StateOfRegret

I can definitely relate to this. I sometimes (this morning, for instance) wake up to a tapestry of coloured, sparkling dots, somewhat regularly arranged and moving slowly in unison. The first couple of times I thought my HPPD had sky-rocketed for good, but it turned out not to be the case.

Welcome to the forum, Mike. A great first post, I must say :-) I'm very interested in hearing about your dizziness. Can you describe it? Dizziness is one of my main symptoms, so I'm very interested in hearing from others suffering from it. My dizziness can be described variously as feeling as if I'm on a boat or being pushed. It happens whether standing, seated or lying down.

Excuse me for derailing, but this reminds me very much of the Doctor Who episode "The Long Game" where people are promoted only to be never seen again (dead) :-P On topic: I actually wrote a message to jay on this topic about a month ago, and he said "it looks like David has deleted that entire area of the site... I will try and find out about it.", which doesn't bode well (the deletion part, that is) :-( (jay: I hope it's alright by you that I quote our private conversation here? :-) Otherwise, feel free to delete my post!)

Hi Sam93 - Thanks for sharing, this is very interesting. The upregulation of alpha2 sub-receptors sounds almost too good to be true (and also somewhat counter-intuitive) :-) The suspected SNRI action worries me a bit, though.

It doesn't sound like my HPPD. My visuals are sometimes geometric in nature, but never resemble objects. They're mostly splotches of colour, static and strong after-images

Sam93: Very elemental question, I know, but please remind me; Are ligand receptor affinities defined as the equilibrium constant for the process of formation of receptor-ligand complex or for the dissociation of complex into unbound ligand + receptor? Also; If you're a chemistry buff, perhaps you recognize my avatar? :-P

If you're vomiting blood, I'd say get some medical help.

Cyclizine. An antihistamine with some anticholinergic properties.

I've now read it. First: Splendid work! I have a few comments, but I'm on the phone ATM, so they'll have to wait a bit. One question, though: If the cholinergic hypothesis is correct, why do anticholinergics not greatly exacerbate symptoms of HPPD? They are certainly not beneficial, but a few users here (including myself) have taken them without serious adverse effects.

I suffer greatly from dizziness and feelings of movement as well, so I'll look into it as well. Wasn't flunarizine known for causing parkinsonism? I'm on the phone (on the bus) so I can't be bothered to look it up right now. :-P

Will probably read it later, I have ~3 hour ride in public transport (bus+train) ahead of me (going home from visiting parents).

Looking forward to reading the whole thing!

What would you like to study? I study physics and mathematics, and am going back to university in a couple of weeks. I got HPPD on the very first day of summer vacation, so I can't tell you what studying with HPPD will be like just yet. But I'm somewhat anxious about it - mostly the social situations, though! I've been reading a bit of mathematical physics (this book), and I've found that I'm able to comprehend it just about as well as before, though I do find myself re-reading some paragraphs a few times. It should be noted, I guess, that I was somewhat of a "straight A student" in physics/mathematics before acquiring HPPD. I'm determined not to let this crap get in the way of doing what I like!

Don't you mean gustatory, then? :-P

mikezero has got his info wrong. The tor network is absolutely fine (I'm using it this very moment) and so is Silk Road. All that was taken down was tormail, which is just an e-mail service. This is sad, of course, but as long as you use good encryption (PGP springs to mind) you're safe - even if (when) the authorities read your private e-mails, they won't be able to decrypt them. You're much less likely to be scammed on SR than using one of these shady online pharmacies, as long as you use it correctly. Think about it: On SR there is an extensive "reputation/review" system, including a forum where you can read of other people's experiences with specific products and vendors. As if that wasn't enough, there's also an escrow system, meaning that your funds are "locked" upon making a purchase, but they're not transferred to the vendor before you release them. Some vendors require you to release your funds upon dispatch (known as FE for "Finalize early") if you're a newcomer, but this shouldn't be a problem. Another great thing is that all funds go through the bitcoin system - this eliminates the threat of credit card fraud, which is quite common with online pharmacies. With SR you're also much more likely to find a local vendor and your level of privacy is much, much higher. Also; learn to use PGP/GPG encryption!

Glad to hear it! And yes, HPPD does sometimes get better on its own - let us never forget that :-) Have you been taking any medication of any kind? Also, I'm begging you to not smoke cannabis. It was due to a synthetic cannabinoid that my low-grade, mainly visual HPPD turned into full-on HPPD. I mean, why would you even take a chance like that, seeing that you know that you're susceptible to HPPD.

Thanks for keeping us updated - very interesting stuff :-)

I have this book as a PDF if anybody is interested. I hope I'm not breaking a forum rule by offering this.

It's not about blindly trusting any one source (Doctors are frequently wrong as well). If you don't believe Wikipedia, then locate some primary literature on the topic :-) The benzodiazepine receptor does indeed occupy a different site on the GABAA receptors from the one targeted by barbiturates, but that is not to say that there is no cross tolerance. If the mechanism of tolerance is a reduction in GABAA receptor density, then it seems reasonable, at least, that there would be cross tolerance.

Thanks Odisa - I'm still reading the first link. Huperzine A was what led me to look into NMDA antagonists, but it would of course be preferable to use a more selective drug (i.e. one with a profile of NMDA antagonism only), if one were mostly interested in its properties as an NMDA antagonist, seeing how most of the supposed dangers stem from its action as an acetylcholinesterase inhibitor.

Has anyone looked into using Huperzine A as an adjunct to HPPD treatment? It is an acetylcholinesterase inhibitor (and as such prevents the breakdown of acethylcholine, thus increasing the available acetylcholine). Just as importantly, it is an NMDA antagonist, a class of drugs which have been shown to reduce benzodiazepine dependence, including tolerance and withdrawal symptom severity, something I'm sure would benefit many HPPD'ers. Note that some NMDA antagonists are well-known dissociatives (such as Ketamine, PCP and DXM), but from what I can gather, it is entirely possible to reap the benefits of NMDA antagonism without experiencing psychotropic effects (please bear in mindt that the three examples mentioned are not purely NMDA antagonists, but have more complex pharmacodynamics, with affinities for several different receptor systems which may all contribute to their unwanted psychotropic effects). I've collected a few articles on the effect of NMDA antagonists on benzodiazepine dependence, and highlighted some bits pertaining to NMDA antagonist treatment of benzodiazepine dependence in blue. I've also highlighted a few sentences pertaining to treatment of benzodiazepine dependence with AMPA antagonists in red - another area worth investigating further. Effect of NMDA antagonists on rapid tolerance to benzodiazepines We have reexamined the effect of NMDA antagonists [(+)MK-801 and ketamine] on rapid tolerance to chlordiazepoxide. (+)MK-801 and ketamine blocked the development of rapid tolerance to chlordiazepoxide, but this effect was dependent on the dose ratio of the NMDA antagonist to that of the benzodiazepine used to produce rapid tolerance. Furthermore, NMDA antagonists blocked both learned and unlearned tolerance to chlordiazepoxide. It appears that in addition to impairment of memory and learning, NMDA antagonists may also influence some other mechanism involved in the production of drug-tolerance. http://www.ncbi.nlm.nih.gov/pubmed/8971413 The NMDA receptor competitive antagonist CPP modulates benzodiazepine tolerance and discontinuation Benzodiazepine discontinuation is characterized by a syndrome of increased activity and reduced seizure threshold that is similar to effects mediated by the glutamatergic system. To elucidate the involvement of the glutamatergic system in benzodiazepine tolerance and discontinuation, we administered lorazepam, the NMDA antagonist CPP, and the combination of these compounds either concomitantly or consecutively to mice via osmotic pumps and evaluated pentylenetetrazole-induced seizure threshold, open-field activity, and benzodiazepine receptor binding during and after chronic administration. Animals receiving lorazepam alone developed partial tolerance at 7 days and complete tolerance at 14 days to the anticonvulsant effects of lorazepam. This effect was partly attenuated by CPP coadministration with lorazepam. This combination produced only partial tolerance. A reduction in seizure threshold was observed 4 days after discontinuation of lorazepam alone. This effect was abolished by coadministration of CPP with lorazepam and by CPP administration during the withdrawal period. Benzodiazepine binding in most structures examined was significantly reduced at 14 days during chronic lorazepam administration (versus 1 day), and coadministration of CPP did not alter this decrement. After lorazepam discontinuation, binding was increased at 4 and 7 days versus chronically treated animals and versus vehicle within the cerebral cortex. This effect was abolished by coadministration of CPP as well as by CPP administration during the lorazepam withdrawal period. These data support the involvement of the glutamatergic system in benzodiazepine tolerance and discontinuation. http://www.ncbi.nlm.nih.gov/pubmed/9399331 Diazepam dependence prevented by glutamate antagonists Long-term treatment leads to tolerance to and dependence on benzodiazepines. Abrupt termination of benzodiazepine administration triggers the expression of signs of dependence. Mice withdrawn from chronic treatment with diazepam showed a time-related evolution of anxiety, muscle rigidity, and seizures between days 4 and 21 after treatment discontinuation. A period between withdrawal days 1 and 3 was symptom-free. Surprisingly, during this "silent phase" the susceptibility of mice to alpha-amino-3-hydroxy-5-tert-butyl-4-isoxazolepropionate (ATPA) and kainate seizures and the magnitude of monosynaptic reflexes mediated by non-N-methyl-D-aspartate (NMDA) mechanisms were enhanced. In apparent contrast, the "active phase", between withdrawal days 4 and 21, was characterized by increased susceptibility to NMDA seizures and enhanced magnitude of polysynaptic reflexes, which are NMDA dependent. Treatment of mice with alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) antagonists 1-(4-aminophenyl)-4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine (GYKI 52466) or 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo(f)quinoxaline but not with the NMDA antagonist 3-[(+/-)-2-carboxypiperazin-4-yl]-propyl-1-phosphonate (CPP) during the silent phase prevented signs of dependence. In contrast, treatment with CPP but not with GYKI 52466 during the active phase prevented the symptoms. The development of tolerance to and dependence on diazepam was prevented by concurrent treatment of mice with CPP but was not prevented by GYKI 52466. These data indicate that NMDA-dependent mechanisms contribute to the development of tolerance to diazepam and to the expression of signs of dependence in mice after termination of long-term treatment with diazepam. Nevertheless, the non-NMDA-mediated silent phase is essential for triggering the symptoms. Therefore, AMPA antagonists may offer a therapeutic approach for preventing dependence on benzodiazepines that is an alternative to NMDA antagonism. http://www.ncbi.nlm.nih.gov/pubmed/8341715 If anyone is interested, I'd be more than willing to upload the full texts of the mentioned articles. Also, speculation (as to mechanisms and whatnot) is most welcome! :-)

Hey Puppeteer! Did you give up on the thread? I'm still very interested in hearing about your experiences with the various supplements :-)

Are you sure about that? I have no real sources, but I've always understood "oral administration" to mean "swallowed". The Wikipedia entry for "Sublingual administration" specifically compares "sublingual" and "oral" ("Sublingual administration has certain advantages over oral administration [...]"). Looking at Wikipedia's "Routes of administration" chart seems to indicate that oral administration is indeed an umbrella term including, among other things, sublingual administration, so you're probably right :-) By the way; how is obtaining some coluracetam coming along? :-)

No, thank you for doing the research - my help was a minor factor

Thanks for sharing your experience, though I'm unlikely to repeat it. I sometimes fantasize about trying something similar, since my HPPD was the "slowly developing kind", which worsened over the course of more than 100 trips (yeah, I'm an idiot, I'm aware of it), so I figured that one trip more or less was hardly going to do much of a difference. But I'd be much too scared to actually do it - I'm almost positive that the moment I got into the tripping "frame of mind" I'd start obsessing about the trip worsening my symptoms, which would invariably lead to a bad experience, thus perhaps making it a self-fulfilling prophecy...