Abstract

The current study aimed to confirm whether probable rapid eye movement sleep behavior disorder (pRBD) is associated with a specific pattern of striatal dopamine depletion in an international, multicenter, prospective cohort of patients with Parkinson’s disease (PD). Two hundred and seventy de novo, drug-naïve patients with PD underwent dopamine transporter (DAT) single photon emission computed tomography with 123I-FP-CIT at baseline and 1, 2, and 4 years after the initial scan. The diagnosis of pRBD was based on the 10-item RBD Screening Questionnaire. Striatal DAT binding levels and their rates of decline were compared between patients with pRBD and those without. At baseline, patients in the PD-pRBD+ group showed lower striatal DAT binding in the caudate (which was more pronounced in the less-affected hemisphere) and in the putamen. During the 4-year follow-up, patients in the PD-pRBD+ group consistently exhibited greater DAT loss than patients in the PD-pRBD− group with comparable disease duration in all four striatal subregions. These patients also exhibited a more rapid decrease in DAT binding in the caudate and a less prominent interhemispheric asymmetry in the putamen. The distinct pattern of striatal DAT depletion may contribute to a more malignant phenotype of PD associated with RBD, specifically faster progression of motor symptoms.

Highlights

  • Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia characterized by elaborate motor manifestations related to unpleasant dreams and loss of muscle atonia during REM sleep (Hogl et al, 2018)

  • Patients with RBD Screening Questionnaire (RBDSQ) scores of five or less at all four visits were classified as the Parkinson’s disease (PD)-probable RBD (pRBD)− group (n = 135)

  • The remaining 98 patients with RBDSQ scores of six or higher on more than one visit were classified as the PDpRBD+ group

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Summary

Introduction

Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia characterized by elaborate motor manifestations related to unpleasant dreams and loss of muscle atonia during REM sleep (Hogl et al, 2018). While longitudinal data suggest that RBD is associated with faster progression of motor and non-motor symptoms (Chahine et al, 2016; Pagano et al, 2018), the underlying pathophysiology remains unclear. There are other studies reporting no differences in dopamine transporter (DAT) levels between patients with and without RBD in PD (Kotagal et al, 2012; Salsone et al, 2014; Zoetmulder et al, 2016). We aimed to investigate whether the presence of RBD is associated with a more severe dopaminergic deficit and a faster decline in dopaminergic binding as PD progresses. We compared baseline and serial DAT levels in patients with and without probable RBD (pRBD) in an international, multicenter, prospective cohort study of de novo, drug-naïve PD patients

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