shaolinbomber

Most likely what has happened in the brain with people who experience HPPD. From the sensitivity to visual distortions meaning the brain is having a difficult time filtering out useless visual stimuli to the over thinking and anxiety ridden disorders people develop also to the DP/DR phenomenon all suggest that 5ht2a receptors were upregulated either during the drug experience or afterwards as a defense response by the brain to compensate for the chaotic conditions that hallucinogenic drugs produce. On another note, I may take this to my doctor and, after having kinda given up looking for new medications to help me for 5 or so years, I may yet again take up and gauntlet and start trying stuff again as recently my HPPD has been getting the better of me and have been bringing me down,

I take Kratom a few times a week. It helps me and is not as extreme as true opiates although it has some activity at specific opioid receptors.

Personally I experienced tremendous, almost 100%, relief from opiates. But this is not a viable option as it can quickly lead to an unsustainable and unmanageable addiction.

Drug seeking for a non-psychoactive substance? Tolcapone increases dopaminergic activity in the brain but not fast enough as to warrant a feeling of euphoria like illicit drugs do.... AtleAst that's what I understand of it.

Sometimes people need a break from worrying about it and stressing all the time. That's the main reason I stopped posting as much as I used to and I used to post ALOT like 4 years ago.

^^^ damn loratemazepam? Where can I get some of that? Sounds like a super benzo.

Interesting interview, especially the part about pupil dilation being, on average, bigger in hppd patients. I've always believed that opiates/oids, while being highly addictive, can help hppd symptoms and dp/dr because not only do they drastically shrink pupil size but they also cause a flood of dopamine in the brain and anytime I've done them in the past I feel the dp/dr slip away as well as watching my visuals lessen quite a bit with it.

It's a real strong anticholinergic. They would put it in as a cut with Asian #4 heroin back in the 70s to stop the histamine release that dope causes when you shoot.

I'm in Fort Worth texas and know of a couple mds and psychiatrists. Pm me if u want their names.

my mother also suffers from migraines with aura. It's a hell of a coincidence if it is one.

I don't think ingesting more substances that are known to cause the condition is the answer at all and suggesting it on a wide open internet forum is dangerous advice. DOn't take offense to my post but im just stating my opinion.

I'm pretty sure this has atleast something todo with what causes it. It fits the bill for people who develop visuals who never have tried drugs in their entire life.

I would stick to the basic knowledge that we've obtained thus far pertaining to the problem, ie. Genetic alteration to neuronal inihibition.

My doctor wanted me to try this along with my kpins.... I told him no because of its activity at the 5-ht sites.

From the information I'm gathering now the Heat-shock proteins are supposed to be a protective response to acute body temperature rise or what the brain perceives to be upcoming damaging conditions.. The last research article I posted clearly stated that LSD and other excitotoxic chemicals, when introduced into humans, causes the reaction to take place and produces these little RNA "shields" to make sure important parts of our neurons aren't burnt out and killed off. I'm not sure if a semi-permanent to permanent alteration by these RNA proteins could cause a change in genetic coding of proteins from within the cell to adapt to the chaotic environment that LSD and similar drugs produce within the brain. This article here:http://www.ncbi.nlm.nih.gov/books/NBK6614/ explains all about the nature of this reaction in the brain and which genes produce it. It would be interesting to know whether or not David or Dr. A have taken a look at this as a possbility for the cause of the disorder. Any thoughts or feedback would be appreciated as I'd like to discuss this further with someone else.

http://www.pnas.org/content/82/4/1281.full.pdf The article explains how IV LSD administered to rabbits produces a "heat shock protein" which is produced in the nerve cells in the retina and slowly travels down to the superior colliculus. The Superior Colliculus pathway here travels throughout the visual cortex...all the way to the bottom of it. This protein that is synthesized due to acute increases in body temperature during LSD and other similar hallucinogenic drugs can alter parts of the cells in which it binds with. These nerve pathways connect all the way to the back of the brain and inside, from what I understand, part of the most sensitive areas of the visual cortex.... The lowest levels. If I'm not mistaken by memory then this would mean that this would put these heat-shock porteins in contact with the innermost inihibitory interneurons that have been theorized to control the inhibitory actions of our visual processing in the brain. The interneurons containing the highest amount of 5-ht receptors. These researchers say that this protein synthesized can take anywhere as long as 10 days to reach its destination or as little as 24 hours and could remain for up to 30 days possibly continuing to "alter" whatever its binding to. The authors of the article also go on to mention that this production of cells can be triggered by other environmental stressors such as " Perturbations other than hyperthermia can induce synthesis of a major heat shock protein in organs of the intact mammal. A toxic agent such as sodium arsenite, which does not elevate body temperature of rabbits at the dosages employed, induces synthesis of a 74-kDa protein in various organs within 1 hr after intravenous injection (39). Other factors such as amino acid analogs, heavy metal ions, sulfhydryl reagents, and chelating agents have been reported to induce heat shock proteins in tissue culture systems (1, 2, 40-44). A trauma-induced protein of 71 kDa, which shows tissue-specific charge variants, has been reported to be induced in incubated organ slices and in tissues of hyperthermic rat (10, 14, 44-46). It appears that a common set of proteins is induced by diverse treatments as a general cellular reaction to stress." There are several parts of the article I'd like to put in quotations to break it down so the next reader does not have to do as much work but I always strongly believed this process could have a high chance at the atleast ONE of the causes of the disorder. I typed this out quickly and did not look over it much because I just wanted to get the idea out here again ASAP so others could have a chance to look at it and give some feedback for discussion. From WIKI: " Neural circuit The microstructure of the optic tectum / superior colliculus varies across species. As a general rule, there is always a clear distinction between superficial layers, which receive input primarily from the visual system and show primarily visual responses, and deeper layers, which receive many types of input and project to numerous motor-related brain areas. The distinction between these two zones is so clear and consistent that some anatomists have suggested that they should be considered separate brain structures.

I enjoyed that very much. Thank you for sharing that with us David. As always you lead the way for the outbreaks of progress within the community. The problems I had with the paper have already been outlined by a couple of the other members. Particularly the part in the article that states that this disorder is only anxiety driven and, as they basically put it, "all in your head". Well I would love to give whoever has that opinion of this disorder just ONE day with true HPPD and we will see if they're opinion on it is the same. However, I am glad that they followed that piece up with the physiological findings of disinhibition in the neural processing of visual stimuli in the brain with neurological circuitry made to measure electrical activity.

Are you saying you enjoy the real FULL agonist opiates or you don't like them? Kratom isn't a full agonist opiate in the truse sense because, like you said, it activates other receptors which totally ruin the opiate experience. Opiates can be a great tool for mental relaxation and a way to take a break from the daily struggle of HPPD. This is something, in my opinion the medical field has foolishly overlooked. Opiates aren't just a medication to treat physical injury. In fact I would go so far as to say their ability to heal or assist in helping making mental adjustions to mental trauma is stronger than their ability to numb out pain fom physical injuries. Just watch the usage because that relief can quickly turn into an addiction. All in moderation..... As they say.

I never got anything from just the Sinemet alone and I want to try the Tolcapone just once with the Sinemet to see if it alleviates anything for me. If I were to get instantaneous reduction in symptoms from that combo I would be convinced that the problem lies within the activation or lack thereof of the Dopaminergic part of the nerual networks that have been changed/damaged/altered/however you'd like to explain it. but as for right now I remain skeptical for that as a for sure treatment for ALL HPPD sufferers.

This is Phenobarbital right?

pupil constriction plays a big role that the opiates cause in how your visuals are affected.

Count your blessings. I fell into full blown Heroin addiction so remember that it can always be worse. Trust me on that one.

Sinemet is probably going to be useless to you. I'm sorry to dampen your spirits but it hurts that much more to get something new and expect it to work only to feel the same.

I'm right there with you.