Localized Cortical Thinning in Patients with Obstructive Sleep Apnea Syndrome
Adult
Cerebral Cortex
Male
Sleep Apnea, Obstructive
Polysomnography
Neuroimaging
Middle Aged
Neuropsychological Tests
Magnetic Resonance Imaging
Young Adult
03 medical and health sciences
0302 clinical medicine
Case-Control Studies
Humans
Cognition Disorders
DOI:
10.5665/sleep.2876
Publication Date:
2013-07-31T19:57:51Z
AUTHORS (5)
ABSTRACT
To investigate differences in cortical thickness in patients with obstructive sleep apnea (OSA) syndrome and healthy controls.Cortical thickness was measured using a three-dimensional surface-based method that enabled more accurate measurement in deep sulci and localized regional mapping.University hospital.Thirty-eight male patients with severe OSA (mean apnea-hypopnea index > 30/h) and 36 age-matched male healthy controls were enrolled.Cortical thickness was obtained at 81,924 vertices across the entire brain by reconstructing inner and outer cortical surfaces using an automated anatomical pipeline.Group difference in cortical thickness and correlation between patients' data and thickness were analyzed by a general linear model.Localized cortical thinning in patients was found in the orbitorectal gyri, dorsolateral/ventromedial prefrontal regions, pericentral gyri, anterior cingulate, insula, inferior parietal lobule, uncus, and basolateral temporal regions at corrected P < 0.05. Patients with OSA showed impaired attention and learning difficulty in memory tests compared to healthy controls. Higher number of respiratory arousals was related to cortical thinning of the anterior cingulate and inferior parietal lobule. A significant correlation was observed between the longer apnea maximum duration and the cortical thinning of the dorsolateral prefrontal regions, pericentral gyri, and insula. Retention scores in visual memory tests were associated with cortical thickness of parahippocampal gyrus and uncus.Brain regions with cortical thinning may provide elucidations for prefrontal cognitive dysfunction, upper airway sensorimotor dysregulation, and cardiovascular disturbances in OSA patients, that experience sleep disruption including sleep fragmentation and oxygen desaturation.
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