穿支动脉粥样硬化病课件.pptx

BAD Related Ischemic Stroke朱佳佳2017-8-31进展性卒中END24一半病因尚未明确，发生率13.8%（24h内再通，4分）；大动脉粥样硬化性31%，心源性23%，腔梗9%进展性腔梗But in 20–30% of patients with LS, neurological deficits worsen in hours or even days following stroke onset.Deterioration involves especially motor function and often terminates leaving an important disability.Lacunar Stroke Is the Major Cause of Progressive Motor DeficitsProgressive Motor DeficitsPMD was defined as an increase of at least 2 points on the motor item of the NIHSS score persisting for at least 24 hours within 5 days of stroke onset.Deep perforating artery infarct was more frequently associated with PMD (35.8%) compared with large artery disease (27.3%) and cardioembolism (5.3%). Multiple logistic analysis found that deep perforating artery infarct was independently associated with PMD. Deep perforating artery infarct is the major cause of PMD.SSSI（孤立皮层下小梗死）Neuroimaging Markers for END in SSSIEarly neurological deterioration (END) occurs in ≥20% of single small subcortical infarctions.Patients with relevant artery stenosis and branch atheromatous lesions had significantly higher odds of exhibiting END.Branch atheromatous disease and its association with progressive motor deficitsBADBAD亚洲国家多发，研究集中于日本、韩国；早期END比例较高；缺乏统一定义，目前诊断主要依赖梗死灶分布、大小、形态；高分辨MRI研究较少；与大动脉粥样硬化性比较，危险因素无显著差异。概念由主干动脉分出的穿通支入口部发生动脉粥样硬化引起的狭窄或闭塞。强调这种梗塞在病理上与高血压所致的脂质透明变性不同, 而以动脉粥样硬化为主要的改变。BAD的病理机制Caplan LR. Intracranial branch atheromatous disease: A neglected, understudied, and underused concept, Neurology 1989A 主干动脉斑块堵塞分 支动脉入口B 主干动脉斑块延伸到 分支动脉结合部斑 块C 分支动脉入口处斑块A BAD，病灶延伸到脑桥腹侧表面B 脂质透明变性脑桥腔隙性脑梗死。Caplan LR. Intracranial branch atheromatous disease: A neglected, understudied, and underused concept, Neurology 1989临床表现以运动障碍为主要表现；急性期症状波动、反复；急性期症状加重、病灶逐渐扩大的病例多见。High-resolution MRI findings in patients withcapsular warning syndromeCapsular warning syndromeThe exact pathogenic mechanism of CWS has not been fully understood. Various mechanisms have suggested, including small vessel disease, embolism