Abstract

Mrs B is a 65-year-old, married, white woman with long-standing history of bipolar disorder type I who achieved mood stability with chronic lithium treatment. She developed end-stage renal disease, which was suspected to be the result of chronic lithium exposure in the context of medical comorbidity, and subsequently required renal transplantation. Following transplantation and discontinuation of lithium, Mrs B was unable to achieve mood stability with multiple medication trials and required more than 40 medical and psychiatric hospitalizations with eventual transition to skilled nursing care. After much discussion among the psychiatric treatment team, the patient, and her husband, primary care provider, nephrologist, and renal transplant surgeon, the decision was made to restart the patient on lithium given her previous treatment success. The purpose of this case report is to discuss the use of lithium following renal transplantation. In this case, a multidisciplinary approach was used to assist the patient in carefully weighing the risks and benefits of her treatment decisions. The consensus of the patient, her husband, and her providers was that the benefit of mood stabilization outweighed the potential risks of renal toxicity. Although treatment with lithium after renal transplant is not a first-line treatment option, this case illustrates that lithium could be considered in certain cases.

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Drug-induced parkinsonism is defined as the appearance of parkinsonism on treatment with pharmaceutical agents. Symptoms typically manifest within a few days, and 90% of cases emerge within 3 months. The patient was a 68-year-old white man with a past psychiatric history significant for bipolar I versus cyclothymic disorder. The patient presented with pressured speech, flight of ideas, distractibility, delusions, and disorganized thinking. He was started on risperidone and, due to a subclinical response, was cross-tapered from risperidone to olanzapine, and divalproex was started. The patient was then given paliperidone 234 mg long-acting injection (LAI) and a second loading dose of 156 mg 1 week later. The patient's cognitive and functional status subsequently declined, all neuroleptics were discontinued, and he was diagnosed with drug-induced parkinsonism. After a complicated hospital course the patient died approximately 5 months after the administration of paliperidone LAI. Although there are several confounding factors, due to the temporal relationship of events it is likely that paliperidone LAI was a contributing factor for the development of severe parkinsonism. Practitioners should be cognizant of the potential long-term consequences of paliperidone LAI.

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