The Florey Institute of Neuroscience and Mental Health, Melbourne, VIC, Australia; University of Melbourne, Melbourne, VIC, Australia.
The Florey Institute of Neuroscience and Mental Health, Melbourne, VIC, Australia; University of Melbourne, Melbourne, VIC, Australia.
Sleep Med. 2021 Jul;83:45-53. doi: 10.1016/j.sleep.2021.04.011. Epub 2021 Apr 15.
OBJECTIVE/BACKGROUND: Sleep-wake dysfunction is bidirectionally associated with the incidence and evolution of acute stroke. It remains unclear whether sleep disturbances are transient post-stroke or are potentially enduring sequelae in chronic stroke. Here, we characterize sleep architectural dysfunction, sleep-respiratory parameters, and hemispheric sleep in ischemic stroke patients in the chronic recovery phase compared to healthy controls.
PATIENTS/METHODS: Radiologically confirmed ischemic stroke patients (n = 28) and matched control participants (n = 16) were tested with ambulatory polysomnography, bi-hemispheric sleep EEG, and demographic, stroke-severity, mood, and sleep-circadian questionnaires.
Twenty-eight stroke patients (22 men; mean age = 69.61 ± 7.4 years) were cross-sectionally evaluated 4.1 ± 0.9 years after mild-moderate ischemic stroke (baseline NIHSS: 3.0 ± 2.0). Fifty-seven percent of stroke patients (n = 16) exhibited undiagnosed moderate-to-severe obstructive sleep apnea (apnea-hypopnea index >15). Despite no difference in total sleep or wake after sleep onset, stroke patients had reduced slow-wave sleep time (66.25 min vs 99.26 min, p = 0.02), increased time in non-rapid-eye-movement (NREM) stages 1-2 (NREM-1: 48.43 vs 28.95, p = 0.03; NREM-2: 142.61 vs 115.87, p = 0.02), and a higher arousal index (21.46 vs 14.43, p = 0.03) when compared to controls. Controlling for sleep apnea severity did not attenuate the magnitude of sleep architectural differences between groups (NREM 1-3=ηp2 >0.07). We observed no differences in ipsilesionally versus contralesionally scored sleep architecture.
Fifty-seven percent of chronic stroke patients had undiagnosed moderate-severe obstructive sleep apnea and reduced slow-wave sleep with potentially compensatory increases in NREM 1-2 sleep relative to controls. Formal sleep studies are warranted after stroke, even in the absence of self-reported history of sleep-wake pathology.
目的/背景：睡眠-觉醒障碍与急性中风的发病和演变呈双向相关。目前尚不清楚睡眠障碍是中风后短暂的还是慢性中风后的潜在持久后遗症。在这里，我们比较了处于慢性恢复期的缺血性中风患者与健康对照者的睡眠结构障碍、睡眠呼吸参数和半球性睡眠。
患者/方法：对经影像学证实的缺血性中风患者（n=28）和匹配的对照组参与者（n=16）进行了动态多导睡眠图、双半球睡眠脑电图以及人口统计学、中风严重程度、情绪和睡眠-昼夜节律问卷的测试。
28 名中风患者（22 名男性；平均年龄 69.61±7.4 岁）在轻度至中度缺血性中风后 4.1±0.9 年进行了横断面评估（基线 NIHSS：3.0±2.0）。57%的中风患者（n=16）患有未确诊的中重度阻塞性睡眠呼吸暂停（呼吸暂停低通气指数>15）。尽管中风患者的总睡眠时间和睡眠后觉醒时间无差异，但他们的慢波睡眠时间减少（66.25 分钟 vs 99.26 分钟，p=0.02），非快速眼动（NREM）1-2 期时间增加（NREM-1：48.43 分钟 vs 28.95 分钟，p=0.03；NREM-2：142.61 分钟 vs 115.87 分钟，p=0.02），觉醒指数更高（21.46 次/分钟 vs 14.43 次/分钟，p=0.03）。与对照组相比。控制睡眠呼吸暂停严重程度并不能减轻组间睡眠结构差异的幅度（NREM 1-3=ηp2>0.07）。我们观察到同侧与对侧评分的睡眠结构没有差异。
57%的慢性中风患者患有未确诊的中重度阻塞性睡眠呼吸暂停，与对照组相比，慢波睡眠减少，而 NREM 1-2 睡眠可能代偿性增加。即使没有睡眠-觉醒病理的自我报告病史，中风后也应进行正式的睡眠研究。
