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So I'm trying to do some homework on neurotransmitters to get a better understanding of what supplements and medications may benefit me most. I know my symptoms are always better in the morning and worse at night, that I don't respond well to stimulants (even medical ones prescribed by doctors), that I've had anxiety for years and my adrenals are likely fatigued, and that I do respond well to calming agents, as is the case with most people here. I do think one of my main problems is lack of dopamine, but I also know other neurotransmitters play a huge role in HPPD as well. So I guess I was just wondering what the consensus is on all this. I hear GABA thrown around a lot, but I have no idea how GABA works. Is more GABA better or less? And what about serotonin? Any responses are much appreciated. I've tried rummaging through the boards to read up about this stuff but there doesn't seem to be any single particular thread that summarizes all this briefly so perhaps someone could enlighten me. Not looking for anything too extensive, just a quick recap. Thanks.

Dear Community, The initial results are public. Dr. Abraham presented the report at the Annual Meeting of the Biological Psychiatry Society earlier this year. I have included a copy of the Abstract in this post and providing a link to Dr. Abraham's additional discussion and graphs at the bottom. My emphasis added, but to restate Dr. Abraham's website: "This study is NOT the gold standard of proof that this approach works. . .These medications are not approved for use in HPPD. Any interest in them should be discussed with your physician." I know we have discussed COMT, genetic variations and watched the board's discussion move from the serotonin system to the dopaminergic system having originally focused on the GABAergic system. These are not systems locked in single compartments, single receptors and single cell types, but have complex interactions and as you are aware we are just touching the surface of Neural Science and Behavior/Perception. However, the basic discussion was on target: Dr. Abraham hypothesized that inhibition of COMT would reduce symptoms in HPPD. Consequently, COMT inhibitors were tolcapone and Sinemet Again, these are not approved for HPPD and should only be tried with a clinician. Here is the abstract from the conference: Catechol-O-Methyl Tranferase Inhibition Reduces Symptoms of Hallucinogen Persisting Perception Disorder Henry D. Abraham, Psychiatry, Tufts University, Boston, MA Background: Hallucinogen persisting perception disorder (HPPD) is a poorly understood disorder arising from the use of hallucinogens. It is characterized by continuous visual disturbances which can be lifelong. There is no known treatment. Studies of HPPD patients with qEEG mapping show that the disorder is represented by disinhibition in the cerebral cortex. Inhibition of catechol-O-methyl transferase (COMT) increases inhibition of sensory input in humans carrying the G/G polymorphism. Accordingly, I hypothesized that inhibition of COMT would reduce symptoms in HPPD. Methods: A single-dose, open label trial of a tolcapone, carbidopa, and L-dopa was conducted in 17 consecutive HPPD subjects. Visual symptoms in each subject were coded on a 0 to 7 Likert scale before, and two hours after, drug administration. A paired Student t-test was used to determine statistical significance. Results: The mean pre-drug visual symptom score for the entire sample was 4.7 +/- 2.6, compared to the post-drug score of 3.7 +/- 2.8 (P= .001). A post hoc median split of the percent response of each subject was 51% symptom reduction in the upper half of responders compared to 1% in the lower half, suggesting a bimodal sample. Conclusions: Inhibition of COMT is a novel approach in the treatment of HPPD. The bimodal treatment response is consistent with the action of a functional polymorphism in the COMT gene. Future directions include a double blind, placebo controlled trial of this treatment and a determination of COMT polymorphism in responders and non-responders. Keyword(s): HPPD, COMT, tolcapone, carbidopa, DOPA (Retrieved from Convention eBook downloaded from: http://www.sobp.org/...?pageid=345267; Kindle Locations 21096-21098. SOBP. Kindle Edition.) LINK TO Dr. Abraham's Web Page regarding this study: http://amrglobal.pow...atment-for-hppd Best wishes, - David Kozin

I believe there are others on this forum suffering from bipolar disorder also... I am wondering if any of you have noticed changes in your hppd symptoms during depressive and manic episodes? I was on Lamictal for about a year and it helped with both, but at the beginning of this summer I quitted cold after forgetting to take it for several days and thinking I was still feeling ok. The hppd symptoms came back after a while, but they didn't bother me much so I somehow delayed taking my meds until today.... I guess lately I've been going through my first hypomanic episode since I got hppd, and during this time it seems like my hppd symptoms got better. Which scares me, because I've been impulsively doing drugs again... (When I'm depressed, I don't do any drugs because even before hppd, everything I did led to panic attacks) I actually feel quite ok, It feels nice to be able to do drugs and have fun again... I sometimes think that maybe it's just me being paranoid, maybe I'm actually cured... But I recognized this pattern a few days ago, after my second lsd trip this month. The last time I was feeling and acting this way, I ended up having HPPD. I'm scared of what could happen after this illusion of feeling good is gone. I started taking Lamictal again today, I hope that it will help the way it did before... I would like to hear about your experiences... Also, I know that same neurotransmitters are affecting both conditions in some way, but I don't understand the mechanisms that much and would like to learn about it more. Any reading suggestions?

For those looking for new solutions, a bit can be learned from old solutions ... Quinine has been in use since the 1800's. Its main purpose is to treat malaria. However, it used to be used as a general tonic. Today it is still readily available in tonic water, as those of you who love G&Ts (Gin and Tonic) might know. It is derived from the bark of Cinchona trees/bushes. Like most meds, they don't know how it works for malaria. It relaxes smooth muscle like an anticholergenic. It does affect dopamine activity. It seems to alter the ANS as well as the CNS (See posts regarding Ca, Mg, and K such as #39 http://hppdonline.com/index.php?/topic/1959-spitting-out-yet-another-theory-magnesium/) It isn't a med to take high amounts unless you have malaria (~2g per day). See http://www.aspenpharma.com.au/product_info/pi/PI_Quinate.pdf However, as stated above, it is in genuine tonic water with amounts limited to about 80mg per quart. And they haven't issued any warning about too many G&Ts - Twenty Five quarts a day would treat malaria . I've only worked with 75mg at a time ... and then only a few times (will let you know if anything significant occurs, good or bad). It reduces DR (defined in this case as the feeling of disconnection, as if there is a transparent barrier between the world and self) and is relaxing - all this without the Gin. Can be quite sedative. Feels like a cross between Keppra and Sinemet. Hope this is helpful. Have fun and enjoy your G&T! Miscellaneous bedtime reading: http://www.ncbi.nlm.nih.gov/pubmed/2759182 http://onlinelibrary.wiley.com/doi/10.1111/j.1471-4159.1992.tb10993.x/abstract http://www.ncbi.nlm.nih.gov/pubmed/1357098 http://www.ncbi.nlm.nih.gov/pubmed/11797417 http://www.progressivehealth.com/rls-quinine.htm http://www.nourishing-the-soul.com/2010/06/mood-food-connection/ http://www.sciencedirect.com/science/article/pii/0306362377900118 http://link.springer.com/article/10.1007%2FBF00688932

Hey guys, I just wanted to post this before I forgot, unfortunately I don't have the time to view it in its entirety as I have finish some articles and do some studying, but I found this highly interesting: http://www.slideshare.net/AakratiGupta1/ppt-on-vanilloid-receptors Potential applications from research on vanilloid 'receptors' and vanilloids - it seems to affect brain inflammation as well as affect Dopamine and has some interesting effects in the brain/nervous system (similar to CBD1 receptors), thus could potentially hold value in fear/anxiety problems. I'd like to get full access of this: http://pubs.acs.org/doi/pdf/10.1021/jm00070a002 I'm still searching for things that can help me - I believe my problems lie within NMDA because the weekend that I believe made HPPD stick with me incorporated abuse of tons of NMDA-antagonists; perhaps serotonin as well, but I find conflicting results in how MDMA affects the serotonergic system. I thought I had acetylcholine problems due to being laced with PCP/embalming fluid, yet that only has moderate anti-cholinergic activity and very potent NMDA-antagonism. Pregnenolone is an option, as is collagen/gelatin and glycine (bone broth and gelatinous meat). Hope this catches the eyes of some of you intelligent members!

Ok so I know that this is a weird topic. Please don't judge me...but in all seriousness, for as long I can remember I have had a dramatic increase in sexual desire since I got HPPD. Does anyone have this same thing? It's like I feel like I have to. I've tried to stop for awhile because I thought maybe masturbating made it worse but when I do I just get really panicky, racing thoughts, and increase of anxiety. I know masturbation has a lot to do with neurotransmitters in the brain. It releases dopamine and also does something with the acetylcholine receptors...so my question is can anybody relate to this? Does anyone feel that it makes them feel worse or better? For me, I can't tell...I tend to associate whackin off as a negative thing and I usually acquire some psychological guilt with it, mainly because I simply don't know if it's pulling me in the right direction or not, but I also feel that it does relieve some of the stress and anxiety. I feel that if I have an increased sexual desire than my body's telling me that it needs dopamine and those extra hormones to deal with the stress in order to deal with HPPD. ANY INSIGHTS?