It is such a shocking experience to hear someone talking about having their walls moving in the side of their vision but they never go anywhere or one day have perfect vision and the next day and beyond have blurred vision. I hope that helps
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