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Cerebrovascular Reactivity in Young Subjects with Sleep Apnea

睡眠呼吸暂停 睡眠(系统调用) 医学 阻塞性睡眠呼吸暂停 呼吸暂停 反应性(心理学) 心脏病学 听力学 心理学 内科学 麻醉 替代医学 计算机科学 操作系统 病理
作者
John Buterbaugh,Charles Wynstra,Natalie Provencio,Daniel Combs,Michael Gilbert,Sairam Parthasarathy
出处
期刊:Sleep [Oxford University Press]
卷期号:38 (2): 241-250 被引量:29
标识
DOI:10.5665/sleep.4406
摘要

Regional brain alterations may be involved in the pathogenesis and adverse consequences of obstructive sleep apnea (OSA). The objectives for the current study were to (1) determine cerebrovascular reactivity in the motor areas that control upper airway musculature in patients with OSA, and (2) determine whether young patients with OSA have decreased cerebrovascular reactivity in response to breath holding. Case-control study. Academic center. Twelve subjects with OSA (age 24–42 y; apnea-hypopnea index 17; interquartile range [IQR] 9, 69 per hour) and control subjects (n = 10; age 29–44 y; AHI 2; IQR 1, 3 per hour). Subjects underwent blood oxygen level-dependent functional magnetic resonance imaging (BOLD-fMRI) while awake, swallowing, and breath holding. In subjects with OSA, during swallowing, there was less activity in the brainstem than in controls (P = 0.03) that remained reduced after adjusting for cortical motor strip activity (P = 0.036). In OSA subjects, brain regions of increased cerebrovascular reactivity (38; IQR 17, 96 cm3) was smaller than that in controls (199; IQR 5, 423 cm3; P = 0.01). In OSA subjects, brain regions of decreased cerebrovascular reactivity during breath hold was greater (P = 0.01), and the ratio of increased-to-decreased brain regions was lower than that of controls (P = 0.006). Adjustment for cerebral volumes, body mass index, and white matter lesions did not change these results substantively. In patients with obstructive sleep apnea (OSA), diminished change in brainstem activity during swallowing and reduced cerebrovascular reactivity may contribute to the etiopathogenesis and adverse cerebrovascular consequences, respectively. We speculate that decreased cerebral auto-regulation may be causative of gray matter loss in OSA.

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