Department of Neurology, Medical School of Hannover, Germany.
Ann N Y Acad Sci. 2010 Oct;1207:116-22. doi: 10.1111/j.1749-6632.2010.05738.x.
Infections after ischemic stroke are known to complicate the clinical course and worsen the outcome. Neuroinflammation is one of the predominant mechanisms of secondary progression of brain injury and infection and is far from being well understood. Experimental data demonstrate that ischemic stroke patients are at a higher risk for systemic infections if they show a pronounced anti-inflammatory response after the event, which is considered an indication of a stress-mediated reduction of immune competence. Only a small number of studies describe the time course of inflammation mediators after ischemic stroke in patients with early poststroke infections. Levels of inflammation mediators after the event of stroke differ, depending on clinical severity and concomitant infectious diseases. Thus, sequential dynamics of early inflammation must be considered in the development of both mechanism-targeting anti-inflammatory and anti-infectious treatment strategies in ischemic brain damage.
感染是缺血性脑卒中的常见并发症，可使临床病程恶化，预后变差。神经炎症是脑损伤和感染继发进展的主要机制之一，但目前人们对此仍知之甚少。实验数据表明，如果缺血性脑卒中患者在事件发生后表现出明显的抗炎反应，他们发生全身感染的风险更高，这被认为是应激导致免疫能力下降的一个迹象。只有少数研究描述了早期脑卒中后感染患者的炎症介质在缺血性脑卒中后的时间进程。炎症介质的水平因临床严重程度和并发感染性疾病的不同而有所差异。因此，在缺血性脑损伤的靶向抗炎和抗感染治疗策略的开发中，必须考虑早期炎症的动态变化。
