I think I know a possible cure

[windscar]

Before anything, sorry for my bad english. With some effort I'm sure you can understand. Well I'm an engineer student, not a biologist. But I used to be a very good student and my best hability was, probably, that of finding a solution to a problem before being exposed to the answer (as opposed of how students are teachen nowadays). So I can be completly wrong on what I'll say, but, who knows, I can be right somewhere.<br><br>There is an study where researchers did the following:<br>They got a marine animal (I don't remember the specie) whose brain is very simple. That animal has an reflex that is activated when you touch certain part of its body (don't remember what). It contracts itself as a defensive response. As every reflex, it is an automatic response, that is, the animal have no control of it, just like us when we touch a hot object.  They performed 4 tests on that animal:<br>1. They touched that part of the animals body several times in a short period of time. They realized that, after some attempts, that animal decreased its response to the stimuli, but, after a few hours, that response was back to normal.<br>2. They touched that part of the animal several times spaced over a long period of time. They realized that, after some attempts, the animal decreased its response to the stimuli and maintained this behavior for a few weeks.<br>3. They touched that part of the animals body several times in a short period of time and, imediatelly after each attempt, they exposed the animal to an eletrical current that caused pain. They realized that, this time, after some attemtps, the animal increased its response to the stimuli, but, after some hours, it was back to normal.<br>4. They touched that part of the animals body several times spaced over a long period of time, applying the eletrical current after every attempt. The animal increased its response to the stimulii and maintained that behavior for weeks.<br><br>Ok. How can we explain that? Simple. The brain of that animal does have a mechanism that regulates that unvoluntary response. Remember, the purpose of that reflex is to protect the animal. If the reflex is activated but nothing happens the brain of the animal adapts itself to stop reacting to the touch. If he gets eletrified its brain adapts to react more intensively to the touch. Remember, it is an unvoluntary response, so its not the animal remembering what to do... it is, de facto, the structure of its neurons that is changing. Even more interesting is that the response does return to normal if the animal gets touched for a brief period of time but it doesn't when the period is long enough.<br><br><b>It was shown, later, that this stimuli response regulation mechanism is a common feature to (almost?) every brain of any living being.</b> <br><br>So, what does this have to so with hppd?<br><br>First, let's think about the afterimages. Why do they happen? It is very probable that they are not a physical limitation of our eyes (read the article about palinopsia on wikipedia for sources). So its something programmend into us. As such, they happen because they are necessary - they are a FEATURE of our brain. So what they're necessary for? Well I'm not sure yet but very probably it does have a role on our perception of motion. Know when you move your fingers very hapidly back and forth? It's so fast for your eye to know where exactly is your finger so you see a hybrid mesh of everywhere it passed though. This is possibly possible because of the afterimages. <br><br>And floaters? What are them? Well. You know that we are made from cells. But cells die. What do you think would happen if a cell just died above the surface of your eye? Well if it was close enough it would cast a shadow on it. But people, usually, do not see lots of black spots floating over their vision! How's that possible, if there ARE shadows being cast on the vision of all of us? There's only one explanation. Our brain removes them automatically. It FILLS the space where the shadows are cast.<br><br>Well, so, what do both of those have on common? Well. They are both FEATURES of our vision and they are UNCONCIOUS. That is, it's something that our brain does automatically, with a specific function that is important to our proper working. Wow, wait!  Isn't that just what is, too, our marine animal's reflex?<br><br>Remember, neural networks does have a way of regulating it's responses to an input. It does not even have to be an extern stimuli. Internal inputs ("functions") are regulating themselves everytime on our brain so we can function correctly. It means that <b>there is, probably, a system that regulates the strength of our afterimages, floaters, etc - and, more probably, that regulation is based on what we see. If the afterimages we see are not doing their job, whatever it is (probably the job of softening movement), then our brain will adjust increasing or decreasing their strength.<br><br></b>Now this can be used to explain almost everything that happens on HPPD. <br><br>Why do HPPD happen? When we are in a trip we suddenly experience an alterated vision. Suddenly everything we see is not supposed to be how it is. Our brain then perceives that it's efforts to see correctly are not working and tries to adapt. For instance, when it realizes we can still see trails of objects (hindu deities effect) even when the "afterimages system" (motion softening system) was supposed to be working properly, it does naturally increase the strength of our afterimages. But the trip will go away while those changes won't. That's what configures the persistend perceptual disoreders.<br><br>Why is it often triggered by hallucinogens, but is often seen in people who never used them? Because HPPD is not caused by hallucinogens. HPPD is caused by "seeing wrongly". If anything makes someone sees wrongly for long enough, then he can get HPPD. So we can exect antidepressives, migraine auras, perhaps even bad nutrition or traumatic events cause HPPD for susceptible individuals and, guess what? That's just what happens.<br><br>Why some people use lots of LSD and never get sick, while others get HPPD from their first trip? Because HPPD is not caused by the drug but by the fact of seeing everything messed up long enough. If someone have a less visual trip, he won't develop HPPD. If someone doesn't trip long enough, he won't develop LSD. So, if someone doesn't develop HPPD on their first attempts, that person will probably become resistent (both physically and psychologically) to psychodelics in a way that it's very unlikely that he sometime will have a trip strong enough for long enough to decelop HPPD. That would make us conclude that ONE EASY WAY TO DEVELOP HPPD WOULD BE DOSING STRONG IN YOUR FIRST TRIP. And, guess what? That is, indeed, the case of many people!<br><br>Why some are cured after some time while others aren't? Because, as evidenced by the experiences with the marine specime, our brain can adapt to longer or short terms to a disturption of its functioning. If someone is exposed to visual changes long enough for their brains to adapt in a long term, then they HPPD will last longer. It can last very short. <br><br>Why each HPPD is different? Because every trip is different. I can <br><br>What about depersonalization, anxiety and stuff? If a trip is long enough then <br><br>Why do some remedies work? Trips, generally speaking, disinhibits and inhibits some parts of our brains. So we can expect that the ADAPTATIONS that our brains make during a trip will involve disinhibiting and inhibiting those parts accordingly. So it's not a surprise that some remedies coincidentally causes disinhibition and inhibition of the same parts that are misconfigured. For instance, some suggest that afterimages are strengtened by a disinhibition on certain neurons of our visual cortex. Benzodiazepines inhibit our neurons in a general way, principally those that are overactive. So it's not a surprise that they will somewhere inhibit strongly those neurons involved on the generation afterimages. This is not a cure. It's just a temporary relief. Why? *Well, I'm an eletrical engineering student." But I would guess that long terms adaptations are made when our neurons move closer or further away from each other by stretching their dentrites/axoms, changing the strength of the signal being sent by a neuron to other. This way, short term adaptations would be when there is a change on receptors density, again changing the strength of a signal, and being something that seems very reversible to me. So, as a remedy will act on our receptors, they can change the functioning of our brain while they are on their effects, but, as they do not change our perception strong/long enough for that "natural adaptation" of our brain to take place, they won't have long term effects.<br><br>OK enough. Now the interesting part. THE CURE!<br><br>If you understood what I said <br>

[windscar]

then you probably realized that a possible way of obtaining a cure would be doing the opposite of what gave us HPPD. That is, seeing wrongly, long enough, for our brain to adapt in the inverse way it did when we tripped.

Thinking this way I tried the following: I looked into a strong light for very long until I couldn't handle it anymore. Then I looked again, and again, and again. I realized tat every time I made this, my vision became softer and cleaner (except for that burn in the middle of my vision, of course). After some time, I did my usual afterimage tests and, guess what? I WAS COMPLETLY FREE FROM PALINOPSIA! Trust me, my vision was never so clear since HPPD. No halos, no trails, nothing.

Well I'm completly exhausted as I'm writing this so I must go. As you can see, I wrote it straight with no formatting, no consulting the dictionary, no nothing. I just wanted to share my thoughts. I'll come here later to edit and summarize this into something decent (you are, of course, welcome to help me if possible) and add more info. If someone read this, please, try that exercise. But beware not to harm your vision. See you.

[Rozzer]

Hello

Please give an update on this.. This sounds very interesting..

[gill]

I think the whole process is more complex. Sure hallucinogens excite cells, but this whole process leads to gene expression changes. Who knows, maybe a bunch of cells just became all interconnected that weren't supposed to because lsd goes in there and tells the cell to grow out a branch that it shouldn't normally do.... Ugh, crazy stuff.....

[Loky]

I think the whole process is more complex. Sure hallucinogens excite cells, but this whole process leads to gene expression changes. Who knows, maybe a bunch of cells just became all interconnected that weren't supposed to because lsd goes in there and tells the cell to grow out a branch that it shouldn't normally do.... Ugh, crazy stuff.....

Bit of a newbie here, but could you briefly elaborate on this? What is your source? Cheers

[gill]

http://www.nature.com/npp/journal/v26/n5/full/1395848a.html

[Loky]

thanks mate

[alice-acid]

hmm that makes alot of sense to me but wheres the cure in all that?

[Sara]

Yeah..Im a little bit confused :S but I would like to know more...

[mbellamy09]

im not even trying to be mean but i cannot read all of that honestly...