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Has patients affected by REM sleep Behavior Disorder a specific brain glucose metabolism pattern?

C. Liguori, R. Ruffini, E. Olivola, A. Chiaravalloti, F. Izzi, O. Schillaci, N. Mercuri, F. Placidi (Rome, Italy)

Meeting: 2018 International Congress

Abstract Number: 866

Keywords: Dementia with Lewy bodies (DLB), Parkinsonism, Rapid eye movement(REM)

Session Information

Date: Sunday, October 7, 2018

Session Title: Other

Session Time: 1:45pm-3:15pm

Location: Hall 3FG

Objective: This study aimed at evaluating brain glucose metabolism in patients affected by REM sleep behavior disorders (RBD) compared to Parkinson’s Disease (PD), Lewy Body Dementia (LBD), Alzheimer’s Disease (AD) and elderly controls (EC).

Background: RBD is a complex parasomnia, characterized by the pathological lack of atonia during REM sleep associated with enacting dreams. Several longitudinal studies revealed that a high proportion of RBD patients convert to α-synucleinopathies such as PD or LBD. [18F]FDG-PET is currently the most accurate in-vivo method for the investigation of regional human brain metabolism. [18F]FDG-PET studies revealed that in RBD patients brain glucose abnormalities are associated with the phenoconversion to neurodegenerative diseases.

Methods: Differences in brain [18F]FDG uptake were analyzed using statistical parametric mapping (SPM8; Wellcome Department of Cognitive Neurology, London, UK) implemented in Matlab R2012b using the MMSE scores, UPDRS motor section scores, sex and age, as covariates. The following voxel-based comparisons were performed using a ‘two-sample t test’ design model: RBD versus PD; RBD versus LBD; RBD versus AD; RBD versus EC.

Results: 35 RBD, 31 PD, 10 LBD, 32 AD, and 32 EC were included in this study. We documented significant brain [18F]FDG uptake changes in RBD patients compared to all groups. In particular, RBD patients showed brain glucose hypometabolism in the precuneus, middle temporal gyrus, parietal and occipital lobes compared to EC. Considering the other comparisons, RBD patients mainly showed cerebral glucose hypometabolism in frontal areas compared to AD patients; temporal glucose hypometabolism compared to LBD; and frontal, cerebellar and subcortical brain glucose hypometabolism compared to PD patients. These comparisons were extremely different and thus RBD patients seems to show a different cerebral glucose metabolism pattern than all the other groups.

Conclusions: This study documented the alteration of brain [18F]FDG uptake in RBD patients, as expected in a preclinical neurodegenerative process. Moreover, RBD patients showed a distinctive pattern of cerebral [18F]FDG uptake, which is different from AD, LBD or PD. These findings further support the hypothesis that RBD may represent a preclinical stage of neurodegeneration in which biomarkers changes already occur. Longitudinal studies may help in identifying different patterns of [18F]FDG uptake predictive of a specific neurodegenerative process.

To cite this abstract in AMA style:

C. Liguori, R. Ruffini, E. Olivola, A. Chiaravalloti, F. Izzi, O. Schillaci, N. Mercuri, F. Placidi. Has patients affected by REM sleep Behavior Disorder a specific brain glucose metabolism pattern? [abstract]. Mov Disord. 2018; 33 (suppl 2). https://www.mdsabstracts.org/abstract/has-patients-affected-by-rem-sleep-behavior-disorder-a-specific-brain-glucose-metabolism-pattern/. Accessed May 13, 2025.
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