2021-03-26
Journal:frontiers in neurology
Publication type: Original Research
IF(IF): 4.003
PMID: 33841304 Link To Pubmed Full text Download
研究背景: 卒中被报告为全球第二大最常见死亡原因和第三大最常见的伤残调整生命年降低原因,也是2017年以来影响全中国死亡和伤残调整生命年最主要的原因[1, 2]。 近些年有研究发现睡眠时长会影响卒中的发生。一项纳入15项前瞻性队列的荟萃分析显示,短时间和长时间的睡眠都是卒中的独立危险因素,呈现出U型关系[3-5]。也有研究发现卒中发生只与长时间睡眠存在相关性,呈J型关系[6]。短时间睡眠会影响夜间自主神经功能调节和昼夜节律,进而影响瘦素和生长激素释放肽水平,促进皮质醇激素增加和生长激素改变,加速肥胖的发生,影响血压、血脂、血糖的水平,促进动脉粥样硬化形成。短时间睡眠(<6.8h)也会增大大脑中动脉的搏动指数[7]。另外短时间睡眠还会激活体内炎症反应、自主神经系统、下丘脑-垂体-肾上腺轴,影响血流动力学波动,以上因素均会促使卒中的发生[3, 8, 9]。而长时间的睡眠可能因为睡眠呼吸暂停等因素增加卒中发生风险[10]。 研究发现睡眠呼吸暂停、失眠等睡眠疾病会影响卒中患者的预后。不仅会增加脑血管病的死亡、残疾风险,还会影响患者的情绪水平[1, 11]。动物实验发现卒中后第一天睡眠会激活GABA受体,为病灶周围提供一个保护区。另外睡眠时神经突触联系增强,对白天的运动学习进行巩固,睡眠时间的长短会影响大脑记忆巩固的时间,进而影响卒中患者肢体康复的效果[12]。研究也发现卒中后失眠患者平衡功能恢复较差[13]。动物研究发现卒中后动物REM睡眠减少,而在卒中前给与急性睡眠剥夺的动物在卒中后REM增加,且黑色素、食欲素系统激活,利于梗死病灶缩小,保护神经功能[14]。短时间睡眠会导致体内炎症水平和氧化应激反应增加[15],从而影响卒中的远期预后。研究发现长时间的睡眠剥夺、睡眠结构紊乱会增加脑损伤,损害神经可塑性[16],促进睡眠的药物对神经可塑性和卒中恢复有良好的作用[17]。但日本一项研究发现更长的睡眠时间(≥9h)与缺血性卒中的死亡率增加有关[18]。 目前研究主要集中在睡眠障碍与卒中发生的相关性,而关于卒中预后的研究较少,且研究主要集中在睡眠呼吸暂停,对于睡眠时长,尤其是卒中急性期的睡眠时长与卒中预后的相关性研究较少,而且样本量较少,结论不一致。早期认识和治疗睡眠障碍是很重要的。 研究目的: 本文的研究目的是探讨卒中急性期睡眠时间长短对卒中3个月预后的影响,是否存在U型或J型曲线。
Nationally representative samples from the Third China National Stroke Registry were used to examine cognition and sleep impairment after AIS (CNSR-III-ICONS). Based on baseline sleep duration before onset of stroke as measured by using the Pittsburgh Sleep Quality Index (PSQI), 1446 patients were divided into four groups: >7, 6-7, 5-6 and <5 hours of sleep. Patients were followed up with the General Anxiety Disorder-7 (GAD-7) and Patient Health Questionnaire-9 (PHQ-9) for 3 months. Post-stroke anxiety (PSA) was defined as GAD-7 of ≥5 and post-stroke depression (PSD) as PHQ-9 of ≥5. The association of sleep duration with PSA and PSD were evaluated using multivariable logistic regression.
Sleep duration of shorter than 6 hours was predictive of anxiety and depression after ischemic stroke.
The incidences of PSA and PSD were 11.2% and 17.6% at 3 months, respectively. Compared to a sleep duration of >7 hours, 5-6 hours and <5 hours of sleep were identified as risk factors of PSA (odds ratio, OR 1.95, 95% confidence interval, CI, 1.24-3.07, P<0.01; and OR 3.41, 95% CI 1.94-6.04, P<0.01) and PSD (OR 1.47, 95% CI 1.00-2.17, P=0.04; and OR 3.05, 95% CI 1.85-5.02, P<0.01), while 6-7 hours of sleep was associated with neither PSA (OR 1.09, 95% CI 0.71-1.67, P=0.68) nor PSD (OR 0.92, 95% CI 0.64-1.30, P=0.64). In interaction analysis, the impact of sleep duration on PSA and PSD was not affected by gender (P=0.68 and P=0.29, respectively).