Psychogenic Polydipsia and Bupropion

“Mr. A” is a 48-year-old man with past psychiatric history of major depressive disorder with psychotic features and alcohol dependence, currently in full remission, who developed irresistible urges to drink excess water, up to an average of 10 L–15 L per day, in 2004. He reported that it helped him calm down. He had episodes of confusion and bizarre behavior secondary to hyponatremia, for which he had three admissions to the medical ICU from 2004 to 2007. During his fourth admission, in 2007, he developed central pontine myelinolysis. He recovered partially, but was left dysarthric and wheelchair-bound after the last admission. During this time, he was treated with risperidone, olanzapine, ziprasidone, aripiprazole, and clonazepam, but to no significant benefit for his polydipsia. He continued to experience irresistible urges to drink water to help him calm down, and his polydipsia continued even after he suffered from central pontine myelinolysis. In 2007, he was discharged to long-term care, where he received fluid restriction, behavioral interventions, and pharmacotherapy, primarily with ziprasidone, bupropion, and clonazepam. His polydipsia continued, although it was less severe, and he was drinking up to 6–8 L of water per day. He was in long-term care for 2 years and was discharged home in Aug 2009 on ziprasidone, bupropion, and clonazepam. At home, he continued to struggle with polydipsia. His brother noticed that he was very drowsy, so he discontinued ziprasidone and clonazepam without consulting a doctor, and he continued to give him bupropion XL 300 mg po qd. About a month after being at home and being only on bupropion XL, the patient’s polydipsia completely subsided, with minimal urges to drink excessive water. In addition to bupropion, his brother also kept him on fluid restriction, to 1.2 L per day. The patient has been followed at our outpatient psychiatric clinic with no relapses of depression, psychosis, or polydipsia for the past 2 years.

Literature study reveals the etiology of psychogenic polydipsia to be the hypersensitive dopamine receptors⁵ or malfunction of hypothalamic thirst center. Case reports reveal that polydipsia usually develops in chronic schizophrenic after patients have been on an antipsychotic for a long time. The antipsychotics, with their antagonist action on dopamine receptors, increase their sensitivity. We hypothesize that bupropion, being an inhibitor of neuronal uptake of dopamine and norepinephrine, increases the dopamine available at the dopamine receptors. This causes decrease in the sensitivity of dopamine receptors responsible for mediating thirst, thus playing a therapeutic role in psychogenic polydipsia in the long term. In our patient, concomitant use of bupropion with different antipsychotics neutralized this effect of bupropion, as a result of which our patient continued to have polydipsia in spite of earlier treatment with bupropion. Polydipsia improved on the solitary treatment with bupropion. However, more studies are needed to support this action of bupropion, and, given that psychogenic polydipsia is a very difficult entity to treat, the treating psychiatrist should be aware of the few available agents, including bupropion, which have shown to be helpful.