Hurvitz Brain Sciences Program, Sunnybrook Research Institute, University of Toronto, Toronto, ON, Canada.
Hurvitz Brain Sciences Program, Sunnybrook Research Institute, University of Toronto, Toronto, ON, Canada.
Sleep Med. 2021 Jul;83:83-88. doi: 10.1016/j.sleep.2021.03.043. Epub 2021 Apr 19.
Recent studies suggest that interindividual genetic differences in glial-dependent CSF flow through the brain parenchyma, known as glymphatic flow, may trigger compensatory changes in human sleep physiology. In animal models, brain perivascular spaces are a critical conduit for glymphatic flow. We tested the hypothesis that MRI-visible PVS volumes, a putative marker of perivascular dysfunction, are associated with compensatory differences in real-world human sleep behavior.
We analyzed data from 152 cerebrovascular disease patients from the Ontario Neurodegenerative Disease Research Initiative (ONDRI). PVS volumes were measured using 3T-MRI. Self-reported total sleep time, time in bed, and daytime dysfunction were extracted from the Pittsburgh Sleep Quality Index.
Individuals with greater PVS volumes reported longer time in bed (+0.85 h per log10 proportion of intracranial volume (ICV) occupied by PVS, SE = 0.30, p = 0.006) and longer total sleep times (+0.70 h per log10 proportion of ICV occupied by PVS volume, SE = 0.33, p = 0.04), independent of vascular risk factors, sleep apnea, nocturnal sleep disturbance, depression, and global cognitive status. Further analyses suggested that the positive association between PVS volumes and total sleep time was mediated by greater time in bed. Moreover, despite having on average greater total sleep times, individuals with greater basal ganglia PVS volumes were more likely to report daytime dysfunction (OR 5.63 per log10 proportion of ICV occupied by PVS, 95% CI: 1.38-22.26, p = 0.018).
Individuals with greater PVS volumes spend more time in bed, resulting in greater total sleep time, which may represent a behavioral compensatory response to perivascular space dysfunction.
最近的研究表明，胶质细胞依赖的脑实质脑脊液流动的个体间遗传差异，即神经胶质淋巴系统，可能引发人类睡眠生理学的代偿性变化。在动物模型中，脑周细胞空间是神经胶质淋巴系统的一个关键通道。我们检验了这样一个假设，即 MRI 可见的 PVS 体积（一种血管周围功能障碍的假定标志物）与现实世界中人类睡眠行为的代偿性差异有关。
我们分析了来自安大略省神经退行性疾病研究倡议（ONDRI）的 152 名脑血管病患者的数据。使用 3T-MRI 测量 PVS 体积。从匹兹堡睡眠质量指数中提取自我报告的总睡眠时间、卧床时间和白天功能障碍。
PVS 体积较大的个体报告的卧床时间更长（每增加 1 个颅内体积（ICV）的 PVS 比例的对数，增加 0.85 小时，SE=0.30，p=0.006），总睡眠时间更长（每增加 1 个 ICV 的 PVS 体积比例的对数，增加 0.70 小时，SE=0.33，p=0.04），独立于血管危险因素、睡眠呼吸暂停、夜间睡眠障碍、抑郁和整体认知状态。进一步的分析表明，PVS 体积与总睡眠时间之间的正相关关系是由卧床时间增加介导的。此外，尽管平均总睡眠时间较长，但 PVS 体积较大的基底节区个体更有可能报告白天功能障碍（每增加 1 个 ICV 的 PVS 比例的对数，OR 为 5.63，95%CI：1.38-22.26，p=0.018）。
PVS 体积较大的个体卧床时间更长，导致总睡眠时间更长，这可能代表对周细胞空间功能障碍的行为代偿反应。
