The Relationship between Cerebral Vasoreactivity and Post-Concussive Symptom Severity
The Relationship between Cerebral Vasoreactivity and Post-Concussive Symptom Severity
复制标题
DOI：
10.1089/neu.2017.5060
复制
发表时间：
2017-10-01
影响因子：
4.2
通讯作者：
Tan, Can Ozan
中科院分区：
文献类型：
--
作者：
Albalawi, Tamadher;Hamner, Jason W.;Tan, Can Ozan
虽然脑震荡后症状负担的病理生理学尚不清楚，但数据表明脑血管功能障碍可能是罪魁祸首之一。我们试图确定脑血管缓冲动脉气体变化（血管反应性）的能力受损程度是否与脑震荡症状相关。在15名被诊断为脑震荡的参与者（19 +/- 5岁，受伤后1周至1年）中，我们从逐搏大脑中动脉血流速度（经颅多普勒超声）与潮气末CO2（空气再呼吸）进行性增加期间潮气末CO2的线性关系的斜率评估血管反应性。使用脑震荡后症状量表评估症状负担。随后，我们通过线性模型探讨了血管反应性与脑震荡后头痛严重程度和认知困难之间的关系。在再呼吸期间，CO2从32.6 +/- 1.6增加到46.8 +/- 1.8mmHg，脑血管传导（即，流速/压力）从0.48 +/- 0.04增加到0.74 +/- 0.06 cms（-1）mmHg（-1）。在CO2的增加和电导率的增加之间存在强线性关系（R-2 = 0.81 +/- 0.05; p < 0.05）。平均而言，脑血管反应性为0.018 +/- 0.003 cm（-1）s（-1）mmHg CO2-1。尽管渐进参与者的血管反应性倾向于略高（0.019 +/- 0.003 vs. 0.015 +/- 0.005 cm（-1）s（-1）mmHg CO2-1），但该差异无统计学显著性（p = 0.48）。血管反应性越高，头痛越严重（R-2 = 0.57; p < 0.01），认知症状越差（R-2 = 0.71; p < 0.01）。因此，脑血管反应性与脑震荡后头痛和认知症状负担密切相关。这对于理解脑震荡后症状负担的病理生理学和设计有效的治疗方案具有重要意义。
While pathophysiology underlying post-concussion symptom burden is unknown, data suggest that cerebrovascular dysfunction may be among the culprits. We sought to determine whether the degree of impairment in the ability of cerebrovasculature to buffer against changes in arterial gases (vasoreactivity) is associated with concussion symptoms. In 15 participants (19 +/- 5 years, 1 week to 1 year post-injury) diagnosed with concussion, we assessed vasoreactivity from the slope of the linear relationship of beat-by-beat middle cerebral artery blood flow velocity (transcranial Doppler ultrasound) to end-tidal CO2 during progressive increases in end-tidal CO2 (air rebreathing). Symptom burden was assessed using the Post-Concussion Symptom Scale. Subsequently, we explored the relationship between vasoreactivity and the severity of post-concussion headache and cognitive difficulties by linear models. During rebreathing, CO2 increased from 32.6 +/- 1.6 to 46.8 +/- 1.8mmHg and cerebrovascular conductance (i.e., flow velocity over pressure) increased from 0.48 +/- 0.04 to 0.74 +/- 0.06 cms(-1) mmHg(-1). There was a strong linear relationship between the increase in CO2 and in conductance (R-2 = 0.81 +/- 0.05; p < 0.05). On average, cerebral vasoreactivity was 0.018 +/- 0.003 cm(-1) s(-1) mmHg CO2-1. Although vasoreactivity tended to be somewhat higher in the asymptotic participants (0.019 +/- 0.003 vs. 0.015 +/- 0.005 cm(-1) s(-1) mmHg CO2-1), this difference was not statistically significant (p = 0.48). Higher vasoreactivity was strongly associated with more severe headaches (R-2 = 0.57; p < 0.01) and worse cognitive symptoms (R-2 = 0.71; p < 0.01). Thus, cerebral vasoreactivity relates strongly to post-concussive headache and cognitive symptom burden. This has significant implications for understanding the pathophysiology underlying post-concussive symptom burden and for devising effective treatment options.