A Precision Medicine Approach to Cerebral Edema and Intracranial Hypertension after Severe Traumatic Brain Injury: Quo Vadis?
A Precision Medicine Approach to Cerebral Edema and Intracranial Hypertension after Severe Traumatic Brain Injury: Quo Vadis?
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DOI：
10.1007/s11910-018-0912-9
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发表时间：
2018-11-07
影响因子：
5.6
通讯作者：
Kochanek PM
中科院分区：
文献类型：
--
作者：
Jha RM;Kochanek PM
用于治疗严重TBI后的脑水肿和颅内高压的标准临床方案在过去几十年中保持非常相似。脑水肿和颅内高压可互换治疗，实际上颅内压（ICP）不仅代表脑水肿，也代表其他过程，如肿块病变程度、脑积水或脑血容量。多种分子机制的复杂相互作用导致严重TBI后的脑水肿，并且这些不能通过当前临床可用的工具测量或靶向。解决这些基础可能是预防或治疗脑水肿和改善严重TBI后结果的关键。本文首先概述了水肿和ICP之间关系的基本原则，包括Monro-Kellie学说和颅内顺应性/弹性的概念。随后简要讨论了国际比较方案监测/管理的现行准则。然后，我们将大部分的审查集中在一个不断发展的精确医学方法对脑水肿和颅内高压后TBI。个性化的侵入性神经监测参数，包括ICP波形分析，脉冲幅度，压力反应，和纵向轨迹。随后讨论脑水肿亚型（离子性/细胞毒性/血管源性水肿和进行性继发性出血的连续体）。本文综述了脑外伤后脑水肿的分子机制。对于每一个目标，我们提出了从临床前模型的研究结果，并评估其作为生物标志物和脑水肿减少的治疗目标的临床效用。这一选择代表了有希望的候选人，来自不同研究小组的证据，与其他途径的重叠/相互关联，以及临床/翻译潜力。我们概述了一个不断发展的精确医学和翻译方法对脑水肿和颅内高压后，严重的TBI。
Standard clinical protocols for treating cerebral edema and intracranial hypertension after severe TBI have remained remarkably similar over decades. Cerebral edema and intracranial hypertension are treated interchangeably when in fact intracranial pressure (ICP) is a proxy for cerebral edema but also other processes such as extent of mass lesions, hydrocephalus, or cerebral blood volume. A complex interplay of multiple molecular mechanisms results in cerebral edema after severe TBI, and these are not measured or targeted by current clinically available tools. Addressing these underpinnings may be key to preventing or treating cerebral edema and improving outcome after severe TBI. This review begins by outlining basic principles underlying the relationship between edema and ICP including the Monro-Kellie doctrine and concepts of intracranial compliance/elastance. There is a subsequent brief discussion of current guidelines for ICP monitoring/management. We then focus most of the review on an evolving precision medicine approach towards cerebral edema and intracranial hypertension after TBI. Personalization of invasive neuromonitoring parameters including ICP waveform analysis, pulse amplitude, pressure reactivity, and longitudinal trajectories are presented. This is followed by a discussion of cerebral edema subtypes (continuum of ionic/cytotoxic/vasogenic edema and progressive secondary hemorrhage). Mechanisms of potential molecular contributors to cerebral edema after TBI are reviewed. For each target, we present findings from preclinical models, and evaluate their clinical utility as biomarkers and therapeutic targets for cerebral edema reduction. This selection represents promising candidates with evidence from different research groups, overlap/inter-relatedness with other pathways, and clinical/translational potential. We outline an evolving precision medicine and translational approach towards cerebral edema and intracranial hypertension after severe TBI.
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影响因子：
15.1
作者：
Cui J;Chen S;Zhang C;Meng F;Wu W;Hu R;Hadass O;Lehmidi T;Blair GJ;Lee M;Chang M;Mobashery S;Sun GY;Gu Z
通讯作者：
Gu Z
DOI：
10.12659/msm.898190
发表时间：
2016-12-08
期刊：
Medical science monitor : international medical journal of experimental and clinical research
影响因子：
--
作者：
Chen JQ;Zhang CC;Jiang SN;Lu H;Wang W
通讯作者：
Wang W
影响因子：
38.9
作者：
Badri, Shide;Chen, Jasper;Treggiari, Miriam M.
通讯作者：
Treggiari, Miriam M.
影响因子：
4.1
作者：
Bullock, R;Zauner, A;Young, HF
通讯作者：
Young, HF
影响因子：
4.8
作者：
Carney, Nancy;Totten, Annette M.;Ghajar, Jamshid
通讯作者：
Ghajar, Jamshid