痴呆MRI的诊断课件

ThispresentationwillfocusontheroleofMRIinthediagnosisofdementiaandrelateddiseases.

Wewilldiscussthefollowingsubjects:SystematicassessmentofMRindementiaMRprotocolfordementiaTypicalfindingsinthemostcommondementiasyndromesAlzheimer'sdisease(AD)VascularDementia(VaD)Frontotemporallobedementia(FTLD)Shortoverviewofneurodegenerativedisorderswhichmaybeassociatedwithdementia这次讲座将集中在痴呆和相关疾病的MRI诊断上。将讨论以下论题：系统性评价MR在痴呆中的应用MR诊断痴呆的协定最常见的痴呆综合征的典型表现阿尔茨海默病血管性痴呆额颞叶痴呆和痴呆相关神经变性病的简要回顾海马的冠状位图像Theroleofneuroimagingindementianowadaysextendsbeyonditstraditionalroleofexcludingneurosurgicallesions.

Radiologicalfindingsmaysupportthediagnosisofspecificneurodegenerativedisordersandsometimesradiologicalfindingsarenecessarytoconfirmthediagnosis.

ItisachallengeforneuroimagingtocontributetotheearlydiagnosisofneurodegenerativediseasessuchasAlzheimer'sdisease.

Earlydiagnosisincludesrecognitionofpre-dementiaconditions,suchasmildcognitiveimpairment(MCI).

Inaddition,earlydiagnosisallowsearlytreatmentusingcurrentlyavailabletherapiesornewtherapiesinthefuture.

NeuroimagingmayalsobeusedtoassessdiseaseprogressionandisadoptedincurrenttrialsinvestigatingMCIandAD.Thecoronalimageshowsthehippocampus,themainstructureinvolvedinmanyformsofdementia.如今神经影像学在痴呆中的作用已远远超过了它传统的在神经外科的作用。影像特点可能支持特异性神经变性的诊断，有时甚至在确定诊断上是必须的。神经影像在早期诊断神经变性病比如AD上是一个挑战。早期诊断包括识别痴呆前状态，例如轻度认知功能障碍。除此之外，早期诊断能用现在流行有效的或以后治疗方式的进行治疗。神经影像也可用于评估疾病进程并在现在探索MCI和AD的试验中采用。这个冠状位图像显示海马，是多种形式痴呆的主要结构。Coronal-obliqueT1-weightedimagesareusedfortheassessmentofmedialtemporallobeandhippocampalatrophy.

Theyareobtainedinaplaneorthogonaltothelongaxisofthehippocampus;thisplaneisorientatedparalleltothebrainstem.

Theseshouldbethin-sectionimagesandareideallyobtainedbyreformattingasagittal3DT1sequencethroughtheentirebrain.

Additionalsagittalreconstructionswillenabletheassessmentofmidlinestructuresaswellasparietalatrophy,whichmaybeinvolvedincertainneurodegenerativedisorders.FLAIRimagesareusedtoassessglobalcorticalatrophy(GCA),vascularwhitematterhyperintensitiesandinfarctions.

T2-weightedimagesareusedtoassessinfarctions,inparticularlacunarinfarctionsinthethalamusandbasalganglia,whichcanbemissedonFLAIRimages.T2*-weightedimagesarenecessarytodetectmicrobleedsinamyloid

angiopathy.Theseimagescanalsodepictcalcificationsandirondeposition.DWIshouldbeconsideredasasupplementalsequenceinyoungpatientsorinrapidlyprogressiveneurodegenerativedisorders(DD-vasculitis,CJD).冠状-斜位T1加权图像用于评估内侧颞叶和海马萎缩。沿着海马长轴位垂直的平面得到图像；这些平面平行于脑干。最理想的是薄层扫描病通过整个脑干进行矢状位的3D重建。其他矢状位重建将增强对一些有可能涉及中线结构的神经变性病例如顶叶萎缩的评估。FLAIR图像将用于整个皮质萎缩，血管性白质高信号和梗死。T2加权图像将用于评估梗死，特别是发生在丘脑和基底节的腔隙性梗死，这些可能在FLAIR图像被漏掉。T2*加权图像在检测微出血和淀粉样血管病时是必须的，这些图像同样可用于对钙化和铁沉积的描述。DWI被认为是一类在青中年患者及快速进行的神经变性病（血管炎，CJD）中的补充序列。CTprotocolCTcanbeusefulwhencontraindicationspreventMRIorwhentheonlyreasonforimagingistoruleoutsurgicallytreatablecausesofcognitivedecline.

Inthetransverseplanethescanangleshouldbeparalleltothelongaxisofthetemporallobe.

Useofmulti-detectorCTwillenablecoronallyreformattedimagestobereconstructedperpendiculartothelongaxisofthetemporallobeforoptimalvizualisationofthehippocampus.CT评定在当患者有MRI检查的禁忌症或只是排除外伤性可治疗认知下降的原因时，可应用CT.轴位平面扫描角可平行于颞叶的长轴。应用多探测器能增强冠状位格式的图像用于重建垂直颞叶长轴显示海马的视角。CT负角扫描显示海马Useofmulti-detectorCTwillenablecoronallyreformattedimagestobereconstructedperpendiculartothelongaxisofthetemporallobeforoptimalvizualisationofthehippocampus.应用多探测器能增强冠状位格式的图像用于重建垂直颞叶长轴显示海马的最佳视角。AnMR-studyofapatientsuspectedofhavingdementiamustbeassessedinastandardizedway.

Firstofall,treatablediseaseslikesubdural

hematomas,tumorsandhydrocephalusneedtobeexcluded.Nextweshouldlookforsignsofspecificdementiassuchas:Alzheimer'sdisease(AD):medialtemporallobeatrophy(MTA)andparietalatrophy.FrontotemporalLobarDegeneration(FTLD):(asymmetric)frontallobeatrophyandatrophyofthetemporalpole.VascularDementia(VaD):globalatrophy,diffusewhitematterlesions,lacunesand'strategicinfarcts'(infarctsinregionsthatareinvolvedincognitivefunction).DementiawithLewybodies(DLB):incontrasttootherformsofdementiausuallynospecificabnormalities.SowhenwestudytheMRimagesweshouldscoreinasystematicwayforglobalatrophy,focalatrophyandforvasculardisease(i.e.infarcts,whitematterlesions,lacunes).

怀疑患者有痴呆须用标准途径评估MR表现。首先，可治疗疾病像硬膜下血肿和脑积水须被排除。其次寻找特殊痴呆的表现如：AD：内侧颞叶（MTA）和顶叶萎缩。额颞叶痴呆（FTLD）：非对称性额叶和颞叶萎缩。血管性痴呆（VaD）：全脑萎缩，弥散像白质病变，腔梗和关键部位脑梗死。路易体痴呆（DLB）：对比其他类型痴呆通常没有什么特异性。所以当研究MR图像时，我们应该对全脑性萎缩、局造型萎缩和血管性疾病（梗死，白质病变，腔梗）进行评分。

ThisstandardizedassessmentoftheMRfindingsinapatientsuspectedofhavingacognitivedisorderincludes:GCA-scaleforGlobalCorticalAtrophyMTA-scaleforMedialTemporallobeAtrophyKoedamscoreforparietalatrophyFazekasscaleforWMlesionsLookingforstrategicinfarcts对怀疑认知功能下降的的患者MR特点标准化评估时包括：GCA-全脑性萎缩标准MTA-内侧颞叶萎缩的标准Koedam-顶叶萎缩将平分FazekasWM病灶的标准寻找关键部位梗死GCA-scaleforGlobalCorticalAtrophyGCAscaleisthemeanscoreforcorticalatrophythroughoutthecompletecerebrum:0:nocorticalatrophy1:mildatrophy:openingofsulci

2:moderateatrophy:volumelossofgyri

3:severe(end-stage)atrophy:'knifeblade'atrophy.GCA-全脑性萎缩标准GCA标准时整个大脑皮质萎缩的平均评分0：没有皮质萎缩1：轻度萎缩：脑沟开放2：中度萎缩：脑回容量减少3：重度（终末期）萎缩：刀片样萎缩

CorticalatrophyisbestscoredonFLAIRimages.

Insomeneurodegenerativedisorderstheatrophyisasymmetricandoccursinspecificregions.

Aradiologicalreportshouldmentionanyregionalatrophyorasymmetry.

Whenassessingatrophyindifferentregionskeepinmindthatcranially,thecentralsulcusliesmoreposteriorlythanyouwouldexpect(figure).皮层萎缩在FLAIR上最好评估。在一些神经变性病中萎缩是不对称的并发生在特殊部位。影像学报告需要设及到哪些区域萎缩和是否对称。当评估不同部位萎缩时，记住颅内中央沟比想象的要靠后（箭头）。MTA-scaleforMedialTemporallobeAtrophyTheMTA-scoreshouldberatedoncoronalT1-weightedimagesataconsistentsliceposition.

Selectaslicethroughthecorpusofthehippocampus,attheleveloftheanteriorpons.<75years:MTA-score2ormoreisabnormal(i.e.1canbestillnormal)

>75years:MTA-score3ormoreisabnormal(i.e.2canstillbenormalatthisage)Datafromastudywith222controlsandpatientswithvariousformsofdementiainwhichthisvisualratingscalewasusedtoassesstemporallobeatrophysuggestthatsensitivitiesandspecificitiesof85%canbeobtainedforpatientswithAD.MTA-内侧颞叶萎缩标准MTA需要在冠状T1持续扫描图像上评分，选择通过海马体部在脑桥前层面评估。<75岁：MTA2分或更多为异常（1分可被认为仍正常）>75岁：MTA评分3分或以上为异常（2分可认为正常）在一项222对照者和不同形式痴呆患者的研究发现这种评价内颞叶萎缩在AD患者中可达到85%的敏感性和特异性Thescoreisbasedonavisualratingofthewidthofthechoroidfissure,thewidthofthetemporalhorn,andtheheightofthehippocampalformation.score0:noatrophyscore1:onlywideningofchoroidfissurescore2:alsowideningoftemporalhornoflateralventriclescore3:moderatelossofhippocampalvolume(decreaseinheight)score4:severevolumelossofhippocampusScrollthroughtheimagesforexamplesofMTAscore0-4.这个得分依赖于对脉络膜裂，颞角宽度，海马高度的视觉评估。0分：没有萎缩1分：仅有脉络膜裂增宽2分：伴有侧脑室颞角的增宽3分：中度海马体积的减低（高度降低）4分：中度海马的萎缩图片显示0-4分的例子。AhighMTA-scoreisverysensitiveforthediagnosisofAlzheimerdiseaseandispresentinthevastmajorityofpatientswithAD,whileincontrolsapositivescoreisalmostalwaysabsent。

ThereforeitisagoodtesttodiscerncontrolsfrompatientswithAD.

ThistestisnotcompletelyspecificforADhowever,asMTAcanalsobefoundinotherformsofdementias(7).

Ontheotherhandifapatientwithmildcognitiveimpairment(MCI)apossible'prodromalstateofAD'hasanegativeMTA-score,itisveryunlikelythatthispatientwilldevelopAD(highsensitivityyieldshighnegativepredictivevalue),exceptinveryyoungsubjects,inwhomamoreposteriorpatternofatrophycanbeobservedinAD.高的MTA得分对AD的诊断有很高的敏感性，并且出现在大多数的AD患者中；然而在对照组中几乎没有。因此这是在AD患者中一个很好的鉴别试验。这项测试对AD并不是完全特异的，因为在出现在其他形式痴呆中。另一方面，如果一个有AD前状态的轻度认知功能障碍的患者有阴性的MTA值，那这个患者几乎不会发展为AD（高敏感性，高的阴性预测值），除了在年轻的患者中，后萎缩形式可出现AD。IfthereisastrongsuspicionofAlzheimer'sdisease,itcanbeusefultorepeattheexaminationtoseeifthereisanyprogressofthe(medialtemporallobe)atrophy.

Theimagesshowafollow-upexaminationat18and36monthsinapatientwhowasatriskforfamilialAD,demonstratingprogressionofthedisease.

AnalternativeapproachwouldbetoperformaSPECT-orPET-scantolookforchangesinperfusion/metabolismofthetemporo-parietalcortex,asthesechangesprecedethedevelopmentofatrophy.如果高度怀疑AD，重复MR检查来观察内侧颞叶萎缩是否进展是有用的。上图显示了一个有家族性AD危险因素的患者18个月和36个月的随访检查，证明了疾病的进展。另一个替代的方法可用SPECT或PET扫面寻找颞顶叶皮质灌注和代谢的改变，这些变化可出现在萎缩之前。FazekasscaleforWMlesions

Fazekas白质病变的评分标准FazekasscaleforWMlesionsOnMR,whitematterhyperintensities(WMH)andlacunes-bothofwhicharefrequentlyobservedintheelderly-aregenerallyviewedasevidenceofsmallvesseldisease.TheFazekas-scaleprovidesanoverallimpressionofthepresenceofWMHintheentirebrain.

ItisbestscoredontransverseFLAIRorT2-weightedimages.

Score:Fazekas0:NoneorasinglepunctateWMHlesionFazekas1:MultiplepunctatelesionsFazekas2:Beginningconfluencyoflesions(bridging)Fazekas3:LargeconfluentlesionsFazekas白质病变的评分标准在MR上，脑白质高信号（WMH）和腔梗-在老年患者中很常见，被认为是小血管病变。Fazekas评分标准提供了一个整个脑白质病变的整体印象。在FLAIR和T2加权像上可以很好的评分。

得分Fazekas0分：没有或单个点状白质病灶Fazekas1分：多发点状病灶Fazekas2分：病灶开始融合（桥状）Fazekas3分：大片融合TheFazekasscaleforWMlesionspredictsfuturedisabilityinelderly.

Fazekas脑白质评分对老年未来残疾的预测。Fazekas1isconsiderednormalintheelderly.

Fazekas2and3arepathologic,butmaybeseeninnormallyfunctioningindividuals.

Theyarehowever,athighriskfordisability.In600normallyfunctioningelderlypeopletheFazekasscorepredicteddisabilitywithinoneyear(table).IntheFazekas3group25%wasdisabledwithinoneyear.

Threeyearfollow-upshowsthatseverewhitematterchangesindependentlyandstronglypredictrapidglobalfunctionaldecline.Fazekas1级被认为是老年患者的正常表现。Fazekas2和3级分是病理性的，但是在正常功能个体也可见到，不过增加了致残率。在600位正常功能老年个体，一年内的Fazekas值预测残疾率。在Fazekas3级分患者在一年内25%致残。3年随访观察显示中度白质改变独立很强的预测了脑功能下降。Capsandbands帽和带Alimitedamountofwhitematterhyperintensitiesmayalsooccurinthenormallyageingbrain(Fazekasgrade1).

Lacunesarealwayspathological.有限的白质高信号亦可发生在正常老化的大脑（Fazekas1级）腔隙性梗死灶往往是病理性的。NormalageingThefindingsinanormallyagingbraincanoverlapwithfindingsindementia.

Asimplicatedearlier,theremaybesomedegreeofatrophy,thoughmainlyofthewhitematterwithincreasingprominenceoftheperivascular(Virchow-Robin)spacesandnon-specificfronto-parietalsulcalwidening.

Theremayalsobesomedegreeofmedialtemporallobeatrophy.

AMTA-scoreof2forindividualsolderthan75yearsofagemaybenormal.Asthebrainages,thereisanincreasingdepositionofironinspecificareasofthebrain:mainlythebasalganglia,nucleusruberandparsreticluarisofthesubstantia

nigra.

TherealsomaydeveloparimofhighsignalintensityonT2WandFLAIRimagesaroundtheventricles,knownascapsandbands(figure).正常老化正常老化大脑的和痴呆的影像表现可有一定的交叉。在相关早期，可有一些萎缩，尽管主要涉及突出的周围血管间隙和非特异性的额顶沟的加宽。这也会出现一定程度的内侧内叶的萎缩。一个MTA评分2分的超过75岁的患者可能是正常的。随着大脑的老化，有越来越多的铁沉积在大脑的特定区域：主要是基底节，黑质的致密部和网状部。这同样会在T2和FLAIR像上形成沿着脑室高的信号边缘，成为帽和带。StrategicinfarctionsStrategicinfarctionsareinfarctionsinareasthatarecrucialfornormalcognitivefunctioningofthebrain.

Theseareasaresummarizedinthetable.关键部位的梗死关键部位的梗死指影响脑认知功能区域的梗死。这些区域在表中概括。StrategicinfarctionsarebestseenontransverseFLAIRandT2Wsequences.

Theimagesshowbilateralthalamicinfarctions-lesionsoftenassociatedwithcognitivedysfunction.关键部位梗死在FLAIR和T2W加权序列上。图像显示双侧丘脑梗死伴随认知功能下降Studytheimagesoftwodifferentpatients.

Thencontinuereading.TheimageonthefarleftshowsaninfarctinthevascularterritoryofthePosteriorCerebralArtery(PCA),withinvolvementoftheinferiormedialtemporallobewhichincludesthehippocampus.

Thisisastrategicinfarction,sinceitisinthedominanthemisphere,itwillresultincognitivedysfunction.TheimagenexttoitisatransverseFLAIRimageshowinganotherinfarctinthePCA-territory,withinvolvementofthetemporo-occipitalassociationarea.

Thisisanotherexampleofastrategicinfarctionthatcanresultincognitivedysfunction.先看两例不同的病人，然后继续往下读:左侧图像显示了大脑后动脉的区域梗死，累及内侧颞叶包括海马。这是一例关键部位的梗死，因为这是主要大脑半球，这将导致认知功能下降。另一幅轴位FLAIR图像显示大脑后动脉前部梗死，影响了颞顶相连的部位。这是另一例关键部位梗死导致认知下降。KoedamscoreforParietalAtrophyInadditiontomedialtemporallobeatrophy,parietalatrophyalsohasapositivepredictivevalueinthediagnosisofAD.

AtrophyoftheprecuneusisparticularlycharacteristicofAD.

ThisisparticularlythecaseinyoungpatientswithAD(presenileAD),whomayhavenormalMTA-scores.

TheKoedamscaleratesparietalatrophy-assessedinsagittal,coronalandaxialplanes.

Intheseplanes,wideningoftheposteriorcingulateandparieto-occipitalsulciaswellasparietalatrophy(includingtheprecuneus)israted(Table).顶叶萎缩的Koedam评分除了内侧颞叶萎缩，顶叶萎缩在AD的诊断中同样有阳性预测值。楔前叶的萎缩时AD的一个特征性表现。这是一个特殊的青年AD患者（早老性AD）的病例，可能有正常的MTA值。Koedam值对顶叶分级要评估矢状位、冠状位和轴位图像。在这些平面中，后扣带回和顶枕沟的增宽和顶叶萎缩（包括楔前叶）被评定。Koedamscalegrade0-1

SagittalT1-,axialFLAIR-andcoronalT1-weightedimagesillustratingtheKoedamscaleofposterioratrophy.

Whendifferentscoresareobtainedindifferentorientations,thehighestscoremustbeconsideredKoedam标准0-1级矢状位T1，轴位FLAIR和冠状T1加权图像显示后部萎缩的Koedam标准。当不同的分数在不同方向不同时，取其最高值。Koedamscalegrade2-3

SagittalT1-,axialFLAIR-andcoronalT1-weightedimagesillustratingtheKoedamscaleofposterioratrophy.

Theyellowarrowspointtoextremewideningoftheposteriorcingulateenparieto-occipitalsulciinapatientwithgrade3posterioratrophy.Koedam标准2-3级矢状位T1，轴位FLAIR和冠状T1图像显示后部萎缩。黄色箭头显示在3级患者后部扣带回与顶枕沟末端加宽。FDG-PETInadditiontoclinicalfindings,CSFandMRI,PET-imagingisusefulindiagnosingAD.

InADFDG-PETcanshowhypometabolisminthetemporoparietalregionsand/ortheposteriorcingulum.

ThismayhelpdifferentiateADfromFTD,whichshowsfrontalhypometabolismonFDG-PET.

TheimagesshowFDG-PETandaxialFLAIRimagesofanormalsubjectandofpatientswithADandFTD.FDG-PET(toprow)andaxialFLAIRimagesofanormalsubjectandofADandFTDpatients.

InADthereisadecreasedmetabolismoftheparietallobes(yellowarrows),whereasinFTD,thereisfrontalhypometablism(redarrows).FDG-PET除了临床发现以外，CSF和MRI，PET图像诊断AD也是有益的。在AD患者中，FDG-PET显示颞顶叶区域和或后部扣带的低灌注。这或能帮助鉴别AD和FTD，FTD中显示FDG-PET的额叶低灌注。这张图像显示了正常个体、AD和FTD患者的FDG-PET和轴位FLAIR图像。正常个体、AD和FTDFDG-PET患者的FDG-PET和轴位FLAIR图像。在AD患者，顶叶代谢率降低，而在FTD患者，额叶低灌注。Theprevalenceofspecificformsofdementiaisage-dependent.

Inpatients<65yearstherearemorecasesoffamilialandpresenileprogressiveformsofADandmorecasesofFTLD.

Inpatients>65yearstherearemorecasesofsenileADandvasculardementia.

InmanyolderpatientswithmanifestADthereisco-existingvasculardisease,whichcontributestothedementedstate.特异形式痴呆的流行因素是年龄。在小于65岁患者，更多的是AD家族性和早老性进程与更多的FTLD。在大于65岁患者，有更多的早老性AD和血管性痴呆。在很多老年患者有AD特征和血管性疾病共存，这加重了痴呆状态。AlzheimersDiseaseADaccountsfor50%-70%ofallcasesofdementiaintheelderlypopulation.

Ageisastrongriskfactor,withthediseaseaffectingapproximately8%ofindividualsovertheageof65and30%overtheageof85years.

TheprogressionofADisgradualandtheaveragepatientlives10yearsaftertheonsetofsymptoms.

Withtheincreasingpercentageofelderlyinthepopulation,theprevalenceofADisexpectedtotripleoverthenext50years.Inend-stageADthereiswidespreadatrophy,whichisnodifferentfromotherend-stagedementias.

InimagingwethereforehavetotrytoidentifyADinanearlierstageandwehavetoconcentrateonthehippocampusandthemedialtemporallobe,becausethatiswhereADstarts.

TheroleofMRIinthediagnosticprocessofADistwofold:Ruleoutothercausesofcognitiveimpairment.IdentifyearlyonsetADforpossibleinnovativetherapyandcounseling阿尔茨海默病AD占老年人群所有痴呆的50%-70%。年龄是一个很强的危险因素，随着年龄增加，AD影响了8%的大于65岁的患者和30%的大于85岁人群。AD是逐渐进展的过程，症状发作后患者平均生存10年。随着老年患者比例的增加，预计在未来50年AD的发病率增加3倍。在AD的终末期广泛的萎缩，和其他类型痴呆的晚期相似。在影像学上我们需要在早期发现AD，为此我们更加关注颞叶内侧皮质和海马，因为那是AD起始处。MR对AD的诊断过程是双重的：1、排除其他认知下降的原因。2、确认早期AD以便早期治疗和参考Studytheimage,thencontinuereading.ThefindingsareconsistentwiththediagnosisofendstageAD,becausethereis:Extremehippocampalandmedialtemporallobeatrophy(MTAscore:4)Severeglobalatrophy(GCAscale:3)

ItisnotspecificforADhowever,sincesevereGCAoccursinotherend-stagedisordersaswell学习图像，然后往下读.这些发现和AD的诊断一致，因为：明显的海马和内侧颞叶的萎缩(MTA4分）重度全脑萎缩（GCA3级）但这对AD并不是特异的，因为重度GCA可发生在其他痴呆的终末期。PresenileADPresenileAD(<65y)hasadifferentpresentation.

Althoughthereusuallyissomemildhippocampalatrophy,themoststrikingfindingisparietalatrophywithatrophyoftheposteriorcingulumandtheprecuneus;thehippocampuscanbenormal.早老性AD早老性AD（小于65岁）有不同的表现。尽管有轻度的海马萎缩，最重要的发现是伴随后部扣带和楔前叶的顶叶萎缩。海马可正常MildCognitiveImpairment(MCI)Mildcognitiveimpairmentisarelativelyrecenttermusedtodescribepeoplewhohavesomeproblemswiththeirmemory,butdonotactuallyhavedementia,sincedementiaisdefinedashavingproblemsintwoormorecognitivedomains.

SomeofthesepatientswillbeintheearlystagesofAlzheimer'sdiseaseoranotherdementia,soitisimportanttoidentifythem.

FindingMTAisastrongrisk-factorforprogressiontodementia.轻度认知功能障碍（MCI）轻度认知功能障碍是最近被用于描述那些有记忆障碍，但是并没有痴呆的患者，因为痴呆被定义为有两个或更多领域的认知障碍。这些患者可能处于AD的早期阶段或其他类型的痴呆，所以识别他们很重要。MTA表现是进行性痴呆的一个重要的危险因素。PCAinfarctioninvolvingthemedialtemporallobe.

脑后动脉梗死影响到颞叶内侧皮质VascularDementia(VaD)Vasculardementia(VaD)isthoughttobethesecondmostcommoncauseofdementiaafterAlzheimer'sdisease.

ItcansometimesbedistinguishedfromADbyamoresuddenonsetandassociationwithvascularriskfactors.

VaDcanbecharacterizedbyitsstepwisedeteriorationwithperiodsofstabilityfollowedbysuddendeclineincognitivefunction.

Mostpatients,however,havesmallvesseldisease,whichistypifiedbyamoregradualandsubtlepatternofdeterioration.

Controlofvascularriskfactorsisthetreatmentofchoice,butcholinesteraseinhibitors(drugsthatarebeingusedinAD)arealsoincreasinglybeingusedtotreatvasculardementia.TheimagesshowapatientwithastrategicPCAinfarctioninvolvingthehippocampus.

Thistypeofinfarctcanresultinsuddendementiaiflocatedinthedominanthemisphere.

Itwillusuallynotresultindementiaifitoccursinthenon-dominanthemisphere.血管性痴呆血管性痴呆被认为是仅此于AD的痴呆的第二大原因。有时可通过突然发病和有血管危险因素与AD鉴别。血管性痴呆以渐进性恶化有稳定期和突然的认知功能下降。大多数的患者，有小血管疾病，这以渐进性和明显恶化为特征。控制血管因素是治疗的一个选择，但是胆碱酯酶抑制剂也同样越来越多被用于治疗血管性痴呆。这幅图像显示了累及海马的关键区域的大脑后动脉梗死。这种类型的梗死可导致突然的痴呆如果位于优势半球。如果发生在非优势半球一般不引起痴呆。InmostpatientswithVaDthereisdiffusewhitematterdiseasewithlargeconfluentlesions(Fazekas3).

Insomeofthesepatientstheventriclesmaybedilatedduetoglobalatrophyandsomewillalsohavemedialtemporallobeatrophy.

TheimagesareofapatientwhohadVaD,butthemedialtemporallobewasnormal.在大多数血管性痴呆的患者，往往有弥散性白质融合病灶（Fazekas3级）在一些这类病人中，会因脑萎缩而引起脑室的扩张，仍伴随内侧颞叶萎缩。这幅图像是一个有血管性痴呆的患者，但是内侧颞叶正常。StrategicinfarctsandsmallvesseldiseaseCognitivedysfunctioninVaDcanbetheresultof:Largevesselinfarctions:Bilateralintheanteriorcerebralarteryterritory.Parietotemporal-andtemporo-occipitalassociationareasofthedominanthemisphere(angulargyrusincluded)PosteriorcerebralarteryterritoryinfarctionoftheparamedianthalamicregionandinferiormedialtemporallobeofthedominanthemisphereWatershedinfarctionsinthedominanthemisphere(superiorfrontalandparietal)Smallvesseldisease:Multiplelacunar

infactionsinfrontalwhitematter(>2)andbasalganglia(>2)WMLs(atleastmorethan25%ofWM)Bilateralthalamiclesions关键部位的梗死和小血管病变血管性认知功能下降可由下面原因引起：大血管梗死：双侧大脑前动脉供应区。顶颞和颞枕交界区（包括角回）大脑后动脉供血区的丘脑内侧旁和优势半球颞叶后内侧部的梗死优势半球分水岭梗死（额上部和顶叶）小血管疾病额叶白质(>2)和基底节(>2)的多发腔梗。广泛白质病变（至少超过25%的白质病变）双侧丘脑病变Thereisanincreasingawarenessfortheimportanceofsmallvesseldiseaseasapredictorofcognitivedeclineanddementia.

Moreover,itseemstoamplifytheeffectsofpathologicchangesofAlzheimer'sdisease.

OntheleftweseeapatientwhowasdiagnosedashavingVaD.

WhitematterdiseaseisseenassevereWMH(hypointenseonT1)intheperiventricularregions.

Inadditiontothesevascularchanges,thereisalsoMTA.

PresumablythispatienthasbothVaDandAD,afindingseeninmanyelderlypatients.

Thesefindingsshouldbedescribedseparatelyasitmayhavetherapeuticconsequences.在预测认知功能下降和痴呆方面小血管疾病正越来越受重视。然而，很多时候把AD的病理改变扩大化了。上面的图像诊断为血管性痴呆。白质疾病可看到严重的脑室周围的白质病变（T1低信号），除了这些血管性改变，同样也有内侧颞叶的萎缩。假设这个病人既有VaD又有AD，这个情况可在很多老年患者中见到。这些表现因治疗的不同应该单独描述。Theproblemhoweveris,thatwhitematterhyperintensitiesandlacunesarealsofrequentlyobservedinnon-dementedelderlyandatsomelevelcanberegardedasnormalfindingsinaging.

ToovercomethisproblemtheNINDS-AIRENInternationalWorkGrouphasformulatedcriteriaforthehistoryandphysical,radiological,(seeabove)andpathologicalexaminationtoclassifypatientsashavingpossible,probableanddefiniteVaD.

HoweverconsiderableinterobservervariabilityexistsfortheassessmentoftheradiologicalpartoftheseNINDS-AIRENcriteriaandsomeleveloftrainingismandatory.

问题是白质高信号和腔梗在非痴呆的老年人常见，甚至在一定程度上被认为随年龄变化的正常表现。为了克服这个问题，NINDS-AIREN协会基于病史、体格检查、影像学表现和病理改变制定了可能的、很可能的和明确的血管性痴呆。然而，在评估NINDS-AIREN标准重影像学部分时存在相当大的观察者观察变异，一些观察水平也是强制性的。Themedialnucleiofthethalamusplayanimportantroleinmemoryandlearning.

Alargeunilateralinfarctionorbilateralinfarctionsinthisregioncancausedementia.

Youhavetopayspecialattentiontotheseareastofindthesesmallinfarctions.丘脑内侧核团在学习和记忆中扮演重要角色。大的单侧梗死和双侧的梗死可引起痴呆。要特别注意这些区域的小的梗死灶。OnFLAIRimagesyouwilleasilymisstheseinfarctions,becausetheycanbeisointensetothesurroundingstructures(8).

AhighresolutionT2WIisneededtodetectthesethalamicinfarcts.

FLAIRintheinfratentorialregionandinthespinalcordisoflimitedvalueasitsuppressesnotonlythesignalofwater,butalsopathologywithalongT1-relaxationtime.

ThisphenomenoncanalsobeseeninthedetectionofMultipleSclerosis,whereFLAIRisoflimitedvalueintheinfratentorialregionandofnouseinthespinalcord.在FLAIR图像上很容易漏掉梗死灶，，因为它们和周围信号相同。检测丘脑的梗死需要高分辨率的T2图像。FLAIR在幕区和脊髓中价值不大，因为它不仅抑制水的信号，而且引起长的T1弛豫时间。这种现象在多发性硬化中也可以见到，FLAIR在幕区和脊髓中价值不大。CerebralAmyloid

Angiopathy(CAA)DementiamaybetheclinicalpresentationinCAA,aconditioninwhichß-amyloidisdepositedinthevesselwallsofthebrain.

Theresultishemorrhage,usuallymicrohemorrhages,butalsosubarachnoidhemorrhageorlobarhematomasmayoccur.OnMR,theT2*sequencewillshowmultiplemicrohemorrhages,typicallyinaperipherallocation(asopposedtohypertensivemicrohemorrhages,whichareusuallymorecentrallylocated,e.g.inthebasalgangliaandthalami).

Inaddition,FLAIRwillrevealmoderatetoseverwhitematterhyperintensities(Fazekasgrade2or3)T2*imagesinapatientwithCAAshowmultipleperipherallylocatedmicrobleeds.脑淀粉样血管病（CAA）痴呆可能是CAA的临床表现，由ß淀粉样蛋白沉积引起。CAA容易出血，往往是微出血，同样可引起蛛网膜下腔出血和脑叶的血肿。在MR上，T2*序列上显示多发微出血，典型的事周围部位（对比高血压出血，常发生在中央部位，如基底节区和丘脑）除此之外，FLAIR将显示中道重度白质高信号（(Fazekas2或3级）T2*图像显示CAA病人多发外周微出血。FLAIRimagesofthesamepatientshowFazekas2whitematterhyprintensities.

FLAIR图像显示同一个病人Fazekas2级的白质高信号。T2*imagesinapatientwithCAAmicrobleeds.

T2*图像显示CAA患者微出血。T2*imagesdemonstratemultiplelobarmicrobleedsinapatientwithCAA.

T2*图像证明了在CAA病人中多发脑叶微出血的存在。FrontotemporalLobarDegeneration(FTLD)FTLD,formerlycalledPick'sdisease,isaprogressivedementia,thataccountsfor5-10%ofcasesofdementia.,andoccursrelativelymorefrequentlyinpresenilesubjects

FTLDisclinicallycharacterizedbybehavioralandlanguagedisturbancesthatmayprecedeorovershadowmemorydeficits.

Thereiscurrentlynotreatmentforthiscondition.Imagingplaysanimportantroleinthediagnosisasthefindingsareeasytorecognize.

Radiologicalfindingsarepronouncedatrophyoffrontaland/ortemporallobes.

InsomeformsofFTLDtheatrophymightbestrikinglyasymmetric,e.g.inSemanticDementia,adiseasesubtypewithprogressiveaphasiaandleft-sidedtemporallobedegeneration.额颞叶痴呆（FTLD）FTLD，之前被称作匹克病，是一种进行性痴呆，占痴呆的5-10%，发生在相对年轻的群体。FTLD临床上以行为和语言障碍为主，一定程度上掩盖了记忆缺陷。至今没有针对此的治疗。图像在诊断上有重要作用，因为易于识别。影像学的主要表现是额叶与颞叶的萎缩。在另一些形式的FTLD中萎缩可明显不对称，如语义性痴呆，一个进行性失语和左侧颞叶变性的亚型。Theimagesareofapatientwithprogressiveaphasia.

Themostprominentfindingisthestrikingasymmetricatrophyofthetemporallobeontheleftsidewithnotonlyatrophyofthehippocampus,butalsothetemporalpoles.

Theatrophyhasresultedingyrithatappearassharpasknives('knifebladeatrophy').

ThereisalsosomeincreasedsignalintensityseenontheFLAIRimage,probablyduetogliosis.

ThesefindingsarepathognomonicforthediagnosisofFTLD.Patientswithleft-sidedtemporalatrophyareusuallyclinicallyobvious.

Right-sidedatrophyisusuallynotaseasilyrecognizedasthesepatientsonlypresentwithsubtledisturbancesinrecognizingfaces.这是一个渐进性失语患者的图像。最主要的发现是明显的左侧颞叶前部和海马的非对称性萎缩。萎缩使得脑回如刀片样（刀片样萎缩）在FLAIR相上，可能由于胶质的增生可见高信号区。这是发现是诊断FTLD的特殊特征。左侧颞叶萎缩的病人往往有明显的临床特征。右侧萎缩往往不好识别，因为病人表现出轻微的异常。路易体痴呆路易体痴呆占痴呆的25%，和PSP/MSA同为非典型的帕金森综合征。路易体痴呆的临床特征可类似于AD或帕金森病相关的痴呆。患者通