It might be time to let cooler heads prevail after mild traumatic brain injury or concussion.
It might be time to let cooler heads prevail after mild traumatic brain injury or concussion.
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在轻度脑外伤或脑震荡之后，也许是时候让冷静的头脑占上风了。
DOI：
10.1016/j.expneurol.2015.02.019
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发表时间：
2015
影响因子：
5.3
通讯作者：
Jackson,TravisC
中科院分区：
文献类型：
--
作者：
Kochanek,PatrickM;Jackson,TravisC
在医学上，很少有条件比轻度创伤性脑损伤（mTBI）或脑震荡更能引起人们的兴趣。几十年来，对TBI的病理生物学和治疗的研究经常被神经科学界视为“太混乱而无法理解”或“缺乏解剖损伤和行为后果之间的明确关系”，并且主要由数量有限的专门研究小组进行，主要是（尽管不是唯一的）集中于严重TBI的挑战性问题。然而，已经认识到在诸如运动性脑震荡或战斗伤员护理的环境中mTBI的急性和亚急性后果代表了巨大的公共卫生问题，以及最近认识到mTBI和/或重复性mTBI可以作为神经变性疾病谱中的许多重要病症的发展或恶化的隐性触发因素，所述神经变性疾病包括阿尔茨海默病、帕金森病、肌萎缩性侧索硬化、慢性创伤性脑病以及可能的其他病症，已经产生了令人感兴趣的大漩涡，并且对于TBI领域，临床前和临床研究都是早就应该进行的（DeKosky等人，2013年，Robertson等人，2014年，Skolnick等人，2014年，Smith等人，2013年，Kochanek等人，2015年）。mTBI领域的这种顿悟产生了具有许多新认识的研究的黄金时代，以及开发新疗法的令人兴奋的潜在机会，并且部分地受到对该研究的财政支持的欢迎激增的驱动，特别是来自美国陆军和国立卫生研究院（Diaz-Arrastia et al.，2014 a，Diaz-Arrastia等人，2014 b，Kochanek等人，2011年，McMahon等人，2014年）。因此，对于跨TBI的严重性和表型谱的新疗法的成功开发存在新的希望，其将降低目前观察到的急性和慢性发病率和/或死亡率，并且还用于鉴定可能阻止TBI后慢性神经退行性疾病发展的疗法。在这一期的《实验神经学》中，Titus及其同事（Titus等人，2015），来自道尔顿·迪特里希博士的实验室，几十年来，他一直是实验性脑损伤低温领域的领先研究者，为我们提供了另一个合乎逻辑、简单且有点可怕的mTBI观察结果--但可能会产生相当大的临床后果。
Few conditions in medicine have garnered more recent interest in the lay press than mild traumatic brain injury (mTBI) or concussion. For decades, investigation into the pathobiology and therapy of TBI has often been viewed by the neuroscience community as “too messy to understand” or “lacking a clear relationship between anatomical injury and behavioral consequences” and has been carried out largely by a limited number of dedicated investigative groups, primarily (albeit not exclusively) focused on the challenging problem of severe TBI.However, the acute and sub-acute consequences of mTBI in settings such as sports concussion or combat casualty care have been recognized to represent an enormous public health problem, and the recent realization that mTBI and/or repetitive mTBI may serve as occult triggers to the development or exacerbation of a number of important conditions across the spectrum of neurodegenerative disease including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, chronic traumatic encephalopathy, and possibly others, has produced a maelstrom of interest and both pre-clinical and clinical investigation that–for the field of TBI—is long overdue (DeKosky et al., 2013, Robertson et al., 2014, Skolnick et al., 2014, Smith et al., 2013, Kochanek et al., 2015). This epiphany in the field of mTBI has produced a golden age of investigation with many new realizations, and exciting potential opportunities to develop novel therapies, and has been driven in part by a welcome surge in financial support for this research particularly from both the United States Army, and the National Institutes of Health (Diaz-Arrastia et al., 2014a, Diaz-Arrastia et al., 2014b, Kochanek et al., 2011, McMahon et al., 2014). There is, thus, new hope for the successful development of novel therapies across the severity and phenotypic spectra of TBI that will reduce the acute and chronic morbidity, and/or mortality that is currently observed, and also for the identification of therapies that might stop chronic neurodegenerative diseases from developing after TBI. In this issue of Experimental Neurology, Titus and co-workers (Titus et al., 2015), from the laboratory of Dr. Dalton Dietrich, who has been a leading investigator in the area of hypothermia in experimental brain injury for decades, provide us with another logical, simple, and somewhat frightening observation in mTBI—yet one that might have considerable clinical consequence.