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"Permanently" upregulated 5-HT2a after using of THC & Psilos on top of an O-PCM binge

dopamimetic

Bluelighter
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"Permanently" upregulated 5-HT2a after using of THC & Psilos on top of an O-PCM binge

Hi folks,

the following is a personal issue of which I simply don't know where or with whom to talk about. Of course it should be a doctor, and I know that bluelight can't nor shouldn't replace one, but I am afraid of that for now because of how some people react when it comes to hearing voices.. they aren't exactly voices, more an asynchronous second train of thought over which I only have very limited control (but can talk with, sometimes, also in limited amount). No pitch, just words.

This started when I was addicted to O-PCM and took a "Dutch tour". One or two joints on day one, another one and psilocybe tampaensis on day two. Of course mixed with my beloved PCM, and contrary to the plan I emptied the whole box of truffles within a few hours (should have known better, yay). None of these were new to me, had good experiences with truffles years ago and not so good ones with weed but every drug alone was tolerated. Also I have mixed O-PCM before with a handful of other things although never these other two.

The first hours nothing unexpected happened, some delusions but no real hallucinations. Then black-out, next thing I remember is being out in the stairwell, thinking it was a psych ward where I would have lived forever and just woke up off a dream of my real life. More black-outs followed, after 12h or so I was back to reality but felt weird. Nothing too special, just that it lasts up to today (10 months). The voices come and go, they are worse when I am stressed and it takes just a tiny fraction of what I used to tolerate, for extreme stress reactions like stuttering, headache, pounding heartbeat, fucking strong anxiety. Concentration's on holidays and cognition slows down too often.. social withdrawal etc, guess it's your usual negative/positive symptoms..

Antipsychotics don't cut it, some with 5-ht2a antagonism do lower the frequency though (chlorprothixen, dipiperon). Risperidone 2mg caused a worsening (over 10 days). Recently I found CBD to be more helpful. Lisdexamphetamine helps with the cognitive issues, but does worsen the voice phaenomen when coming down .. SSRIs did just increase inner tension until I started the dipiperon. Pregabalin doesn't to help on the long run either.

My theory is that I experienced some kind of seizures due to overexcitation mediated by (also) the 5-HT2a and CB1 receptor couple, and glutamate autoreceptors blocked.. in an oversimplification. Is this possible? And what might help?

Oh, missed something. I am on morphine maintenance, 300mg. Was an attempt to get me off the PCM that didn't hit it, have been taking both for a while until the symptoms got too bad. I can't withdraw at the time being because even before the runny nose these damn thoughts and extreme tension set in. In retrospective I feel like the opioids (bupe first, then morphine) potenciated the (acute) delusional effects from dissos.

I'd be thankful about some supplement working of course. Sarcosine, Agmatine maybe?
I am taking a B-complex now and will switch to a multivitamine after that.

Otherwise from the prescription drugs, a 5-HT2a reverse agonist maybe (does one exist that is available)? Rimonabant being a CB1 reverse one. Or rather glutamatergic modulators, I made mixed to good experienced with memantine against overexcitability years ago..
I won't experiment with more than supplements for now, just want to understand what's happened or might have happened, to be able to convince a doctor to help me more than just label me a psychotic episode..

Thanks!
Dopa
 
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I'm not sure if it makes sense to think of this in such purely neurochemical terms. Perhaps 5-HT2A upregulation is the cause of your symptoms, perhaps not, but if it is it's just the neurological mechanism behind what sounds to me like a fairly unremarkable case of feeling slightly scattered for some time after an unexpectedly intense experience on several powerful psychoactive substances... to put it mildly. That being the case, the appropriate treatment is likely to be much the same as that for any lingering symptoms from such an event, whether they be PTSD, HPPD or something else less well defined - ie, giving yourself some time to recover, and just keeping on trying to do all the things you know you should do for yourself even if you don't want to. By which I mean of course, good diet, exercise, mentally stimulating activities, some meditation perhaps, and just wait for your scrambled mind to figure out how to put itself back together again.

Some other substance might well help you out in the short term, or even the longer term, but realistically it's just going to be guesswork because you can't really feel something as specific as 5HT2A upregulation directly even if you might surmise that what you CAN feel in yourself is connected to that, and there's just not enough research into these substances' interactions to say whether or not this is even likely to be case, let alone the best way to treat it.

Just my opinion of course based on no controlled studies whatsoever.
 
Risperidone can sometimes paradoxically make HPPD worse. Actually, the atypicals don't block all of the psychoactive effects of 5-HT2A agonists even when there are those meds in your system when you're dosing the psychedelic, so maybe they bind to a different place on the receptor and disable only one secondary messenger pathway. It's probably safest to avoid any unnecessary drugs/pharmaceuticals until the HPPD problem is gone.
 
Risperidone can sometimes paradoxically make HPPD worse. Actually, the atypicals don't block all of the psychoactive effects of 5-HT2A agonists even when there are those meds in your system when you're dosing the psychedelic, so maybe they bind to a different place on the receptor and disable only one secondary messenger pathway. It's probably safest to avoid any unnecessary drugs/pharmaceuticals until the HPPD problem is gone.

"Atypical" antipsychotic is a pretty arbitrary classification, though.

The irony here is that in terms of its effects, risperidone's balance between serotonergic and dopaminergic antagonist effects make it not that much different from a "typical" thioxanthene antipsychotic like chlorprothixen, while pipamperon, despite sharing the butyrophenone backbone of the infamous typical antipsychotic haloperidol, behaves much more like an atypical in terms of its selectivity for 5HT2a over dopaminergic receptors.

Honestly, I'd be surprised if the "atypical" antipsychotics really performed worse at blocking trips due to weaker 5HT2a antagonism... more likely, the typical antipsychotics simply generally pack an extra punch against all sorts of craziness due to their generally stronger dopamine antagonism.

I could see the third-generation-antipsychotics like aripiprazole (which are usually also classed as "atypical" antipsychotics) failing to block psychedelics though, since they mostly act via a sort of partial agonist action at specific dopamine receptor subtypes.

Anyway, getting back to OP's question: There is indeed a highly effective inverse agonist for 5HT2a that is even widely used in psychiatric medicine: olanzapine, better known under the trade name "Zyprexa".

Still, I would like to echo the sentiments of the previous about how you shouldn't be too certain that your issues are solely related to 5HT2a upregulation: Smoking weed can certainly exacerbate psychoses, and binging on all those dissociatives may have affected all sorts of glutaminergic pathways (there is a reason they use MK-801, a powerful NMDA antagonist, to induce psychotic behavior in animal studies).
 
Hodor, according to Wikipedia, the risperidone's affinity for 5-HT2A is tens of times greater than for any dopamine receptor (0.17 nanomoles per liter compared to over 3 nmol/L). With quetiapine the ratio isn't that large but significant anyway. I remember an article where it was claimed that 1 mg of risperidone is enough to pretty much saturate the 5-HT2A while usual therapeutic doses of quetiapine block less than 60% of the receptors.
 
Hodor, according to Wikipedia, the risperidone's affinity for 5-HT2A is tens of times greater than for any dopamine receptor (0.17 nanomoles per liter compared to over 3 nmol/L). With quetiapine the ratio isn't that large but significant anyway. I remember an article where it was claimed that 1 mg of risperidone is enough to pretty much saturate the 5-HT2A while usual therapeutic doses of quetiapine block less than 60% of the receptors.

The thing about risperidone is that its effects on the D2 receptor cannot be described in terms of its binding affinity alone; despite the relatively low binding affinity, there is a significantly higher incidence of extrapyramidal side-effects and hyperprolactinemia than with other "atypical" antipsychotics. Apparently, this is because risperidone reaches more deeply into the binding pockets of the receptor than other atypicals, as was recently demonstrated by the same team that did the famous crystallography study on the way LSD gets "stuck" in the human 5ht2b receptor (another substance whose extreme potency could not be adequately explained merely as a function of binding affinity).
 
the appropriate treatment is likely to be much the same as that for any lingering symptoms from such an event

You're absolutely right... if I just could. I don't have a real place called home where I could go through a hefty withdrawal time and on too many days I can't stand these basic all-day challenges.do.. Somehow I think to feel that the opioids made things worse right from the beginning, I have had probably more than one respiratory depression, although this was "before" and as long as O-PCM put everything in silk I didn't think much about everything.. this spring I had signs of liver damage, well I didn't care enough to keep up eating and stuff like that. Then I went to therapy to discover that the insurance only pays 8 weeks unless I'd go into drug rehab which is 6 months of strict structure for what I don't feel like being able to do..

Isn't HPPD mostly about rather mild, but disturbing to the new, symptoms that last as long as one focuses to them and are meant to pass slowly when letting them go.. and mostly visual things? Does this include voices waking me up from sleep?

Going down just 1/3 on the morphine (400mg/d total) strongly intensifies the feeling of my brain 'frying' (I know it doesn't work that way, and while it's not exactly the first such moment, it for sure is the first that lasts for months, even weeks..), migraine-like headaches and sickness, on top of that these voices ... before the physical w/d even starts.

I fear of loosing control, being admitted to psych again and put under a medication I don't have the ability to deny if it makes things worse inside.. and of additional damage.

I have been away from any dissociative chem for maybe 4 months, with the hardest time being the end of the first week (insane craving) and progress being mostly limited to the first few weeks. While before it required just a few days of abstinence for most lingering after-symptoms to fade, now I don't tolerate just a regular anti-cough dose of DXM anymore.

Thankfully my cognition appears to recover to an acceptable degree. The emotions don't. It won't work that way, yet I hope there's something powerful enough to reverse the most dysfunctional stuff so that I am able to go through the whatever amount of time it needs ... hell, even if it just blocks the voices. It's quiet right now but I know it won't take much to flip back and D2 antags don't cut it, for me. Can't assure it but I'd say a pure 5ht2a inverse agonist would help more than the most selective D2 one. Or maybe I should give haloperidal a try .... had it once, in a low dose, just to immediately requiring that antidote to dyskinesia..


Lisdexamphetamine (just 30mg, prescribed to aid with fatigue, since they didn't know about voices) made myself feel on the track again at first but for one day of life there were two days of feeling deadly sick, so much that I was afraid of taking it on day 3. Nothing psychotic though despite the dopamine.

Anyway, getting back to OP's question: There is indeed a highly effective inverse agonist for 5HT2a that is even widely used in psychiatric medicine: olanzapine, better known under the trade name "Zyprexa".
Thank you, I will remember this for a future appointment.

(there is a reason they use MK-801, a powerful NMDA antagonist, to induce psychotic behavior in animal studies).
I know. Yet up to named coincidence, the NMDA antags always were the seemingly only chems that truly calmed me down whatever situation I had to face. Unless I was on a binge with sleep deprivation, or just overdosed, there were never any signs of psychosis. For years I was in (not really felt) fear of loosing my GABAergic interneurons what whyever didn't became apparent until with one boom everything changed. That's why I come up with so much theory stuff, cognitive understanding happens to my way of accepting things too..

Actually I thought of the 5-HT2a/CB1 circuit leading to a glutamate dysregulation in.. whatever part of the brain processing auditory stimuli (temporal or frontal lobe?). I had noticed before that my left-sided tinnitus almost indicates some sort of activity. It changed according to the level of dissociation and amount of active chems, becoming louder when I am stressed and the more it fades, the better I am.. Usually I need some quiet music to fall asleep, otherwise I'd listen to the tinnitus and thought stream, making it worse. Active noise-isolating headphones are a godsend here..
Note that I am susceptible to noise now, that kind of noise an amplifier produces whilst on but no music playing. Let me fall asleep with headphones on and no shut off timer set, and I'll dream weird, weird things of ghosts haunting me, and the voices even infecting dreams.. at some time I dreamed of my brain needing me to put these headphones off.. years ago I found it fun to listen to isochronic tones and such stuff from youtube to get more intense dreams, yet never anything remotely as threatening like now.

--

(little off-topic.. I know, no drug screen topics here, so feel free to ignore it. They sell full spectrum CBD drops here with 22% CBD and 0.8% THC. The shop staff tells they're safe and won't show up on usual drug screens, what I doubt. Didn't the natural hemp, before human breed it for higher levels, also contain THC in low single digit range? These 'just a few drops a day' will sum up and I don't need to find out the hard way. I'm not driving, it's therapeutical reasons for testing.)
 
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Isn't HPPD mostly about rather mild, but disturbing to the new, symptoms that last as long as one focuses to them and are meant to pass slowly when letting them go.. and mostly visual things? Does this include voices waking me up from sleep?

As far as I know, HPPD is indeed mostly associated with mild visual changes such as "visual snow", which is when you start seeing "static" similar to an old CRT TV set tuned to a dead channel, except it tends to be multi-coloured instead of white (visual snow can be annoying, as it basically tends to decrease the "signal-to-noise"-ratio of your eyes, especially in the dark). Other symptoms could be e.g. tracers or distortions in perspective, but also cognitive/emotional phenomena like sensations of deja vu and deja senti.

Hearing voices, I would say, is already entering substance-induced psychosis territory, unfortunately.

Going down just 1/3 on the morphine (400mg/d total) strongly intensifies the feeling of my brain 'frying' (I know it doesn't work that way, and while it's not exactly the first such moment, it for sure is the first that lasts for months, even weeks..), migraine-like headaches and sickness, on top of that these voices ... before the physical w/d even starts.

Stress (such as when one is going through drug withdrawal) can often exacerbate psychiatric and psychosomatic symptoms.

I have been away from any dissociative chem for maybe 4 months, with the hardest time being the end of the first week (insane craving) and progress being mostly limited to the first few weeks. While before it required just a few days of abstinence for most lingering after-symptoms to fade, now I don't tolerate just a regular anti-cough dose of DXM anymore.

Addiction is every bit of a mental thing as it is a physical thing. IMO it is fairly unlikely that a medicinal dose of DXM bumping into your NMDA receptors causes your symptoms to recur... but just the thought of it being a dissociative may trigger so many unpleasant memories and feelings of shame that you're getting serious nocebo effects.

Thankfully my cognition appears to recover to an acceptable degree. The emotions don't. It won't work that way, yet I hope there's something powerful enough to reverse the most dysfunctional stuff so that I am able to go through the whatever amount of time it needs ... hell, even if it just blocks the voices. It's quiet right now but I know it won't take much to flip back and D2 antags don't cut it, for me. Can't assure it but I'd say a pure 5ht2a inverse agonist would help more than the most selective D2 one. Or maybe I should give haloperidal a try .... had it once, in a low dose, just to immediately requiring that antidote to dyskinesia..

Good to hear you're recovering. I knew someone who was suffering from hearing voices who benefitted massively from adding a very low dose of haloperidol to her high-dose quetiapine regimen. But as you said, being a dopamine antagonist, haloperidol can often make the voices shut right up, but its efficacy comes at a price. Olanzapine, as I've mentioned, is also highly effective, although here the side-effects are usually related to weight gain (to the point where some patients develop type II diabetes).
You could also try getting back on risperidone, which offers a balance between serotonergic and dopaminergic antagonism - maybe your dose was just too low back then?

IMO it might be more helpful in your situation to see your condition as a form of residual substance-induced psychosis, where recurring symptoms are greatly exacerbated by your stress levels. Rather than trying to make a hypothesis specifically linking your condition to specific receptors, you could try to achieve a regimen where you combine medication and therapy to decrease your feelings of anxiety and guilt, aiming for consistency and stability in your life. (there is, of course, nothing wrong with looking up which meds might potentially be helpful, but often the initial phase requires a certain degree of trial and error, and trusting in your psychiatrist's years of experience).

I once met a woman who had been treated with high-dose haloperidol in her youth, and she eventually managed to minimize her dose by essentially training herself to apply Occam's Razor to the voices (i.e. telling the voices from the get-go that Jesus probably has better things to do than phone her brain while she's having a psychotic episode), and treating any re-appearance of the voices as a signal to re-adjust her life, that it was in everyone's best interest not to overstress herself on behalf of others.

That said, I am fully aware of how trite this sounds and how it is obviously more easily said than done. However, you did quit a pretty massive disso habit and came out of it with a functioning bladder, so that speaks to your resolve. :)
 
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As far as I know, HPPD is indeed mostly associated with mild visual changes such as "visual snow", which is when you start seeing "static" similar to an old CRT TV set tuned to a dead channel, except it tends to be multi-coloured instead of white (visual snow can be annoying, as it basically tends to decrease the "signal-to-noise"-ratio of your eyes, especially in the dark). Other symptoms could be e.g. tracers or distortions in perspective, but also cognitive/emotional phenomena like sensations of deja vu and deja senti.

Hearing voices, I would say, is already entering substance-induced psychosis territory, unfortunately.
That's what I thought too. I know HPPD symptoms by myself but never feared them and so they were gone before I could change my mind ... if I'd experienced HPPD my first time together with the mindset I had recently, though, it'd be the complete opposite. Maybe this says something about background mechanisms. Could too much glutamate (to take another over-simplification) be the real player?

The second topic, too. Fuck these voices. I am really curious about what they really are, where they come from and so on. If it is complete noise, a partially wrong phaenomen (as it appears sometime, like a .. badly interpreted bot, that tries to speak with oneself, maybe you get it), or whatever..
Yeah I tried to cope with them, never fully believed that they are higher spirits or something like that, maybe yes but not one to one communicating with me. It was easy to lead them to absurdity and thus realize it's just some brain circuits doing whatever they weren't constructed to do.. sometimes much more than at other times though. They're a true chameleon. And in the end I realized that they might be a mirror of myself, like hunting for my shadow.... at least they are deeply coupled to my emotions and feelings. If I'm happy and at ease, my mind is also mostly silent and if there's residual noise, then it's positive thought fragments not negative ones. But if I am stressed, down, at the limit then it becomes much much worse. But I couldn't manage to control that. Not by a tiny amount, until now.

Okay, I couldn't stop me from trying one more medication, albeit one that I knew already: Memantine. 20mg/d. I truly didn't have much hope for it, and as you pointed out about the DXM, it probably won't be placebo .... nevertheless, I get better and better with every day. It's indescribable and incredible. I am so much faster, calmer, more positive ... already than I hoped I could ever become again, just to see how far away I am from what I was. So, at the moment the memantine is a godsend to me. And I know that I'll tolerate it pretty easily.

Just ...... might it be that I made myself vulnerable by using memantine (20-30mg/d) before (3-4 years ago, for maybe 10 months straight, cause of impulsive disorder symptoms and stuff like that) and then abruptly discontinuing it, cause some genius psych doc decided so when my long time ex threw me out on the street and I was the most vulnerable in my adult life so I didn't fight for it.. developed full-on mania, got hooked on fucking cigs (from which I'm clear now again) and on valproic acid, 600-900mg for half a year - until most of my head hair fell out, and I felt true physical malaise for maybe the first time in my life so I tapered off that again. Well straight on from the discontinuation of memantine I was more time on other dissociatives than off them (DXM, MXE, K, O-PCx, ...... alcohol ........ also something I've never liked before)..

And what would the implications be? Could I be fine just taking memantine for the next years or maybe for life, or will it eventually lead to the next downfall? It appears to be everything it needs for a psychosis (NMDA antagonism, equal or stronger D2 agonism, even anticholinergic, nicotine though) but it feels like the essence of haloperidol to me just with nearly all the bad stuff cut out.. it makes me hungry (wait? it's supposed to be a dopaminergic.), a bit drowsy and sleepy while interfering with real sleep which is unnerving but yeah, laughable in comparison. Also I mean to feel how it somehow stops dopamine from overdriving just that it does halt it in the opposite direction than usual antipsychotics.. both are ataxic but here it's almost enjoyable, no akathasia and most is gone as of day.. 7 or so. Who can say that about any random antidopaminergic?

What I was interested in before too, years ago even, was riluzole. This again comes to the front of my mind now, with its unique profile of reducing glutamatergic toxicity, so many apparently unheard (why?) positive study results for exactly the thing I need- mental health problems, anxiety, overwhelming emotions, psychosis and so on .. few real side effects, appears to be even stimulative .. and (at least to me, being a chemical novice) looking like some serotonergic thing.
Just, why is it maybe the only psychoactive with such an unique study to personal / anecdotal evidence situation, with usually the first being relatively low and the latter sky-high but here it's inverse. No one appears to have used riluzole, just these guys doing the publications.

That said, I am fully aware of how trite this sounds and how it is obviously more easily said than done.
I know but apparently you know what you're talking about, I am thankful for that.

Oh, I'm more than 1/2 down on the morphine side (the required amount varies a bit from day to day so I can only tell for sure after there's a true change, and there is one). No symptoms to speak of. None. Okay, less need for sleep. Some restlessness, and tachycardia. Missing some parts of the habit. But as I finally feel like myself again since years, it's next to nothing. And a few hours of sleep feel like more rest than a whole day in bed on morphine.

Now I just need to get a prescription for this stuff. Oh well. You can get a RX for methadone, morphine and lisdexamphetamine, even pure 5mg amph tablets, with no real afford. But something that really helps, like memantine, or riluzole, no way. Lovely how things work.
Just, well.. ITS A DISSO. Hoping this one is really different enough, with not producing any psychotomimetic signs.

(shit. I realize that I have felt before like I was on some sort of antidopaminergic. Before the memantine. Regardless of the real ones I've tried (and used, in respect to the dipiperone). This was more intensive now cause I was severly slowed down (and admitted that to the morphine) but it was even present the first time I've tried memantine, back then I was opioid naive and not on antipsychotics. Like antidopaminergics just exacrebates symptoms that are already there. Weird.)

Sorry for wall of text (yay I'm back!). Hopefully somebody manages his/her way through :\
 
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As far as I know, HPPD is indeed mostly associated with mild visual changes such as "visual snow", which is when you start seeing "static" similar to an old CRT TV set tuned to a dead channel, except it tends to be multi-coloured instead of white (visual snow can be annoying, as it basically tends to decrease the "signal-to-noise"-ratio of your eyes, especially in the dark). Other symptoms could be e.g. tracers or distortions in perspective, but also cognitive/emotional phenomena like sensations of deja vu and deja senti.

Indeed, this. But I really don't mind it; I quite love it.

From my understanding this arises from COMT enzyme suppression.
 
It's known as "eigengrau" and is the result of your receptors for light being small enough that thermal noise can cause them to trigger in the absence of light.
 
https://www.hearing-voices.org

I hope these people can help. I believe it was originally a Dutch group and it is beginning to look like a lot of people hear voices. I can only say that neuroleptics are quite blunt instruments but medical specialists generally only think of medication as part of any treatment. In most cases too much DOPAC (dopamine metabolite) and/or too little NMDA are found in the cerebrospinal fluid of people experiencing these things. By no means do we fully understand the range of conditions or other causes so I suppose only you know what is best for you. As long as you get the help you want, that's the important thing - not ticking the DSM-V boxes.
 
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It's truly weird that the voices go away with blocking NMDA receptors for me (and even agonizing D2, with memantine). They'd also go away if I did K but with your usual disso there's kind of a rebound/crash which memantine seems to lack (thankfully).

Cause it all escalated after that NL trip and I've combined dissos & tryptamines before w/o problems, while having had anxiety issues from THC, I am blaming that. So a load of rimonabant?? :sus:
 
It's truly weird that the voices go away with blocking NMDA receptors for me (and even agonizing D2, with memantine). They'd also go away if I did K but with your usual disso there's kind of a rebound/crash which memantine seems to lack (thankfully).

Cause it all escalated after that NL trip and I've combined dissos & tryptamines before w/o problems, while having had anxiety issues from THC, I am blaming that. So a load of rimonabant?? :sus:

I know back in the bad old days (people in secure mental units were fair game for trials), some so-called medicinal chemists gave people with such symptoms both PCP & K. PCP reliably brought on the whole set of positive symptoms, K didn't. I'm guessing that it's a spike in dopamine (too much DOPAC) is quite reliable. I do a lot of HR work and opiates are neuroleptics so a GUESS that the opiate activity of K offsets the dopamine... but it's all guesses. I really wish I had more to give you. If common neuroleptics are of no value, clozapine is that drug-of-last-resort because of it's NMDA activity but that stuff is the worst of what I feel is an awful set of drugs. Stuff that would NEVER be licensed if it wasn't treatment for such a debilitating (for some) condition.

That you are remain aware of what is going on IS a very positive sign. I've met people whose voices are pretty much all positive, some who just take the meds when it's bad, some who just take the meds and the refractive people. If you are able to ground yourself without medicines, that IS an accepted treatment in many nations (sadly not all, not even most). A friend who is a psychologist teaches people self-analysis. He's someone who see's meds as overused, a file-and-forget answer and something he isn't happy with.

If I could suggest 1 thing to try? Don't take ANYTHING. I mean no caffeine, no nicotine (the side-effects of neuroleptics are reduced by nicotine so I am employed looking into agents with similar activity) and no sugar. Just drop everything for a good 12-13 weeks IF you can. If you have tried and it made things worse, forget I wrote, but taking out everything to do with imbibed sources is of diagnostic benefit.
 
Thanks for your input.. Unfortunately I yet have to come into the situation of being able to simply plainly being able to handle 12-13 weeks of dropping everything / taking absolutely nothing, without becoming insane (hahahaha). I don't have friends / family / work / a life to speak of which could distract me, I have to do everything by myself and that was the primary reason why I started doing drugs in the beginning. (it tended to improve, massively, then the legal repercussions began and my relationship blow and everything I had and built up fell apart so fast),

clubcard said:
PCP reliably brought on the whole set of positive symptoms, K didn't
Interesting. Any links / sources for that to dig deeper? It's not just about not bringing up the whole set of symptoms but I'd have bet that NMDA antags can have antipsychotic properties (negative & positive) before but just everywhere the opposite is written.. as in my case they absolutely had. They made my "psychotic"* anxiety, fears and depression go away in first line. But do you say the difference is mainly about dopamine? How can then memantine be antipsychotic (and it is, for me. No voices now anymore, since days - it's never been so long before and that without severe dysphoria or slowdown).

* (at least the intensity wasn't from this world)
 
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It's known as "eigengrau" and is the result of your receptors for light being small enough that thermal noise can cause them to trigger in the absence of light.

Jesus you're so intelligent. I remember taking neuropsych and I'm trying to wrap my mind around this.

Can someone elaborate?

Eigengrau (German: "intrinsic gray", lit. "own gray"; also called Eigenlicht (Dutch and German: "own light"), dark light, or brain gray, is the uniform dark gray background that many people report seeing in the absence of light. The term Eigenlicht dates back to the nineteenth century, but has rarely been used in recent scientific publications. Nowadays, the phenomenon is more commonly referred to as "visual noise" or "background adaptation" because it is accompanied by perception of an ever-changing field of tiny black and white dots.

Eigengrau is perceived as lighter than a black object in normal lighting conditions, because contrast is more important to the visual system than absolute brightness. For example, the night sky looks darker than eigengrau because of the contrast provided by the stars.

So is the implication is that everyone sees some level of visual snow in the dark?
 
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So is the implication is that everyone sees some level of visual snow in the dark?

Yes, it's pretty much the same as Brownian motion. If you put a small speck of dust on water and look at it with a microscope, it will do sudden random movements now and then when a water molecule with more than average kinetic energy hits it. The same thing happens with the light receptors on your retina - random collisions with surrounding molecules can cause false excitations of the receptors and this is seen as "static" in the visual field.
 
I do also see visual snow in cloudy sunlight etc. this increases with dissociation usually but it's always there and I've just accepted it as being some 'feature' of my body being made out of tiny cells doing all the time their best just for me and thus having some imperfections, like seeing my own receptors working and am thankful for that I am able to see & recognize this, eyesight is a very precious gift imho (I have severe myopia, -10 etc..) as is cognitive processing power..

And the 'voices', they are usually just a second stream of thought which helps me grasp things and logic faster, be kinda of 'one step ahead'.. it's a feature, not a bug :) :\ that got out of control, sadly.. now the feature is bugged, or so. I've been severly slowed down without this ability of parallel processing due to one part being psychotic..... and maybe, maybe it's slowly improving (strangely, using dissos or not using them appears to be an irrelevant factor. It's much more important for me not to use other classes of drugs, e.g. opioids(!)/mu agonists and yeah I know many dissos also have mu affinity but behave or feel very different )

Yet interesting to read about the science behind..

And nice to see German words in English =D as we have just so many anglicisms in everyday language.
 
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https://doi.org/10.1016/S0006-8993(03)02777-X
https://doi.org/10.1016/0306-4522(91)90196-U
https://doi.org/10.1016/S0893-133X(98)00060-8
DOI: 10.1007/s00406-011-0280-9
https://doi.org/10.1046/j.1471-4159.2000.0742049.x

I just want to make it clear that the above were chosen by keyword & impact factor. The last time I looked (a couple of decades ago) there was just 1 paper on the topic and a second in which it was mentioned. The takeaway for me was that PCP & K resulted in totally different outcomes for a group of in-patients. As I mentioned, dual-diagnosis (opioid dependence + mental health issue) makes up over ⅓ of the homeless in the UK. Right now the nasty, non-selective CB1/CB2 ligands being sold as 'Spice' are wreaking havoc on people.

http://michaellinnell.org.uk/michae...tal_illness/david_out_of_your_head_guide.html

The above are a few years old but are still a great blueprint for good HR information. Like Michael Linnell, I'm not interested in judging other people. I just try to do what I can to help which is more or less just information.
 
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