Cotard's Syndrome in a Young Male Bipolar Patient
Case Report
A 20-year-old male was diagnosed as having a bipolar disorder because of three manic episodes suffered during the year prior to admission. No previous depressive episodes were detected. He had a family history of bipolar disorder in a second-degree relative. While he was on treatment with lithium carbonate 800 mg/day, the patient suffered a short period of overactivity. Progressively over a 2-week period he became more isolated; he had a depressed mood, lost his appetite, and started to lie in bed most of the time, presenting a severe psychomotor retardation. Two days before his admission he showed nihilistic delusions concerning his body (“my liver and stomach are being destroyed,” “my heart doesn't beat,” “I don't have muscles”) and concerning existence (“I am dead”). The family brought the patient to our emergency room.On admission to our inpatient psychiatric unit his most prominent psychopathology was a flat affect, psychomotor retardation, ideas of negation, and delusions of being dead. Physical examination was normal. Laboratory assessment (complete blood count, electrolyte and creatinine levels, and thyroid hormones) was within normal values. At this time lithium levels were 0.56 mEq/l. The dexamethasone suppression test was negative. Brain CT did not demonstrate any pathology. A diagnosis was made of bipolar disorder, severe depressive episode with psychotic symptoms (DSM-IV).Imipramine was added at a daily dosage of 225 mg. Three days after initiating treatment with imipramine, the patient became mute, refused to eat and drink, and presented a marked psychomotor inhibition and muscular rigidity (a catatonic state). Electroconvulsive therapy (ECT) with bilateral electrode placement and brief pulse stimulus was initiated on a 3 days/week basis. Lithium treatment was discontinued because of the potential risk for developing a confusional state in association with ECT. After the sixth ECT session the patient's condition improved promptly. A hypomanic episode appeared progressively after the eighth ECT session. Because of the presence of this hypomania, the patient's family decided that ECT sessions should be interrupted at the 10th session, with a total convulsive time of 574 seconds. Imipramine dose was decreased to 150 mg/day.Two days after discontinuing ECT, the patient progressively developed slowness in movements and speech, and 2 days later, he relapsed with hypochondriacal delusions (that his muscles were degenerating, that his tonsils were deteriorating, that his heart had become smaller). He also showed a feeling of derealization and depersonalization.At this point, we decided to add haloperidol 8 mg/day to the treatment. Because of an oculogyric crisis, biperiden 4 mg/day was also added. After 3 days the symptoms began to improve. The patient was discharged 14 days later, in a state of almost full remission.
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