Voxel-based magnetic resonance imaging study of structural brain changes in patients with idiopathic REM sleep behavior disorder
Introduction
Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia characterized by loss of normal skeletal muscle atonia during REM sleep and prominent motor activity while dreaming [1]. Structural lesions occur in the dorsolateral tegmental portion of the pons, and in particular the subcoeruleus region and laterodorsal tegmental nuclei have been proposed as the regions responsible for the occurrence of RBD [1]. RBD occurs either as an idiopathic disease or in association with neurodegenerative diseases, particularly alpha-synucleinopathies.
There have been few studies examining structural brain changes in patients with iRBD. Previous magnetic resonance imaging (MRI) studies have failed to show specific brain stem lesions which could play a role in the occurrence of the loss of muscle atonia during REM sleep except for unspecific findings such as white matter (WM) lesions and generalized cerebral atrophy [2]. Recent studies have shown microstructural WM changes of the brain stem in iRBD patients using diffusion tensor imaging [3], [4]. In the present study, we measured gray matter (GM) volume in patients with iRBD using voxel-based morphometry (VBM) MRI to determine structural brain alterations associated with the disorder.
Section snippets
Subjects
We recruited 22 consecutive untreated patients having iRBD, which was diagnosed based on thorough clinical interviews and one night video-polysomnographic (PSG) findings by sleep disorder expert physicians, according to the criteria of the International Classification of Sleep Disorders, Second Edition [5]. PSG and video monitoring were performed simultaneously as the patients slept. However, we studied only 20 patients (17 men and 3 women; mean age ± SD: 68 ± 7 years; mean RBD duration ± SD:
Results
Clinical, neuropsychological, and PSG data for patients with iRBD are given in Table 1. The frequency of RBD symptoms was 1–2 nights/month in 4 patients, 1–2 nights/week in 9 patients, 3–5 nights/week in 4 patients, and 6–7 nights/week in 3 patients. Significantly reduced GM volume in patients with iRBD compared with controls was found in the anterior lobes of the right and left cerebellum, tegmental portion of the pons, and left parahippocampal gyrus (Table 2, Fig. 1). No significant
Discussion
We found reduced GM volume in the anterior lobes of the right and left cerebellum, tegmental portion of the pons, and left parahippocampal gyrus in patients with iRBD.
There are limited reports of MRI findings in patients with iRBD. Olson et al. [2] described brain imaging (CT and MRI) findings in 52 patients who showed RBD symptoms. They found that only 4 patients had brain stem pathology and all 4 of these patients also had a neurodegenerative disorder known to be associated with RBD. Other
Conflict of interest
The authors report no conflict of interest.
Acknowledgments
We are grateful to Mr. Roderick J. Turner, Assistant Professor Edward F. Barroga and Professor J. Patrick Barron of the Department of International Medical Communications of Tokyo Medical University for their review of the manuscript.
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2020, NeuroImage: ClinicalCitation Excerpt :Since MRI is a non-invasive and widely available technique that could be used for this purpose, there is a growing interest to better characterize brain changes in IRBD patients. Brain structure in IRBD has previously been studied by means of voxel-based morphometry, cortical thickness and diffusion-tensor imaging, suggesting changes in both cortical (Campabadal et al., 2019; Hanyu et al., 2012; Park et al., 2018; Pereira et al., 2019; Rahayel et al., 2018b, 2018a, 2015; Unger et al., 2010) and subcortical (Ellmore et al., 2010; Hanyu et al., 2012; Park et al., 2018; Rahayel et al., 2018b, 2018a; Scherfler et al., 2011; Unger et al., 2010) structures. Regarding resting-state functional MRI (rs-fMRI), a prior work, using a seed-based approach focused on the substantia nigra, identified altered nigrostriatal and nigrocortical connectivity (Ellmore et al., 2013).