Gyawali Prajwal, Hinwood Madeleine, Chow Wei Zhen, Kluge Murielle, Ong Lin Kooi, Nilsson Michael, Walker Frederick Rohan
School of Biomedical Sciences and Pharmacy and Priority Research Centre for Stroke and Brain Injury, The University of Newcastle, Callaghan, NSW, Australia.
Hunter Medical Research Institute, New Lambton Heights, NSW, Australia.
Brain Behav Immun Health. 2020 Oct 9;9:100157. doi: 10.1016/j.bbih.2020.100157. eCollection 2020 Dec.
The precise mechanisms underlying the aetiology of post-stroke fatigue remain poorly understood. Inflammation has been associated with clinically significant fatigue across a number of neurological disorders; however, at present there is a lack of evidence regarding the association of fatigue and inflammation in the chronic phase of stroke recovery.
The aim of this study was to examine fatigue in a cohort of stroke survivors in the chronic phase of stroke, compared with matched controls, and to explore associations between the pro-inflammatory cytokine interleukin-6, high-sensitivity C-reactive Protein and fatigue.
We performed an exploratory cross-sectional study of 70 people in the chronic phase of stroke recovery, and 70 age matched controls. Fatigue was assessed using the Fatigue Assessment Scale. Interleukin-6 was measured in serum using a commercially available enzyme immunoassay kit. Both outcome measures were assessed contemporaneously.
Clinically significant fatigue, defined as a score ≥24 on the Fatigue Assessment Scale, was reported by 60% of stroke survivors, and 15.7% of controls. The odds of experiencing clinically significant fatigue was 8.04 times higher among stroke survivors compared to control participants (odds ratio 8.045; 95% CI: 3.608, 17.939; < 0.001). The fatigue score was significantly correlated with the level of both interleukin-6 and high-sensitivity c-reactive protein, however once entered into a linear regression model with cardiovascular covariables, this relationship was no longer statistically significant.
This study shows that fatigue may be associated with systemic inflammation in the chronic phase of stroke. The pathological mechanisms underlying post-stroke fatigue and its clinical implications require further study.
中风后疲劳的病因的确切机制仍知之甚少。炎症与多种神经系统疾病中具有临床意义的疲劳有关;然而,目前缺乏关于中风恢复慢性期疲劳与炎症之间关联的证据。
本研究的目的是在中风慢性期的一组中风幸存者中检测疲劳情况,并与匹配的对照组进行比较,同时探讨促炎细胞因子白细胞介素-6、高敏C反应蛋白与疲劳之间的关联。
我们对70名处于中风恢复慢性期的患者和70名年龄匹配的对照组进行了一项探索性横断面研究。使用疲劳评估量表评估疲劳情况。使用市售酶免疫分析试剂盒测定血清中的白细胞介素-6。这两种结果指标均同时进行评估。
60%的中风幸存者报告有临床显著疲劳,定义为疲劳评估量表得分≥24分,而对照组为15.7%。与对照组参与者相比,中风幸存者出现临床显著疲劳的几率高8.04倍(优势比8.045;95%置信区间:3.608,17.939;P<0.001)。疲劳得分与白细胞介素-6和高敏C反应蛋白水平均显著相关,然而,一旦将心血管协变量纳入线性回归模型,这种关系就不再具有统计学意义。
本研究表明,疲劳可能与中风慢性期的全身炎症有关。中风后疲劳的病理机制及其临床意义需要进一步研究。