急性缺血性脑卒中患者静脉溶栓后发生早期神经功能恶化的研究进展

Research Progress on Early Neurological Deterioration after Intravenous Thrombolysis in Patients with Acute Ischemic Stroke

摘要: 本综述全面回顾了急性缺血性脑卒中患者在静脉溶栓治疗后发生早期神经功能恶化(END)的研究进展。END是静脉溶栓后常见的并发症，其发生机制复杂，包括血液流动障碍、炎症反应激活和机体平衡破坏等多方面因素。END的定义和诊断标准尚未统一，目前多依据NIHSS评分进行评估，其发生率在不同患者群体中差异显著，约为5%~40%。研究表明，患者年龄、血糖、血压、心房颤动及入院时NIHSS评分等均是END的重要危险因素。此外，炎症因子和实验室指标(如C反应蛋白和血清同型半胱氨酸)也在END的发生中扮演关键角色。静脉溶栓虽然能够恢复脑部血液供应，但也可能通过增加血液粘稠度和微血栓形成导致血流再堵塞，加重脑组织损伤。目前，对END的预测多集中在单一因素的分析，缺乏综合性预测模型；对其预防和治疗也尚无统一策略，现有研究建议通过个性化评估患者病情、优化治疗方案以及使用抗氧化剂和抗炎药物进行干预，以降低END的发生率并改善患者预后，未来研究方向应包括END综合预测体系的建立、多维度病理机制的探索以及新型治疗药物的开发。

Abstract: This review comprehensively examines the research progress on early neurological deterioration (END) in patients with acute ischemic stroke after intravenous thrombolysis. END is a common complication following intravenous thrombolysis, with complex underlying mechanisms including blood flow disturbances, activation of inflammatory responses, and disruption of homeostasis. The definition and diagnostic criteria for END have not yet been unified, and currently, it is primarily assessed using the NIHSS score. The incidence of END varies significantly among different patient populations, ranging from approximately 5% to 40%. Studies have shown that patient age, blood glucose levels, blood pressure, atrial fibrillation, and NIHSS scores at admission are important risk factors for END. Additionally, inflammatory cytokines and laboratory indicators (such as C-reactive protein and serum homocysteine) also play crucial roles in the occurrence of END. While intravenous thrombolysis can restore cerebral blood flow, it may also lead to re-occlusion of blood flow by increasing blood viscosity and microthrombus formation, thereby exacerbating brain tissue damage. Currently, predictions of END mostly focus on the analysis of single factors, lacking a comprehensive predictive model. There are also no unified strategies for its prevention and treatment. Existing research suggests personalized assessments of patient conditions, optimization of treatment protocols, and the use of antioxidants and anti-inflammatory drugs for intervention to reduce the incidence of END and improve patient prognosis. Future research directions should include the establishment of a comprehensive predictive system for END, exploration of multidimensional pathological mechanisms, and the development of novel therapeutic drugs.