Pramipexole-induced psychosis in Parkinson's disease
PRAMIPEXOLE, LIKE OTHER dopamine agonists for treating Parkinson's disease (PD), has a tendency to induce psychotic symptoms due to central dopaminergic stimulation.1 A meta-analysis demonstrated that, relative to placebo, pramipexole increased the risk of hallucinations (odds ratio 5.2).2 There is no report detailing the psychosis formation in terms of the dosage of pramipexole that causes it. Here we present a case of PD in which the psychotic symptoms were exacerbated after increasing pramipexole dosage.
The patient was an 89-year-old man with a 6-year history of PD. Two years previously he began to receive amantadine and selegiline. Three months later, pramipexole (0.25 mg/day) was added to his treatment regimen to combat his persistent tremor and bradykinesia, and the dosage was increased to 0.5 mg/day in 2 weeks. One month after the dosage was titrated to 0.5 mg/day, visual hallucinations (VH) developed. He could see faces of people and ghosts in different sizes and colors. The occurrence of VH was mostly limited to night time, when he was fully conscious and aware, but he did not inform others about these symptoms. In terms of his prominent motor symptoms, pramipexole was titrated up to 2.25 mg/day 5 months before this admission. After 2 months on this regimen he experienced an increased frequency of complex VH, and also had olfactory hallucinations, delusions of being poisoned, delusions of persecution, and destructive behaviors. All these psychotic symptoms persisted under normal consciousness. Amantadine and selegiline were discontinued. Pramipexole was decreased to 1.5 mg/day and quetiapine 25 mg/day was prescribed. However, all the psychotic symptoms remained the same for 1 week under the regimen. He was then admitted to the geropsychiatric ward. After admission pramipexole was discontinued and, due to his vivid psychotic symptoms and agitation, quetiapine was increased gradually to 300 mg/day in 10 days. Three weeks after admission his psychotic symptoms gradually resolved. After discharge, quetiapine dosage was reduced gradually without psychotic exacerbation. In addition, no antiparkinsonian drug was used for his tremor and bradykinesia, which were reported as tolerable.
To our knowledge this is the first case report of pramipexole-induced olfactory hallucinations and delusions of persecution in addition to auditory and visual hallucinations. The patient's psychosis developed after addition of pramipexole and were exacerbated after increasing the dosage. His psychosis recovered gradually after discontinuing pramipexole and applying quetiapine. Animal study has demonstrated that pramipexole dose-dependently evoked hyperactivity that was inhibited by antipsychotics, such as haloperidol.3 This report highlights the importance of monitoring and screening the psychotic symptoms in patients treated with pramipexole, especially for elderly patients.
