Taylor Keri S, Millar Philip J, Murai Hisayoshi, Haruki Nobuhiko, Kimmerly Derek S, Bradley T Douglas, Floras John S
Department of Medicine, University Health Network and Mount Sinai Hospital, University of Toronto, Toronto, Ontario, Canada.
Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada.
Sleep. 2018 Feb 1;41(2). doi: 10.1093/sleep/zsx208.
The sympathetic excitation elicited acutely by obstructive apnea during sleep (OSA) carries over into wakefulness. We hypothesized that OSA induces structural changes in the insula and cingulate, key central autonomic network elements with projections to brainstem sympathetic premotor regions. The aims of this study were to (1) apply two distinct but complementary methods (cortical thickness analysis [CTA] and voxel-based morphometry [VBM]) to compare insula and cingulate gray matter thickness in participants without and with OSA; (2) determine whether oxygen desaturation index (ODI) relates to cortical thickness; and (3) determine whether cortical thickness or volume in these regions predicts muscle sympathetic nerve activity (MSNA) burst incidence (BI). Overnight polysomnography, anatomical magnetic resonance imaging, and MSNA data were acquired in 41 participants with no or mild OSA (n = 19; 59 ± 2 years [Mean ± SE]; six females; apnea-hypopnea index [AHI] 7 ± 1 events per hour) or moderate-to-severe OSA (n = 22; 59 ± 2 years; five females; AHI 31 ± 4 events per hour). Between-group CTA analyses identified cortical thinning within the left dorsal posterior insula and thickening within the left mid-cingulate cortex (LMCC), whereas VBM identified thickening within bilateral thalami (all [p < .05]). CTA revealed inverse relationships between ODI and bilateral dpIC and left posterior cingulate cortex (LPCC) or precuneus thickness. Positive correlations between BI and LMCC gray matter thickness or volume were evident with both methods and between BI and left posterior thalamus volume using VBM. In OSA, the magnitude of insular thinning, although a function of hypoxia severity, does not influence MSNA, whereas cingulate and thalamic thickening relate directly to the intensity of sympathetic discharge during wakefulness.
睡眠期间阻塞性呼吸暂停（OSA）急性引发的交感神经兴奋会延续至清醒状态。我们推测，OSA会导致脑岛和扣带回发生结构变化，这两个结构是中枢自主神经网络的关键组成部分，且向脑干交感神经运动前区投射。本研究的目的是：（1）应用两种不同但互补的方法（皮质厚度分析[CTA]和基于体素的形态学测量[VBM]）比较无OSA和有OSA参与者的脑岛和扣带回灰质厚度；（2）确定氧去饱和指数（ODI）是否与皮质厚度相关；（3）确定这些区域的皮质厚度或体积是否可预测肌肉交感神经活动（MSNA）爆发发生率（BI）。对41名无或轻度OSA（n = 19；59±2岁[均值±标准误]；6名女性；呼吸暂停低通气指数[AHI]为每小时7±1次事件）或中度至重度OSA（n = 22；59±2岁；5名女性；AHI为每小时31±4次事件）的参与者进行了整夜多导睡眠图监测、解剖磁共振成像和MSNA数据采集。组间CTA分析发现，左侧背侧后脑岛皮质变薄，左侧中扣带回皮质（LMCC）增厚，而VBM发现双侧丘脑增厚（均为[p <.05]）。CTA显示ODI与双侧背侧后岛叶皮质（dpIC）以及左侧后扣带回皮质（LPCC）或楔前叶厚度呈负相关。两种方法均显示BI与LMCC灰质厚度或体积呈正相关，VBM显示BI与左侧后丘脑体积呈正相关。在OSA中，脑岛变薄的程度虽然是缺氧严重程度的函数，但不影响MSNA，而扣带回和丘脑增厚与清醒期间交感神经放电强度直接相关。
