Tardive psychosis

Tardive psychosis is a term for a hypothetical form of psychosis, proposed in 1978.[1] 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.

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."[2][3]

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. A hypothetical condition related to tardive psychosis, tardive dysmentia, has also been questioned.[4]

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.

In addition to dopaminergic upregulation in the nigrostriatal tracts, many investigators have suggested that dopaminergic upregulation may occur in mesolimbic or mesocortical tracts, leading to a worsening of psychosis beyond the original level. This phenomenon has been called 'tardive psychosis' or 'supersensitivity psychosis'.[5]

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.

See also

References
  1. McCarthy, John J. (1978). "Tardive Psychosis". American Journal of Psychiatry. 135 (5): 625–626. doi:10.1176/ajp.135.5.625-b. ISSN 0002-953X.
  2. Palmstierna, T; Wistedt, B (1988). "Tardive psychosis: Does it exist?". Psychopharmacology. 94 (1): 144–5. doi:10.1007/BF00735897. PMID 2894699.
  3. "Tardive psychosis: does it exist?" (pdf download link)
  4. Wilson, I. C; Garbutt, J. C; Lanier, C. F; Moylan, J; Nelson, W; Prange, A. J (1983). "Is There a Tardive Dysmentia?". Schizophrenia Bulletin. 9 (2): 187–92. doi:10.1093/schbul/9.2.187. PMID 6135252.
  5. Ross, David E (2004). "Clozapine and Typical Antipsychotics". American Journal of Psychiatry. 161 (10): 1925–6. doi:10.1176/ajp.161.10.1925-a. PMID 15465996.
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