OP, you
may have had a brief psychotic episode related to DXM, which is not all that unusual especially in persons with your history, "psychosis" may actually be too strong a term for what you exprienced although perhaps you are the better judge having been psychotic before—the essential difference seems that your recent experience was brief, you had a degree of insight, organization and orientation to reality despite intrusive and delusional thoughts. Technicalities don't really matter, what you experienced was obviously distressing and I don't think that I need to tell you that it could have been much worse or might be next time, while they have different activities DXM and MA both can cause flat out psychosis. Are you formally diagnosed (in order to be taking the risperidone?) Combination of antidopaminergics with DXM might actually have some
unpleasant or even problematic effects that are not very well known or appreciated in the general net.drugs scene.
You seem to have taken away the right thing from your experience though: you have a brain with certain predispositions and certain experiences (and, remember, each time you have a psychotic episode, particularly when relating to either using drugs or discontinuing medications, your brain does change structurally in such a way that further episodes will be worse, sort of like the phenomenon of "kindling" in seizures.) Be careful out there. NMDA and dopamine are clearly not good targets in your brain for you to be hitting, especially as you are taking medications with the literal opposite effects for therapeutic reasons. I'd advise avoiding drug use altogether, but
particularly to avoid stimulants and dissociatives. Classical psychedelics are not a good idea either but the milder ones might be
slightly less risky but still not a good idea. I'd also recommend against marijuana use as it has an association with psychosis that is much downplayed by it's advocates.
It doesn't help that the mechanism through which dxm works is the exact mechanism in the brain responsible for scizophrenic symptoms. ^That is why they are used to model psychosis: because NMDA hypofunction is the cause of schizophrenia, and NMDA antagonists mimic all the symptoms by synthetically inducing NMDAR hypofunction.
It actually gets even better than that, PCP, notorious for being one of the most psychotomimetic "street drugs," as well as some of the novel dissociatives, are not only NMDA antagonists but dopamine reuptake inhibitors, thus combining the
two best models we have of psychosis—OP has now experienced both, having previously had an MA related psychosis. Must keep in mind though these models are
not perfect, saying "NMDA hypofuntion is the
cause of scz" is a bold and unsupported statement. But anyway look at the molecular structures of PCP and MPA and you'll see what I'm talking about, overlaps of the sort of "archetypes" of the dissociatives and the DRIs. But I digress. DXM is not a DRI except very mildly at low doses, it actually as a tertiary effect thru NMDA and 5HT is a mild dopamine
blocker in high doses, but this clearly doesn't mitigate any risk of psychosis. Welcome to Bluelight, BTW, depending on your level of interest and education about this stuff your may want to check out our
Advanced Drug Discussion forum.
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