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睡眠中断与创伤性脑损伤相关的后遗症。

Sleep disruption and the sequelae associated with traumatic brain injury.

作者信息

Lucke-Wold Brandon P, Smith Kelly E, Nguyen Linda, Turner Ryan C, Logsdon Aric F, Jackson Garrett J, Huber Jason D, Rosen Charles L, Miller Diane B

机构信息

The Center for Neuroscience, West Virginia University School of Medicine, Morgantown, WV 26506, USA; Department of Neurosurgery, West Virginia University School of Medicine, Morgantown, WV 26506, USA.

Department of Basic Pharmaceutical Sciences, West Virginia University School of Pharmacy, Morgantown, WV 26506, USA; The Center for Neuroscience, West Virginia University School of Medicine, Morgantown, WV 26506, USA.

出版信息

Neurosci Biobehav Rev. 2015 Aug;55:68-77. doi: 10.1016/j.neubiorev.2015.04.010. Epub 2015 May 6.

Abstract

Sleep disruption, which includes a loss of sleep as well as poor quality fragmented sleep, frequently follows traumatic brain injury (TBI) impacting a large number of patients each year in the United States. Fragmented and/or disrupted sleep can worsen neuropsychiatric, behavioral, and physical symptoms of TBI. Additionally, sleep disruption impairs recovery and can lead to cognitive decline. The most common sleep disruption following TBI is insomnia, which is difficulty staying asleep. The consequences of disrupted sleep following injury range from deranged metabolomics and blood brain barrier compromise to altered neuroplasticity and degeneration. There are several theories for why sleep is necessary (e.g., glymphatic clearance and metabolic regulation) and these may help explain how sleep disruption contributes to degeneration within the brain. Experimental data indicate disrupted sleep allows hyperphosphorylated tau and amyloid β plaques to accumulate. As sleep disruption may act as a cellular stressor, target areas warranting further scientific investigation include the increase in endoplasmic reticulum and oxidative stress following acute periods of sleep deprivation. Potential treatment options for restoring the normal sleep cycle include melatonin derivatives and cognitive behavioral therapy.

摘要

睡眠中断,包括睡眠缺失以及质量不佳的碎片化睡眠,常常伴随创伤性脑损伤(TBI)出现,在美国每年影响大量患者。碎片化和/或中断的睡眠会加重TBI的神经精神、行为和身体症状。此外,睡眠中断会损害恢复过程并可能导致认知衰退。TBI后最常见的睡眠中断是失眠,即难以保持睡眠状态。受伤后睡眠中断的后果从代谢组学紊乱和血脑屏障受损到神经可塑性改变和神经变性不等。关于睡眠为何必要有几种理论(例如,类淋巴系统清除和代谢调节),这些理论可能有助于解释睡眠中断如何导致脑内神经变性。实验数据表明,睡眠中断会使过度磷酸化的tau蛋白和淀粉样β斑块积聚。由于睡眠中断可能作为一种细胞应激源,值得进一步科学研究的目标领域包括急性睡眠剥夺期后内质网增加和氧化应激。恢复正常睡眠周期的潜在治疗选择包括褪黑素衍生物和认知行为疗法。

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