癡呆MRI的診斷課件

ThispresentationwillfocusontheroleofMRIinthediagnosisofdementiaandrelateddiseases.

Wewilldiscussthefollowingsubjects:SystematicassessmentofMRindementiaMRprotocolfordementiaTypicalfindingsinthemostcommondementiasyndromesAlzheimer'sdisease(AD)VascularDementia(VaD)Frontotemporallobedementia(FTLD)Shortoverviewofneurodegenerativedisorderswhichmaybeassociatedwithdementia這次講座將集中在癡呆和相關(guān)疾病的MRI診斷上。將討論以下論題：系統(tǒng)性評價MR在癡呆中的應(yīng)用MR診斷癡呆的協(xié)定最常見的癡呆綜合征的典型表現(xiàn)阿爾茨海默病血管性癡呆額顳葉癡呆和癡呆相關(guān)神經(jīng)變性病的簡要回顧海馬的冠狀位圖像Theroleofneuroimagingindementianowadaysextendsbeyonditstraditionalroleofexcludingneurosurgicallesions.

Radiologicalfindingsmaysupportthediagnosisofspecificneurodegenerativedisordersandsometimesradiologicalfindingsarenecessarytoconfirmthediagnosis.

ItisachallengeforneuroimagingtocontributetotheearlydiagnosisofneurodegenerativediseasessuchasAlzheimer'sdisease.

Earlydiagnosisincludesrecognitionofpre-dementiaconditions,suchasmildcognitiveimpairment(MCI).

Inaddition,earlydiagnosisallowsearlytreatmentusingcurrentlyavailabletherapiesornewtherapiesinthefuture.

NeuroimagingmayalsobeusedtoassessdiseaseprogressionandisadoptedincurrenttrialsinvestigatingMCIandAD.Thecoronalimageshowsthehippocampus,themainstructureinvolvedinmanyformsofdementia.如今神經(jīng)影像學(xué)在癡呆中的作用已遠遠超過了它傳統(tǒng)的在神經(jīng)外科的作用。影像特點可能支持特異性神經(jīng)變性的診斷，有時甚至在確定診斷上是必須的。神經(jīng)影像在早期診斷神經(jīng)變性病比如AD上是一個挑戰(zhàn)。早期診斷包括識別癡呆前狀態(tài)，例如輕度認知功能障礙。除此之外，早期診斷能用現(xiàn)在流行有效的或以后治療方式的進行治療。神經(jīng)影像也可用于評估疾病進程并在現(xiàn)在探索MCI和AD的試驗中采用。這個冠狀位圖像顯示海馬，是多種形式癡呆的主要結(jié)構(gòu)。Coronal-obliqueT1-weightedimagesareusedfortheassessmentofmedialtemporallobeandhippocampalatrophy.

Theyareobtainedinaplaneorthogonaltothelongaxisofthehippocampus;thisplaneisorientatedparalleltothebrainstem.

Theseshouldbethin-sectionimagesandareideallyobtainedbyreformattingasagittal3DT1sequencethroughtheentirebrain.

Additionalsagittalreconstructionswillenabletheassessmentofmidlinestructuresaswellasparietalatrophy,whichmaybeinvolvedincertainneurodegenerativedisorders.FLAIRimagesareusedtoassessglobalcorticalatrophy(GCA),vascularwhitematterhyperintensitiesandinfarctions.

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

angiopathy.Theseimagescanalsodepictcalcificationsandirondeposition.DWIshouldbeconsideredasasupplementalsequenceinyoungpatientsorinrapidlyprogressiveneurodegenerativedisorders(DD-vasculitis,CJD).冠狀-斜位T1加權(quán)圖像用于評估內(nèi)側(cè)顳葉和海馬萎縮。沿著海馬長軸位垂直的平面得到圖像；這些平面平行于腦干。最理想的是薄層掃描病通過整個腦干進行矢狀位的3D重建。其他矢狀位重建將增強對一些有可能涉及中線結(jié)構(gòu)的神經(jīng)變性病例如頂葉萎縮的評估。FLAIR圖像將用于整個皮質(zhì)萎縮，血管性白質(zhì)高信號和梗死。T2加權(quán)圖像將用于評估梗死，特別是發(fā)生在丘腦和基底節(jié)的腔隙性梗死，這些可能在FLAIR圖像被漏掉。T2*加權(quán)圖像在檢測微出血和淀粉樣血管病時是必須的，這些圖像同樣可用于對鈣化和鐵沉積的描述。DWI被認為是一類在青中年患者及快速進行的神經(jīng)變性?。ㄑ苎祝珻JD）中的補充序列。CTprotocolCTcanbeusefulwhencontraindicationspreventMRIorwhentheonlyreasonforimagingistoruleoutsurgicallytreatablecausesofcognitivedecline.

Inthetransverseplanethescanangleshouldbeparalleltothelongaxisofthetemporallobe.

Useofmulti-detectorCTwillenablecoronallyreformattedimagestobereconstructedperpendiculartothelongaxisofthetemporallobeforoptimalvizualisationofthehippocampus.CT評定在當(dāng)患者有MRI檢查的禁忌癥或只是排除外傷性可治療認知下降的原因時，可應(yīng)用CT.軸位平面掃描角可平行于顳葉的長軸。應(yīng)用多探測器能增強冠狀位格式的圖像用于重建垂直顳葉長軸顯示海馬的視角。CT負角掃描顯示海馬Useofmulti-detectorCTwillenablecoronallyreformattedimagestobereconstructedperpendiculartothelongaxisofthetemporallobeforoptimalvizualisationofthehippocampus.應(yīng)用多探測器能增強冠狀位格式的圖像用于重建垂直顳葉長軸顯示海馬的最佳視角。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).

懷疑患者有癡呆須用標準途徑評估MR表現(xiàn)。首先，可治療疾病像硬膜下血腫和腦積水須被排除。其次尋找特殊癡呆的表現(xiàn)如：AD：內(nèi)側(cè)顳葉（MTA）和頂葉萎縮。額顳葉癡呆（FTLD）：非對稱性額葉和顳葉萎縮。血管性癡呆（VaD）：全腦萎縮，彌散像白質(zhì)病變，腔梗和關(guān)鍵部位腦梗死。路易體癡呆（DLB）：對比其他類型癡呆通常沒有什么特異性。所以當(dāng)研究MR圖像時，我們應(yīng)該對全腦性萎縮、局造型萎縮和血管性疾?。üＫ溃踪|(zhì)病變，腔梗）進行評分。

ThisstandardizedassessmentoftheMRfindingsinapatientsuspectedofhavingacognitivedisorderincludes:GCA-scaleforGlobalCorticalAtrophyMTA-scaleforMedialTemporallobeAtrophyKoedamscoreforparietalatrophyFazekasscaleforWMlesionsLookingforstrategicinfarcts對懷疑認知功能下降的的患者MR特點標準化評估時包括：GCA-全腦性萎縮標準MTA-內(nèi)側(cè)顳葉萎縮的標準Koedam-頂葉萎縮將平分FazekasWM病灶的標準尋找關(guān)鍵部位梗死GCA-scaleforGlobalCorticalAtrophyGCAscaleisthemeanscoreforcorticalatrophythroughoutthecompletecerebrum:0:nocorticalatrophy1:mildatrophy:openingofsulci

2:moderateatrophy:volumelossofgyri

3:severe(end-stage)atrophy:'knifeblade'atrophy.GCA-全腦性萎縮標準GCA標準時整個大腦皮質(zhì)萎縮的平均評分0：沒有皮質(zhì)萎縮1：輕度萎縮：腦溝開放2：中度萎縮：腦回容量減少3：重度（終末期）萎縮：刀片樣萎縮

CorticalatrophyisbestscoredonFLAIRimages.

Insomeneurodegenerativedisorderstheatrophyisasymmetricandoccursinspecificregions.

Aradiologicalreportshouldmentionanyregionalatrophyorasymmetry.

Whenassessingatrophyindifferentregionskeepinmindthatcranially,thecentralsulcusliesmoreposteriorlythanyouwouldexpect(figure).皮層萎縮在FLAIR上最好評估。在一些神經(jīng)變性病中萎縮是不對稱的并發(fā)生在特殊部位。影像學(xué)報告需要設(shè)及到哪些區(qū)域萎縮和是否對稱。當(dāng)評估不同部位萎縮時，記住顱內(nèi)中央溝比想象的要靠后（箭頭）。MTA-scaleforMedialTemporallobeAtrophyTheMTA-scoreshouldberatedoncoronalT1-weightedimagesataconsistentsliceposition.

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

>75years:MTA-score3ormoreisabnormal(i.e.2canstillbenormalatthisage)Datafromastudywith222controlsandpatientswithvariousformsofdementiainwhichthisvisualratingscalewasusedtoassesstemporallobeatrophysuggestthatsensitivitiesandspecificitiesof85%canbeobtainedforpatientswithAD.MTA-內(nèi)側(cè)顳葉萎縮標準MTA需要在冠狀T1持續(xù)掃描圖像上評分，選擇通過海馬體部在腦橋前層面評估。<75歲：MTA2分或更多為異常（1分可被認為仍正常）>75歲：MTA評分3分或以上為異常（2分可認為正常）在一項222對照者和不同形式癡呆患者的研究發(fā)現(xiàn)這種評價內(nèi)顳葉萎縮在AD患者中可達到85%的敏感性和特異性Thescoreisbasedonavisualratingofthewidthofthechoroidfissure,thewidthofthetemporalhorn,andtheheightofthehippocampalformation.score0:noatrophyscore1:onlywideningofchoroidfissurescore2:alsowideningoftemporalhornoflateralventriclescore3:moderatelossofhippocampalvolume(decreaseinheight)score4:severevolumelossofhippocampusScrollthroughtheimagesforexamplesofMTAscore0-4.這個得分依賴于對脈絡(luò)膜裂，顳角寬度，海馬高度的視覺評估。0分：沒有萎縮1分：僅有脈絡(luò)膜裂增寬2分：伴有側(cè)腦室顳角的增寬3分：中度海馬體積的減低（高度降低）4分：中度海馬的萎縮圖片顯示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得分對AD的診斷有很高的敏感性，并且出現(xiàn)在大多數(shù)的AD患者中；然而在對照組中幾乎沒有。因此這是在AD患者中一個很好的鑒別試驗。這項測試對AD并不是完全特異的，因為在出現(xiàn)在其他形式癡呆中。另一方面，如果一個有AD前狀態(tài)的輕度認知功能障礙的患者有陰性的MTA值，那這個患者幾乎不會發(fā)展為AD（高敏感性，高的陰性預(yù)測值），除了在年輕的患者中，后萎縮形式可出現(xiàn)AD。IfthereisastrongsuspicionofAlzheimer'sdisease,itcanbeusefultorepeattheexaminationtoseeifthereisanyprogressofthe(medialtemporallobe)atrophy.

Theimagesshowafollow-upexaminationat18and36monthsinapatientwhowasatriskforfamilialAD,demonstratingprogressionofthedisease.

AnalternativeapproachwouldbetoperformaSPECT-orPET-scantolookforchangesinperfusion/metabolismofthetemporo-parietalcortex,asthesechangesprecedethedevelopmentofatrophy.如果高度懷疑AD，重復(fù)MR檢查來觀察內(nèi)側(cè)顳葉萎縮是否進展是有用的。上圖顯示了一個有家族性AD危險因素的患者18個月和36個月的隨訪檢查，證明了疾病的進展。另一個替代的方法可用SPECT或PET掃面尋找顳頂葉皮質(zhì)灌注和代謝的改變，這些變化可出現(xiàn)在萎縮之前。FazekasscaleforWMlesions

Fazekas白質(zhì)病變的評分標準FazekasscaleforWMlesionsOnMR,whitematterhyperintensities(WMH)andlacunes-bothofwhicharefrequentlyobservedintheelderly-aregenerallyviewedasevidenceofsmallvesseldisease.TheFazekas-scaleprovidesanoverallimpressionofthepresenceofWMHintheentirebrain.

ItisbestscoredontransverseFLAIRorT2-weightedimages.

Score:Fazekas0:NoneorasinglepunctateWMHlesionFazekas1:MultiplepunctatelesionsFazekas2:Beginningconfluencyoflesions(bridging)Fazekas3:LargeconfluentlesionsFazekas白質(zhì)病變的評分標準在MR上，腦白質(zhì)高信號（WMH）和腔梗-在老年患者中很常見，被認為是小血管病變。Fazekas評分標準提供了一個整個腦白質(zhì)病變的整體印象。在FLAIR和T2加權(quán)像上可以很好的評分。

得分Fazekas0分：沒有或單個點狀白質(zhì)病灶Fazekas1分：多發(fā)點狀病灶Fazekas2分：病灶開始融合（橋狀）Fazekas3分：大片融合TheFazekasscaleforWMlesionspredictsfuturedisabilityinelderly.

Fazekas腦白質(zhì)評分對老年未來殘疾的預(yù)測。Fazekas1isconsiderednormalintheelderly.

Fazekas2and3arepathologic,butmaybeseeninnormallyfunctioningindividuals.

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

Threeyearfollow-upshowsthatseverewhitematterchangesindependentlyandstronglypredictrapidglobalfunctionaldecline.Fazekas1級被認為是老年患者的正常表現(xiàn)。Fazekas2和3級分是病理性的，但是在正常功能個體也可見到，不過增加了致殘率。在600位正常功能老年個體，一年內(nèi)的Fazekas值預(yù)測殘疾率。在Fazekas3級分患者在一年內(nèi)25%致殘。3年隨訪觀察顯示中度白質(zhì)改變獨立很強的預(yù)測了腦功能下降。Capsandbands帽和帶Alimitedamountofwhitematterhyperintensitiesmayalsooccurinthenormallyageingbrain(Fazekasgrade1).

Lacunesarealwayspathological.有限的白質(zhì)高信號亦可發(fā)生在正常老化的大腦（Fazekas1級）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腦的和癡呆的影像表現(xiàn)可有一定的交叉。在相關(guān)早期，可有一些萎縮，盡管主要涉及突出的周圍血管間隙和非特異性的額頂溝的加寬。這也會出現(xiàn)一定程度的內(nèi)側(cè)內(nèi)葉的萎縮。一個MTA評分2分的超過75歲的患者可能是正常的。隨著大腦的老化，有越來越多的鐵沉積在大腦的特定區(qū)域：主要是基底節(jié)，黑質(zhì)的致密部和網(wǎng)狀部。這同樣會在T2和FLAIR像上形成沿著腦室高的信號邊緣，成為帽和帶。StrategicinfarctionsStrategicinfarctionsareinfarctionsinareasthatarecrucialfornormalcognitivefunctioningofthebrain.

Theseareasaresummarizedinthetable.關(guān)鍵部位的梗死關(guān)鍵部位的梗死指影響腦認知功能區(qū)域的梗死。這些區(qū)域在表中概括。StrategicinfarctionsarebestseenontransverseFLAIRandT2Wsequences.

Theimagesshowbilateralthalamicinfarctions-lesionsoftenassociatedwithcognitivedysfunction.關(guān)鍵部位梗死在FLAIR和T2W加權(quán)序列上。圖像顯示雙側(cè)丘腦梗死伴隨認知功能下降Studytheimagesoftwodifferentpatients.

Thencontinuereading.TheimageonthefarleftshowsaninfarctinthevascularterritoryofthePosteriorCerebralArtery(PCA),withinvolvementoftheinferiormedialtemporallobewhichincludesthehippocampus.

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

Thisisanotherexampleofastrategicinfarctionthatcanresultincognitivedysfunction.先看兩例不同的病人，然后繼續(xù)往下讀:左側(cè)圖像顯示了大腦后動脈的區(qū)域梗死，累及內(nèi)側(cè)顳葉包括海馬。這是一例關(guān)鍵部位的梗死，因為這是主要大腦半球，這將導(dǎo)致認知功能下降。另一幅軸位FLAIR圖像顯示大腦后動脈前部梗死，影響了顳頂相連的部位。這是另一例關(guān)鍵部位梗死導(dǎo)致認知下降。KoedamscoreforParietalAtrophyInadditiontomedialtemporallobeatrophy,parietalatrophyalsohasapositivepredictivevalueinthediagnosisofAD.

AtrophyoftheprecuneusisparticularlycharacteristicofAD.

ThisisparticularlythecaseinyoungpatientswithAD(presenileAD),whomayhavenormalMTA-scores.

TheKoedamscaleratesparietalatrophy-assessedinsagittal,coronalandaxialplanes.

Intheseplanes,wideningoftheposteriorcingulateandparieto-occipitalsulciaswellasparietalatrophy(includingtheprecuneus)israted(Table).頂葉萎縮的Koedam評分除了內(nèi)側(cè)顳葉萎縮，頂葉萎縮在AD的診斷中同樣有陽性預(yù)測值。楔前葉的萎縮時AD的一個特征性表現(xiàn)。這是一個特殊的青年AD患者（早老性AD）的病例，可能有正常的MTA值。Koedam值對頂葉分級要評估矢狀位、冠狀位和軸位圖像。在這些平面中，后扣帶回和頂枕溝的增寬和頂葉萎縮（包括楔前葉）被評定。Koedamscalegrade0-1

SagittalT1-,axialFLAIR-andcoronalT1-weightedimagesillustratingtheKoedamscaleofposterioratrophy.

Whendifferentscoresareobtainedindifferentorientations,thehighestscoremustbeconsideredKoedam標準0-1級矢狀位T1，軸位FLAIR和冠狀T1加權(quán)圖像顯示后部萎縮的Koedam標準。當(dāng)不同的分數(shù)在不同方向不同時，取其最高值。Koedamscalegrade2-3

SagittalT1-,axialFLAIR-andcoronalT1-weightedimagesillustratingtheKoedamscaleofposterioratrophy.

Theyellowarrowspointtoextremewideningoftheposteriorcingulateenparieto-occipitalsulciinapatientwithgrade3posterioratrophy.Koedam標準2-3級矢狀位T1，軸位FLAIR和冠狀T1圖像顯示后部萎縮。黃色箭頭顯示在3級患者后部扣帶回與頂枕溝末端加寬。FDG-PETInadditiontoclinicalfindings,CSFandMRI,PET-imagingisusefulindiagnosingAD.

InADFDG-PETcanshowhypometabolisminthetemporoparietalregionsand/ortheposteriorcingulum.

ThismayhelpdifferentiateADfromFTD,whichshowsfrontalhypometabolismonFDG-PET.

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

InADthereisadecreasedmetabolismoftheparietallobes(yellowarrows),whereasinFTD,thereisfrontalhypometablism(redarrows).FDG-PET除了臨床發(fā)現(xiàn)以外，CSF和MRI，PET圖像診斷AD也是有益的。在AD患者中，F(xiàn)DG-PET顯示顳頂葉區(qū)域和或后部扣帶的低灌注。這或能幫助鑒別AD和FTD，F(xiàn)TD中顯示FDG-PET的額葉低灌注。這張圖像顯示了正常個體、AD和FTD患者的FDG-PET和軸位FLAIR圖像。正常個體、AD和FTDFDG-PET患者的FDG-PET和軸位FLAIR圖像。在AD患者，頂葉代謝率降低，而在FTD患者，額葉低灌注。Theprevalenceofspecificformsofdementiaisage-dependent.

Inpatients<65yearstherearemorecasesoffamilialandpresenileprogressiveformsofADandmorecasesofFTLD.

Inpatients>65yearstherearemorecasesofsenileADandvasculardementia.

InmanyolderpatientswithmanifestADthereisco-existingvasculardisease,whichcontributestothedementedstate.特異形式癡呆的流行因素是年齡。在小于65歲患者，更多的是AD家族性和早老性進程與更多的FTLD。在大于65歲患者，有更多的早老性AD和血管性癡呆。在很多老年患者有AD特征和血管性疾病共存，這加重了癡呆狀態(tài)。AlzheimersDiseaseADaccountsfor50%-70%ofallcasesofdementiaintheelderlypopulation.

Ageisastrongriskfactor,withthediseaseaffectingapproximately8%ofindividualsovertheageof65and30%overtheageof85years.

TheprogressionofADisgradualandtheaveragepatientlives10yearsaftertheonsetofsymptoms.

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

InimagingwethereforehavetotrytoidentifyADinanearlierstageandwehavetoconcentrateonthehippocampusandthemedialtemporallobe,becausethatiswhereADstarts.

TheroleofMRIinthediagnosticprocessofADistwofold:Ruleoutothercausesofcognitiveimpairment.IdentifyearlyonsetADforpossibleinnovativetherapyandcounseling阿爾茨海默病AD占老年人群所有癡呆的50%-70%。年齡是一個很強的危險因素，隨著年齡增加，AD影響了8%的大于65歲的患者和30%的大于85歲人群。AD是逐漸進展的過程，癥狀發(fā)作后患者平均生存10年。隨著老年患者比例的增加，預(yù)計在未來50年AD的發(fā)病率增加3倍。在AD的終末期廣泛的萎縮，和其他類型癡呆的晚期相似。在影像學(xué)上我們需要在早期發(fā)現(xiàn)AD，為此我們更加關(guān)注顳葉內(nèi)側(cè)皮質(zhì)和海馬，因為那是AD起始處。MR對AD的診斷過程是雙重的：1、排除其他認知下降的原因。2、確認早期AD以便早期治療和參考Studytheimage,thencontinuereading.ThefindingsareconsistentwiththediagnosisofendstageAD,becausethereis:Extremehippocampalandmedialtemporallobeatrophy(MTAscore:4)Severeglobalatrophy(GCAscale:3)

ItisnotspecificforADhowever,sincesevereGCAoccursinotherend-stagedisordersaswell學(xué)習(xí)圖像，然后往下讀.這些發(fā)現(xiàn)和AD的診斷一致，因為：明顯的海馬和內(nèi)側(cè)顳葉的萎縮(MTA4分）重度全腦萎縮（GCA3級）但這對AD并不是特異的，因為重度GCA可發(fā)生在其他癡呆的終末期。PresenileADPresenileAD(<65y)hasadifferentpresentation.

Althoughthereusuallyissomemildhippocampalatrophy,themoststrikingfindingisparietalatrophywithatrophyoftheposteriorcingulumandtheprecuneus;thehippocampuscanbenormal.早老性AD早老性AD（小于65歲）有不同的表現(xiàn)。盡管有輕度的海馬萎縮，最重要的發(fā)現(xiàn)是伴隨后部扣帶和楔前葉的頂葉萎縮。海馬可正常MildCognitiveImpairment(MCI)Mildcognitiveimpairmentisarelativelyrecenttermusedtodescribepeoplewhohavesomeproblemswiththeirmemory,butdonotactuallyhavedementia,sincedementiaisdefinedashavingproblemsintwoormorecognitivedomains.

SomeofthesepatientswillbeintheearlystagesofAlzheimer'sdiseaseoranotherdementia,soitisimportanttoidentifythem.

FindingMTAisastrongrisk-factorforprogressiontodementia.輕度認知功能障礙（MCI）輕度認知功能障礙是最近被用于描述那些有記憶障礙，但是并沒有癡呆的患者，因為癡呆被定義為有兩個或更多領(lǐng)域的認知障礙。這些患者可能處于AD的早期階段或其他類型的癡呆，所以識別他們很重要。MTA表現(xiàn)是進行性癡呆的一個重要的危險因素。PCAinfarctioninvolvingthemedialtemporallobe.

腦后動脈梗死影響到顳葉內(nèi)側(cè)皮質(zhì)VascularDementia(VaD)Vasculardementia(VaD)isthoughttobethesecondmostcommoncauseofdementiaafterAlzheimer'sdisease.

ItcansometimesbedistinguishedfromADbyamoresuddenonsetandassociationwithvascularriskfactors.

VaDcanbecharacterizedbyitsstepwisedeteriorationwithperiodsofstabilityfollowedbysuddendeclineincognitivefunction.

Mostpatients,however,havesmallvesseldisease,whichistypifiedbyamoregradualandsubtlepatternofdeterioration.

Controlofvascularriskfactorsisthetreatmentofchoice,butcholinesteraseinhibitors(drugsthatarebeingusedinAD)arealsoincreasinglybeingusedtotreatvasculardementia.TheimagesshowapatientwithastrategicPCAinfarctioninvolvingthehippocampus.

Thistypeofinfarctcanresultinsuddendementiaiflocatedinthedominanthemisphere.

Itwillusuallynotresultindementiaifitoccursinthenon-dominanthemisphere.血管性癡呆血管性癡呆被認為是僅此于AD的癡呆的第二大原因。有時可通過突然發(fā)病和有血管危險因素與AD鑒別。血管性癡呆以漸進性惡化有穩(wěn)定期和突然的認知功能下降。大多數(shù)的患者，有小血管疾病，這以漸進性和明顯惡化為特征。控制血管因素是治療的一個選擇，但是膽堿酯酶抑制劑也同樣越來越多被用于治療血管性癡呆。這幅圖像顯示了累及海馬的關(guān)鍵區(qū)域的大腦后動脈梗死。這種類型的梗死可導(dǎo)致突然的癡呆如果位于優(yōu)勢半球。如果發(fā)生在非優(yōu)勢半球一般不引起癡呆。InmostpatientswithVaDthereisdiffusewhitematterdiseasewithlargeconfluentlesions(Fazekas3).

Insomeofthesepatientstheventriclesmaybedilatedduetoglobalatrophyandsomewillalsohavemedialtemporallobeatrophy.

TheimagesareofapatientwhohadVaD,butthemedialtemporallobewasnormal.在大多數(shù)血管性癡呆的患者，往往有彌散性白質(zhì)融合病灶（Fazekas3級）在一些這類病人中，會因腦萎縮而引起腦室的擴張，仍伴隨內(nèi)側(cè)顳葉萎縮。這幅圖像是一個有血管性癡呆的患者，但是內(nèi)側(cè)顳葉正常。StrategicinfarctsandsmallvesseldiseaseCognitivedysfunctioninVaDcanbetheresultof:Largevesselinfarctions:Bilateralintheanteriorcerebralarteryterritory.Parietotemporal-andtemporo-occipitalassociationareasofthedominanthemisphere(angulargyrusincluded)PosteriorcerebralarteryterritoryinfarctionoftheparamedianthalamicregionandinferiormedialtemporallobeofthedominanthemisphereWatershedinfarctionsinthedominanthemisphere(superiorfrontalandparietal)Smallvesseldisease:Multiplelacunar

infactionsinfrontalwhitematter(>2)andbasalganglia(>2)WMLs(atleastmorethan25%ofWM)Bilateralthalamiclesions關(guān)鍵部位的梗死和小血管病變血管性認知功能下降可由下面原因引起：大血管梗死：雙側(cè)大腦前動脈供應(yīng)區(qū)。頂顳和顳枕交界區(qū)（包括角回）大腦后動脈供血區(qū)的丘腦內(nèi)側(cè)旁和優(yōu)勢半球顳葉后內(nèi)側(cè)部的梗死優(yōu)勢半球分水嶺梗死（額上部和頂葉）小血管疾病額葉白質(zhì)(>2)和基底節(jié)(>2)的多發(fā)腔梗。廣泛白質(zhì)病變（至少超過25%的白質(zhì)病變）雙側(cè)丘腦病變Thereisanincreasingawarenessfortheimportanceofsmallvesseldiseaseasapredictorofcognitivedeclineanddementia.

Moreover,itseemstoamplifytheeffectsofpathologicchangesofAlzheimer'sdisease.

OntheleftweseeapatientwhowasdiagnosedashavingVaD.

WhitematterdiseaseisseenassevereWMH(hypointenseonT1)intheperiventricularregions.

Inadditiontothesevascularchanges,thereisalsoMTA.

PresumablythispatienthasbothVaDandAD,afindingseeninmanyelderlypatients.

Thesefindingsshouldbedescribedseparatelyasitmayhavetherapeuticconsequences.在預(yù)測認知功能下降和癡呆方面小血管疾病正越來越受重視。然而，很多時候把AD的病理改變擴大化了。上面的圖像診斷為血管性癡呆。白質(zhì)疾病可看到嚴重的腦室周圍的白質(zhì)病變（T1低信號），除了這些血管性改變，同樣也有內(nèi)側(cè)顳葉的萎縮。假設(shè)這個病人既有VaD又有AD，這個情況可在很多老年患者中見到。這些表現(xiàn)因治療的不同應(yīng)該單獨描述。Theproblemhoweveris,thatwhitematterhyperintensitiesandlacunesarealsofrequentlyobservedinnon-dementedelderlyandatsomelevelcanberegardedasnormalfindingsinaging.

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

HoweverconsiderableinterobservervariabilityexistsfortheassessmentoftheradiologicalpartoftheseNINDS-AIRENcriteriaandsomeleveloftrainingismandatory.

問題是白質(zhì)高信號和腔梗在非癡呆的老年人常見，甚至在一定程度上被認為隨年齡變化的正常表現(xiàn)。為了克服這個問題，NINDS-AIREN協(xié)會基于病史、體格檢查、影像學(xué)表現(xiàn)和病理改變制定了可能的、很可能的和明確的血管性癡呆。然而，在評估NINDS-AIREN標準重影像學(xué)部分時存在相當(dāng)大的觀察者觀察變異，一些觀察水平也是強制性的。Themedialnucleiofthethalamusplayanimportantroleinmemoryandlearning.

Alargeunilateralinfarctionorbilateralinfarctionsinthisregioncancausedementia.

Youhavetopayspecialattentiontotheseareastofindthesesmallinfarctions.丘腦內(nèi)側(cè)核團在學(xué)習(xí)和記憶中扮演重要角色。大的單側(cè)梗死和雙側(cè)的梗死可引起癡呆。要特別注意這些區(qū)域的小的梗死灶。OnFLAIRimagesyouwilleasilymisstheseinfarctions,becausetheycanbeisointensetothesurroundingstructures(8).

AhighresolutionT2WIisneededtodetectthesethalamicinfarcts.

FLAIRintheinfratentorialregionandinthespinalcordisoflimitedvalueasitsuppressesnotonlythesignalofwater,butalsopathologywithalongT1-relaxationtime.

ThisphenomenoncanalsobeseeninthedetectionofMultipleSclerosis,whereFLAIRisoflimitedvalueintheinfratentorialregionandofnouseinthespinalcord.在FLAIR圖像上很容易漏掉梗死灶，，因為它們和周圍信號相同。檢測丘腦的梗死需要高分辨率的T2圖像。FLAIR在幕區(qū)和脊髓中價值不大，因為它不僅抑制水的信號，而且引起長的T1弛豫時間。這種現(xiàn)象在多發(fā)性硬化中也可以見到，F(xiàn)LAIR在幕區(qū)和脊髓中價值不大。CerebralAmyloid

Angiopathy(CAA)DementiamaybetheclinicalpresentationinCAA,aconditioninwhich?-amyloidisdepositedinthevesselwallsofthebrain.

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

Inaddition,FLAIRwillrevealmoderatetoseverwhitematterhyperintensities(Fazekasgrade2or3)T2*imagesinapatientwithCAAshowmultipleperipherallylocatedmicrobleeds.腦淀粉樣血管?。–AA）癡呆可能是CAA的臨床表現(xiàn)，由?淀粉樣蛋白沉積引起。CAA容易出血，往往是微出血，同樣可引起蛛網(wǎng)膜下腔出血和腦葉的血腫。在MR上，T2*序列上顯示多發(fā)微出血，典型的事周圍部位（對比高血壓出血，常發(fā)生在中央部位，如基底節(jié)區(qū)和丘腦）除此之外，F(xiàn)LAIR將顯示中道重度白質(zhì)高信號（(Fazekas2或3級）T2*圖像顯示CAA病人多發(fā)外周微出血。FLAIRimagesofthesamepatientshowFazekas2whitematterhyprintensities.

FLAIR圖像顯示同一個病人Fazekas2級的白質(zhì)高信號。T2*imagesinapatientwithCAAmicrobleeds.

T2*圖像顯示CAA患者微出血。T2*imagesdemonstratemultiplelobarmicrobleedsinapatientwithCAA.

T2*圖像證明了在CAA病人中多發(fā)腦葉微出血的存在。FrontotemporalLobarDegeneration(FTLD)FTLD,formerlycalledPick'sdisease,isaprogressivedementia,thataccountsfor5-10%ofcasesofdementia.,andoccursrelativelymorefrequentlyinpresenilesubjects

FTLDisclinicallycharacterizedbybehavioralandlanguagedisturbancesthatmayprecedeorovershadowmemorydeficits.

Thereiscurrentlynotreatmentforthiscondition.Imagingplaysanimportantroleinthediagnosisasthefindingsareeasytorecognize.

Radiologicalfindingsarepronouncedatrophyoffrontaland/ortemporallobes.

InsomeformsofFTLDtheatrophymightbestrikinglyasymmetric,e.g.inSemanticDementia,adiseasesubtypewithprogressiveaphasiaandleft-sidedtemporallobedegeneration.額顳葉癡呆（FTLD）FTLD，之前被稱作匹克病，是一種進行性癡呆，占癡呆的5-10%，發(fā)生在相對年輕的群體。FTLD臨床上以行為和語言障礙為主，一定程度上掩蓋了記憶缺陷。至今沒有針對此的治療。圖像在診斷上有重要作用，因為易于識別。影像學(xué)的主要表現(xiàn)是額葉與顳葉的萎縮。在另一些形式的FTLD中萎縮可明顯不對稱，如語義性癡呆，一個進行性失語和左側(cè)顳葉變性的亞型。Theimagesareofapatientwithprogressiveaphasia.

Themostprominentfindingisthestrikingasymmetricatrophyofthetemporallobeontheleftsidewithnotonlyatrophyofthehippocampus,butalsothetemporalpoles.

Theatrophyhasresultedingyrithatappearassharpasknives('knifebladeatrophy').

ThereisalsosomeincreasedsignalintensityseenontheFLAIRimage,probablyduetogliosis.

ThesefindingsarepathognomonicforthediagnosisofFTLD.Patientswithleft-sidedtemporalatrophyareusuallyclinicallyobvious.

Right-sidedatrophyisusuallynotaseasilyrecognizedasthesepatientsonlypresentwithsubtledisturbancesinrecognizingfaces.這是一個漸進性失語患者的圖像。最主要的發(fā)現(xiàn)是明顯的左側(cè)顳葉前部和海馬的非對稱性萎縮。萎縮使得腦回如刀片樣（刀片樣萎縮）在FLAIR相上，可能由于膠質(zhì)的增生可見高信號區(qū)。這是發(fā)現(xiàn)是診斷FTLD的特殊特征。左側(cè)顳葉萎縮的病人往往有明顯的臨床特征。右側(cè)萎縮往往不好識別，因為病人表現(xiàn)出輕微的異常。路易體癡呆路易體癡呆占癡呆的25%，和PSP/MSA同為非典型的帕金森綜合征。路易體癡呆的臨床特征可類似于AD或帕金森病相關(guān)的癡呆?；颊咄?/p>