Tardive psychosis
Tardive psychosis is a term for a hypothetical form of psychosis, proposed in 1978.[by whom?] It was defined as a condition caused by long term use of neuroleptics, noticeable when the medication had become decreasingly effective, requiring higher doses, or when not responding to higher doses.[citation needed]
Evaluation suggests that tardive psychosis as a whole is a combination of "several different and not necessarily correlated phenomena related to neuroleptic treatment of schizophrenia."[1][2]
Some articles equate tardive psychosis to supersensitivity psychosis. However, descriptions of symptoms of the latter do not match the former. Specific supersensitivity psychosis articles only address psychotic episodes in the wake of psychotic medication withdrawal associated with Clozapine. They do not mention medication resistance, which is the cornerstone of tardive psychosis theory.[citation needed] A hypothetical condition related to tardive psychosis, tardive dysmentia, has also been questioned.[3]
Description
The theoretical tardive psychosis is distinct from schizophrenia and induced by the use of current (dopaminergic) antipsychotics by the depletion of dopamine and related to the known side effect caused by their long-term use, tardive dyskinesia.[citation needed]
Tardive psychosis was researched in 1978 and 1989, and sporadic research continues. Some studies have found it to be associated with psychotic depression and potentially, dissociation. For people with any tardive conditions clozapine remains an option but since it can create blood dyscrasias, which require frequent blood work, as well as other severe side effects, it is used increasingly less in clinical practice. Although tardive psychosis continues to be studied, it still has not been established as a fact but it is known that the study classes of antipsychotics such as the NMDA receptor modulators (glutamate antagonists) in not creating tardive dyskinesia will not create this condition.
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