I would argue that stimulant psychosis is indicative of toxicity--it's something about adrenergic or TAARs becoming hyper-sensitive.
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N&PD Moderators: Skorpio
Perplexed by the relationship of Stimulant Psychosis to Neurotoxicity.
- Thread starter BathedinMercury
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dopamimetic
Bluelighter
Do you have a source for the adrenergic hyper-sensitivity thing?
I actually get psychosis from neuroleptics. Repeatedly. Immediatly after a decent dose of a stronger one takes full effect- and to the extent where I don´t remember anything of these hours. In contrast, I seem to tolerate huge amounts of dopamine (just get hyper-focused and a bit compulsive if it´s too much, e.g. from repeated cocaine or HDMP-28 use).
But I´d totally agree that many of the negative effects from stimulants actually originate in adrenergic circuits. While it seems to flatten stimulants somewhat, I found clonidine to be a very good additive that makes me to tolerate multi-day binges with feeling almost normal. I don´t do this anymore but it was remarkable.serotonin2A
Bluelighter
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I'm curious regarding the specific symptoms of psychosis that you experience after taking neuroleptics? Have you tried atypical antipsychotics?
The hypothesis about adrenergic involvement in stimulant psychosis is easy enough to test -- it should be possible to block it with adrenergic antagonists. As far as I am aware, that has been attempted but it doesn't work.
One hypothesis of why people use cocaine compulsively is that the adrenergic effects outlast the dopaminergic effects. This makes people feel anxious as they start to come down and encourages continued use to relieve the negative symptoms associated with adrenergic hyperactivity. Clonidine would probably be an excellent way to counteract those effect sof cocaine.Last edited:
dopamimetic
Bluelighter
Oh how I love technical devices...now it threw my draft away cause I forgot to check that 'remind me' box at login... will replace later.
This is exactly what I meant. And indeed it works! Forgot to mention that because it feels so clear to me, but probably it´d be different if I knew nothing about pharmacology and/or had tried cocaine earlier...
Indeed I get (nor)adrenergic tension, slight anxiety and restlessness from many NDRIs- ethylphenidate (very pronounced), alpha-pvp, also methylphenidate and clonidine suppresses a good part of these after effects. I´ve always been on memantine when I did cocaine and accordingly experienced smooth come down- don´t know exactly why, but for me that anti-tolerance thing really works.. probably also against the tachyphylaxis, prolonging effects of dopaminergics and therefore also opioids to some extent..
Taking cocaine on memantine and maybe some clonidine (usually 75mcg are enough, it takes 30min or more to take effect even if administered sublingually) feels almost nonaddictive in the way that it is nice, but easy and painless to stop- being concentrated or distracted I just forgot about it..Last edited:https://en.wikipedia.org/wiki/Kynurenic_acid#Role_in_disease
This is a substance that I find is often overlooked when discussing the dopamine/nmda debate, and may offer further insight into how these systems are interrelated.
Cotcha Yankinov
Bluelight Crew
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That's very interesting it gets worse with neuroleptics Dopamimetic, I do wonder what overlap some of these symptoms might have with HPPD. Risperdal is known to make HPPD worse, while drugs that inhibit COMT helped about 1/3 of HPPD sufferers, although you would think drugs that increased dopamine and such would make something similar to the psychosis spectrum worse. HPPD was theorized to be from a dysregulation of COMT though, an un-inhibition, while some Parkinson's drugs inhibit COMT.
Something just to point out in theory here is that it might not be the individual neuron that counts as much as how one brain structure is communicating with the others, the amygdala and so forth I thought was typically different functionally in schizophrenics (aside from total brain volume being typically smaller), although I might be thinking of bipolar type 2 regarding the amygdala...
The point is it might not be a matter of (for example) you have "1000 units" of dopamine in someone's system and they are normal but when you hit 10,000 some individuals are temporarily schizophrenic/psychotic but it's not solely the number of cell firings that matter but that when you hit 10,000 the brain cells for some people are firing in a schizophrenic/psychotic PATTERN. There might be people who can go up to 10,000 and be fine and then there might be people who are firing in a "psychotic pattern" at only 1000 units.
And then there might be people who actually need more dopamine for their cognitive faculties which sounds like some HPPD people possibly. But in theory this could do with an uneven spread of cells throughout the brain, not enough prefrontal cortex dopamine/glutamate to think a delusional thought through the higher faculties etc. a channel of cell firings that is not run through the best structures of the brain for filtering out noise essentially.
Anyways I do believe brain waves are important, thalamocortical resonance for one, after all the thalamus is the sensory gate. Unfortunately EEG readings from the deeper brain are hard to read through the skull/scalp