Tardive psychosis

Tardive psychosis is a form of psychosis 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'.

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. Although tardive psychosis and the little understood hypothetical condition tardive dysmentia have been used by the anti-psychiatry movement as reasons why antipsychotics are too dangerous for use in clinical practice, others see the side effects as reasons for continued research and the realization of new antipsychotics that do not create them. There are also experimental treatments for tardive dyskinesia such as ondansetron, which is also being researched to treat psychosis from Parkinsons' disease, and the natural remedy rhodiola which is also being researched for Parkinson's disease and tardive dyskinesia.