Late-life parkinsonism in bipolar disorder.

Abstract

Aim: Parkinsonism is a frequently encountered symptom in individuals with bipolar disorder (BD). It can be drug-induced, co-occurring with Parkinson's disease (PD), or a genuine motor abnormality of BD itself. This study aims to address the primary pathophysiology of parkinsonism in BD.

Methods: Sixteen patients with BD and parkinsonism were recruited from consecutive patients who were referred to a neurology clinic at a tertiary psychiatric centre. The patients underwent clinical assessments, dopamine transporter single-photon computed tomography (DAT-SPECT), cardiac 123I-metaiodo-benzylguanidine (MIBG) scintigraphy, and morphometric magnetic resonance imaging (MRI). The positivity or negativity of Lewy body disease (LBD) biomarkers was determined based on the visual assessment of DAT-SPECT and heart-to-mediastinum ratio on cardiac MIBG scintigraphy. Four out of the 16 participants received 300-600 mg of levodopa.

Results: Thirteen patients were diagnosed with BD type 1, and 12 had experienced >5 previous mood episodes. Parkinsonism developed more than 10 years after the onset of BD and after the age of 50 years in all patients. Four cases were positive for LBD biomarkers. Six patients with negative LBD biomarkers showed reduced striatal uptake with z-scores below -2.0. MRI morphometry revealed varying degrees of brain atrophy in most patients. Three of the four patients did not respond to 600 mg of levodopa.

Conclusions: The results of this study indicate that the majority of parkinsonism observed in BD is not a consequence of PD/LBD. Instead, it may represent a genuine motor abnormality of BD in late life.