穿支动脉粥样硬化病-PPT课件.pptx

1、BAD Related Ischemic Stroke2017-8-31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 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 impo

2、rtant 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 f

3、requently 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）Neuroimagin

4、g Markers for END in SSSI Early 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 progress

5、ive 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A A 主干动脉斑块堵塞主干动脉斑块堵塞分分 支动脉入口支动脉入口B B 主干动脉斑块延伸主干动脉斑块延伸到到 分支动脉结合部分支动脉结合部斑斑 块块C C 分支动脉入口处斑分支动脉入口处斑块块Cap

6、lan LR. Intracranial branch atheromatous disease: A neglected, understudied, and underused concept, Neurology 1989A 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

7、重、病灶逐渐扩大的病例多见。High-resolution MRI findings in patients withcapsular warning syndromeCapsular warning syndrome The 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 depol

8、arization, 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 in

9、farct, especially in Asian. The fluctuating course of stereotyped symptoms was thought to be the result of hemodynamic compromise due to the origin occlusion.BAD诊断标准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 伸的扇形病灶。3 支配病灶区的主干动脉无严重狭窄(50%) 或闭塞，无明显心源性栓子来源。北川一夫，脳卒中 2009;3

10、1(6)：552陈谅.Branch atheromatous disease.日本医学介绍2007 年第28 卷第2 期Clinical Evaluation of LI and BAD LI 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

11、slices or a lesion extending to the surface of the pontine base observed on diffusion-weighted magnetic resonance imaging.Clinical Evaluation of LI and BADBAD 与 大动脉狭窄堵塞穿支 父辈动脉有无严重狭窄； 临床危险因素、波动/进展等难以鉴别。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、内皮细胞功能障碍； 炎症、水肿。The Impact of Diagnosing Branch Atheromatous Diseas

12、e for 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 com

13、pared 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.Different Characteristics of Anterior and Poste

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

15、dictive 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.Lipid and hyperglycemia factors in first-everpenetrating artery infarction, a comparison between different subtypes治疗 快速波动、

16、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。Stuttering Lacunes: An Acute Role for Clopidogrel?双抗血小板预防作用？Cilostazol for the Prevention of BAD双抗优于单抗Treatment of Progressive Stroke withTirofiban Experience in 35 Patients Safety and Preliminary Efficacy of Early TirofibanTreatment After Alteplase in

17、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

18、body weight per minute for at least 24 hours.Safety and Preliminary Efficacy of Early TirofibanTreatment After Alteplase in Acute Ischemic Stroke Patients tPA did not adequately prevent END, and did not show better outcome in LSA infarction due to BAD compared with antiplatelet therapy only. 小结 亚洲高发，尤其老年女性糖尿病患者； 运动障碍为主，早期快速波动、进展，内囊或桥脑预警； 急性期进展风险大，可致残，部分患者预后不良； 病理生理机制上治疗以溶栓、强化抗血小板为主，日本推荐鸡尾 酒疗法； 出血转化风险低，溶栓后可考虑24小时内抗血小板治疗预防进展。