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Lesion network mapping of REM Sleep Behaviour Disorder
H Odd1, C Dore1, S H Eriksson2
1Functional Imaging Laboratory, Department of Imaging Neuroscience, UCL Queen Square Institute of Neurology, University College London, UK.
Neuroimage. Clinical
|February 15, 2025
Summary
REM Sleep Behaviour Disorder (RBD) is linked to brainstem damage disrupting sleep atonia. This study identifies a brainstem disconnection syndrome, suggesting damage along specific white matter tracts causes RBD, explaining disease variability.
Area of Science:
- Neuroscience
- Sleep Medicine
- Neurology
Background:
- REM Sleep Behaviour Disorder (RBD) involves loss of muscle paralysis during REM sleep, leading to dream enactment.
- Idiopathic RBD is a significant risk factor for future alpha-synucleinopathies, such as Parkinson's disease.
- The precise neuroanatomical underpinnings of RBD in humans are not fully understood, despite animal studies identifying brainstem structures involved in sleep atonia.
Purpose of the Study:
- To empirically define a candidate anatomical network for RBD using lesion network mapping.
- To test the hypothesis that RBD results from damage to specific brainstem nodes, their white matter connections, or other brain regions.
- To identify the critical brainstem regions and tracts involved in maintaining REM sleep atonia.
Main Methods:
- Reviewed published cases of secondary RBD with discrete brain lesions to create lesion masks (n=25).
- Utilized MRI lesion masks from pontine strokes without RBD (n=15) as an exclusion mask.
- Employed lesion network mapping, probabilistic tractography, and warping to the Human Connectome dataset to identify and characterize the RBD network.
Main Results:
- Lesions associated with RBD were predominantly located in the brainstem, with significant variability.
- 72% of RBD lesions directly intersected with white matter tracts derived from pontine regions of interest (ROIs) overlapping the locus coeruleus.
- 92% of lesions were at or caudal to the maximal overlap region, suggesting a critical tract connecting the rostral locus coeruleus and medulla.
Conclusions:
- RBD appears to be a brainstem disconnection syndrome, where damage to the tract connecting the rostral locus coeruleus and medulla impairs sleep atonia.
- This model aligns with animal literature and may explain the variability in neuroimaging findings and clinical presentation of idiopathic RBD.
- Understanding this network provides insights into the pathophysiology of RBD and its association with alpha-synuclein disorders.
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