onelovez

https://speakwisdom.wordpress.com/2015/07/15/apex-type-a-tdcs-device-review/ - here you can find a nice review of it . I gonna buy it within next few days and do some tests. It looks solid and the price is reasonable. let me know anybody if there is other interesting models in similar price range.

Thanks for sharing all the info with us!

This one looks interesting. I wrote about it before in a different post, but decided to make a new one. It looks safe and it's description hits few interesting keywords, glutamate caused excitability and been anecdotally reported to work on tinnitus, which is an HPPD symptom, and might therefore be implicated in its pathophysiology. Drug's name: Acamprosate Drug class: NDMA modulator, depending on concentration/dose applied (possibly weak antagonism action at NMDA receptor) Effect on Calcium Channels Neuroprotective Effects Used as treatment for: Alcohol dependence/withdrawal Tinnitus Effect on HPPD (Anecdotal experiences): No references on HPPD communities, one reference on Those With Visual Snow forum Not any known anecdotal experiences, open to experimentation Side effects: Diarrhea, nausea, anxiety, depression Study: Role of acamprosate in sensorineural tinnitus http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3271548/ http://www.dovepress.com/acamprosate-for-treatment-of-alcohol-dependence-mechanisms-efficacy-an-peer-reviewed-article-TCRM Acamprosate has low bioavailability, but also has an excellent tolerability and safety profile. Mechanism of action of acamprosate. Part I. Characterization of spermidine-sensitive acamprosate binding site in rat brain. http://www.ncbi.nlm.nih.gov/pubmed/9660304 ... The results show that acamprosate binds to a specific spermidine-sensitive site that modulates the NMDA receptor in a complex way. Together, with data from al Quatari et al. (see next paper), this work suggests that acamprosate acts as "partial co-agonist" at the NMDA receptor, so that low concentrations enhance activation when receptor activity is low, whereas higher concentrations are inhibitory to high levels of receptor activation. This may be relevant to the clinical effects of acamprosate in alcohol-dependent patients during abstinence. http://onlinelibrary.wiley.com/doi/10.1111/j.1527-3458.2003.tb00260.x/pdf page 10: Initial studies postulated that acamprosate might affect central neurones through an activation of the GABA neurotransmission (19,20). However, this hypothesis has been practically ruled out. Acamprosate does not seem to affect GABAA receptor mediated trans mission. Since approximately 1997, investigators re-directed their efforts and explored three possible mechanisms of action of acamprosate (31,60): — interaction of acamprosate with N-methyl-D-aspartate (NMDA) receptors; — blockade of voltage-dependent Ca2+ channels; — changes in NMDA receptor subunit composition. In this section we review data that support these three hypotheses. ....However, it is not clear whether acamprosate enhances or inhibits NMDA re- ceptor function.... Zeise et al. (66),using in vivo electrophysiological recordings and in vitro techniques, reported in 1993 that acamprosate reduces the activation of synapses controlled by L-glutamate (L-Glu) in the rat neocortex. These authors showed, for the first time, that acamprosate potently and reversibly reduces depolarizing responses induced by several excitatory amino acids, including L-Glu and NMDA. The interaction of acamprosate with NMDA receptors has also been studied using other in vitro techniques. So, Allgaier et al. (1) studied the effect of the drug on the Ca2+ influx evoked by NMDA in cultured neurons. The results obtained by these authors clearly show that acamprosate significantly reduces NMDA-induced elevation in free intracellular Ca2+ concentration. Similarly, Al-Qatari et al. (3) showed that acamprosate inhibits glutamate-induced calcium entry in cultures of neocortical neurons without affecting glutamate... .... Taken together, it seems clear that acamprosate reduces glutamatergic neurotransmission.... Blockade of Voltage-Dependent Ca2+Channels In addition to the above described interaction with the NMDA receptors, acamprosate has been found to block the voltage-gated Ca2+ channels. This effect could also be responsible for the reduction of neuronal hyperexcitability by acamprosate during alcohol withdrawal. Initially, it has been reported that acamprosate displaces Ca2+ channel antagonists from a low-affinity site on brain membranes and inhibits the upregulation of Ca2+channels in alcohol-withdrawn rats (4). More recently, Allgaier et al. (1) reported that in rat cultured mesencephalic neurons acamprosate antagonizes K+ -induced increase in intracellular Ca2+ concentration in a concentration-dependent manner Taken together, it seems clear that acamprosate reduces glutamatergic neurotransmission. At this moment it is not clear whether these effects are a result of a direct interaction with the NMDA receptor channel or with the polyamines-sensitive binding site at the NMDA receptor. Acamprosate seems to act as a functional antagonist at the NMDA receptor system counterbalancing chronic ethanol-induced changes. This would lead to a reduction of neuronal hyperexcitability during the true and the conditioned ethanol withdrawal. Blockade of Voltage-Dependent Ca2+ Channels In addition to the above described interaction with the NMDA receptors, acamprosate has been found to block the voltage-gated Ca2+ channels. This effect could also be responsible for the reduction of neuronal hyperexcitability by acamprosate during alcohol withdrawal. Initially, it has been reported that acamprosate displaces Ca2+ channel antagonists from a low-affinity site on brain membranes and inhibits the upregulation of Ca2+ channels in alcohol-withdrawn rats (4). More recently, Allgaier et al. (1) reported that in rat cultured mesencephalic neurons acamprosate antagonizes K+ -induced increase in intracellular Ca2+ concentration in a concentration-dependent manner. Changes in NMDA Receptor Subunit Composition In 2001, Rammes et al. (51) reported that acute acamprosate (and other well estab- lished NMDA antagonists such as memantine and MK-801) increased the expression of specific NMDA-receptor subunits in selected brain areas. This phenomenon could con- stitute a novel pharmacological explanation of the mechanism of action of this drug. Importantly, upregulation has been selectively observed in the cortex and hippocampus and no changes were detected in the brainstem. In the cortex, the changes in protein expression were detected after a single i.p. dose of 200 mg/kg of acamprosate; they affected mainly the NMDAR1–3/1–4 and NMDAR2B subunits. In the hippocampus two injections of acamprosate, 200 mg/kg i.p., separated by a 12-h interval, increased protein expression of all subunits investigated (NMDAR1–1/1–2; NMDAR1–3/1–4; NMDAR2B). These data strongly suggest that NMDA-receptor subunit expression can be rapidly and region-dependently increased after acute exposure to acamprosate. Provided that changes in NMDA-receptor subunits composition could induce changes in functional characteristics of these receptors in the brain regions affected, the modulation induced by acamprosate may constitute a novel explanation of the mode of action of this drug. However, more experiments are necessary to properly characterize the neurochemical consequences of these changes in the transcription of NMDA receptor subunits. A new hypothesis to explain the mechanism of action of acamprosate has been recently proposed (26). According to this hypothesis acamprosate exerts its effects through interactions with the group I metabotropic receptors for glutamate (I mGluR). Harris et al. (26) found that acamprosate inhibits the binding of trans-ACPD (a well recognized agonist of the group I and II metabotropic glutamate receptors) to AP2 membrane preparations of several rat brain areas. Moreover, acamprosate was neuroprotective against trans-ACPD induced neurotoxicity in organotypic hippocampal slice cultures. Hence, in the opinion of the authors, acamprosate’s binding and functional characteristics are consistent with it being a group I mGluR antagonist.

I have a bad reaction with most meds even clonazepam. I might give lomerizine a go, but first I wanna try to get some relief with natural supplements for another few months. But if anybody here feels strong enough to try, go for it.

Ok but which supplements have you tried for longer than one month?

What do you guys think of this? I don't know how much different it is from other calcium channel blockers. It just that it acts on 5HT2a receptors, antagonizes them right? From what I have heard agonising and antagonising of 5HT2a receptors both downregulates these receptors.. And a very interesting thing - in wiki it says "serotonin-induced contraction of the basilar artery, which can lead to migraines." If serotonin can contract the basilar artery, maybe.. since people with HPPD seem to be somehow oversensetive to drugs (many of those people anyway), could the agonisation of serotonin receptors by psychodelics/other drugs, cause some constriction of some blood vessels, seriously restricting the blood flow and doing something to our brain? Ischemia, dysreguletion of something, anything. As I said many times before - I did scintigraphy examination of the brain which shows focal hypoperfusions in two places.. (those responsible for cognition and language etc). Could that be caused by the "serotonin-induced contraction"? It's like.. if any of the drug did restrict the blood flow - the restriction stayed until months/years later. Is that possible? more about the drug itself: https://en.wikipedia.org/wiki/Lomerizine : Lomerizine (INN) (also known as KB-2796) is a diphenylpiperazine class L-type and T-type calcium channel blocker.[1] This drug is currently used clinically for the treatment of migraines, while also being used experimentally for the treatment of glaucoma and optic nerve injury. Mechanism of ActionLomerizine works as a calcium antagonist[3] by blocking voltage-dependent calcium channels.[4] A study using [3H]Nitrendipine showed that lomerizine allosterically inhibits binding in calcium channels at a site different than the 1,4 dihydropyridine binding site.[5] However, its antimigraine effects are believed to be due not to the blocking of calcium channels, but to the antagonizing effects of lomerizine on the 5HT2A receptor. The drug was shown to competitively inhibit binding of [3H]spiperone to 5-HT2A receptors, inhibiting the 5-HT driven release of Ca2+. Lomerizine treatment of 5-HT2A expressing cells led to the inhibition of Ca2+ release in response to 5-HT, while Ca2+ release in response to ATP was unaffected.[6] By preventing the release of Ca2+, lomerizine prevents serotonin-induced contraction of the basilar artery, which can lead to migraines. Lomerizine has also been shown to possess neuroprotective effects, specifically in the case of retinal damage. Doses of .03 mg/kg given intravenously as a pretreatment were shown to prevent glutamate-induced neurotoxicity, while also providing protection against NMDA-induced and kainate-induced neurotoxicity. Lomerizine was shown to have little affinity for NMDA or kainate receptors, so its protectivity against neurotoxicity in these cases is believed to be due to the blocking of Ca2+ influx through voltage-dependent calcium channels.[7] By blocking these channels and preventing Ca2+ release, lomerizine increases circulation in the optic nerve head. These effects show that lomerizine may prove to be a useful treatment for ischemic retinal diseases, such as glaucoma.[7] Lomerizine also shows neuroprotective effects against secondary degeneration resulting from injury in retinal ganglion cells. In this case, increased membrane depolarization, in conjunction with the inability of the sodium-calcium exchanger to function due to depleted ATP stores, causes the activation of calcium-dependent signal transduction. These processes lead to cell death through either apoptosis or necrosis.[4] Lomerizine's role in blocking Ca2+ can rescue these cells from death by preventing excitotoxicity. Decreased intracellular calcium also prevents necrosis by decreasing permeability, and apoptotic death is reduced through the reduction of calcium-dependent apoptotic agents.[4] While some calcium-channel blockers, such as flunarizine, act on the dopaminergic system, lomerizine is ineffective in vivo at inhibiting the release of dopamine. However, it has been observed to weakly inhibit the binding of [3H]spiperone to D2 dopamine receptors in vitro.[8] While researchers are unsure of the reason for this difference, one hypothesis is that the doses administered cannot reach a high enough concentration in the brain to affect D2 receptors.[8]

I haven't heard about anybody being told he is schizophrenic why only having HPPD. Those conditions are very, very distinguishable. Schizophrenics are not aware that they hallucinations are not real, while people with HPPD do (or should I say pseudo-hallucinations).

Hope1 do you still want to be collecting funds for a research of many different conditions apart from HPPD and VS or has anything changed?

Exactly that's human nature. We neither good or bad, we just are the way nature has formed us. However I hate human race and I hate to be human (not because of HPPD), because I BELIEVE we literally are viruses or "machines" programmed with certain mechanism or mechanisms to survive. We are born feeling more or less unhappy, with a need for stimulation or pleasure.. So we look for those pleasures in all the GOOD AND BAD things we do. All of this for sake of surviving and spreading endlessly and for no great reason. (imagine if you were blisfully happy, you probably you wouldnt even fee like going around looking for girls to have sex etc.., so we can't be too happy or our DNA wouldn't carry on). Realizing just that would not be so bad, but knowing that we are doing all the terrible things possible to one another, because we are made to do them... hmm it makes me little confused about life.. Then our mind desperately tries to give our presence some great, wonderfull meaning and justify our presence with stuff like.. we are here to learn, its a test, later after death there will be a reward and whatnot.. but it's all bulshit based on nothing.. this is another mechanism of ours to cope with this meaningless life. It feels so lonely here cause it seems like nobody else seems to realize/agree that THIS really could be the case ;p

lamictal is found to decrease perfusion in the brain. I don't know is it happening in the relevant areas though.. https://en.wikipedia.org/wiki/Lomerizine this is something that interests me.. used for treating migraines, improves perfusion, blocks Ca2+ channels - sounds like a perfect candidate I have focal hypoperfusion and i have a feeling other ppl with hppd could have it too as the hypoperfused areas of the brain are resposible for language, communication (even with yourself) and planning, thinking etc...which correlates with the symptoms of hppd. ... mycall81 headache can be a symptom of inadequate blood flow in the brain

Oh ya right now im in a phase of retesting some things like vinpocetine in really low doses... Maybe my brain gets too much of something at a time and needs to get used to it.. I have read that with even replenishing neurotransmitter, worsening of symptoms can be experienced before the actual improvement. I gonna take whatever supplements that protect against reperfusion injury as I have hypoperfusion in 2 regions in the brain, maybe those regions somehow do not tolerate sudden increase of bloodflow/increse of neurotransmitters... I don't know, these are my wild guesses.

Oh ya right now im in a phase of retesting some things like vinpocetine in really low doses... Sorry, wrong thread.

Sinemet, Clonazepam - They worsened my hppd slightly, but im almost sure, "permanently". Lamictal, Flunarizinium - they give me stinging in my head and worsen my cognition temporarily Piracetam - makes me irritable and increases ghosting big time. Lion's Mane, Vinpocetine, Ginkgo Biloba, Kudzu - also gives me stinging in my head als worsens cogniotion temporarily (although lions mane first improved it) CoQ10 - Took it for more than a week. First few days it felt like its improving my congition, now I take one pill and it makes me slower. Possibly worsened my memory or visual reaction slightly and more like longterm. L-arginine - also worsens symptoms slightly very weird thing - Flaxseed oil and fermented fish oil - after taking them, instantly it triggers hppd somehow - kills my thinking, increases ghosting, decreases visual reaction time. (somebody knows why could that be the case???????) I think even ascorbic acid 1000mg or Magnesium Malate 2-4g makes me little spaced out, but I continue to take them at lower doses hoping for some long term benefits. One thing that I keep taking and gives me no side effects or worsening of symptoms is 2g of grape seed extract everyday. I gonna add few supplements to it about which you can read here: http://www.evernote.com/l/AbRcCksdg0BC46TZDRI0_7mxXXsN2lStOwE/ 1. I start to think that anything that increases bloodflow in the brain makes me feel spaced out, worsens my cognition etc. 2. Also anything that increases/agonizes serotonin (gingko/kudzu/St. Johns Wort), gaba (clonazepam), dopamine (sinemet) - has some bad effect on me - although the mentioned herbs only affect me temporarily. the list is longer, but I don't those are the most important ones I guess..

I had a 35 h trip from brazil to europe.. I took clonazepam twice on it (small doses, but it affects me a lot). I think it increased my tinnitus from the level of tolerable to really annoying.. It became first thing I hear after waking up in the morning - just like somebody slapped me in my ear.. fuck VS increased slightly too. (cause I don't think its the grape seed extract or qoenzym Q10 causing it, that I am taking right now, but who knows..) If thats the case then so far: Sinemet worsened my symptoms permanently (only tried it for few days). Clonazepam (also things like xanax, valium - i was taking them sometimes before and I think they contributed A LOT to worsening of my HPPD). And like.. I can smoke weed sometimes and feel shit for few days/weeks, but the effects of it will wear off and it will be more or less back to the baseline. Thats not the case with the meds/other drugs though.

Lethargic acid have you done much yoga for any longer periods of time?? I think hanging upside down/ headstands etc could help in HPPD, or at least address the problem of hypoperfusion in some areas of the brain that can cause a cognition fuck up I guess. I think increasing the blood by chilling upside down maybe could help with that? I don't know, but I have heard that it helps with creation of new synapsis in the brain. Also I have heard people that do yoga saying they don't feel right if they don't do the hanging or headstands every few days ;p

Lions mane gave me a nice feeling of learning things, being focused and more talkative (nootropic I guess) though I had some side effects, stinging in my head, after lions mane (but i seem to be the only one) and tried astralagus pills with no effect BUT... I think even if you got the right supplement it would still need more than a month for your brain to heal, hence.. keep trying - if it does no harm I suggest.. keep taking it. Some ppl get helped by sinemet - for me it worsened everything slightly for few weeks, after 3 days taking it.. so everybody can get helped by a different thing. I will highly recommend lions mane to be taken for few months. Astralagus - why not.

I start to think there is more people affected than everyone thinks.. Two of my good friends got HPPD. One got it over really heavy 1 or 2 weeks long alcohol session. The other over few times taking speed.

great idea thank you

I believe if i did worry about my symptoms more then i wouldnt keep taking more drugs and in turn worsening my hppd. So worrying can be good sometimes. For the first two years I was really stressing about the symptoms, checking if I still have them constantly - that was obsessive and thats wrong. But I don't remember them getting worse over it. Once my trailing got triggered out of the blue, while I was checking it out, but I was taking different drugs at that time, so it could be them not me. Today I check my visuals few times a day to see how my excercise affects me, the herbs I try, the diet I am on at the moment etc. I think there is nothing wrong with that, im not stressing about it or being obsessed. Its important to add that it increases the comfort of life when you learn to notice them but not get upset abou them. Its something that comes with time. So I think the key here is some kind of acceptance by learning NOT giving too much thoughts to it. I am saying some kind of acceptance, because I will never fully accept this condition. Its just my "beliefe" system. I personally don't associate myself with anxiety. My cognition is fucked up yes. I may look like im anxious while being in a group of people - too much information going around etc. But thats still not anxiety - thats my brain not being able to handle so many informations etc. Anxiety doesn't have any influence on my cognition or hppd symptoms. Sleep does. Either way - Jogging and skateboarding helps me a lot to relax. It increases comfort of life too, by having that few hours a day that I forget about other matters. I think that is really really important - to have something to do that you really like, that absorbs you. Erythrina Mulungu, - havent tried A combination of l-arginine/l-lysine, - i am going to try l-theanine (you should get: suntheanine ®), - it used to relax me, it was brilliant. Since my hppd got worse - it triggers my HPPD - after l-theaning my brain goes blank. Scutellaria Galericulata (I used this in high doses, however expensive), - havent tried magnesium (400mg daily), - epsom baths decreased my cognitive/visual reaction time slightly, so I stopped. But maybe I should have used less magnesium. -- 5-HTP l-tryptophan ashwaganda, - couldn't think straight after passionflower, california poppy, valerian, - couldn't think straight after lemon balm, hops, gingko biloba, - i think no effect, so maybe I will try taking it again for the long term benefits. GABA - it is somehow amnesiac and didnt go well together with my hppd rhodolia rhodesia, - after this one my brain went wired somehow. When i tried it I was good enough at pool - after rhodolia I couldnt pot 1 ball in one game. chamomile - relax me somehow, but also slows down. the next day I feel slightly wired. check this post out, a very good read on this subject. http://www.longecity.org/forum/topic/54028-treating-anxiety-safely-effectively/

Hi Few days ago I tried Mucuna Pruriens, 400 mg pills 1 a day for 3 days. Day second and third I was getting more spaced out, didnt really absorb what I was reading or listening. Haven't noticed any benefits. Visual reaction time acutally decreased little bit. After images might had been longer too (they still are I think) After day 3 I stopped it because I felt its going in a bad direction. Had 5 days while being off it and I felt terrible.. something like when I took mushrooms around year ago and it made my HPPD skyrocket. Since the next day and every day after I knew I am in big trobule. Now I feel sliightly similar ( you just know when the "HPPD hangover" after taking something doesnt go away for few days, that its there to stay for longer).. Mucuna also increased the stinging feeling inside my head and as well it increased the "tremour" that can be kind of felt in my head too and in my eyes/face muscles. I was sure it was DMT trace content in Mucuna that made my symptoms worse (as I felt little similar like after mushrooms in terms of difficulty in thinking after taking them. Yesterday I had a visit with my doctor, Rafel Higashi. I asked him to prescribe me Sinemet. I thought it will be better to try again to get some benefits of L-dopa in pure form this time. I am taking 1/4 of a 250/25 dose of sinemet a day. Well its second day im taking it and I start to feel aggitated again, spaced out, the stinging feeling appeared today and I am affraid that the situation will repeat. Also there is no benefits. Maybe it is going to get worse tomorrow and once I decide to stop it - again the decreased visual reaction time, afterimages, trailing and difficulty in thinking will persist. ( I must add that after stoping Mucuna I already had some suicidal thoughts everyday - It felt like all the months/weeks of the healing process that might have taken place, although I don't really feel like it, got ruined by the trial with Mucuna). I just have some standards for my life and for bearing the pain associated it. I keep telling myself if it gets a tiny bit worse, it will tip the scale and I might not be able to bear it no more and finish with myself. I think I am sensitive to a lot of things. What I took before that increased the stinging feeling in my head were flunarizinium, lamotrigine or even Lion's Mane. It is always accompanied by a cognition decline, spaciness etc. I stopped taking all of them after 2-3 days, cause it was just getting worse and worse. Although Funarizinium, lamotrigine and lion's mane didnt leave any longterm bad effects. You feel where I am coming from? It somehow seems to worsen my hppd long-term. I mean maybe it would go back to normal after 2-3 weeks, but we don't know that. I get this bad feeling about it. Im sure some of you had it too after taking some recreational drugs, you just know its not going to get as good as it was. I am affraid maybe agonising of the dopamine receptors somehow will downregulate them or something and worsen my hppd? But then again. They say some drugs you have to keep taking for the sideeffects to subside and for the benefits to appear. Could that be the case with sinemet???

sup. I have some news for you guys. Doctor Rafael Higashi in Rio De Janeiro, who is a neurologist, nutritionist and a specialist in TMS/tDCS that I have started consultations with. He seems to be a very decent person with a great approach towards his profession. After the first consultation I received a 25 pages long and in-depth form to fill out with many very detailed questions about my body and mental health. This is first time I came across such detailed examination. Every doctor that consider his job serious should be doing the same. Doctor Rafael got me to do scintigraphy examination before proceeding with tDCS. It is similar to SPECT/PET, but from what he said - Scintigraphy only shows underactivity in the brain. I think he said SPECT - can show both over and underactivity. I did the examination and this is what came up (in portuguese): A analise das imagens tomograficas (cortes transversais, sagitais e coronais) e da reconstrucao tridimensional obtidas apos a administracao EV do radiotracador (99m Tc - ECD) evidencia areas de hipoperfusao na projecao do lobo front-paretial superior (bilateral) e fronto temporal (esquerdo, discreta), bem observado nos cortes tomograficos transversais nos 11 ao 13, coronais 16 ao 18 e sagitais 7 ao 10, bem como nas reconstrucoes tridimensionais. Translation by google: The analysis of CT images (cross sections, sagittal and coronal) and three-dimensional reconstruction obtained after the administration of EV radiotracer (99mTc - ECD) evidence of hypoperfusion areas in the projection of the upper front-paretial wolf (bilateral) and fronto temporal (left , discrete) and observed in cross-sectional tomographic cuts 11-13, coronal and sagittal 16-18 7-10 as well as in three-dimensional reconstructions. Hypoperfusion for those who don't know is a decreased blood flow through an organ. Since I showed him the studies about HPPD and VS and he assumes that I do have overactivity in the occipital area as shown in one of the studies, hence the visual hallucinations. Doctor Rafael explained to me one of the affected parts of the brain is responsible for language, but he indicated that its to do with the thoughts we hear/think to ourselves and the other area being responsible for planning (and so I guess critical thinking). I am not sure what fronto temporal stands for, but I will find out later (looks like wrong translation). I am going to be treated with tDCS - he said this could activate those areas. I asked him what he thinks about HPPD, why those areas have less activity, is it that some receptors became damaged? He answered that he doesn't think its a damage of receptors - if that was the case I would not be functioning properly (biologogically I guess). He added that it's more to do with insufficient production of neurotransmitters and that tDCS could increase it. He picked a protocol for me of tDCS. The anode (+) will be located at FZ point (between front and middle of the head) and the cathode somewhere at the back of the head. The anode will stimulate one part/increase the activity and the cathode will lessen the activity in occipital area. Fingers crossed ! I am starting the treatment tomorrow. Will let you know of the progress. A friend got a very bad reaction with one session of tDCS, his hppd worsened so that he felt like after taking ayahuasca (in terms of hppd symptoms) for day or two, but I think it went back to normal after few days. He discontinued the therapy. He had a different protocol though. It was for depression instead of for the parts affected by hppd specifically. I also asked the doctor to prescribe me Sinemet which I will make another post about, because I have some worries about it and how it can affect me. Regarding the evidences - I haven't heard about hypoperfusion in any person with HPPD. Is my case different or am I the first one to have this kind of examination done? I hope this will shine some light on our understanding of HPPD. New things to wonder about.. why those parts of the brain undergo hypo/hyper perfusion and what mechanism could cause it? How could it be dealt with? I hope tDCS is some kind of answer to the last question.

These are the studies I presented to my doctor which is a neurologist and tDCS, TMS treatments specialist, when I was explaining him what is HPPD. Any suggestions/modifications are welcome. Later anybody can use it as a quick introduction when talking to a doctor. Study: Stable quantitative EEG difference in post-LSD visual disorder by split-half analysis: evidence for disinhibition (10/7/1996)- http://www.ncbi.nlm.nih.gov/pubmed/8912957?dopt=Abstract Study: EEG coherence in post-LSD visual hallucinations (10/1/2001)- http://www.ncbi.nlm.nih.gov/pubmed/11566431?dopt=Abstract pdf: http://www.lycaeum.org/research/researchpdfs/2001_abraham_1.pdf Study: Hallucinogen persisting perception disorder in neuronal networks with adaptation (2/2012)- http://www.ncbi.nlm.nih.gov/pubmed/21671074?dopt=Abstract Study: Hallucinogen Persisting Perception Disorder (HPPD) and Flashback-are they Identical? http://esciencecentral.org/journals/hallucinogen-persisting-perception-disorder-hppd-and-flashback-are-they-identical-jaldd.1000121.pdf Good explanation with a reference to many drug trials. Recommended read. Flashbacks and HPPD: A Clinical-oriented Concise Review (2014) - http://doctorsonly.co.il/wp-content/uploads/2015/01/13_Flashbacks-and-HPPD.pdf Very good summary of hppd definitions and treatments - must read.

Hey guys. To those that sit in a corner and cry and to those that came out of the corner and start living life again, but still feel that things could be better: lets do start trying some new things! Lets experiment with amino acids. I haven't seen too any people trying them. Firstly, with your help, I wanna make a list of all amino acids that we think could be helpful and write out their potential benefits and side effects. Then we should start trying them and report the effects. I gonna order L-Lysine, L-arginine soon and L-Citrulline soon (Visual has inquired about them in another post and i got interested. L-Lysine Source: https://en.wikipedia.org/wiki/Lysine Lysine has a anxiolytic action through its effects on serotonin receptors in the intestinal tract, and is also hypothesized to reduce anxiety through serotonin regulation in the amygdala.[40] One study on rats[41] showed that overstimulation of the 5-HT4 receptors in the gut are associated with anxiety-induced intestinal pathology. Lysine, acting as a serotonin antagonist and therefore reducing the overactivity of these receptors, reduced signs of anxiety and anxiety-induced diarrhea in the sample population. Another study showed that lysine deficiency leads to a pathological increase in serotonin in the amygdala, a brain structure that is involved in emotional regulation and the stress response.[40] Human studies have also shown correlations between reduced lysine intake and anxiety. A population-based study in Syria included 93 families whose diet is primarily grain-based and therefore likely to be deficient in lysine. Fortification of grains with lysine was shown to reduce markers of anxiety, including cortisol levels; Smiriga and colleagues hypothesized that anxiety reduction from lysine occurs through mechanism of serotonin alterations in the central amygdala; older primary research reports hypothesized lysine to reduce anxiety through the potentiation of benzodiazepine receptors (common targets of anxiolytic drugs such as Xanax and Ativan).[42] (Note that all of these studies were funded by Ajinomoto, Co. Inc., an industrial manufacturer of lysine.) Side effects: http://www.webmd.com/vitamins-supplements/ingredientmono-237-lysine.aspx?activeingredientid=237&activeingredientname=lysine Lysine is POSSIBLY SAFE for most people when taken by mouth at recommended doses for up to one year, or when applied to the skin short-term. It can cause side effects such as stomach pain and diarrhea. Anecdote: http://www.curezone.org/forums/am.asp?i=1929281 L-Citrulline Source: http://www.webmd.com/vitamins-supplements/ingredientmono-1245-l-citrulline.aspx?activeingredientid=1245&activeingredientname=l-citrulline L-citrulline is used for Alzheimer’s disease, dementia, fatigue, muscle weakness, sickle cell disease, erectile dysfunction, high blood pressure, and diabetes. It is used for heart disease, body building, increasing energy, and for improving athletic performance. How does it work?L-citrulline is a naturally occurring amino acid found in food, such as watermelons, and also made in the body. Our bodies change L-citrulline into another amino acid called L-arginine and also to nitric oxide. L-citrulline might help increase the supply of ingredients the body needs to making certain proteins. It might also help open up veins and arteries to improve blood flow and reduce blood pressure. Side effects: L-citrulline is POSSIBLY SAFE when used appropriately by adults and children. I will be updating this post soon myself and with the stuff anybody sends.

same here.

there had been periods of weeks or even months that I experienced this mess in my head every night while falling asleep (few years ago when Id take drugs from time to time) although my hppd got permamently worse (visuals and cognition) after iboga and mushrooms I think I don't experience it so much mess before falling asleep anymore (unless after taking some kinds of medicine / herb, can't remember if thats the case with alcohol) however after iboga when I wake up in the morning my thoughts feel messy/random sometimes (especially after alcohol)