穿支動(dòng)脈粥樣硬化病

BADRelated

IschemicStroke朱佳佳2017-8-31進(jìn)展性卒中END24一半病因尚未明確，發(fā)生率13.8%（24h內(nèi)再通，4分）；大動(dòng)脈粥樣硬化性31%，心源性23%，腔梗9%進(jìn)展性腔梗Butin20–30%ofpatientswithLS,neurologicaldeficitsworseninhoursorevendaysfollowingstrokeonset.Deteriorationinvolvesespeciallymotorfunctionandoftenterminatesleavinganimportantdisability.LacunarStrokeIstheMajorCauseofProgressiveMotorDeficitsProgressiveMotorDeficitsPMDwasdefinedasanincreaseofatleast2pointsonthemotoritemoftheNIHSSscorepersistingforatleast24hourswithin5daysofstrokeonset.DeepperforatingarteryinfarctwasmorefrequentlyassociatedwithPMD(35.8%)comparedwithlargearterydisease(27.3%)andcardioembolism(5.3%).Multiplelogisticanalysisfoundthatdeepperforatingarteryinfarct

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

hadsignificantlyhigheroddsofexhibitingEND.BranchatheromatousdiseaseanditsassociationwithprogressivemotordeficitsBADBAD亞洲國家多發(fā)，研究集中于日本、韓國；早期END比例較高；缺乏統(tǒng)一定義，目前診斷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(dòng)脈粥樣硬化性比較，危險(xiǎn)因素?zé)o顯著差異。概念由主干動(dòng)脈分出的穿通支入口部發(fā)生動(dòng)脈粥樣硬化引起的狹窄或閉塞。強(qiáng)調(diào)這種梗塞在病理上與高血壓所致的脂質(zhì)透明變性不同,而以動(dòng)脈粥樣硬化為主要的改變。BAD的病理機(jī)制A主干動(dòng)脈斑塊堵塞分支動(dòng)脈入口B主干動(dòng)脈斑塊延伸到分支動(dòng)脈結(jié)合部斑塊C分支動(dòng)脈入口處斑塊CaplanLR.Intracranialbranchatheromatousdisease:Aneglected,understudied,andunderusedconcept,Neurology1989ABAD，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。CaplanLR.Intracranialbranchatheromatousdisease:Aneglected,understudied,andunderusedconcept,Neurology1989臨床表現(xiàn)以運(yùn)動(dòng)障礙為主要表現(xiàn)；急性期癥狀波動(dòng)、反復(fù)；急性期癥狀加重、病灶逐漸擴(kuò)大的病例多見。High-resolutionMRIfindingsinpatientswith

capsularwarningsyndromeCapsularwarningsyndromeTheexactpathogenicmechanismofCWShasnotbeenfullyunderstood.Variousmechanismshavesuggested,includingsmallvesseldisease,embolismfromtheheart,vasospasm,peri-infarctdepolarization,and,inrareinstances,atheroscleroticdiseaseoftheMCA.SmallperforatorarterydiseaseisproposedtobethemostcommoncauseoftheCWS.Recently,morestudiessuggestedthatintracranialatheroscleroticdiseaseplaysanimportantroleinthedevelopmentofsmallstratiocapsularinfarct,especiallyinAsian.Thefluctuatingcourseofstereotypedsymptomswasthoughttobetheresultofhemodynamiccompromiseduetotheoriginocclusion.BAD診斷標(biāo)準(zhǔn)1豆紋動(dòng)脈供血區(qū)BAD型梗死：水平位頭顱MRI上梗死灶達(dá)三個(gè)層面以上2腦橋旁正中動(dòng)脈供血區(qū)BAD型梗死：梗死灶與腦橋腹側(cè)表面相接、向被蓋部延伸的扇形病灶。3支配病灶區(qū)的主干動(dòng)脈無嚴(yán)重狹窄(<50%)

或閉塞，無明顯心源性栓子來源。北川一夫，脳卒中2009;

31(6)：552陳諒.Branchatheromatousdisease.日本醫(yī)學(xué)介紹2007年第28卷第2期ClinicalEvaluationofLIandBADLIwasdefinedasanintracerebrallesion,15mmindiameterandfewerthan3slicesoralesionwithinthepontineparenchyma.BADwasdefinedasanintracerebrallesionof15mmindiameterandmorethan3slicesoralesionextendingtothesurfaceofthepontinebaseobservedondiffusion-weightedmagneticresonanceimaging.ClinicalEvaluationofLIandBADBAD與大動(dòng)脈狹窄堵塞穿支父輩動(dòng)脈有無嚴(yán)重狹窄；臨床危險(xiǎn)因素、波動(dòng)/進(jìn)展等難以鑒別。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)胞功能障礙；炎癥、水腫。TheImpactofDiagnosingBranchAtheromatousDiseaseforPredictingPrognosisNeurologicworseningwasobservedatasignificantlyhigherrateinBADcomparedwiththeLIpatientsinboththeLSAandPPAgroups(45.1%versus22.6%and46.7%versus0%).IntheLSAgroup,theenlargementoftheischemiclesionwassignificantlymorefrequentinBADcomparedwiththeLIpatients(66.2%and34.0%).Therewasasignificantrelationbetweentheenlargementofthelesionandtheworseningofneurologicdeficits.Moreover,theclinicalfeatures,whichpredictthelesionenlargement,wereBADandolderage.DifferentCharacteristicsofAnteriorandPosteriorBADwithorwithoutEND高齡、女性、肥胖PredictivefactorsforprogressivemotordeficitsinpenetratingarteryinfarctionsintwodifferentarterialterritoriesThefemalesexandinitialNIHSSscore5ormorepersistsignificantaftermultivariateanalysisforbothgroups.ThespecificindependentpredictivefactorsfortheLSAgroupweresingleinfarctswithoutconcomitantsilentlacunarinfarctsandprecedinglacunarTIAs;andthosefortheAPAgroupwasdiabetesmellitus.Lipidandhyperglycemiafactorsinfirst-ever

penetratingarteryinfarction,acomparisonbetweendifferentsubtypes治療快速波動(dòng)、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。StutteringLacunes:AnAcuteRoleforClopidogrel?雙抗血小板預(yù)防作用？？CilostazolforthePreventionofBAD雙抗優(yōu)于單抗TreatmentofProgressiveStrokewith

Tirofiban–Experiencein35PatientsSafetyandPreliminaryEfficacyofEarlyTirofiban

TreatmentAfterAlteplaseinAcuteIschemicStrokePatients絕大部分入選患者是穿支血管病變Alteplase(0.9mg/kg)thrombolysisimmediatelyfollowedbyintravenoustirofibaninfusion.Tirofibanwasadministeredinabody-weight-adjusteddosagewithabolusof0.4μg/kgbodyweightperminutefor30minutesfollowedbyacontinuousinfusionof0.1μg/kgbodyweightperminuteforatleast24hours.SafetyandPreliminaryEfficacyofEarlyTirofiban

TreatmentAfterAlteplaseinAcuteIschemicStrokePati