Bromocriptine, an ergot derivative with dopamine agonist actions, lowers prolactin levels in the blood (Mehta and Tolis 1979). It is FDA-approved in the United States for the short-term treatment of amenorrhea-galactorrhea that is associated with hyperprolactinemia and is without demonstrable evidence of pituitary tumors. Until recently, the first line of treatment in prolactin-secreting adenomas was surgery or radiotherapy. However, there is now evidence that bromocriptine causes tumor regression and resolution of visual field defects (Bergh et al. 1978; Thorner and Besser 1978). Its ongoing administration has been associated with inducing psychosis, both in patients with no such prior history (Serby et al. 1978) and in those with past history of psychosis in symptomatic remission (Tamminga and Schaffer 1979; Frye et al. 1982). We describe another bromocriptinerelated psychosis in a patient with prolactin adenoma and the use of valproate in combination with low-dose haloperidol in the treatment of the psychosis. The patient, currently a 31-year-old woman, first came to psychiatric attention 5 years ago. In 1978, she developed amenorrhea, galactorrhea, hyperprolactinemia, and hirsutism and was successfully treated by her gynecologist with bromocriptine, 2.5 mg qd for 10 months. At the time, there was no CT evidence of a pituitary adenoma. She tolerated the drug well, with return of menses and cessation of galactorrhea and further abnormal hair growth. The patient had no psychiatric history. She was a well-adapted young woman, employed successfully by a television company, and was social and personable. Family history for affective disorder or psychosis was negative. Unintentionally, the bromocriptine was abruptly discontinued. Within 5 days, she became acutely psychotic and was placed in custody by the police, because she was lying naked on a local beach stating she was waiting for Jesus to impregnate her. On admission to the acute inpatient psychiatric unit, a mental status examination revealed acute agitation, confusion, visual and auditory hallucinations, and preoccupation with religious and bizarre delusions. A diagnosis of atypical psychosis was made by DSM-III criteria. At the time, her prolactin level was 32.5 ng/ml. There was no evidence of other endocrine dysfunction, and CT scans and EEG prior to treatment were negative. She continued to remain psychotic despite several pharmacological and somatic treatments, including lithium, readministrations of bromocriptine, and ECT. Only partial clinical response was achieved with doses of haloperidol up to 60 mg qd. In March 1980, during an acute exacerbation of symptoms, precipitated by lowering the dosage of haloperidol in order to perform sensitive neu