Ziprasidone-Related Tardive Dyskinesia
Ms. A, a 70-year-old woman with chronic hepatitis C without cirrhosis (she had had interferon therapy in 1990) and no past psychiatric history was admitted to our hospital because of a first severe major depressive episode with mood-congruent psychotic features. Her psychiatric symptoms were judged not to be the direct physiological consequence of the chronic hepatitis C. A neurological examination, analysis of CSF, and magnetic resonance imaging, including proton magnetic resonance spectroscopic studies, yielded normal results. Therapy with citalopram, 40 mg/day, and haloperidol, 6 mg/day, was begun. After 6 days, she suffered from akathisia; haloperidol was stopped and replaced by quetiapine, which was gradually increased to a maintenance dose of 400 mg/day. Concomitantly, vitamin E (α-tocopherol, 500 IU/day) was given. She received ziprasidone as an alternative to quetiapine when the latter was discontinued after 12 months of treatment because of fatigue and a mildly depressed mood. The ziprasidone dose was gradually increased to 100 mg/day, and Ms. A’s depressive symptoms remitted. Repetitive involuntary jaw and toe movements were noticeable within 9 weeks of the initiation of ziprasidone treatment.
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