The Bidirectional Link Between Sleep Disturbances and Traumatic Brain Injury Symptoms: A Role for Glymphatic Dysfunction?

The Bidirectional Link Between Sleep Disturbances and Traumatic Brain Injury Symptoms: A Role for Glymphatic Dysfunction?
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DOI:
10.1016/j.biopsych.2021.06.025
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发表时间:
2022-03-01
影响因子:
10.6
通讯作者:
Lim MM
Lim MM
中科院分区:
医学1区
文献类型:
--
作者:
Piantino JA;Iliff JJ;Lim MM

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轻度创伤性脑损伤(mTBI),通常称为脑震荡,是全球发病率和死亡率的主要原因。mTBI后睡眠障碍很常见。此外,在mTBI后出现主观睡眠抱怨的受试者也报告了更严重的躯体、心理健康和认知障碍,并且需要更长的时间从mTBI后遗症中恢复。尽管许多先前的研究解决了睡眠在mTBI后发病率中的作用,但将睡眠与mTBI后恢复联系起来的机制仍然知之甚少。胶质淋巴系统是一个全脑网络,支持通过脑实质的液体运动以及从脑中清除间质溶质和废物。值得注意的是,胶质淋巴系统主要在睡眠期间活跃。清除与躯体、精神健康和神经退行性过程相关的细胞副产物(例如,淀粉样蛋白-β和tau等)部分依赖于完整的胶质淋巴功能,其在mTBI后受损。在这个观点中,我们回顾了目前的知识,睡眠障碍和后mTBI症状之间的关联。我们还讨论了胶质淋巴功能障碍作为mTBI,睡眠中断和创伤后发病率之间的潜在联系的作用。我们概述了一个模型,其中由mTBI引起的胶质淋巴功能障碍和睡眠中断可能对废物清除产生叠加效应,导致脑功能障碍和恢复受损。最后,我们回顾了正在开发的新技术,以检查人类的胶质淋巴功能,并探索潜在的干预措施,以改变胶质淋巴交换,可能提供一种新的治疗方法,那些患有睡眠不佳和mTBI后症状延长。
Mild traumatic brain injury (mTBI), often referred to as concussion, is a major cause of morbidity and mortality worldwide. Sleep disturbances are common after mTBI. Moreover, subjects who develop subjective sleep complaints after mTBI also report more severe somatic, mental health, and cognitive impairment and take longer to recover from mTBI sequelae. Despite many previous studies addressing the role of sleep in post-mTBI morbidity, the mechanisms linking sleep to recovery after mTBI remain poorly understood. The glymphatic system is a brain-wide network that supports fluid movement through the cerebral parenchyma and the clearance of interstitial solutes and wastes from the brain. Notably, the glymphatic system is active primarily during sleep. Clearance of cellular byproducts related to somatic, mental health, and neurodegenerative processes (e.g., amyloid-β and tau, among others) depends in part on intact glymphatic function, which becomes impaired after mTBI. In this viewpoint, we review the current knowledge regarding the association between sleep disturbances and post-mTBI symptoms. We also discuss the role of glymphatic dysfunction as a potential link between mTBI, sleep disruption, and post-traumatic morbidity. We outline a model where glymphatic dysfunction and sleep disruption caused by mTBI may have an additive effect on waste clearance, leading to cerebral dysfunction and impaired recovery. Finally, we review the novel techniques being developed to examine glymphatic function in humans and explore potential interventions to alter glymphatic exchange that may offer a novel therapeutic approach to those suffering from poor sleep and prolonged symptoms after mTBI.
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