Movement Disorders (revue)

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Patterns of cortical thinning in idiopathic rapid eye movement sleep behavior disorder.

Identifieur interne : 000124 ( Main/Exploration ); précédent : 000123; suivant : 000125

Patterns of cortical thinning in idiopathic rapid eye movement sleep behavior disorder.

Auteurs : Shady Rahayel [Canada] ; Jacques Montplaisir ; Oury Monchi ; Christophe Bedetti ; Ronald B. Postuma ; Simona Brambati ; Julie Carrier ; Sven Joubert ; Véronique Latreille ; Thomas Jubault ; Jean-François Gagnon

Source :

RBID : pubmed:24676967

Abstract

Idiopathic rapid eye movement sleep behavior disorder is a parasomnia that is a risk factor for dementia with Lewy bodies and Parkinson's disease. Brain function impairments have been identified in this disorder, mainly in the frontal and posterior cortical regions. However, the anatomical support for these dysfunctions remains poorly understood. We investigated gray matter thickness, gray matter volume, and white matter integrity in patients with idiopathic rapid eye movement sleep behavior disorder. Twenty-four patients with polysomnography-confirmed idiopathic rapid eye movement sleep behavior disorder and 42 healthy individuals underwent a 3-tesla structural and diffusion magnetic resonance imaging examination using corticometry, voxel-based morphometry, and diffusion tensor imaging. In the patients with idiopathic rapid eye movement sleep behavior disorder, decreased cortical thickness was observed in the frontal cortex, the lingual gyrus, and the fusiform gyrus. Gray matter volume was reduced in the superior frontal sulcus only. Patients showed no increased gray matter thickness or volume. Diffusion tensor imaging analyses revealed no significant white matter differences between groups. Using corticometry in patients with idiopathic rapid eye movement sleep behavior disorder, several new cortical regions with gray matter alterations were identified, similar to those reported in dementia with Lewy bodies and Parkinson's disease. These findings provide some anatomical support for previously identified brain function impairments in this disorder.

DOI: 10.1002/mds.25820
PubMed: 24676967


Affiliations:


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