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As soon as he abruptly stopped 20 mg/day of metoclopramide after taking it for three months, a 65-year-old man experienced hallucinations and delusions (Lu et al., 2002). This happened likewise to a 74-year-old man after a six-month course of the same. Previously these men had never been psychotic. They cleared with a brief low-dose course of an antipsychotic medication (Lu et al., 2002). This is tardive psychosis.
Elderly patients are markedly more sensitive to developing tardive dyskinesia (TD) from dopamine-blocking drugs such as metoclopramide. Apparently, they similarly readily develop tardive psychosis, in view of , the low doses and short courses of metoclopramide in these two cases. Such high sensitivity can provide a particularly short and clear path between cause and effect, specifically that dopamine blockers can cause tardive psychosis. There are other reports of new-onset psychotic symptoms attributable to antipsychotic drugs, but none as simple.
In young adults followed prospectively, new onset of mood-incongruent psychotic phenomena developed after three or more years of taking dopamineblocking antipsychotic drugs for resistant nonpsychotic mania (Downs et al., 1993). Although this was longer than the three to six months for the patients on metoclopramide, the psychosis was breakthrough, not withdrawal. That is, tardive psychosis appeared while the patients were actively taking an antipsychotic drug and despite its effects, so the psychotic effect was much stronger. Its occurrence in this manner implies the troubling possibility that a course of worsening psychotic symptoms can be tardive psychosis, regardless of the primary diagnosis. Breakthrough tardive psychosis is analogous to TD starting while taking a dopamine blocker (e.g., Bressan et al., 2004).
Similarly, three separate reports describe new onset of psychotic symptoms in patients who received years of high-dose antipsychotics for Tourette's syndrome (Caine et al., 1978; Lawlor et al., 1987; Suva et al., 1993). In these cases psychosis did not appear until the antipsychotic drug was decreased or stopped. Suva et al. (l 993) reported that a patient with Tourette's syndrome took dopamine blockers for 17 years, including haloperidol (Haldol) 45 mg/day, switched to increasing pimozide (Orap) doses, eventually to 14 mg/day (steadystate haloperidol equivalent of 140 mg/day) (Swartz, 1997). With a halflife of 4.6 days, pimozide levels gradually taper when doses stop. That agitated psychosis appeared just three days...