Fawkinchit

Yah about that. The issue at hand is dealing with something in the nervous system, recovery of these types of tissue is done in about that time, most tissues fully recover or scar within 3 months. Anything else after two years would most like be some form of external remediation. Like for example Jeep Cherokee sports seem to have some chemical in the materials used that acts as a strong stmulant. So they may own it for three years and then sell it, all of a sudden their anxiety improves after 3 years for some reason. So strictly im referring to just body healing.

Vision? Lol, I had static for a month or two. visual disturbances really arent the worst of it. Anxiety and DP/DR is the hard stuff. If you are only dealing with visuals I'd say you dont have the worst end of it all, so be glad about that. But maybe you aren't noticed the effects of anxiety vs visual snow.

Not sure if I understand the question properly but DSM will probably affect different areas of the brain than MDMA, Hallucinogens, etc. So yes the "criteria" may be different. By criteria I think you mean symptoms. They are somewhat varying in different degrees in all of us. Some have worse visuals, some have worse anxiety.

Mine got worse for about a month of two, and then they will seem to flat line, then they started getting better. Hard to say exactly what will happen though cause this is neuronal stuff. Its different for everyone.

Lemon balm will help with the anxiety, its a natural GABA Agonist. BTW, Excess Magnesium will create alot of balances elswhere in the body. Such as calcium. To much of anything is bad.

Its just speculation, its most probable that its wrong as well, as if it were there are drugs that can realter GABA and dopamine, but they dont solve the problem. So it is elsewhere. EDIT ^^^Thats how I felt for the first 3 months! lol.

Somewhat of a metaphor I thought of of the feeling. Theres anxiety and visuals but theres something else going on there. Someone explained it really well in an older post, he explained that theres a siren going off in the brain, and the sedatives help to dim it, which is nice, but its still there.

If they are aware of the condition they will be more receptive, if they arent they wont really know anything about it. The only treatment basically that they will likely offer is sedatives, aka GABA agonists. They will help you to calm down but the burning of the brain will still be there. They do help though, especially for times when it gets really bad. You could try herbal remedies as well. Thats what I generally use. Lemon balm, and a few other natural gaba agonists will help, I cant remember what the other ones are but you can look them up.

My opinion is that the largest sum of recovery should occur in 3-12months. 2 years would most likely be the cutoff point in my opinion.

I think you might be overreacting a little bit, its most probable that its a reaction from the drops at the eye doctor. Be patient. Your eye will itch drastically if you have an infection in it.

Im pretty sure this has more to do with all the stimulant related homrones like adrenaline that are released.

BTW Anyone that wants to add me to facebook send me a link in a PM.

Um, yah, this would be a great thing to inform them of. Basically is all you would need to do is copy and paste the information that I posted to them. Couple problems there though are that, honestly, most modern day scientists are just mainstream method followers, they generally are most likely to be about getting funding, they dont want to do research that may tarnish their reputation, and, youll need to make sure that it was already made public information what you;re sending them so they dont try say they came up with the idea lol. Seriously though I wouldnt be surprised hahaha. This system really is a failure.

This actually isnt a bad probabillity, its definitely possible that instead of apoptosis is caused some malfunction in neuronal resonance, maybe there is some sort of scarring involved. Hard to say. Mainly the post was to make the connections of how the problem most probably occurs. Its definitely open to enterperit the end result. Apoptosis was the best I could come up with, though it definitely could be some other form of damage. Also would MRIs pick up scattered apoptosis? I think they are generally only capable of showing large clusters of the brain tissue death. But I could be wrong about this.

Friiiick I started losing my hair from this too! No one in my family is bald either. Sucks.

Thats a pretty big find! NeuroD1 retrovirus

lol mg why did you remove your picture?

Is anyone else having this problem?

Wow! Thats great Mg. Ha. Just wanted to check up and see how everyone is doing. Been a while since I have been here. Hope you're all doing well.

asdf

Edited

Thanks hope. I couldn't have put it better myself.

Ok here is the full laid out explanation of HPPD The Cerebellum Connection In the rat cerebellum, 5ht2a receptors have been found in the Golgi cells of the granular layer, and in the Purkinje cells. This shows that the cerebellum will be effect in specific cells under the influence of hallucinogens. Purkinje cells are a class of GABAergic neurons located in the cerebellar cortex. People with cerebellar ataxia may initially present with poor balance, which could be demonstrated as an inability to stand on one leg or perform tandem gait. As the condition progresses, walking is characterized by a widened base and high stepping, as well as staggering and lurching from side to side. People with damage to the cerebellum from strokes also have vertigo and other similar balance disorders and problems have been reported with anxiety I believe as well. Symptoms of HPPD have been known to exhibit balance disorders. This gives an obvious full line of connections for the cerebellum being a critical center that is effected by HPPD. Now on to golgi cells in the cerebellum Golgi cells are inhibitory interneurons found within the granular layer of the cerebellum. This ties in with the inhibitory feedback that I was talking about in the beginning of this thread(push pull idea), that there may have been damage to these inhibitory cells, and the brain now lacks the ability to modulate anxiety! That sums up most of the cerebellum Lets take a look at other areas in the brain affected. Newer findings reveal that psychoactive effects of classic psychedelics are mediated by the receptor heterodimer 5-HT2A–mGlu2 and not by monomeric 5-HT2A receptors. The mGluRs perform a variety of functions in the central and peripheral nervous systems: For example, they are involved in learning, memory, anxiety, and the perception of pain. They are found in pre- and postsynaptic neurons in synapses of the hippocampus, cerebellum, and the cerebral cortex, as well as other parts of the brain and in peripheral tissues. This shows other areas in the brain that are going to be negatively affected by hallucinogens. The hipp, cere, cere cortext, and other parts, most likely visual related. So, now we know all the areas of the brain being affected by hallucinogens. Lets take an even closer looks at where and what the 5ht2a receptors do. 5-HT2A is expressed widely throughout the central nervous system. It is expressed near most of the serotoninergic terminal rich areas, including neocortex(mainly prefrontal, parietal, and somatosensory cortex) and the olfactory tubercle. Especially high concentrations of this receptor on the apical dendrites of pyramidal cells in layer V of the cortex may modulate cognitive processes, by enhancing glutamate release followed by a complex range of interactions with the 5-HT1A, GABAA, adenosine A1, AMPA, mGluR2/3, mGlu5, and OX2 receptors. In the rat cerebellum, the protein has also been found in the Golgi cells of the granular layer, and in the Purkinje cells. In the periphery, it is highly expressed in platelets and many cell types of the cardiovascular system, in fibroblasts, and in neurons of the peripheral nervous system. Additionally, 5-HT2A mRNA expression has been observed in human monocytes. I bolded the parts that are the more important keys to showing what causes HPPD. Not also that the golgi and purkinje cells are brought up again. Also note that one of the main functions of the 5ht2a receptor when activated is to enhance the release of glutamate, and effects the AMPA receptor. Lets tie it all up now. Excitotoxicity is the pathological process by which nerve cells are damaged and killed by excessive stimulation by neurotransmitters such as glutamate and similar substances. This occurs when receptors for the excitatory neurotransmitter glutamate such as the NMDA receptor and AMPA receptor are overactivated by glutamatergic Storm. So, hallucinogens extremely high agonist(push) affinity for 5ht2a receptors will overstimulate the receptor, causing a higher than normal release of glutamate, leading to a glutamatergeic storm of all the areas listed above, thus leading to excitotoxicity of those areas, and causing apoptosis to occur to specific sites in the brain. The brain then no longer has the ability to regulate certain stimuli and electromagnetism. Hence, the symptoms of HPPD. That should clear it all up for you guys.

Edited

Edited