onedayillsailagain

Hmm yes, but visually I don't see this method improving much. But mentally/emotionally/spiritually it might be of worth investigating indeed. I'm not trying to shun it. On the contrary actually, if one were to proceed properly and safely with such undertakings (unlike how I did with Iboga), it might prove to be very worthwhile. Thanks for that FPS article, I'll have something to read tomorrow! Finding the cure.. I've been dreaming about that since I befell upon this parallel universe! Treatment would suffice if sustainable, but an actual cure! Personally I'm leaning towards Coluracetam having that potential, for a number of reasons. Perhaps not a cure in the sense of never having to take it again, but a cure in the sense of completely eradicating all symptoms, instead of being merely palliative as most current treatments are. I'm very eager to give it a try. No one with HPPD has yet tried it. IIRC a person even used it concurrently with a psychedelic and reported far less visual distortions than usual. Well, if it has such a profound effect with acute psychedelic ingestion, one could only imagine what it might be able to do for the chronic yet milder nature of HPPD visual distortions. Even if Levetiracetam would prove to work for me, I would gladly enjoy a few weeks of normalcy, to then quit again, only for the sake of giving Coluracetam a fair trial. Perhaps even more valuable would be the ability to compare improvements! Coluracetam being as novel as it is, and having a unique (!) MOA, might just prove to be a new (possibly better) treatment for HPPD. Derailed to off-topic stuff there, haha. Bit too excited about Coluracetam. Back on-topic: If one were to explore that path, indeed perhaps shrooms might be the best way to go. Honestly though, seems that there are little cases of, say, psilocybin or peyote induced HPPD. It would seem that the majority of HPPD cases involved man-made hallucinogens, rather than natural hallucinogens. Thus it would only seem wise that if one must try such approaches, naturally occurring psychedelics should be used preferentially. Perhaps I might add that while a second trip on XTC made my HPPD worse for a substantial period of time, doing Iboga did not. Perhaps for a day or three, but after that my visuals went back to baseline. I was just scared as shit though, to be blatantly honest, and was totally unprepared for a real hallucinogen. Bad timing and all that. Micro-dosing Iboga however, well that could be considered as useful. Which was my initial plan, but impatience lead me to make bad decisions. It left me with the feeling that, if only I had done Iboga instead of XTC, I probably wouldn't have ended up with HPPD, and I would've probably cherished the experience for life. Just a retrospective view on what might've been had I not been so reckless. That said, finding a universal cure for HPPD would bring more joy to my life than a thousand sunsets could ever do. Yet again I emphasize that psychedelic treatment will most likely not benefit the visual aspects of HPPD, but it may be beneficial to the common co-morbid symptoms. Personally I've just accepted that drugs (hallucinogens in particular) will never again be able to be part of my life. And I'm okay with that, knowing that I will find another way to resolve this issue, most likely thanks to neuroscience, whether it takes me a year, a decade, or a lifetime. Preferably tomorrow though, haha! Besides, hallucinogens are not necessary for spiritual growth. Meditation might actually provide a better sense of accomplishment than simply ingesting a substance, but that's just my take on it. Gee, where was I heading with this? It's a sign: time for bed. Cheers.

Hmm.. you know once I read something about shamans trying to cure people of schizophrenia with Ayahuasca. This just reminded me of that. But I sincerely doubt munching down shrooms would be helpful. I too at first thought: well.. maybe I just need to do a session with hallucinogens to get back to normal. Tried Iboga, that's a story for another day though. But in the end, it didn't help. I get the "fight fire with fire" approach, but I just don't see how taking shrooms would be remotely close to a smart idea if you have HPPD, no offense.

NO NO NO I'll expand on this later, but just NO. source: experience edit: well, I talked a bit about it in this post. Micro-dosing might be safe, so as to not have a full-blown, I-can-barely-walk, psycho-spiritual journey. And if you want to try everything, as you said, then try tDCS first. I had an occasion where I was DP-free for at least 15 minutes. The short effect duration might be due to the fact that it was a home-made device and placement might've been improper. HD-tDCS has a lot more potential than tDCS, so it might also be able to have profounder, longer lasting effects than regular tDCS. In any case, if done correctly, tDCS is completely harmless. Tends to make it climb the ladder of preferability a little.

http://www.ncbi.nlm.nih.gov/pubmed/10564367 Wiki quote of that study: http://en.wikipedia.org/wiki/Acetylcholine#Role_in_decision_making Why is this relevant? For the sake of convenience, I'll post a quote from "EEG coherence in post-LSD visual hallucinations": http://www.lycaeum.org/research/researchpdfs/2001_abraham_1.pdf Well my brain just pooped out on me, but hopefully you'll be able to see how this is relevant without me trying to disambiguate the context.

Well that picture drew me to the article. Click on the picture to read the article. “We found that the brain indexes vividness pretty quickly – about a 5th of a second after seeing a picture, which suggests it’s about seeing and not just thinking. Emotion alters activity in the visual cortex, which in turn influences how we see.” Just one of the many interesting quotes in there.

qaiphyx: How do you know the excitotoxicity is no longer present? I don't have anything to support this (yet), but it could be that through genetic alterations or other mechanisms, that some kind of excitotoxic "cycle" is taking place. Hyperexcitability/pre-seizural activity, can be/is, accompanied by excitotoxicity. What use is neurogenesis when apoptosis is still taking place then? Besides, neurogenesis mainly takes place in the hippocampus, and AFAIK never in adult visual cortex. By saying that neurogenesis is the true and only fix, you're simultaneously saying that there is no fix. If as you say the inhibitory cells are dysfunctional/damaged, then that would only trigger a cascading event of excitotoxicity I'd suppose. Also there's enough evidence suggesting the cerebellum (where most of these cells are located) is intrinsically involved with vision, so it wouldn't only affect anxiety and balance. Just some thoughts straight out of bed here.. back to the tea

http://digital.library.adelaide.edu.au/dspace/bitstream/2440/56315/1/02whole.pdf Yep.. insomnia is to blame for me finding that. Really nothing to say about it, besides that ACh is always interesting. Haven't read through it myself yet, but seems quite extensive and should prove to be a good read.

Wwhy do I have to feel so loopy now? I thought I somehow found a way to provide an end to the cycle. Well, let me try regardless. Acetylcholine and hallucinations: disease-related compared to drug-induced alterations in human consciousness Relevance of S-N-R can be found here and here for those of you cognitively more competent than I am (at this moment). So.. correct me if I'm wrong, but acetylcholine enhances signal-to-noise ratio (possibly synonymous to: "reduces neuronal noise"). Epiphany? Perhaps. Soooo.. damnit I lost all my relevant arguments. But it basically came down to: Coluracetam (High-Affinity Choline Uptake Enhancer/ AcetylCholine biosynthesis enhancement) + PRL-8-53 (Positive Allosteric Modulator for ACh receptors / potentiates the effects of ACh) = Super cholinergic synergy + protection from excitotoxicity = probably pretty darn awesome for our case. I got too excited and closed some pretty awesome pages by accident, and can't seem to retrieve them. Damn, damn, and damn. Hoping one of you can make use of this sparse information, and that I might be able to expand on this tomorrow. Perhaps also of interest (although it's on retinal neurons.. but w/e): http://www.iovs.org/content/45/5/1531.full

Damn.. nice find qaiphyx! So then one could try and go about modulating metabotropic glutamate receptors or gene expression (which would probably prove to be extremely difficult). One thing that keeps coming back is the excitotoxicity though. Seeing as this would be easier to treat, I'd expect that taking the right combination of supplements/medications would be enough to reduce symptoms. Maybe this is partly the reason why Keppra works so well for some: http://www.ncbi.nlm.nih.gov/pubmed/17408599 And it of course inhibits pre-synaptic calcium channels. On mitochondrial damage and excitotoxicity from wikipedia: It would seem to be that supporting mitochondrial function, by example, would be beneficial in mitigating excitotoxicity.. Or anything that could limit or reverse the excitotoxic damage really: http://www.ncbi.nlm.nih.gov/pubmed/9541286 I'll look into this later, but it's definitely interesting, thank you!

Actually Ketamine is a NMDA antagonist, meaning it blocks its function basically. However it can't be ruled out that some glutamatergic storm took place, or that there has been a long-term alteration in glutamatergic transmission. But I like your defense-mechanism theory as to why there's dissociation! Following your neurochemical theory though; if there's still NMDA overload taking place, then an agonist would only worsen symptoms. Glutamate is seen as the basic excitatory neurotransmitter, and seeing as there's believed to be pre-epileptic/convulsant/hyperexcitability involved in HPPD, I doubt there's a thereapeutic potential in NMDA agonists. From what I've learned, it's best to focus not on a single neurotransmitter, but more on regional excitability and focal therapy (like tDCS: regional excitability changes.. I've had marginal succes with that, particularly for the DP/DR symptoms). Indeed I believe DP/DR is closely related to anxiety as well, and there might be some dysfunction of the fear response. Personally I notice that after a period of anxiety, my DP/DR gets worse. When there's little anxiety, it doesn't get much better though, it just plateaus I suppose. If you don't have anxiety, my guess is that raising excitability in your frontal regions (especially ventromedial PFC) would be beneficial. Sam, I'm not in any position to make recommendations, but you might want to consider tDCS if you're not planning on medication. It's a non-invasive (and of its class, the least invasive) form of brain stimulation. Again, my experiences were.. how to say.. profound but very transient. Like I flashed back to reality for a few minutes, and then it was gone. But I must note that the device I used was homemade, moreover was the positioning done by myself (could've been that it wasn't directly over the correct region). I'm very eager to see HD-tDCS come to the market soon, as it provided for much better "aiming" and less (almost no) effects in the surrounding (non-targetted) regions. Some believe HPPD is a form of Toxic Encephalitis or (glutamatergic/NMDA) excitotoxicity. Mitochondrial supporting supplements I suppose would help in this regard, limiting excitotoxicity to possibly reversing it (don't quote me on that, but I'm sure it won't hurt). Anyway, I'd stay away from the NMDA agonists if I were you. Have a glance over at Research Articles for some other theories, and I believe recently I posted something about the neurobiological associations with DP/DR. All the best, Odisa.

I think perhaps he might be referring to some LSD-LTP induced excitotoxicity: Seems that glutamatergic excitotoxicity is what happens with LSD ingestion, be it direct or indirect. His reasoning is actually not strange: http://www.nature.com/npp/journal/v26/n5/pdf/1395848a.pdf Basically the idea was, that changes (neural or genetic, maybe in the form of LTP, doesn't really matter for now) had occured which caused chronic glutamatergic (and thus ionic calcium) excitotoxicity. Hyperexcitability (convulsant activity of substantial degree, as seen in HPPD) tends to involve this as well: http://en.wikipedia.org/wiki/Epilepsy#Pathophysiology. Despite the extremely low dosing, it can't simply be said that Keppra isn't doing anything for him. As he said himself though; he hasn't tried Flunarizine without Keppra, so perhaps you are right. But it could be that because they both interact with calcium transmission, they're working synergistically. Also from his report, it seems that such a low dose was effective for him. Yes, might be placebo. But honestly I think that if he didn't have a profound sustainable revitalizing epiphany of some sorts, he would've been smart enough to know that it was an isolated incidence of placebo, subsequently he would probably haven't gone through the trouble of posting his results. He's obviously tried various things, and would know how to discern between placebo and actual effect. Hate to be talking in the third person though, so maybe @Survey could join the discussion?

Hey Sam, welcome to the forum, and thanks for sharing you story! Seeing as you are hoping to recover without medications, perhaps consider some good supplements to help that process, along with proper nutrition of course. It'll definitely help your cause, and you'll feel better about yourself for investing in pills that are good for you If you need references: Longecity.org, Examine.com and Lef.org are good places to start educating yourself on how to support a healthy lifestyle through nutraceuticals. I wish you the best of luck. Odisa.

Enjoy N.B. Seeing as many HPPD'ers attempt to limit/reverse/repair neural damage, I thought this would be relevant to those considering mitcohondrial supporting supplements. Sadly I can't take any supplements at the moment (Levetiracetam evaluation purposes), but I'm considering this supplement for in the future. Seems pretty damn awesome to me. You can also view some of my findings on CoQ10, PQQ, Resveratrol, and the likes, in this same sub-forum.

Hey Zenith, the symptoms you describe look to me more like you're experiencing a bout of Depersonalization, which can have some visual disturbances as well. Your symptoms seem to be mild in nature, and as such I would presume that it's DP. No after-images, visual snow, and other disturbances? Combined with your anxiety, all evidence seems to point to DP without HPPD. No comment on the Prozac though, but hey if it works for you right! Personally I'd rather investigate other safer, sustainable, healthier options for anxiety management. Either way, good luck recovering from this. When I quit MJ (smoked about 3 joints daily from age 12-14), I as well experienced absurd levels of anxiety and depersonalization/derealization. These subsided with time, after which I felt lucid for the first time in years. And as such I think that doing everything you can to support good health will probably speed up that process. Stress management and proper nutrition alone should provide your body with all it needs to recover. I strongly suggest you read the Marijuana topic on page 301 of the Principles of Pharmacology. Serotonin pop-sciences crown-jewel, as such I suggest you take a step back from that focus, and read more into the pharmacology of cannabiniods. Anyways, I got the actual physical book in front of me, and reading through this it would seem a lot more sensible to use a sympatholytic or an anxiolytic to manage your symptoms, rather than an SSRI. "Cannabinoid use causes a prompt high characterized by euphoria, laughter, giddiness, and depersonalization .... High doses of marijuana can cause anxiety, overt panic reactions, perceptual distortions, impairments in reality testing ... Overt panic reactions are the most common reason cited for stopping marijuana use. Withdrawal from marijuana is generally mild due to its high volume of distribution and long elimination half-life. Withdrawal symptoms can include insomnia, loss of appetite, irritability, and anxiety, perhaps due to activation of corticotropin-releasing factor (CRF) system, particularly in the amygdala." Which would cause arousal of the sympathetic nervous system. Have some searches on endocrinology and the likes, maybe consider Ashwagandha instead of Prozac. Have a look over at http://www.lef.org/search/health-goal.adrenal/index.aspx if you're up to it. Also, do you have any concurrent medical issues or uses other medications? Asthma, Lyme, Pfeiffer, thyroidism, whatever? That would give more insight into why you're experiencing what you are. For example, most Asthma medications are sympathomimetics, which can cause anxiety, and subsequently depersonalization. Getting blood tests, hormone function tests, etc. always contribute to a better picture of your health status. Knowing the pharmacodynamics of the medications you might be taking for other issues is also a wise thing to do, as simply switching medications can make a whole lot of difference. Sometimes (if not more often) doctors overlook these simple factors, so it can be necessary to take responsibility for such matters into your own hands, depending on how dear you hold your health. All the best, Odisa.

Don't be discouraged by the seeming irrelevance of this article! http://www.nature.com/mp/journal/v7/n3/pdf/4001032a.pdf Basically that says, that when you are chronically stressed to the max, your ability to change is severely limited. Moreover, a (chronic) hyperactive stress (SNS) system, directly contributes to dysfunction of the PFC, making it even more of a challenge. To put things in perspective: there are also many studies out there that show that stress-induced damage/alterations can be reversed by various means.

http://www.scribd.com/doc/130535139/Depersonalization-Disorder-a-Functional-Neuroanatomical Hmm.. it's been found that people with DP have an inhibited sympathetic reaction to emotional stimuli. Whatever the case, I know for sure that I, for one, do not have an inhibited sympathetic nervous system. In response to emotional stimuli, perhaps. But in general, I would perceive myself as having a hyperactive SNS. Perhaps the studies focus on 'pure' cases of DP. Quite often though, DP is co-morbidly accompanied by anxiety of various forms and sizes. IME, it's very ambiguous and personal what ANS response you'll have to certain stimuli. Moreover, skin-conductance.. yeah I don't know. Plus it was also an acute stressor. I think there's some better conducted study reviewed further on in the article. There's some other general information in the article, but I just can't Ctrl+F it, and I'm lazy now. But there should be something about vmPFC functioning in there, so that would be good to know. It's pretty extensive, so have a go at it when you've got nothing to do! Cheers.

http://en.wikipedia.org/wiki/Broca's_area Afferent connections from the PFC may be contributing to this, as there has been shown to be a measure of inhibition of non-visual cortical areas in HPPD. The somatosensory link is obviously also of note. PFC dysfunction (regardless the cause) would then be able to contribute to speech problems. Anxiety and stress are detrimental to PFC functioning, so go figure

Thanks for sharing!! Although personally I'm of the view there's not nearly enough neuroplasticity present for this. Maybe in some individuals there is though, IME it sure doesn't seem so. But not everyone's etiology is the same of course, and many still retain most of their higher cortical function, indicating lesser 'damage'. Which is why I think that this might be of (more) value in combination with other therapies (NIBS, nutraceutical/farmaceutical interventions). Either way, nice find! EDIT: ohh.. ja laatmaar je weet hoe ik erover denk didn't see it was you!

Yeah it's a great thread, ScienceGuy is very comptetent. Check out Examine.com as well for info on supplements, also useful

Hello again Kellen, thanks for sharing your story! No comments on Effexor though, my knowledge is rather limited on it. But there are many different options to consider (seeing as you are now off of Effexor). Clonazepam, Lamotrigine, Levetiracetam, and Sinemet, to name a few popular choices. Alpha and Beta blockers are also used, Clonidine being the most common, and Propranolol sometimes is used in people who wish to reduce the physical symptoms of anxiety, more so in those prone to panic attacks. If anxiety is a large portion of your torments, then anxiolysis will be a key component to feeling better, at least in the short-term. There are many anxiolytic medications, supplements, herbs, and therapies.. Finding whatever works for you can be the hard part. But seeing as your new to this all, perhaps try a cup of Kava now and then. Though I would advise not to use it concurrently with Zopiclone. Finding a good doctor willing to help and experiment a little is usually a good step to recovery. To answer your other question: symptoms can differ from person to person. HPPD mainly encompasses visual symptoms. Yet other co-morbid disorders can be Derpersonalization, Derealization, Anxiety, Cognitive Deficits, Panic Attacks... Yeah you get the idea. And not everyone experiences the same visuals. But they are largely similar though, and if I'm not mistaken almost all HPPD'ers have visual snow to some extent.. Too bad we can't take photo's of it; would be interesting to compare, no? So yeah, if you feel up for it.. Print out the HPPD page of the DSM, and head over to your doctor. Sorry, feeling rather tired so my advice is limited for now. Hope to help better later. Cheers mate!

Hey Baseline, welcome to the forum Yes many of us experience Depersonalization and/or Derealization co-morbidly. This can be accompanied by feeling "high" despite being sober. If I'm not mistaken (brand names.. tend to forget those) Attivan is a mild benzodiazepine right? With responsible use it's unlikely to do any damage, and will probably provide short-term relief. Effexor I think was Venlafaxine. Reports are mixed on that one, for some it works great, for others it's a nightmare. I think Visual already commented on that in the other thread you posted. Any improvements yet? All the best, Odisa.

Hey man, considering your taking a sympatholytic, caffeïne would probably not really aid your cause. But I suppose it wouldn't hurt too much if your not that anxiety prone. Idk what the other ingredients are though, can't find the stuff online. Any improvements yet? Lately I've been seriously considering adding a sympatholytic.. Would be cool to know if you've had any success with this. All the best.

Hmm I'll respond at more length later.. I mean yeah, why not right? All things can be considered. Finding something in common (besides drug use) among HPPD'ers would be a good start for finding an actual cure. Anyway, before people start spraying JC virus concentrate onto their tonsils.. Immunodeficiency may cause the JC virus to lead to progessive multifocal leukoencephalopathy. Considering many with HPPD experience high levels of anxiety/stress, they're more prone to being immunodeficient, and as such would be more prone to contracting PML from the JC virus. However I won't common on the likelihood or lack thereof of this, as I have no freaking clue. Obviously chronic stress would never make you as immunodeficient as AIDS for example. Cheers.

Having been mostly sedentary the past year, along with sitting in a chair too small, looking at a screen to small, my back has been killing me lately. A few weeks a go I sprained a muscle, and had to walk to the pharmacy like a hunchback. Anyway, seeing as I've been far less anxious than usual, I managed to gather the courage to make an appointment for a back massage this afternoon. So far it seems it reduces cortisol levels (acutely), and raises serotonin and dopamine levels. Sounds like a win-win situation to me. Here's a comprehensive article on massage studies done in different disorders, including PTSD (some people believe HPPD might be a form of PTSD). I'll add more later, for now I have to take a shower and catch a bus! EDIT: well I got bored with this. But feel free to add anything relevant here.