穿支动脉粥样硬化病

1、BAD Related Ischemic Stroke朱佳佳-8-31第1页进展性卒中END24二分之一病因还未明确，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%第2页进展性腔梗But in 2030% 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 i

2、mportant disability.第3页Lacunar Stroke Is the Major Cause of Progressive Motor Deficits第4页Progressive 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 w

3、as 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.第5页SSSI（孤立皮层下小梗死

4、）第6页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.第7页Branch atheromatous disease and its associati

5、on with progressive motor deficits第8页BAD第9页BAD亚洲国家多发，研究集中于日本、韩国；早期END百分比较高；缺乏统一定义，当前诊疗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，危险原因无显著差异。第10页概念由主干动脉分出穿通支入口部发生动脉粥样硬化引发狭窄或闭塞。强调这种梗塞在病理上与高血压所致脂质透明变性不一样, 而以动脉粥样硬化为主要改变。第11页BAD病理机制A 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Caplan LR. Intracranial bran

6、ch atheromatous disease: A neglected, understudied, and underused concept, Neurology 1989第12页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第13页第14页临床表现以运动障碍为主要表现；急性期症状波动、重复；急性期症状加重、病灶逐步扩大病例多见。第15

7、页High-resolution MRI findings in patients withcapsular warning syndrome第16页Capsular warning syndromeThe exact pathogenic mechanism of CWS has not been fully understood. Various mechanisms have suggested, including small vessel disease, embolism from the heart, vasospasm, peri-infarct depolarization,

8、 and, in rare instances, atherosclerotic disease of the MCA.Small perforator artery disease is proposed to be the most common cause of the CWS. Recently, more studies suggested that intracranial atherosclerotic disease plays an important role in the development of small stratiocapsular infarct, espe

9、cially in Asian.The fluctuating course of stereotyped symptoms was thought to be the result of hemodynamic compromise due to the origin occlusion.第17页BAD诊疗标准1 豆纹动脉供血区BAD型梗死： 水平位头颅MRI上梗死灶达三个层面以上2 脑桥旁正中动脉供血区BAD型梗死： 梗死灶与脑桥腹侧表面相接、向被盖部延 伸扇形病灶。3 支配病灶区主干动脉无严重狭窄(50%) 或闭塞，无显著心源性栓子起源。北川一夫，脳卒中 ;31(6)：552陈谅.Bra

10、nch atheromatous disease.日本医学介绍 年第28 卷第2 期第18页Clinical Evaluation of LI and BADLI was defined as an intracerebral lesion ,15 mm in diameter and fewer than 3 slices or a lesion within the pontine parenchyma. BAD was defined as an intracerebral lesion of 15mmin diameter and more than 3 slices or a les

11、ion extending to the surface of the pontine base observed on diffusion-weighted magnetic resonance imaging.第19页Clinical Evaluation of LI and BAD第20页BAD 与 大动脉狭窄堵塞穿支父辈动脉有没有严重狭窄；临床危险因素、波动/进展等难以鉴别。第21页进展机制血栓延伸；局部低灌注、侧支循环不良；血脑屏障破坏、内皮细胞功效障碍；炎症、水肿。第22页The Impact of Diagnosing Branch Atheromatous Disease fo

12、r Predicting PrognosisNeurologic worsening was observed at a significantly higher rate in BAD compared with the LI patients in both the LSA and PPA groups (45.1% versus 22.6% and 46.7% versus 0%). In the LSA group, the enlargement of the ischemic lesion was significantly more frequent in BAD compare

13、d with the LI patients (66.2% and 34.0%). There was a significant relation between the enlargement of the lesion and the worsening of neurologic deficits. Moreover, the clinical features, which predict the lesion enlargement, were BAD and older age.第23页Different Characteristics of Anterior and Poste

14、rior BAD with or without END高龄、女性、肥胖第24页Predictive factors for progressive motor deficits in penetrating artery infarctions in two different arterial territoriesThe female sex and initial NIHSS score 5 or more persist significant after multivariate analysis for both groups. The specific independent

15、predictive factors for the LSA group were single infarcts without concomitant silent lacunar infarcts and preceding lacunar TIAs; and those for the APA group was diabetes mellitus.第25页Lipid and hyperglycemia factors in first-everpenetrating artery infarction, a comparison between different subtypes第

16、26页治疗快速波动、早期进展，治疗难度大；双抗血小板；抗凝治疗；静脉溶栓；IIb/IIIa；鸡尾酒疗法。第27页Stuttering Lacunes: An Acute Role for Clopidogrel?双抗血小板预防作用？第28页Cilostazol for the Prevention of BAD第29页双抗优于单抗第30页Treatment of Progressive Stroke withTirofiban Experience in 35 Patients 第31页Safety and Preliminary Efficacy of Early TirofibanTrea

17、tment After Alteplase in Acute Ischemic Stroke Patients绝大部分入选患者是穿支血管病变Alteplase (0.9mg/kg) thrombolysis immediately followed byintravenous tirofiban infusion.Tirofiban was administered in a body-weight-adjusted dosage with a bolus of 0.4 g/kg body weight perminute for 30 minutes followed by a continuous infusion of 0.1g/kg body weight per minute for at least 24 hours.第32页Safety and Preliminary Efficacy of Early TirofibanTreatment After Alteplase in Acute Ischemic Stroke Patients第33页第3