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Hallucinogen Persisting Perception Disorder (HPPD) Support Forum


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onedayillsailagain last won the day on August 5 2016

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About onedayillsailagain

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  1. IME, Canchew was quite an efficacious anxiolytic and anti-insomniac. Too bad it's so expensive. CibDex, on the other hand, was rather disastrous in that it made me high. Both are made by MMJ Inc, and purportedly low-THC content, though I guess that wasn't the case with the latter product. I might try some other products soon (e-cig CBD vape sounds like a plan). I saw some CBD liquid in Amsterdam the other day; expensive as hell too. I'll try to find a purer, bulkier deal.
  2. http://journal.frontiersin.org/Journal/10.3389/fnsys.2014.00172/full Yet to read it myself, but I found this interesting considering my earlier endeavours with this concept.. Perhaps there's something in here that was overlooked. edit: credits to /u/shrillthrill over at /r/Nootropics for finding this.
  3. Hi there, good to read you've found something that helps. Regarding your Afobazole use: What's your dosing regimen? How long did it take for effects to become apparent? I have some from AwakeBrain that I never really gave a proper trial, so it's something I'd be up for trying again if I have a period where I'm trialling nothing. Best wishes, odisa
  4. I have a vial of this that I hadn't finished sitting in my fridge, from Ceretropic. I tried it a few times SubQ with a 1 inch needle, but didn't like how unhandy it was, so quit. I have some insulin syringes now (dirt cheap by the way, like 100 for 6 euros), so I'll give it another shot should JDTic prove insufficient. Hope you guys have success with it; the few times I tried it, it seemed to do little.
  5. Thanks for the swift reply! I agree; transcranial neuromodulation poses great oppertunities in terms of treatment, although alas so far only ®TMS has been explored in DPD/VS as far as I know. There are various forms of NIBS (non-invasive brain stimulation) that elicit much higher precision than TMS, and therefore offer a superior chance of specifically targetting the affected areas. Being that the lingual gyrii are deeper that the superficial cortical layer, preferably a level of specificity would be attained that has depth-control. IIRC, TUS (transcranial ultrasound stimulation) offers this, but I may be mistaken in that. Either way, the relatively low specificity of TMS could conflict with any improvements; take for instance the study regarding the right Temporo-Parietal Junction, where the neuromodulation may have extended beyond the targetted region, altering both temporal and parietal regions that also govern perception. The latter is just conjecture at most, but does offer a potential reason why the results with TMS so far have been marginal. By the way; under the Research Articles sections of this site I've added plenty of articles relating to transcranial modulation of the visual modalities and my thoughts thereof, should you be interested. Neuronal excitability has been confirmed to be able to be lowered via these methods; a seemingly recurring marker of visual distortions. Perhaps such methods alter metabolism as well.
  6. Haven't read the article myself, but figured it'd be relevant and of interest: http://onlinelibrary.wiley.com/doi/10.1111/j.1750-3841.2009.01447.x/full
  7. Pramipexole? Interesting. The sleep issues should be able to be reduced by taking it early in the day. The itching is rather unfortunate. Has it subsided?
  8. Interesting stuff, though I can't seem to find any scholarly information regarding it, much less the peptide structure or the proposed mechanism of action through which it should function, and lastly peptides are not orally bioavailable in general. It seems rather expensive as well. Perhaps send IAS an e-mail requesting for further references? I'm sure if there's something published that they would be able to provide you with links etc.
  9. I concur with Ghormeh; I wouldn't partake in Sertindole. I would advise you to inform your doctor of the adverse reactions documented in response to Risperidone etc. NAC and Sarcosine would appear relatively harmless; I've taken both myself without any harm afaik. D-AA is a full agonist, and taking it together with Sarcosine and NAC might be overkill. Also remember that Lamotrigine is Glutamatergic as well; as such it may interfere. If you insist on taking these, I would suggest starting them one by one; taking time to adjust to the necessary dose. Then, if tolerable and no ill effects are noted; progress to the next. I would suggest NAC, then Sarcosine, then if still nothing, perhaps small doses of D-AA that are more closely monitored. Of course consult with your doctor etc. Lastly, magnesium works quite differently from sarcosine. Bit tired to explain now, and to be honest I'd have to have a refresher on that. There's plenty of discussion to be found on all of these (except Sertindole) on the forum though Best, -odisa
  10. Welkom Good to see things are moving forward with your much appreciated efforts, and thank you for taking the time to explain the much misunderstood differences and overlappings between HPPD and VS(S). Not sure I entirely agree with it, but that doesn't really matter much, as both conditions clearly share much in common; therefore any data from either diagnosis will be useful. Would be interesting to see both conglommerate I guess, but then of course; where does one draw the line? Where would DPD/DRD fall in? What about cognitive disruptions? Just something to provoke thought; not necessarily seeking an answer currently personally. Please remind me; was it hypo- or hypermetabolism of the Lingual Gyrus? And did they mention whether it was any specific metabolism? Also, I recall there being a lateral specifier, though I can't recall whether it was right or left. Because I don't know what research Goadsby have in mind, and despite the valuable data, it would of course be worth entertaining the possibility of pursuing (theoretical) treatment based off of this observation (putting it bluntly: to cut to the chase). I'm sure there are ways to locally alter the metabolisms of the lingual gyrus somehow; perhaps that deserves a focus as well? In no way is this intended to devalue any of the studies performed so far, yet having your fate rest in someone else's hands entirely requires a lot of faith. Hmm, I just watched your interview with Dr. Abraham. Many thanks to both of you; it was very informative and it will especially serve as a great resource to those new to the conditions. And I must confess; he is correct about the necessity of a more accurate understanding of the pathophysiology involved.. Though I'd think given the current data it's still possible to derive potential treatments, which then may or may not be implemented clinically depending on invasiveness, finances, etc. Anyhow, I'm tired, so off to bed. Sorry if it was a bit deranged, and best wishes to you! P.S. Just checked; apparently I can only donate via credit card.. Is there a way to pay with PayPal or BitCoin? If not, I'll have to do so later. Is there a deadline?
  11. Missjess is making some good advice there; dissociative drugs aren't exactly recommendable with our condition. In short, what is being hypothesized is that Ketamine induces significant synaptogenesis, thereby mediating its neurotrophic, but also anti-depressant effects. Some researchers suggest neurogenesis may in part be also responsible, as Ketamine causes an induction of BDNF as I recall; a protein that mediates both synapto- and neurogenesis Regardless, there are plenty of new substances on their way that are potent synaptogenic and neurogenic substances (e.g. Dihexa and 7,8-DHF/NSI-189/ISX-9 respectively). To me, it would make more sense to target the underlying mechinisms through which beneficial effects occur, rather than to utilize Ketamine, which seems a bit like an indirect method to achieve them. The latter I'd understand being utilized in depression when it is a time-sensitive issue, but certainly not in dissociative states. edit: Whoops, thought I was posting to DPSH. These forums do look very much alike.
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