Thursday, April 16, 2020

Now treatment-resistant schizophrenia is said to have a different neurobiology from treatment-responsive schizophrenia

Potkin et al (2020) argue that the underlying neurobiology of treatment-resistant schizophrenia (for which they give the acronym TRS) may differ from treatment-responsive schizophrenia. As the article indicates, clozapine's licensed indication is for schizophrenia in patients unresponsive to, or intolerant of, conventional antipsychotic drugs. The review is intended to facilitate the development of new pharmacological treatments.

Dopamine, glutamate and serotonin neurotransmitters are said to be potentially involved (as they have been implicated for schizophrenia in general). Dopamine supersensitivity has been suggested as the mechanism for tardive dyskinesia, and by extension it has been suggested that neuroleptics may cause a dopamine supersensitivity psychosis (DSP). I don't think the article makes as clear as it should do, that by suggesting that DSP may be the cause of TRS, it seems to be implying that antipsychotic medication causes treatment resistance.

Surely it's about time journals, including so-called Nature Partner Journals, stopped publishing such speculation as though it were science. It would also help if science itself gave up its wishful hope to explain mental illness in physico-chemical terms (see eg. previous post).

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