穿支動脈粥樣硬化病

1、BAD Related Ischemic Stroke朱佳佳-8-31第1頁進(jìn)展性卒中END24二分之一病因還未明確，發(fā)生率13.8%（24h內(nèi)再通，4分）；大動脈粥樣硬化性31%，心源性23%，腔梗9%第2頁進(jìn)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頁Lacunar Stroke Is the Major Cause of Progressive Motor Deficits第4頁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頁SSSI（孤立皮層下小梗死

4、）第6頁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頁Branch atheromatous disease and its associati

5、on with progressive motor deficits第8頁BAD第9頁BAD亞洲國家多發(fā)，研究集中于日本、韓國；早期END百分比較高；缺乏統(tǒng)一定義，當(dāng)前診療主要依賴梗死灶分布、大小、形態(tài)；高分辨MRI研究較少；與大動脈粥樣硬化性比較，危險原因無顯著差異。第10頁概念由主干動脈分出穿通支入口部發(fā)生動脈粥樣硬化引發(fā)狹窄或閉塞。強(qiáng)調(diào)這種梗塞在病理上與高血壓所致脂質(zhì)透明變性不一樣, 而以動脈粥樣硬化為主要改變。第11頁BAD病理機(jī)制A 主干動脈斑塊堵塞分 支動脈入口B 主干動脈斑塊延伸到 分支動脈結(jié)合部斑 塊C 分支動脈入口處斑塊Caplan LR. Intracranial bran

6、ch atheromatous disease: A neglected, understudied, and underused concept, Neurology 1989第12頁A BAD，病灶延伸到腦橋腹側(cè)表面B 脂質(zhì)透明變性腦橋腔隙性腦梗死。Caplan LR. Intracranial branch atheromatous disease: A neglected, understudied, and underused concept, Neurology 1989第13頁第14頁臨床表現(xiàn)以運動障礙為主要表現(xiàn)；急性期癥狀波動、重復(fù)；急性期癥狀加重、病灶逐步擴(kuò)大病例多見。第15

7、頁High-resolution MRI findings in patients withcapsular warning syndrome第16頁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頁BAD診療標(biāo)準(zhǔn)1 豆紋動脈供血區(qū)BAD型梗死： 水平位頭顱MRI上梗死灶達(dá)三個層面以上2 腦橋旁正中動脈供血區(qū)BAD型梗死： 梗死灶與腦橋腹側(cè)表面相接、向被蓋部延 伸扇形病灶。3 支配病灶區(qū)主干動脈無嚴(yán)重狹窄(50%) 或閉塞，無顯著心源性栓子起源。北川一夫，脳卒中 ;31(6)：552陳諒.Bra

10、nch atheromatous disease.日本醫(yī)學(xué)介紹 年第28 卷第2 期第18頁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頁Clinical Evaluation of LI and BAD第20頁BAD 與 大動脈狹窄堵塞穿支父輩動脈有沒有嚴(yán)重狹窄；臨床危險因素、波動/進(jìn)展等難以鑒別。第21頁進(jìn)展機(jī)制血栓延伸；局部低灌注、側(cè)支循環(huán)不良；血腦屏障破壞、內(nèi)皮細(xì)胞功效障礙；炎癥、水腫。第22頁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頁Different Characteristics of Anterior and Poste

14、rior BAD with or without END高齡、女性、肥胖第24頁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頁Lipid and hyperglycemia factors in first-everpenetrating artery infarction, a comparison between different subtypes第

16、26頁治療快速波動、早期進(jìn)展，治療難度大；雙抗血小板；抗凝治療；靜脈溶栓；IIb/IIIa；雞尾酒療法。第27頁Stuttering Lacunes: An Acute Role for Clopidogrel?雙抗血小板預(yù)防作用？第28頁Cilostazol for the Prevention of BAD第29頁雙抗優(yōu)于單抗第30頁Treatment of Progressive Stroke withTirofiban Experience in 35 Patients 第31頁Safety and Preliminary Efficacy of Early TirofibanTrea

17、tment After Alteplase in Acute Ischemic Stroke Patients絕大部分入選患者是穿支血管病變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頁Safety and Preliminary Efficacy of Early TirofibanTreatment After Alteplase in Acute Ischemic Stroke Patients第33頁第3