脑卒中后疲劳的病因:综述和涉及致炎因子的假设

脑卒中后疲劳不是一种单一致病因素疾患。脑卒中后疲劳一般认为系中枢性疲劳的一种,而影响基底节、丘脑、边缘系统和高级皮质中枢通路的代谢性和结构性病灶均可参与中枢性疲劳的发生,目前尚没有证据明确疲劳源于哪些脑区的受累。致炎因子,主要包括白细胞介素(IL)-1、肿瘤坏死因子(TNF)-α、IL-6与疲劳间可能存在相互作用。认为脑卒中后疲劳的产生与致炎因子促发的疾病行为有关;其物理方面的疲劳机制可能源于致炎因子对下丘脑-垂体-肾上腺素轴的活化作用;其心理方面,有推断提出致炎因子通过减弱星形神经胶质清除细胞外谷氨酸的能力参与精神疲劳的病理生理过程。

Etiology of Poststroke Fatigue: Review of Literature and Hypothesis Involving Inflammatory Cytokines

Poststroke fatigue is not a single etiology disorder.As a kind of central fatigue,the basal ganglia,thalamencephalon,limbic system and the high grade cortical area man be involved,but none of them can be identified as the fatigue area.Some literature suggest the interrelationship between the proinflammatory cytokines,such as IL-1,TNF-α,IL-6,and fatigue.Since the pathologic process of stroke involving cytokines,the researchers proposed that poststroke fatigue may be related to sickness behavior promoted by proinflammatory cytokines ultimately.The physical fatigue may be associated with the proinflammatory cytokines's activation to hypothalamic-pituitary-adrenal axis,and the psychological fatigue may involve that proinflammatory cytokines decreased the clearance of extracellular glutamate by astroglia.