Structural and functional brain alterations in patients with idiopathic rapid eye movement sleep behavior disorder

Chen, Meijie; Li, Yuan; Chen, Jie; Gao, Linlin; Sun, Junyan; Gu, Zhuqin; Wu, Tao; Chan, Piu

doi:10.1016/j.neurad.2020.04.007

Cited by 29 publications

(42 citation statements)

References 37 publications

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“…Regarding the subcortical gray matter alterations, some studies have reported subcortical gray matter alterations in iRBD, 54,55,57‐59,64 and some other studies reported no such alternations 53,56,65,66 . Our results are consistent with the latter.…”

Section: Discussionsupporting

confidence: 91%

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Impaired Ocular Tracking and Cortical Atrophy in Idiopathic Rapid Eye Movement Sleep Behavior Disorder

et al. 2022

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A BS TRACT: Background: Idiopathic rapid eye movement sleep behavior disorder (iRBD) is a prodromal stage of synucleinopathies. Patients with synucleinopathies frequently display eye movement abnormalities. However, whether patients with iRBD have eye movement abnormalities remains unknown. Objective: The aim of this study was to assess eye movement abnormalities and related gray matter alterations and explore whether such abnormalities can serve as biomarkers to indicate phenoconversion to synucleinopathies in iRBD. Methods: Forty patients with iRBD with early disease progression and 35 healthy control subjects participated in a 15-minute ocular-tracking task that evaluated their control of eye movement abilities. They also underwent clinical assessments for olfactory function, nonmotor symptoms, and autonomic symptoms, all of which are biomarkers to predict phenoconversion to synucleinopathies in iRBD. A subgroup of the participants (20 patients with iRBD and 20 healthy control subjects) also participated in structural magnetic resonance imaging. Results:The ocular-tracking ability in patients with iRBD was inferior to that of healthy control subjects in two aspects: pursuit initiation and steady-state tracking. Cortical thinning in the right visual area V4 in patients with iRBD is coupled with impaired pursuit initiation. Furthermore, prolonged pursuit initiation in patients with iRBD exhibits a trend of correlation with olfactory loss, the earliest biomarker that develops prior to other prodromal biomarkers. Conclusions: We found ocular-tracking abnormalities in patients with iRBD even early in their disease progression that have not been reported before. These abnormalities are coupled with atrophy of brain areas involved in the perception of object motion and might indicate phenoconversion to synucleinopathies in iRBD.

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Section: Discussionsupporting

confidence: 91%

“…We also observed surface expansion in the left LO1 in iRBD. Gray matter enlargement in both cortical and subcortical regions in iRBD has been reported in previous studies 57‐59 . Cortical enlargement is usually observed in the early stage of neurodegenerative diseases, including PD 60,61 and Alzheimer's disease 62,63 .…”

Section: Discussionmentioning

confidence: 57%

Impaired Ocular Tracking and Cortical Atrophy in Idiopathic Rapid Eye Movement Sleep Behavior Disorder

et al. 2022

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“…The results of studies assessing structural and functional MRI (fMRI) studies are summarized, in chronological order, in Table 4 [ 163 , 164 , 165 , 166 , 167 , 168 , 169 , 170 , 171 , 172 , 173 , 174 , 175 , 176 , 177 , 178 , 179 , 180 , 181 , 182 , 183 , 184 , 185 , 186 , 187 , 188 , 189 , 190 , 191 , 192 , 193 , 194 ]. These include sudies of gray matter volume (GMV), cortical thickness, diffusion tensor imaging, dorsal nigral hyperintensity (DNH), neuromelanin-sensitive structural and diffusion MRI, and functional MRI.…”

Section: Structural and Functional Magnetic Resonance Imaging (Mri) Studiesmentioning

confidence: 99%

“…Most studies on GMV have used voxel-based morphometry. Although several of these studies have not shown significant clusters of reduced GMV or similar total brain volumes in between iRBD patients compared with controls [ 164 , 178 , 189 ], others have shown non-homogeneous results in iRBD patients, including smaller bilateral putamen volumes [ 164 ], decreased GMV in the anterior lobes of the right and left cerebellum, tegmental portion of the pons, and left parahippocampal gyrus [ 166 ], decreased GMV in the frontal lobes, anterior cingulate gyri, and caudate nucleus [ 172 ], decreased GMV in the frontal, temporal, parietal, occipital cortices as well as increased GMV in cerebellum posterior lobe, putamen, and thalamus [ 182 ], decreased GMV in the brainstem, anterior cingulate and insula [ 191 ], decreased GMV of the right caudate nucleus [ 194 ], and right hippocampal atrophy [ 177 ]. Bourgouin et al, 2019 [ 176 ] described reduced GMV in the caudate nucleus of iRBD patients with depressive symptoms and in the left amygdala-hippocampus in iRBD patients with anxiety symptoms when compared to iRBD patients without these symptoms and with controls.…”

Section: Structural and Functional Magnetic Resonance Imaging (Mri) Studiesmentioning

confidence: 99%

“…A study on structural connectivity showed decreased measures of the global network, average degree, global efficiency, and local efficiency, and increased measures of characteristic path length in iRBD patients compared to controls [ 175 ]. Two studies measuring amplitude of low-frequency fluctuations (ALFF), showed, respectively, increased ALFF values in the right parahippocampal gyrus [ 182 ], and normal values [ 36 ]. A significant reduction in regional homogeneity in the bilateral putamen of iRBD patients compared with controls has also been described [ 36 ].…”

Section: Structural and Functional Magnetic Resonance Imaging (Mri) Studiesmentioning

confidence: 99%

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Neurochemical Features of Rem Sleep Behaviour Disorder

Jiménez‐Jiménez

Alonso‐Navarro

García‐Martín

et al. 2021

JPM

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Dopaminergic deficiency, shown by many studies using functional neuroimaging with Single Photon Emission Computerized Tomography (SPECT) and Positron Emission Tomography (PET), is the most consistent neurochemical feature of rapid eye movement (REM) sleep behaviour disorder (RBD) and, together with transcranial ultrasonography, and determination of alpha-synuclein in certain tissues, should be considered as a reliable marker for the phenoconversion of idiopathic RBD (iRBD) to a synucleopathy (Parkinson’s disease –PD- or Lewy body dementia -LBD). The possible role in the pathogenesis of RBD of other neurotransmitters such as noradrenaline, acetylcholine, and excitatory and inhibitory neurotransmitters; hormones such as melatonin, and proinflammatory factors have also been suggested by recent reports. In general, brain perfusion and brain glucose metabolism studies have shown patterns resembling partially those of PD and LBD. Finally, the results of structural and functional MRI suggest the presence of structural changes in deep gray matter nuclei, cortical gray matter atrophy, and alterations in the functional connectivity within the basal ganglia, the cortico-striatal, and the cortico-cortical networks, but they should be considered as preliminary.

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Surface‐Based Morphometry Analysis of the Cerebral Cortex in Patients With Probable Idiopathic Rapid Eye Movement Sleep Behavior Disorder

Najafzadeh,

Saeeidian‐Mehr,

Akbari‐Lalimi

et al. 2024

Brain and Behavior

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IntroductionStrong indications support the notion that idiopathic rapid eye movement (REM) sleep behavior disorder (iRBD) acts as a precursor to multiple α‐synucleinopathies, including Parkinson's disease and dementia with Lewy bodies. Despite numerous investigations into the alterations in cortical thickness and the volume of subcortical areas associated with this condition, comprehensive studies on the cortical surface morphology, focusing on gyrification and sulcal depth changes, are scarce. The purpose of this research was to explore the cortical surface morphology in individuals with probable iRBD (piRBD), to pinpoint early‐phase diagnostic markers.MethodsThis study included 30 piRBD patients confirmed using the RBD Screening Questionnaire (RBDSQ) and 33 control individuals selected from the Parkinson's Progression Markers Initiative (PPMI) database. They underwent neurophysiological tests and MRI scans. The FreeSurfer software was utilized to estimate cortical thickness (CTH), cortical and subcortical volumetry, local gyrification index (LGI), and sulcus depth (SD). Subsequently, these parameters were compared between the two groups. Additionally, linear correlation analysis was employed to estimate the relationship between brain morphological parameters and clinical parameters.ResultsCompared to the healthy control (HC), piRBD patients exhibited a significant reduction in CTH, LGI, and cortical volume in the bilateral superior parietal, lateral occipital, orbitofrontal, temporo‐occipital, bilateral rostral middle frontal, inferior parietal, and precentral brain regions. Moreover, a significant and notable correlation was observed between CTH and Geriatric Depression Scale (GDS), letter–number sequencing (LTNS), the Benton Judgment of Line Orientation (BJLO) test, and the symbol digit modalities test (SDMT) in several brain regions encompassing the motor cortex.ConclusionPatients with piRBD displayed widespread atrophy in various brain regions, predominantly covering the motor and sensory cortex. Furthermore, LGI could serve as a prognostic biomarker of disease's progression in piRBD.

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Structural and functional brain alterations in patients with idiopathic rapid eye movement sleep behavior disorder

Cited by 29 publications

References 37 publications

Impaired Ocular Tracking and Cortical Atrophy in Idiopathic Rapid Eye Movement Sleep Behavior Disorder

Impaired Ocular Tracking and Cortical Atrophy in Idiopathic Rapid Eye Movement Sleep Behavior Disorder

Neurochemical Features of Rem Sleep Behaviour Disorder

Surface‐Based Morphometry Analysis of the Cerebral Cortex in Patients With Probable Idiopathic Rapid Eye Movement Sleep Behavior Disorder

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