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将创伤性脑损伤、睡眠障碍和创伤后头痛联系起来:糖胺聚糖途径功能障碍的潜在作用。

Linking Traumatic Brain Injury, Sleep Disruption and Post-Traumatic Headache: a Potential Role for Glymphatic Pathway Dysfunction.

机构信息

Department of Pediatrics, Division of Child Neurology, Doernbecher Children's Hospital, Oregon Health & Science University, 707 SW Gaines St. CDRC-P, Portland, OR, 97239, USA.

Department of Neurology, Department of Medicine, Division of Pulmonary and Critical Care Medicine, Department of Behavioral Neuroscience, Oregon Health & Science University, Portland, OR, USA.

出版信息

Curr Pain Headache Rep. 2019 Jul 29;23(9):62. doi: 10.1007/s11916-019-0799-4.

DOI:10.1007/s11916-019-0799-4
PMID:31359173
Abstract

PURPOSE OF THE REVIEW

Traumatic brain injury (TBI) is a major public health concern in the USA and worldwide. Sleep disruption and headaches are two of the most common problems reported by patients after TBI. In this manuscript, we review the current knowledge regarding the relation between post-traumatic sleep disruption and headaches. We also describe the role of the glymphatic system as a potential link between TBI, sleep, and headaches.

RECENT FINDINGS

Recent studies show a reciprocal relation between post-traumatic sleep disruption and headaches: patients with sleep disruption after TBI report more headaches, and post-traumatic headaches are a risk factor for developing disrupted sleep. Despite this clinical association, the exact mechanisms linking post-traumatic sleep disruption and headaches are not well understood. The glymphatic pathway, a newly described brain-wide network of perivascular spaces that supports the clearance of interstitial solutes and wastes from the brain, is active primarily during sleep, and becomes dysfunctional after TBI. We propose a model where changes in glymphatic function caused by TBI and post-traumatic sleep disruption may impair the clearance of neuropeptides involved in the pathogenesis of post-traumatic headaches, such as CGRP. The relation between TBI, post-traumatic sleep disruption, and post-traumatic headaches, although well documented in the literature, remains poorly understood. Dysfunction of the glymphatic system caused by TBI offers a novel and exiting explanation to this clinically observed phenomenon. The proposed model, although theoretical, could provide important mechanistic insights to the TBI-sleep-headache association.

摘要

目的综述

颅脑损伤(TBI)是美国和全球范围内的一个主要公共卫生问题。睡眠障碍和头痛是 TBI 患者报告的两个最常见问题。在本文中,我们回顾了 TBI 后睡眠障碍和头痛之间关系的现有知识。我们还描述了糖质系统作为 TBI、睡眠和头痛之间潜在联系的作用。

最新发现

最近的研究表明 TBI 后睡眠障碍和头痛之间存在相互关系:TBI 后睡眠障碍的患者报告更多的头痛,而 TBI 后头痛是睡眠障碍的发展的风险因素。尽管存在这种临床关联,但将 TBI 后睡眠障碍和头痛联系起来的确切机制尚不清楚。糖质系统是一个新描述的脑周血管空间网络,支持脑内间质溶质和废物的清除,主要在睡眠期间活跃,TBI 后功能失调。我们提出了一个模型,认为 TBI 和 TBI 后睡眠障碍引起的糖质系统功能改变可能会损害参与 TBI 后头痛发病机制的神经肽的清除,如 CGRP。TBI、TBI 后睡眠障碍和 TBI 后头痛之间的关系尽管在文献中有充分记载,但仍知之甚少。TBI 引起的糖质系统功能障碍为这一临床观察现象提供了一个新颖而令人兴奋的解释。虽然该模型是理论性的,但它可以为 TBI-睡眠-头痛关联提供重要的机制见解。

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Accumulation of Cerebrospinal Fluid, Ventricular Enlargement, and Cerebral Folate Metabolic Errors Unify a Diverse Group of Neuropsychiatric Conditions Affecting Adult Neocortical Functions.脑脊液蓄积、脑室扩大和脑叶酸代谢错误将影响成人新皮质功能的一大类神经精神疾病统一起来。
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