Elevated markers of brain injury as a result of clinically asymptomatic high-acceleration head impacts in high-school football athletes
Elevated markers of brain injury as a result of clinically asymptomatic high-acceleration head impacts in high-school football athletes
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DOI：
10.3171/2017.12.jns172386
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发表时间：
2019-05-01
影响因子：
4.1
通讯作者：
Broglio, Steven P.
中科院分区：
文献类型：
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作者：
Joseph, Jacob R.;Swallow, Jennylee S.;Broglio, Steven P.
目的：对高中橄榄球运动员进行前瞻性观察队列研究，以确定不会导致临床诊断为脑震荡的高加速度头部撞击（HHI）是否仍会导致无症状运动员血清中指示创伤性脑损伤（TBI）的生物标志物水平升高，并确定这些生物标志物在橄榄球赛季过程中的纵向分布。对学校橄榄球运动员进行基线神经认知测试和血液采样，以检测生物标志物tau、泛素C末端水解酶L1（UCH-L1）、神经丝轻蛋白（NF-L）、胶质细胞酸性蛋白（GFAP）和血影蛋白分解产物（SBDP）。所有运动员都戴着头盔加速度计，以测量和记录所有练习和比赛期间的头部撞击数据。在赛季的不同时间点，这些运动员中有6名符合HHI的标准（线性加速度> 95 g和旋转加速度> 3760 rad/sec（2））;在这些运动员中，在发生HHI的运动项目结束时抽取了第二份血样。五名不符合HHI标准的运动员在本赛季最后一场比赛后接受了重复血液采样。在一项单独的分析中，所有在赛季中没有接受脑震荡诊断的运动员（n = 12）在赛季结束后接受了重复的神经认知测试和血液采样。而未接受HHI的运动员为164%+/-35%（p = 0.03）。同样，HHI后运动员的UCH-L1水平增加了738.2%+/-163.3%，而没有HHI的运动员则增加了237.7%+/-71.9%（p = 0.03）。在赛季结束时，研究人员发现tau水平增加了0.6 +/-0.2 pg/ml（p = 0.003），UCH-L1水平增加了144.3 +/-56 pg/ml（p = 0.002）。在基线和运动项目结束或赛季结束采样之间没有观察到血清NF-L、GFAP或SBDP的显著升高（对于所有，p> 0.05）。结论在这项对无症状足球运动员的初步研究中，与对照运动员的值相比，HHI与神经元（UCH-L1）和轴突（tau）损伤的标记物增加相关。在橄榄球赛季之后，这些相同的标记物在非脑震荡运动员中也有所增加。
OBJECTIVE This prospective observational cohort study of high-school football athletes was performed to determine if high-acceleration head impacts (HHIs) that do not result in clinically diagnosed concussion still lead to increases in serum levels of biomarkers indicating traumatic brain injury (TBI) in asymptomatic athletes and to determine the longitudinal profile of these biomarkers over the course of the football season.METHODS Sixteen varsity high-school football athletes underwent baseline neurocognitive testing and blood sampling for the biomarkers tau, ubiquitin C-terminal hydrolase L1 (UCH-L1), neurofilament light protein (NF-L), glial fibrillary acidic protein (GFAP), and spectrin breakdown products (SBDPs). All athletes wore helmet-based accelerometers to measure and record head impact data during all practices and games. At various time points during the season, 6 of these athletes met the criteria for HHI (linear acceleration > 95g and rotational acceleration > 3760 rad/sec(2)); in these athletes a second blood sample was drawn at the end of the athletic event during which the HHI occurred. Five athletes who did not meet the criteria for HHI underwent repeat blood sampling following the final game of the season. In a separate analysis, all athletes who did not receive a diagnosis of concussion during the season (n = 12) underwent repeat neurocognitive testing and blood sampling after the end of the season.RESULTS Total tau levels increased 492.6% +/- 109.8% from baseline to postsession values in athletes who received an HHI, compared with 164% +/- 35% in athletes who did not receive an HHI (p = 0.03). Similarly, UCH-L1 levels increased 738.2% +/- 163.3% in athletes following an HHI, compared with 237.7% +/- 71.9% in athletes in whom there was no HHI (p = 0.03). At the end of the season, researchers found that tau levels had increased 0.6 +/- 0.2 pg/ml (p = 0.003) and UCH-L1 levels had increased 144.3 +/- 56 pg/ml (p = 0.002). No significant elevations in serum NF-L, GFAP, or SBDPs were seen between baseline and end-of-athletic event or end-of-season sampling (for all, p > 0.05).CONCLUSIONS In this pilot study on asymptomatic football athletes, an HHI was associated with increased markers of neuronal (UCH-L1) and axonal (tau) injury when compared with values in control athletes. These same markers were also increased in nonconcussed athletes following the football season.