穿支动脉粥样硬化病

BADRelated

IschemicStroke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Butin20–30%ofpatientswithLS,neurologicaldeficitsworseninhoursorevendaysfollowingstrokeonset.Deteriorationinvolvesespeciallymotorfunctionandoftenterminatesleavinganimportantdisability.LacunarStrokeIstheMajorCauseofProgressiveMotorDeficitsProgressiveMotorDeficitsPMDwasdefinedasanincreaseofatleast2pointsonthemotoritemoftheNIHSSscorepersistingforatleast24hourswithin5daysofstrokeonset.DeepperforatingarteryinfarctwasmorefrequentlyassociatedwithPMD(35.8%)comparedwithlargearterydisease(27.3%)andcardioembolism(5.3%).Multiplelogisticanalysisfoundthatdeepperforatingarteryinfarct

wasindependentlyassociatedwithPMD.DeepperforatingarteryinfarctisthemajorcauseofPMD.SSSI（孤立皮层下小梗死）NeuroimagingMarkersforENDinSSSIEarlyneurologicaldeterioration(END)occursin≥20%ofsinglesmallsubcorticalinfarctions.Patientswithrelevantarterystenosisandbranchatheromatouslesions

hadsignificantlyhigheroddsofexhibitingEND.BranchatheromatousdiseaseanditsassociationwithprogressivemotordeficitsBADBAD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CaplanLR.Intracranialbranchatheromatousdisease:Aneglected,understudied,andunderusedconcept,Neurology1989ABAD，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。CaplanLR.Intracranialbranchatheromatousdisease:Aneglected,understudied,andunderusedconcept,Neurology1989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-resolutionMRIfindingsinpatientswith

capsularwarningsyndromeCapsularwarningsyndromeTheexactpathogenicmechanismofCWShasnotbeenfullyunderstood.Variousmechanismshavesuggested,includingsmallvesseldisease,embolismfromtheheart,vasospasm,peri-infarctdepolarization,and,inrareinstances,atheroscleroticdiseaseoftheMCA.SmallperforatorarterydiseaseisproposedtobethemostcommoncauseoftheCWS.Recently,morestudiessuggestedthatintracranialatheroscleroticdiseaseplaysanimportantroleinthedevelopmentofsmallstratiocapsularinfarct,especiallyinAsian.Thefluctuatingcourseofstereotypedsymptomswasthoughttobetheresultofhemodynamiccompromiseduetotheoriginocclusion.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;

31(6)：552陈谅.Branchatheromatousdisease.日本医学介绍2007年第28卷第2期ClinicalEvaluationofLIandBADLIwasdefinedasanintracerebrallesion,15mmindiameterandfewerthan3slicesoralesionwithinthepontineparenchyma.BADwasdefinedasanintracerebrallesionof15mmindiameterandmorethan3slicesoralesionextendingtothesurfaceofthepontinebaseobservedondiffusion-weightedmagneticresonanceimaging.ClinicalEvaluationofLIandBADBAD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。TheImpactofDiagnosingBranchAtheromatousDiseaseforPredictingPrognosisNeurologicworseningwasobservedatasignificantlyhigherrateinBADcomparedwiththeLIpatientsinboththeLSAandPPAgroups(45.1%versus22.6%and46.7%versus0%).IntheLSAgroup,theenlargementoftheischemiclesionwassignificantlymorefrequentinBADcomparedwiththeLIpatients(66.2%and34.0%).Therewasasignificantrelationbetweentheenlargementofthelesionandtheworseningofneurologicdeficits.Moreover,theclinicalfeatures,whichpredictthelesionenlargement,wereBADandolderage.DifferentCharacteristicsofAnteriorandPosteriorBADwithorwithoutEND高龄、女性、肥胖PredictivefactorsforprogressivemotordeficitsinpenetratingarteryinfarctionsintwodifferentarterialterritoriesThefemalesexandinitialNIHSSscore5ormorepersistsignificantaftermultivariateanalysisforbothgroups.ThespecificindependentpredictivefactorsfortheLSAgroupweresingleinfarctswithoutconcomitantsilentlacunarinfarctsandprecedinglacunarTIAs;andthosefortheAPAgroupwasdiabetesmellitus.Lipidandhyperglycemiafactorsinfirst-ever

penetratingarteryinfarction,acomparisonbetweendifferentsubtypes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。StutteringLacunes:AnAcuteRoleforClopidogrel?双抗血小板预防作用？？CilostazolforthePreventionofBAD双抗优于单抗TreatmentofProgressiveStrokewith

Tirofiban–Experiencein35PatientsSafetyandPreliminaryEfficacyofEarlyTirofiban

TreatmentAfterAlteplaseinAcuteIschemicStrokePatients绝大部分入选患者是穿支血管病变Alteplase(0.9mg/kg)thrombolysisimmediatelyfollowedbyintravenoustirofibaninfusion.Tirofibanwasadministeredinabody-weight-adjusteddosagewithabolusof0.4μg/kgbodyweightperminutefor30minutesfollowedbyacontinuousinfusionof0.1μg/kgbodyweightperminuteforatleast24hours.SafetyandPreliminaryEfficacyofEarlyTirofiban

TreatmentAfterAlteplaseinAcuteIschemicStrokePati