Comprehensive Analysis of Brain Volume in REM Sleep Behavior Disorder with Mild Cognitive Impairment.

BACKGROUND: Rapid-eye-movement sleep behavior disorder (RBD) is a major risk factor for Parkinson's disease and dementia with Lewy bodies. More than a third of RBD patients have mild cognitive impairment (MCI), but their specific structural brain alterations remain poorly understood. OBJECTIVE: This study aimed to investigate the local deformation and volume of gray and white matter tissue underlying MCI in RBD. METHODS: Fifty-two idiopathic RBD patients, including 17 with MCI (33%), underwent polysomnography, neuropsychological, neurological, and magnetic resonance imaging assessments. MCI diagnosis was based on a subjective complaint, cognitive impairment on the neuropsychological battery, and preserved daily functioning. Forty-one controls were also included. Deformation-based morphometry (DBM), voxel-based morphometry (VBM), and regional volume analyses of the corpus callosum and cholinergic basal forebrain were performed. Multiple regression models were also computed using anatomical, cognitive (composite z scores), and motor parameters. RESULTS: Globally, patients with MCI displayed a widespread pattern of local deformation and volume atrophy in the cortical (bilateral insula, cingulate cortex, precuneus, frontal, temporal and occipital regions, right angular gyrus, and mid-posterior segment of the corpus callosum) and subcortical (brainstem, corona radiata, basal ganglia, thalamus, amygdala, and right hippocampus) regions compared to patients without MCI (DBM) or controls (DBM and VBM). Moreover, brain deformation (DBM) in patients were associated with lower performance in attention and executive functions, visuospatial abilities, and higher motor symptoms severity. CONCLUSION: The present study identified novel brain structural alterations in RBD patients with MCI which correlated with poorer cognitive performance. These results are consistent with those reported in patients with synucleinopathies-related cognitive impairment.

Brain atrophy in Parkinson's disease with polysomnography-confirmed REM sleep behavior disorder.

We aimed to investigate cortical and subcortical brain alterations in people with Parkinson's disease with polysomnography-confirmed rapid eye movement (REM) sleep behavior disorder (RBD). Thirty people with Parkinson's disease, including 15 people with RBD, were recruited and compared with 41 healthy controls. Surface-based cortical and subcortical analyses were performed on T1-weighted images to investigate thickness and shape abnormalities between groups, and voxel-based and deformation-based morphometry were performed to investigate local volume. Correlations were performed in patients to investigate the structural correlates of motor activity during REM sleep. People with RBD showed cortical thinning in the right perisylvian and inferior temporal cortices and shape contraction in the putamen compared with people without RBD. Compared with controls, people with RBD had extensive cortical thinning and volume loss, brainstem volume was reduced, and shape contraction was found in the basal ganglia and hippocampus. In comparison to controls, people without RBD showed more restricted thinning in the sensorimotor, parietal, and occipital cortices, reduced volume in the brainstem, temporal and more posterior areas, and shape contraction in the pallidum and hippocampus. In Parkinson's disease, higher tonic and phasic REM sleep motor activity was associated with contraction of the thalamic surface, extensive cortical thinning, and subtle volume reduction in the middle temporal gyrus. In Parkinson's disease, the presence of RBD is associated with extensive cortical and subcortical abnormalities, suggesting more severe neurodegeneration in people with RBD. This provides potential neuroanatomical correlates for the more severe clinical phenotype reported in people with Parkinson's disease with RBD.

Neuroimaging of Rapid Eye Movement Sleep Behavior Disorder.

Idiopathic rapid eye movement sleep behavior disorder (iRBD) is a parasomnia characterized by the loss of muscle atonia and the presence of undesirable motor manifestations during rapid eye movement sleep. Research findings have shown that iRBD is a prodromal stage of synucleinopathies such as Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy. A wide array of neuroimaging techniques have improved our understanding of the prodromal stage of these diseases in patients with iRBD, and identified potential biomarkers. In this chapter, we summarize current knowledge about functional and structural central and peripheral neuroimaging in iRBD, including cross-sectional and longitudinal studies using positron emission tomography, single-photon emission computed tomography, magnetic resonance imaging, and transcranial sonography. Current neuroimaging research has revealed several brain alterations in iRBD similar to those reported in synucleinopathies, thereby improving our understanding of the pathophysiology underlying the clinical presentation and progression of their prodromal stages. Moreover, some abnormalities detected by neuroimaging show promise as potential biomarkers to predict which individuals with iRBD may be at risk of conversion and therefore candidates for inclusion in future clinical trials of neuroprotection.