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Back! Possible Cure Part 2 - No Guarantees But Were Here Anyways


Fawkinchit

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I am one of those nut cases that also suspect infection is the probable cause of HPPD, not maybe for everyone but for many. I had a positive ELISA spinal fluid test for Borreliosis burgdorfi back in 2008 and was diagnosed with neuro borreliosis. Back then I had a bunch of neurological disorders, like Bell's palsy, burning skin, etc. I was treated with two weeks of antibiotics and thought I was fine.

Before the lyme infection I had never had tinnitus but started to develop it after the infection. It's has come in waves through the years, often in connection with some medication but also when not. (I've also since then got joint and nerve pain, increased mental disorders, been diagnosed with bipolar disorder, chronic fatigue syndrome, IBS, etc.)

2016 I did a lot of psychedelics.

End of 2016 I started to notice some slight pattern glare/motion when I stared at certain surfaces with some pattern.

Beginning 2018 I noticed visual snow for the first time. Very slight, only noticeable in the dark. It kept on slowly progressing until I got full blown HPPD January 2019. All the symptoms on the list, plus some more (like textual bombardment, hyperacutis, temporary dyslexia, etc.).

Now today it's worse than ever. Tinnitus and hyperacutis is what's affecting me most, with a 50 % increase past three weeks. It's caused me to become suicidal.

I did not get HPPD suddenly. It's been basically creeping up on me, and is slowly deteriorating. I have tests from this summer from a hospital in Germany that says I am positive for a persistant form of borreliosis plus a number of coinfections, a few which affects the CNS. This has made me question if I really have HPPD. Maybe I would have got visual snow syndrome even if I hadn't used drugs. Maybe the drugs acted as a trigger or enabled it. I don't know.

I've done some herbal treatments this summer and I have responded positively to the treatment in some areas, like my joint/nerve pain has decreased by 90 %, my psoriasis is almost gone, light sensitivity is gone, dp/dr completely gone. Most neurological disorders have though remained unaffected, while visual snow, including tinnitus and hyperacusis has kept on getting worse.

Next up is treating the persistent borreliosis and coinfections with antibiotics. I really hope it helps because otherwise I don't know how long I will be able to go on, not with the constant increase of symptoms, and especially with tinnitus reaching a level that makes life unbearable.

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On 10/2/2019 at 12:05 PM, olivier24445 said:

Ok, interesting. Ever heard of a mother / son transmission,  then,  in those cases ? 

I've read about several cases - anecdotal of course - where both mother and child have VSS. It could indicate a casuality to some sort of infection, that's been transferred at birth. 

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17 hours ago, dasitmane said:

I guess we could also consider like a... viral infection, something that feeds on the receptors? Idk... lmao.

Role in virus endocytosis[edit]

5-HT2A may be a necessary receptor for clathrin mediated endocytosis of the human polyoma virus called JC virus, the causative agent of progressive multifocal leukoencephalopathy (PML), that enters cells such as oligodendrocytes, astrocytes, B lymphocytes, and kidney epithelial cells. These cells need to express both the alpha 2-6–linked sialic acid component of the 5-HT2A receptor in order to endocytose JCV.[8]

This has been mentioned before but it seems like as soon as it is mentioned there is a backlash from several people in the HPPD community, like it is totally absurd to even bring up a possible connection.

If we really want to find a "cure" for HPPD, we really need to dig into everything, even if it is unprobable, to make sure we haven't missed something. 

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5 hours ago, sami said:

I am one of those nut cases that also suspect infection is the probable cause of HPPD, not maybe for everyone but for many. I had a positive ELISA spinal fluid test for Borreliosis burgdorfi back in 2008 and was diagnosed with neuro borreliosis. Back then I had a bunch of neurological disorders, like Bell's palsy, burning skin, etc. I was treated with two weeks of antibiotics and thought I was fine.

Before the lyme infection I had never had tinnitus but started to develop it after the infection. It's has come in waves through the years, often in connection with some medication but also when not. (I've also since then got joint and nerve pain, increased mental disorders, been diagnosed with bipolar disorder, chronic fatigue syndrome, IBS, etc.)

2016 I did a lot of psychedelics.

End of 2016 I started to notice some slight pattern glare/motion when I stared at certain surfaces with some pattern.

Beginning 2018 I noticed visual snow for the first time. Very slight, only noticeable in the dark. It kept on slowly progressing until I got full blown HPPD January 2019. All the symptoms on the list, plus some more (like textual bombardment, hyperacutis, temporary dyslexia, etc.).

Now today it's worse than ever. Tinnitus and hyperacutis is what's affecting me most, with a 50 % increase past three weeks. It's caused me to become suicidal.

I did not get HPPD suddenly. It's been basically creeping up on me, and is slowly deteriorating. I have tests from this summer from a hospital in Germany that says I am positive for a persistant form of borreliosis plus a number of coinfections, a few which affects the CNS. This has made me question if I really have HPPD. Maybe I would have got visual snow syndrome even if I hadn't used drugs. Maybe the drugs acted as a trigger or enabled it. I don't know.

I've done some herbal treatments this summer and I have responded positively to the treatment in some areas, like my joint/nerve pain has decreased by 90 %, my psoriasis is almost gone, light sensitivity is gone, dp/dr completely gone. Most neurological disorders have though remained unaffected, while visual snow, including tinnitus and hyperacusis has kept on getting worse.

Next up is treating the persistent borreliosis and coinfections with antibiotics. I really hope it helps because otherwise I don't know how long I will be able to go on, not with the constant increase of symptoms, and especially with tinnitus reaching a level that makes life unbearable.

4 hours ago, sami said:

I've read about several cases - anecdotal of course - where both mother and child have VSS. It could indicate a casuality to some sort of infection, that's been transferred at birth. 

 

This is all really interesting because I distinctly remember my visual snow not appearing until about 2 weeks after getting HPPD, I didn't have the slightest clue what was going on at the time. In retrospect I just figured it had something to do with macro clean up in the nervous system of the damaged tissue, but it could have been increased growth of infection in the central nervous system.

There is a member on here as well that spoke well of how he did hallucinogens and was fine but then a couple months later got really drunk and bam HPPD, which could be infection breach due to alcohols ability to disrupt the epithelial barrier.

Really interesting stuff. WHen you go back for antibiotic treatment take note of your symptoms. Granted, some bacteria are not susceptible to all antibiotics, so this is a dilemma, and some are multi drug resistant strains, so its possible to see no effect at all.

If anyone has had extensive antibiotic therapy and noticed a difference in symptoms during their treatment please post. Thank you!

Edited by dasitmane
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5 minutes ago, yosoydiego said:

Although I'm up for "original" ideas, I just don't think that 5-HT is involved at all, for many many reasons.

Whats your reason? Theres a decent amount of evidence that its the case at hand. They can prove that it definitely is what causes hallucinations, and antipsychotics that act on the receptor make HPPD symptoms worse in a lot of cases.

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If HPPD is caused by a virus antibotics won't of course help directly, but the virus may be active, or even more aggressive, because the immune system is suppressed. So by helping the immune system heal and fight bacterial infection, it might also get more resources to fight a virus infection. The Epstein Barr virus, a herpes virus most people have becomes latent after initial infection, can become active when the immune system is suppressed. Same could be for other viruses (and bacteria).

LSD may act in an immune suppressive fashion.

This post on reddit mentions a paper from 1994 bringing this up (haven't found the paper myself):

https://www.reddit.com/r/LSD/comments/63mcno/lsds_effects_on_the_immune_system/

Other anecdotals:

https://www.reddit.com/r/LSD/comments/bxdi6c/help_guys/

https://www.reddit.com/r/microdosing/comments/572x1t/negative_effects_of_lsd_on_the_immune_system/

So it's possible a latent virus become active which affects the same parts in the brain that hallucinogenics do. It might be even so that because LSD acts as immune suppresant in those specific parts in the brain where it also causes hallucinations, a virus becomes active in those parts. And that might be the reason some get HPPD after drug use and others don't - it's basically related to the state of our immune system.

There is loads of evidence that lyme, mold, mercury, etc. can cause symptoms similar to HPPD/VSS.

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And a lot of people that seem to get better from HPPD are those that live a healthier life. They stop with drugs, alcohol, nicotine, they eat healthier, they excercise, meditate, etc. What could be going on is that the immune system actually gets a boost, and symptoms start to dissipate.

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2 minutes ago, sami said:

And a lot of people that seem to get better from HPPD are those that live a healthier life. They stop with drugs, alcohol, nicotine, they eat healthier, they excercise, meditate, etc. What could be going on is that the immune system actually gets a boost, and symptoms start to dissipate.

Yah, I'm aware of the virus situation, if its a virus I dont know what to do. I'll read those thread you posted later today to see what they all say.

Healthier life definitely helps, but placebo effect should be considered as well. 

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18 hours ago, dasitmane said:

Whats your reason? Theres a decent amount of evidence that its the case at hand. They can prove that it definitely is what causes hallucinations, and antipsychotics that act on the receptor make HPPD symptoms worse in a lot of cases.

To keep it more ordered, I've created a whole topic replying to that:

http://hppdonline.com/topic/6791-hppd-is-not-serotonergic-in-nature/

 

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HUGE post today. 

Last night I was reading an LSD study and the effects on the brain, going on about areas that are upreg/downreg or something. Anyways the down regulated areas he mentioned are desyncronized. I had to look up what that meant because I had no idea, but it started going on about brain frequencies etc. Basically the neurons in areas pulse with a feed back loop from other areas through resonance, the neurons fire in waves, as groups, its exactly what I was talking about really early on in my first thread. So I started conjecturing that maybe in a few minor users of hallucinogens their brain becomes permanently desynced so to speak, or the harmony between the two areas become discordant, exactly like I used to conjecture, only now there is physical evidence to the idea being possible. So, it comes back to the very first and original posts I made here when I joined 7-8 years ago, about using an antagonist, or maybe even an inverse agonist to "resync" the brain areas. It appears that the issues are predominately in the temporal lobes for people who have anxiety, and the occipital lobes for visual effects. I found a study involving Dr. Abraham where they did EEG studies on post drug users with and without anxiety, most of the users with anxiety showed irregularities in these areas, these are also areas in with patients with seizures can be effected. Dr. Abraham and the other doctor also mentioned how before seizures, patients will report high fear/anxiety. The condition of HPPD could very well be brother/sister relationship with epilepsy interestingly enough.

Then I searched the HPPD forum for any posts involving 5HTP2A receptor antagonists or agonists. What found is shocking. Heres the posts from "Victor"

In my case the disorder healed in two months with risperidone and paroxetine. Paroxetine acting upon anxiety and risperidone over visual distortions. Well you know the risk of self-medicating, do not do that, I had facial spasms with only 3 days of use of quetiapine (prescribed by shrink). Doctors actually know about the disorder, but since it is something very recent and vague hardly anyone is diagnosed with it, even because sequels of psychedelic drugs are not the only reason for the cause of false visual perceptions or other senses without loss of lucidity. So go to the psychiatrist anyway, because only then will you get these medications and then heal. Other than this, physical activities are great for diverting your focus from the problem, but the visual symptoms will only disappear with treatment using remedies. I also suggest meditation and some artistic activity such as writing, drawing, playing an instrument, etc. And also temporary abolition of coffee, alcohol and cigarette consumption.

Posted March 25

Hello !
Your story is very similar to everyone here, including mine. When I had HPPD, I also got the symptoms very fast and only noticed them after smoking marijuana days after my trip with LSD.
What matters is that as quickly as the symptoms came, they left. This is because I did psychiatric treatment, initially using paroxetine for anxiety, risperidone for visual distortions and clonazepam for anxious seizures. Risperidone is an antipsychotic and a major antagonist of LSD as well as quetiapine and chlorpromazine (I have taken all of these, but risperidone was the most effective). In a matter of two months the false hallucinogenic perceptions were gone. With you it would not be different, but for this you need to look for a psychiatrist and explain what happens to you, as he will know the right medication to apply. Please do not self-medicate, as these medicines can have horrible adverse reactions. I for example had facial spasms when I took quetiapine (this I only took for 3 days). I recommend that you do not look for it on the internet, because it is still very vague, unfortunately it is difficult to find information about it and almost all are scary, as it comes from a sensational and anti-drug media. Rest assured, what happens to you is nothing serious and has a cure. Avoid using drugs at this time, including marijuana, alcohol, cigarettes, and coffee.
Stay in peace ! 
 
If you read most of his posts he is very adamant that Risperidone cured his HPPD. I found another poster too...

I have HPPD consisting of marihuana-like derealization, LSD-like movements of surfaces, and optical noise.

The LSD-like movements had gotten much better over the course of 7 years until they were barely noticeable, until I took Ritalin. Within two weeks, the LSD effects were almost as bad as in the beginning. The rest of my visual effects were not affected. I discontinued Ritalin. The LSD effects remained unchanged (other than going through their usual cyclical fluctuation over 5 days (IIRC) for the next few weeks.

Then I started taking low-dose Risperidone (2mg, I think).

For the first two days, nothing happened. On day 3, the LSD effects were basically turned off, back to barely noticeable.

It was like flipping a switch. In the morning they were there, in the afternoon they were almost gone.

I continued taking Risperidone for a few weeks, even increased the dosage, but nothing else happened. There was no effect on my other visuals.

After discontinuing Risperidone, the LSD effects did not return, even when I started taking Ritalin again (strange, huh?).

I've been taking Ritalin for a few years now. The HPPD symptoms are stable.

Caffeine never affected my symptoms.

I also found another poster saying he was cured by 200mg of Lamotrigine, which is an antiseizure medication, but it would be clear that this would only treat the symptoms since they are probably similar to epilepsy like disruptions in the brains resonations.

Also, there are arguements that Risperidone, an inverse agonist of 5HTP2A exasperates symptoms of HPPD, which is also probably very true, as per the drug in itself without history of HPPD can cause palinopsia. I'm guessing the difference is just in the dose, as the one guy listed his dose which was very smart of him, and as far as I'm concerned is a pretty low dose, not the lowest, but pretty low, as the high does is 200mg.

So the answer may very well be in inverse agonists, and maybe even antagonists as well. whichever being the case I'm not entirely sure. Interestingly enough this is probably the "reversal" that hope's research team may have in mind, whether they read my initial ideas/post in my first thread I have no idea, and if that is what they have in mind I'm not entirely sure. But this may very well be it.

The cure for HPPD.

Edited by dasitmane
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10 minutes ago, dasitmane said:

Also, there are arguements that Risperidone, an inverse agonist of 5HTP2A exasperates symptoms of HPPD, which is also probably very true, as per the drug in itself without history of HPPD can cause palinopsia. I'm guessing the difference is just in the dose, as the one guy listed his dose which was very smart of him, and as far as I'm concerned is a pretty low dose, not the lowest, but pretty low, as the high does is 200mg.

Treatment with the atypical antipsychotic medications paliperidone and risperidone normalized basal extracellular glutamate

https://www.ncbi.nlm.nih.gov/pubmed/21699956

 

In line with my other post :)

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Here is another case where the patient is prescribed 1mg of risperidone, and within two months reports that they are cured. Ill post more if I find any. Looks like one month in though they discontinued Risperidone and added the lamotrigine. This is the lamotrigine person I mentioned in the previous post.

Also if anyone has had any EEGs done please do post the results.

Would like to add too that its possible that the Risperidone could exasperate symptoms initially, but then resolve them, sometimes in medicine when there is a cure, the symptoms get worse before better. Not always, but there are cases.

Heres a post from another member, stating that it worsened his symptoms, he doesn't give the dose that he was prescribed though unfortunately.

Posted December 29, 2012

Firstly they gave me risperidone, this amplified my symptoms and i stopped taking them. They then gave me amisulpride, that didnt go well either. Then seroquel, it was the better of the three.Once i got used to the side effects it doesnt seem so bad, although im really not sure how much good its doing me.

Thats pretty much all I could find on the forum, if theres anything else anyone can find please share. Thanks!

If all this is true and accurate, these desyncronization or discordances in the brain could be the cause of a lot of mental disorders. 

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I was put on 200mg Lamotrigine beginning of 2018, when I was diagnosed with bipolar disorder. It was shortly after that that I saw visual snow for the first time. I even brought this up with the prescribing doctor.

At this point I had no idea even what visual snow was. Visual snow got worse during the year, end of 2018 I also had tinnitus and diplopia. Jan 2019 I started to see the visual snow in day time, and I also got palinopsia, light sensitivity, floaters, starbursts, halos, etc. I quit the treatment with Lamitrogine in February. No change. Instead most of my symptoms (except light sensitivity and dp/dr) have been progressing and getting worse since then, and this far nothing I've done has changed that. Quitting all drugs and pharmaceuticals, caffeine, nicotine has had zero effect. Ketogenic diet during six months and intermittent fasting during five months has had zero effect. Living healthy, excercise, meditation has made no change in the progression of the symptoms.

I am ready to try keppra and clonazepam on top of the infection approach, since I am far from convinced infection is the cause, but I got to try something, because as it is... I am slowly deteriorating.

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1 hour ago, sami said:

I was put on 200mg Lamotrigine beginning of 2018, when I was diagnosed with bipolar disorder. It was shortly after that that I saw visual snow for the first time. I even brought this up with the prescribing doctor.

At this point I had no idea even what visual snow was. Visual snow got worse during the year, end of 2018 I also had tinnitus and diplopia. Jan 2019 I started to see the visual snow in day time, and I also got palinopsia, light sensitivity, floaters, starbursts, halos, etc. I quit the treatment with Lamitrogine in February. No change. Instead most of my symptoms (except light sensitivity and dp/dr) have been progressing and getting worse since then, and this far nothing I've done has changed that. Quitting all drugs and pharmaceuticals, caffeine, nicotine has had zero effect. Ketogenic diet during six months and intermittent fasting during five months has had zero effect. Living healthy, excercise, meditation has made no change in the progression of the symptoms.

I am ready to try keppra and clonazepam on top of the infection approach, since I am far from convinced infection is the cause, but I got to try something, because as it is... I am slowly deteriorating.

No Risperidone though?

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In some cases it does appear risperidone makes symptoms worse. Maybe an antagonist would be better.

EDIT: Antagonists like trazodone seem to do nothing, but I was thinking that maybe its nessasary to have a highly specific 5HT2A inverse agonist.

Edited by dasitmane
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5 hours ago, yosoydiego said:

EEGs are, more or less, useless. Fun though :P

As far as I know its pretty useful for epileptics. Granted if these alternative theories are wrong, then its discordance/desyncronization in the feedback loops involved due to white matter neuronal loss, which would be for the most part unrepairable even with neurogenesis.

 

It is a very curious thing though that Risperidone is working in some of these patients...

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22 hours ago, dasitmane said:

No Risperidone though?

No risperidone. I've also been on Mirtazapine (4 yrs) and Zopiclone (6 months). Quit everything back in Jan-Feb after my symptoms turned to worse. Withdrawal from bith meds definitely exaggerated symptoms for a while, and I was off them completely for 5 months. Some symptoms improved after a while, like I mentioned (light sensitivity, dp/dr, also palinopsia got slightly better, was having constant positive afterimages but it was reduced by 50%) but the others have kept on deteriorating (visual snow, tinnitus, halos, starbursts, bfep, pattern glare). I got sleeping issues again after five months (in July) and have since then been back on Zopiclone, lower dose though, and my psychiatrist convinced I should get back on a low dose of Mirtazapine too, and I hate myself that I've done that, because it feels like symptoms have progressed faster since then. But it could just be correlation. Not sure of anything anymore. Now I am trying to get off Mz again, and it may be the cause of some symptoms getting a lot worse past two weeks. I started tapering off 17 days ago, when my tinnitus had already gotten worse. Now it's a lot worse plus the hyperacusis, and today I also started to notice increased palinopsia and diplopia, which hasn't happened since January.

Personally I suspect there are a lot of reasons for my deteriorating condition. It's not only drugs, since I've been off them before I even got visual snow. I suspect it is a combination of drugs, pharmaceuticals and infection, and the neuro borreliosis back in 2008 has been the main kicker.

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  • 1 month later...

More shit, I'm going to try and find any correlations with qEEG and other disorders, that could give some more leads as to the cause of this.

Here's a study where they already did this with 44 HPPD patients. I dont know anything about qEEGs or what everything means, all I made out was "disease severity was highly significant". All I can make out is faster alpha frequency(brainwave), and visual evoked response, which has something to do with LSD induced cortical(outer areas of the brain) disinhibition.

Abstract

Hallucinogen persisting perceptual disorder (HPPD) may follow the ingestion of LSD or other hallucinogens in a subset of users. It is characterized by chronic, intermittent or constant visual hallucinations of many sorts persisting beyond the period of acute drug effects. We studied 44 LSD-induced HPPD subjects and 88 matched controls to search for spectral and evoked potential differences using quantitative EEG (qEEG). HPPD subjects demonstrated faster alpha frequency and shorter VER (visual evoked response) latency, consistent with prior animal and human data on response to acute LSD administration which suggest LSD-induced cortical disinhibition. AER (auditory evoked response) latency was prolonged consistent with a differential LSD effect upon visual and auditory systems. The exploratory T-statistic significance probability mapping (T-SPM) technique demonstrated HPPD-control differences mostly involving temporal and left parietal scalp regions, confirmed by a split-half analysis. Significant variables were all derived from the long latency flash VER and click AER. None were derived from spectral analyzed EEG data. Canonical correlation between SPM-derived measures and variables reflecting disease severity was highly significant. A between-group stepwise discriminant analysis based upon a full set of qEEG measures demonstrated 87% prospective classification success by jackknifing and 88% success in a separate split-half analysis.

https://www.ncbi.nlm.nih.gov/pubmed/8912957

Heres another. "in HPPD, there is widespread cortical inhibition in the eyes-opened state, but localized and isolated occipital disinhibition upon eye closure, a state known to facilitate hallucinatory experiences."

Abstract

LSD use in certain individuals may result in chronic visual hallucinations, a DSM-IV syndrome known as hallucinogen persisting perception disorder (HPPD). We studied 38 HPPD subjects with a mean of 9.7 years of persistent visual hallucinations and 33 control subjects. Measures of local and medium distance EEG spectral coherence were calculated from all subjects. Coherence, a measure of spectral similarity over time, may estimate cortical coupling. In the eyes-open state in HPPD subjects, widespread reduction of coherence was noted. However, upon eye closure, the occipital region demonstrated augmented regional coherence over many frequencies but with reduced coherence of the occipital region to more distant regions. This occipital coherence increase correlated with previously reported shortened occipital visual evoked potential latency for HPPD subjects. We speculate from coherence and known clinical and psychophysical data that, in HPPD, there is widespread cortical inhibition in the eyes-opened state, but localized and isolated occipital disinhibition upon eye closure, a state known to facilitate hallucinatory experiences. An analogy is drawn to findings in the interictal and ictal epileptic focus. In HPPD, we speculate that occipital EEG hypersynchrony resulting from increased regional coherence, when coupled with relative isolation of visual cortex, especially upon eye closure, facilitates hallucinations and illusions.

https://www.ncbi.nlm.nih.gov/pubmed/11566431

Basically the cerebrum(outer parts of the brain/front back and side) is disinhibitied or overreacting for some reason. Very interesting.

Heres a study that probably rules out the GABA interneurons theory. It doesn't definitively, but leans away from the idea more so.

https://www.jneurosci.org/content/jneuro/20/16/6232.full.pdf

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Super fucking interesting

In electroencephalography, the P50 is an event related potential occurring approximately 50 ms after the presentation of a stimulus, usually an auditory click.[1] The P50 response is used to measure sensory gating, or the reduced neurophysiological response to redundant stimuli.

Research has found an abnormal P50 suppression in people with schizophrenia, making it an example of a biological marker for the disorder.[2][3] Besides schizophrenia, abnormal P50 suppression has been found in patients with traumatic brain injury, recreational drug use, and post-traumatic stress disorder.[4]

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What da fawk

Nicotine[edit]

One reason people report they like smoking cigarettes is nicotine's ability to aid their selective attention.[3] In order to alleviate the stress of not being able to gate sensory input, nicotine can correct sensory gating deficits for individuals with schizophrenia, but the effects only last about 30 minutes after nicotine intake.[9] The same self-medication is present among those with attention-deficit/hyperactivity disorder and even those on the autism spectrum as well.

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This is nuts because I always noticed my anxiety would slightly increase as the sun was going down and everything was getting darker, probably effects alpha waves to some degree likened to that of closing of the eyes, and found in high frequencies in our brains.

Alpha waves are neural oscillations in the frequency range of 8–12 Hz[1] arising from the synchronous and coherent (in phase or constructive) electrical activity of thalamic pacemaker cells in humans. They are also called Berger's waves after the founder of EEG.

Alpha waves are one type of brain waves detected either by electroencephalography (EEG) or magnetoencephalography (MEG), and can be quantified using quantitative electroencephalography (qEEG). They predominantly originate from the occipital lobe during wakeful relaxation with closed eyes. Alpha waves are reduced with open eyes, drowsiness and sleep. Historically, they were thought to represent the activity of the visual cortex in an idle state. More recent papers have argued that they inhibit areas of the cortex not in use, or alternatively that they play an active role in network coordination and communication.[2] Occipital alpha waves during periods of eyes closed are the strongest EEG brain signals.

 

These faster alpha waves could be the whole cause of HPPD, and could explain the disinhibition of the cortex/cerebrum.

Visually everything routes through the thalamus too, to be communicated to the visual cortex. Interesting indeed.

Edited by dasitmane
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Super weird that it is out of the brain in 20 minutes....

The drug moves quickly to the brain and throughout the body and acts on both the central and autonomic nervous systems. All traces of the drug disappear from the brain rapidly in about 20 min, although the effects may last many more hours.

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