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Senior Resident, Ranchi Institute of NeuroPsychiatry and Allied Sciences, Ranchi, India, fax 916512450813, rudrapc{at}yahoo.com
Junior Resident, Central Institute of Psychiatry, Ranchi
Published Online, October 9, 2007. www.theannals.com, DOI 10.1345/aph.1K250
Case Report. A 37-year-old Indian man with chronic paranoid schizophrenia was admitted to a closely supervised inpatient unit, owing to severe psychotic symptoms. One year prior to admission, he had received therapy with depot fluphenazine. During the months leading up to admission, he had been treated with a combination of risperidone 8 mg/day, trifluoperazine 5 mg/day, amisulpride 200 mg/day, and trihexyphenidyl 6 mg/day orally. This antipsychotic polypharmacy regimen provided limited therapeutic benefit and induced prominent and persistent nondystonic extrapyramidal symptoms (EPS).
The 3 antipsychotics were discontinued simultaneously and abruptly upon the patient's admission, but trihexyphenidyl was continued at a reduced dose of 4 mg/day. Without any washout period, clozapine was initiated at 25 mg/day and was gradually titrated upward. Within a few days, EPS resolved completely. Suddenly, 9 days later, the patient experienced a witnessed episode of oculogyric crisis (clozapine dosage 150 mg/day), which was successfully treated with 50 mg of intramuscular promethazine.
Because the patient suffered from constipation, the decision was made to gradually discontinue trihexyphenidyl over a 2 week period. Within 48 hours of such discontinuation, he experienced a second episode of oculogyric crisis (on day 25 of clozapine monotherapy; clozapine dose 150 mg/day), which again responded to promethazine. In neither of these 2 oculogyric crises did immediate and follow-up clinical examinations reveal changes in the patient's mental or neurologic status. By the time the second event occurred, his psychopathology was showing moderate improvement.
Discussion. It seems unlikely that these reactions were related to the residual effects of the patient's previous antipsychotic drugs. The oral medications had been discontinued 9 days prior to the first incident and 25 days prior to the second. Moreover, he had not received depot fluphenazine for more than a year. It is also unlikely that he was taking any other medications or substances during the hospitalization, given that he was under close supervision. Thus, clozapine appears to be the cause of the oculogyric crises. This viewpoint is consistent with the Naranjo probability scale, which indicates a probable relationship between the oculogyric crises and clozapine pharmacotherapy.5
Interestingly, anticholinergic agents have been used to treat rare cases of clozapine-induced dystonic reactions,3 but our patient experienced oculogyric crisis while receiving an anticholinergic agent. Another episode of oculogyric crisis occurred after discontinuation of the anticholinergic agent, which is consistent with a previously reported case of clozapine-induced oculogyric crisis.3 We wonder whether the abrupt discontinuation of multiple neuroleptics may have had a role in the development of oculogyric crises. However, since clozapine-induced dystonias/oculogyric crises are so rarely reported, it is impossible to discern patterns and draw conclusions.
References
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