Concussion history in rugby union players is associated with depressed cerebrovascular reactivity and cognition.
Concussion history in rugby union players is associated with depressed cerebrovascular reactivity and cognition.
复制标题
橄榄球联盟球员的脑震荡史与脑血管反应性和认知能力下降有关。
DOI:
10.1111/sms.14046
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发表时间:
2021
期刊:
影响因子:
--
通讯作者:
and Damian M. Bailey.
中科院分区:
文献类型:
--
作者:
Thomas S. Owens;Thomas A. Calverley;Benjamin S. Stacey;George A. Rose;Lewis Fall;Hayato Tsukamoto;Gareth L. Jones;Robin Corkill;Edouard Tuaillon;Christophe Hirtz;Sylvain Lehmann;Nicola Marchi;Christopher J. Marley;and Damian M. Bailey.
Recurrent contact and concussion in rugby union remains a significant public health concern given the potential increased risk of neurodegeneration in later life. This study determined to what extent prior‐recurrent contact impacts molecular‐hemodynamic biomarkers underpinning cognition in current professional rugby union players with a history of concussion. Measurements were performed in 20 professional rugby union players with an average of 16 (interquartile range [IQR] 13–19) years playing history reporting 3 (IQR 1–4) concussions. They were compared to 17 sex‐age‐physical activity‐and education‐matched non‐contact controls with no prior history of self‐reported concussion. Venous blood was assayed directly for the ascorbate free radical (A•−electron paramagnetic resonance spectroscopy) nitric oxide metabolites (NO reductive ozone‐based chemiluminescence) and select biomarkers of neurovascular unit integrity (NVU chemiluminescence/ELISA). Middle cerebral artery blood flow velocity (MCAv doppler ultrasound) was employed to determine basal perfusion and cerebrovascular reactivity (CVR) to hyper/hypocapnia (). Cognition was assessed by neuropsychometric testing. Elevated systemic oxidative‐nitrosative stress was confirmed in the players through increased A•−(p< 0.001) and suppression of NO bioavailability (p< 0.001). This was accompanied by a lower CVR range (;p= 0.045) elevation in neurofilament light‐chain (p= 0.010) and frontotemporal impairments in immediate‐memory (p= 0.001) delayed‐recall (p= 0.048) and fine‐motor coordination (p< 0.001). Accelerated cognitive decline subsequent to prior‐recurrent contact and concussion history is associated with a free radical‐mediated suppression of CVR and neuronal injury providing important mechanistic insight that may help better inform clinical management.