Altered Brain Functional Network in Parkinson Disease With Rapid Eye Movement Sleep Behavior Disorder.

Parkinson disease (PD) with rapid eye movement (REM) sleep behavior disorder (PD-RBD) tend to be a distinct phenotype with more severe clinical characteristics and pathological lesion when compared with PD without RBD (PD-nRBD). However, the pathological mechanism underlying PD-RBD remains unclear. We aim to use the resting-state functional magnetic resonance imaging (rs-fMRI) to explore the mechanism of PD-RBD from the perspective of internal connectivity networks. A total of 92 PD patients and 20 age and sex matched normal controls (NC) were included. All participants underwent rs-fMRI scan and clinical assessment. According to the RBD screening questionnaire (RBDSQ), PD patients were divided into two groups: PD with probable RBD (PD-pRBD) and PD without probable RBD (PD-npRBD). The whole brain was divided into 90 regions using automated anatomic labeling atlas. Functional network of each subject was constructed according to the correlation of rs-fMRI blood oxygenation level dependent signals in any two brain regions and network metrics were analyzed using graph theory approaches. Network properties among three groups were compared and correlation analysis was made using distinguishing network metrics and RBDSQ scores. We found both PD-pRBD and PD-npRBD patients existed small-world characteristics. PD-pRBD showed a wider range of nodal property changes in neocortex and limbic system than PD-npRBD patients when compared with NC. Besides, PD-pRBD showed significant enhanced nodal efficiency in the bilateral thalamus and betweenness centrality in the left insula, but, reduced betweenness centrality in the right dorsolateral superior frontal gyrus when compared with PD-npRBD. Moreover, nodal efficiency in the bilateral thalamus were positively correlated with RBDSQ scores. Both NC and PD patients displayed small-world properties and indiscriminate global measure but PD-pRBD showed more extensive changes of nodal properties than PD-npRBD. The increased centrality role in the bilateral thalamus and the left insula, and disruption in the right dorsolateral superior frontal gyrus may play as a key role in underlying pathogenesis of PD-RBD.