Department of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX, USA.
Cell Mol Neurobiol. 2023 Dec 19;44(1):7. doi: 10.1007/s10571-023-01437-2.
Stroke is the third leading cause of death and long-term disability in the world. Considered largely a disease of aging, its global economic and healthcare burden is expected to rise as more people survive into advanced age. With recent advances in acute stroke management, including the expansion of time windows for treatment with intravenous thrombolysis and mechanical thrombectomy, we are likely to see an increase in survival rates. It is therefore critically important to understand the complete pathophysiology of ischemic stroke, both in the acute and subacute stages and during the chronic phase in the months and years following an ischemic event. One of the most clinically relevant aspects of the chronic sequelae of stroke is its extended negative effect on cognition. Cognitive impairment may be related to the deterioration and dysfunctional reorganization of white matter seen at later timepoints after stroke, as well as ongoing progressive neurodegeneration. The vasculature of the brain also undergoes significant insult and remodeling following stroke, undergoing changes which may further contribute to chronic stroke pathology. While inflammation and the immune response are well established drivers of acute stroke pathology, the chronicity and functional role of innate and adaptive immune responses in the post-ischemic brain and in the peripheral environment remain largely uncharacterized. In this review, we summarize the current literature on post-stroke injury progression, its chronic pathological features, and the putative secondary injury mechanisms underlying the development of cognitive impairment and dementia. We present findings from clinical and experimental studies and discuss the long-term effects of ischemic stroke on both brain anatomy and functional outcome. Identifying mechanisms that occur months to years after injury could lead to treatment strategies in the chronic phase of stroke to help mitigate stroke-associated cognitive decline in patients.
中风是全球第三大致死原因和长期残疾原因。鉴于其主要是一种老年病，随着越来越多的人进入高龄，其全球经济和医疗保健负担预计将会增加。由于急性中风管理方面的最新进展，包括静脉溶栓和机械取栓治疗时间窗的扩大，我们可能会看到存活率的提高。因此，了解缺血性中风的完整病理生理学，包括在急性和亚急性期以及在缺血事件发生后的数月和数年内的慢性期，至关重要。中风慢性后遗症中最具临床相关性的方面之一是其对认知功能的长期负面影响。认知障碍可能与中风后较晚时间点所见的白质恶化和功能障碍重组有关，以及持续的进行性神经退行性变。中风后大脑的脉管系统也会受到严重损伤和重塑，发生的变化可能进一步导致慢性中风病理。尽管炎症和免疫反应是急性中风病理的明确驱动因素，但先天和适应性免疫反应在缺血后大脑和外周环境中的慢性和功能作用在很大程度上仍未得到充分描述。在这篇综述中，我们总结了中风后损伤进展、其慢性病理特征以及认知障碍和痴呆发展背后假定的继发损伤机制的最新文献。我们展示了临床和实验研究的发现，并讨论了缺血性中风对大脑解剖结构和功能结果的长期影响。确定在损伤后数月至数年发生的机制可能会导致中风慢性期的治疗策略，以帮助减轻中风患者的认知能力下降。
