1 Centre d'études avancées en médecine du sommeil, Hôpital du Sacré-Cœur de Montréal, Montreal, Quebec, Canada.
2 Département de psychiatrie.
Am J Respir Crit Care Med. 2017 Jun 1;195(11):1509-1518. doi: 10.1164/rccm.201606-1271OC.
Obstructive sleep apnea causes intermittent hypoxemia, hemodynamic fluctuations, and sleep fragmentation, all of which could damage cerebral gray matter that can be indirectly assessed by neuroimaging.
To investigate whether markers of obstructive sleep apnea severity are associated with gray matter changes among middle-aged and older individuals.
Seventy-one subjects (ages, 55-76 yr; apnea-hypopnea index, 0.2-96.6 events/h) were evaluated by magnetic resonance imaging. Two techniques were used: (1) voxel-based morphometry, which measures gray matter volume and concentration; and (2) FreeSurfer (an open source software suite) automated segmentation, which estimates the volume of predefined cortical/subcortical regions and cortical thickness. Regression analyses were performed between gray matter characteristics and markers of obstructive sleep apnea severity (hypoxemia, respiratory disturbances, and sleep fragmentation).
Subjects had few symptoms, that is, sleepiness, depression, anxiety, and cognitive deficits. Although no association was found with voxel-based morphometry, FreeSurfer revealed increased gray matter with obstructive sleep apnea. Higher levels of hypoxemia correlated with increased volume and thickness of the left lateral prefrontal cortex as well as increased thickness of the right frontal pole, the right lateral parietal lobules, and the left posterior cingulate cortex. Respiratory disturbances positively correlated with right amygdala volume, and more severe sleep fragmentation was associated with increased thickness of the right inferior frontal gyrus.
Gray matter hypertrophy and thickening were associated with hypoxemia, respiratory disturbances, and sleep fragmentation. These structural changes in a group of middle-aged and older individuals may represent adaptive/reactive brain mechanisms attributed to a presymptomatic stage of obstructive sleep apnea.
阻塞性睡眠呼吸暂停引起间歇性低氧血症、血流动力学波动和睡眠片段化，所有这些都可能损害大脑灰质，而这些损害可以通过神经影像学来间接评估。
研究阻塞性睡眠呼吸暂停严重程度的标志物是否与中老年人的灰质变化有关。
71 名受试者（年龄 55-76 岁；呼吸暂停低通气指数 0.2-96.6 次/小时）接受了磁共振成像评估。采用两种技术：（1）体素形态计量学，测量灰质体积和浓度；（2）FreeSurfer（一个开源软件套件）自动分割，估计预定义的皮质/皮质下区域的体积和皮质厚度。在灰质特征与阻塞性睡眠呼吸暂停严重程度标志物（低氧血症、呼吸紊乱和睡眠片段化）之间进行回归分析。
受试者有很少的症状，即嗜睡、抑郁、焦虑和认知缺陷。尽管与基于体素的形态计量学没有关联，但 FreeSurfer 显示出与阻塞性睡眠呼吸暂停相关的灰质增加。较高的低氧血症水平与左侧外侧前额皮质的体积和厚度增加以及右侧额极、右侧外侧顶叶和左侧后扣带回皮质的厚度增加相关。呼吸紊乱与右侧杏仁核体积呈正相关，更严重的睡眠片段化与右侧额下回厚度增加有关。
灰质肥大和增厚与低氧血症、呼吸紊乱和睡眠片段化有关。这些中老年人的结构变化可能代表了阻塞性睡眠呼吸暂停的亚临床阶段的适应性/反应性大脑机制。
