Neural alterations associated with anxiety symptoms in obstructive sleep apnea syndrome

• Published in: Depression and anxiety Vol. 26; no. 5; pp. 480 - 491
• Main Authors: Kumar, Rajesh, Macey, Paul M., Cross, Rebecca L., Woo, Mary A., Yan-Go, Frisca L., Harper, Ronald M.
• Format: Journal Article
• Language: English
• Published: Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.05.2009
• Subjects: Adult; amygdala; Anxiety - physiopathology; Anxiety - psychology; Arousal - physiology; Axons - physiology; Brain - physiopathology; Brain Damage, Chronic - physiopathology; Brain Damage, Chronic - psychology; Brain Ischemia - physiopathology; Brain Ischemia - psychology; Brain Mapping; Dominance, Cerebral - physiology; Emotions - physiology; Female; fornix; hippocampus; Humans; Image Processing, Computer-Assisted; intermittent hypoxia; Magnetic Resonance Imaging; Male; Middle Aged; Nerve Fibers, Myelinated - physiology; Polysomnography; Sleep Apnea, Obstructive - physiopathology; Sleep Apnea, Obstructive - psychology; sleep-disordered breathing
• ISSN: 1091-4269; 1520-6394
• DOI: 10.1002/da.20531

Background: Neuropsychological comorbidities, including anxiety symptoms, accompany obstructive sleep apnea (OSA); structural and functional brain alterations also occur in the syndrome. The objective was to determine whether OSA patients expressing anxiety symptoms show injury in specific brain sites. Methods: Magnetic resonance T2‐relaxometry was performed in 46 OSA and 66 control subjects. Anxiety symptoms were evaluated using the Beck Anxiety Inventory (BAI); subjects with BAI scores>9 were classified anxious. Whole brain T2‐relaxation maps were compared between anxious and nonanxious groups using analysis of covariance (covariates, age and gender). Results: Sixteen OSA and seven control subjects showed anxiety symptoms, and 30 OSA and 59 controls were nonanxious. Significantly higher T2‐relaxation values, indicating tissue injury, appeared in anxious OSA versus nonanxious OSA subjects in subgenu, anterior, and mid‐cingulate, ventral medial prefrontal and bilateral insular cortices, hippocampus extending to amygdala and temporal, and bilateral parietal cortices. Brain injury emerged in anxious OSA versus nonanxious controls in bilateral insular cortices, caudate nuclei, anterior fornix, anterior thalamus, internal capsule, mid‐hippocampus, dorsotemporal, dorsofrontal, ventral medial prefrontal, and parietal cortices. Conclusions: Anxious OSA subjects showed injury in brain areas regulating emotion, with several regions lying outside structures affected by OSA alone, suggesting additional injurious processes in anxious OSA subjects. Depression and Anxiety, 2009. © 2008 Wiley‐Liss, Inc.