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Fawkinchit

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Posts posted by Fawkinchit

  1. So correct me if I'm wrong but you're saying that after 2 years has past there is no chance of recovery?

     

    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.

  2. 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.

    • Upvote 2
  3. 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.

  4. As the title said those three things seem to be getting worse but I'm pretty sure I need to withdrawal off the klonopin I've taken for five years.ive tried twice before and am down a very low dose so I hope symptoms are at a minimum but who knows.

    I'm gonna start the withdrawal after spring break so basically at the start of April. My concern is that the things that are worsening will just get crazy after. Any advice on this?

     

    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.

    • Upvote 1
  5. If anyone cares I've been taking magnesium for a few weeks and unfortunately I think it mad my fogginess,snow,and after images work. Anyone know of any other supplement I can try?

     

    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.

  6. So there is a lot of talk about gaba, dopamine etc etc being disregulated in hppd.  Do we know this for a fact or is it just informed speculation? Is there a way of knowing for a fact - spinal tap, brain scans etc?

     

    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.

  7. What do you mean by "burning of the brain"?

     

    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.

    • Upvote 1
  8. 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.

    • Upvote 2
  9. I've been reading a few posts about estimated normal recovery is like 3 months-5 years. Obviously not measured in any way shape or form though. That leads to the question of how long do you guys think someone could have this before it's "to late" to recover?

     

    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.

  10. Correct me if I'm wrong but if there were ever an approach and modality to help us, wouldn't this be it?

    Someone able to speak science needs to get in touch with these doctors, inform them of this condition and explain how and why their research could probably help us. I could think of you, Qaiphyx, Visual and of course David but there are plenty of others who could articulate the theory behind our problem and perhaps pose a challenge to these scientists that will entice them to solve. Will someone with the smarts contact them please???

     

    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. :lol: Seriously though I wouldnt be surprised hahaha. This system really is a failure.

  11. I think there are some excellent kernels of value and interest in what you say, though the question I have about all this is the failure of any MRI, CAT (I've had both) and possibly PET scans (can someone check?) to detect any cell death.  So I am not sold on neurotoxicity and neuron death as primary factors in HPPD.

     

    BUT:  you bring to mind another possible avenue of research with excellent bona fides: deep brain stimulation, and trans-cranial stimulation.  Both are vetted, with published and verified results in the areas where they have been applied.

     

    For example, 100,000 Parkinsons patients are running experimental devices that SHUT OFF their tremors by stimulating the clusters of neurons responsible for the out-of-whack firing patterns.

     

    What if, instead of cell death, a "malformed" but resonant pattern of firing has been set up amongst groups of neurons, causing the responses that developed during intoxication to return and persist - and what if electrical stimulation would disrupt the resonant pattern and extinguish the misfirings, hence the symptoms?

     

    I have to say, my HPPD has been much less an issue for me since my breakdown and subsequent electro-shock.

     

    Think about it.

     

    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.

  12. Qaiphyx brought to my attention 5ht2a inverse agonists.  It was a great success in FDA trials.  And because of his ideas i invested in a stock that went up 1000%.  

    Thank you!  ....but ofc the money is not as important as something that will help us and other people with nerve based problems.  

     

    This is what I have been interested in now:  a treatment for MDD and stem cells.  The treatment for MDD is a drug called NSI-189.   I'm not sure we have mentioned it before  but there are official trials being performed as we speak.  And i found a site where people were getting the drug from chemical companies and this is some of their "opinions":  http://208.71.46.190/search/srpcache?ei=UTF-8&p=longecity+nsi-189&fr=yfp-t-140&rs=0&u=http://cc.bingj.com/cache.aspx?q=longecity+nsi-189&d=4573935196046048&mkt=en-US&setlang=en-US&w=y653-FeiyYof_A2CyQ0KTNLrnI9JNkzn&icp=1&.intl=us&sig=VNrvcJFPLC2J_zIR6jbtCw--

     

    The company behind these therapies is neuralstem. 

     

    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.

    • Upvote 6
  13. 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.

  14. If hppd isn't bad enough along with the cormirbituties like tinnitus and dp/dr, it's all the other baggage and wear n tear that really makes life hard. 43 may not sound old but add degenerative disc disease, a touch of arthritis from a torn meniscus, anxiety that wobbles like a pendulum: all in all it really makes an already troubling situation that more harrowing. I hope you guys muster the intellect needed to beat this beast because that's what it is: a bloody relentless, heartless beast that simply wants to suck any semblance if normality and happiness away. I hope you guys are successful and hope even more that I can thank you all who helped crack the hppd code.

    I hope...

     

    Edited

  15. Seriously, I'm really living on borrowed time.

    I'm at the end of my rope and at 43 with life literally being in the toilet, lost my marriage and have a son with autism, probably because of hppd, I can't see myself making it to 50 and not because I want to die but because my body can't take the neurological disconnect for much longer. The dysfunction is affecting my physicality, the stress is prematurely aging me and I'm greeting at a rapid pace. With everything that is going on in medicine, this theoretically small community needs and deserved help. I had 27 excellent years of life before getting crucified with this shit but I want to live. I want to help my son, I want to contribute to society, be a good man, lead a good fulfilling life. Never had I would have ever thought I'd be living back home at my age, a disgrace to my family and an utter failure. I know I'm better than this but the damage to my mind makes it virtually impossible for me to keep carrying on the act. Help yourselves by reaching out to tedearchers who can help. Don't let your life go by without having tried because the steps taken now can change the future and the focus on this condition. For all that is good I hope help does come because you don't want to be like me.

     

     

    Edited

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