Abstract
Objective Rapid eye movement (REM) sleep behavior disorder (RBD) is a common symptom in Parkinson's disease (PD), and patients with PD-RBD tend to have an increased risk of cognitive decline and have the tendency to be akinetic/rigidity predominant. At the same time, the mechanisms of RBD in patients with PD remain unclear. Therefore, this study aimed to detect the structural and functional differences in patients with PD-RBD and PD without RBD (PD-nRBD). Methods Twenty-four polysomnography-confirmed patients with PD-RBD, 26 patients with PD-nRBD, and 26 healthy controls were enrolled. Structural and functional patterns were analyzed based on voxel-based morphometry and seed-based functional connectivity (FC). Correlations between altered gray matter volume (GMV)/FC values and cognitive scores and motor impairment scores in PD subgroups were assessed. Results Compared with patients with PD-nRBD, patients with PD-RBD showed relatively high GMV in the cerebellar vermis IV/V and low GMV in the right superior occipital gyrus (SOG). For the FC, patients with PD-RBD displayed lower FC between the right SOG and the posterior regions (left fusiform gyrus, left calcarine sulcus, and left superior parietal gyrus) compared with the patients with PD-nRBD. The GMV values in the right SOG were negatively correlated with the Unified PD Rating Scale-III scores in patients with PD-RBD but positively correlated with delayed memory scores. The GMV values in the cerebellar vermis IV/V were positively correlated with the tonic chin EMG density scores. There were positive correlations between the FC values in the right SOG-left superior parietal gyrus and MoCA and visuospatial skills/executive function scores and in the right SOG-left calcarine sulcus and delayed memory scores. Conclusion Higher GMV in the cerebellum may be linked with the abnormal motor behaviors during REM sleep in patients with PD-RBD, and lower GMV and FC in the posterior regions may indicate that PD-RBD correspond to more serious neurodegeneration, especially the visuospatial–executive function impairment and delayed memory impairment. These findings provided new insights to learn more about the complicated characteristics in patients with PD-RBD.
Highlights
Rapid eye movement sleep behavior disorder (RBD), which is characterized by nightmares, abnormal motor manifestations, and impaired muscle atonia during REM sleep [1], is closely associated with Parkinson’s disease (PD)
We further explored the changes in functional connectivity (FC) among the PD-RBD, PD-nRBD, and healthy controls (HCs) groups based on the significant differences observed between the PD-RBD and PD-nRBD groups in the cerebellar vermis IV/V and right superior occipital gyrus (SOG)
In the PD-RBD group, the gray matter volume (GMV) values in the right SOG were negatively correlated with the UPDRS-III scores (r −0.44, P 0.03), but positively correlated with the language scores (r 0.45, P 0.03) and delayed memory scores (r 0.50, P 0.01); the GMV values in the cerebellar vermis IV/V were positively correlated with the tonic chin EMG density scores (r 0.54, P 0.01). ere were positive correlations between the FC values in the right SOG-left SPG and Montreal Cognitive Assessment (MoCA) (r 0.52, P 0.01) and visuospatial skills/executive function scores (r 0.66, P 0.00) and in the right SOG- left CS and delayed memory scores (r 0.41, P 0.04)
Summary
Rapid eye movement sleep behavior disorder (RBD), which is characterized by nightmares, abnormal motor manifestations, and impaired muscle atonia during REM sleep [1], is closely associated with Parkinson’s disease (PD). Previous studies have proven that the impaired subcoeruleus nucleus and ventral medial medulla are associated with generating abnormal motor behaviors during REM sleep [7, 8]. In normal REM sleep, the ventral medial medulla can inhibit the spinal cord and prevent the motor cortex from generating movements owing to hyperpolarization of the spinal cord. Erefore, the cortical hypothesis proposed that the neocortex can produce movements because of the impaired ventral medial medulla in RBD. Us, the brainstem hypothesis stated that the red nucleus can generate excessive movements on account of the impaired ventral medial medulla in RBD. Guo et al [9] found that increased nodal measures in the neocortex and limbic system may stimulate the ascending reticular activating system, resulting in a “like-arousal” state during REM sleep and generating abnormal motor behaviors in patients with PD-RBD. Li et al [10] showed that decreased activity of the primary motor cortex may lead to poor control of motor behaviors during REM sleep in patients with PD-RBD. ese inconsistent results and different explanations urge us to learn more about the complex mechanisms underlying the RBD symptoms in PD
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