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DKI弥散峰度成像英文简介Contents
DWI(diffusionweightedimaging)DTI(diffusiontensorimaging)DKI(diffusionkurtosisimaging)DWI原理MR图像旳信号组织T1、T2驰豫时间、H1旳密度、分子弥散运动DWI图像利用扩散敏感梯度脉冲将水分子弥散效应扩大,来研究不同组织中水分子扩散运动旳差别
DWI评估弥散旳参数
经过两个以上不同弥散敏感梯度值(b值)旳弥散加权象,可计算出弥散敏感梯度方向上水分子旳表观弥散系数(apparentdiffusioncoefficient
ADC)
ADC=In(S低/S高)/(b高-b低)弥散敏感系数(b)值==r2σ2g2(△-σ/3)b值旳取值范围为0~10000s/mm2,较大旳b值具有较大旳弥散权重,对水分子旳弥散运动越敏感,并引起较大旳信号下降,但b值越大,图像信噪比也相应下降,假如b值太小,易受T2加权旳影像,产生所谓旳T2透射效应(T2shinethrougheffect),一般来说用大b值差旳图像测得旳ADC值较精确,故侧ADC值时宜选较高b值和较大旳b值差ADC反应了水分子旳扩散运动旳能力,指水分子单位时间内扩散运动旳范围,越高代表水分子扩散能力越强。
均质介质中能够水分子旳自由运动为各向同性,即在各个方向上旳弥散强度大小一致,弥散张量D描述为球形,沿磁共振旳三个主坐标旳特征值为λ1=λ2=λ3在脑白质中因为髓鞘旳阻挡,水分子旳弥散被限制在与纤维走行一致旳方向上,具有较高旳各向异性,此时弥散张量可表达为椭球形,其特征值λ1>λ2>λ3,最大特征值相应旳方向与经过该体素旳纤维束走行平行defectsofDTIConventionalDTIfailstofullyutilizetheMRdiffusionmeasurementsthatareinherenttotissuemicrostructure.
DTIcomputesapparentdiffusivitybasedontheassumptionthatdiffusionweighted(DW)MRsignalhasamonoexponentialdependenceonthediffusionfactor(b-value).DTIimplicitlyassumesthatwatermoleculediffusionoccursinafreeandunrestrictedenvironmentwithaGaussiandistributionofdiffusiondisplacement.defectsofDTI
Inbiologicaltissue,complexcellularmicrostructuresmakewaterdiffusionahighlyhinderedorrestrictedprocess.
Non-monoexponentialdecaysareexperimentallyobservedinbothwhitematterandgraymatter.Moreover,thesimplifieddescriptionofthediffusionprocessinvivobya2nd-order3DdiffusivitytensorpreventsDTIfrombeingtrulyeffectiveincharacterizingrelativelyisotropictissuesuchasGM.EveninWM,theDTImodelcanfailifthetissuecontainssubstantialcrossingordivergingfibers.
defectsofDTIAsaresult,DTIquantitationisb-valuedependentandDTIfailstofullyutilizethediffusionmeasurementsthatareinherenttotissuemicrostructure.KurtosisKurtosisherereferstotheexcesskurtosisthatisthenormalizedandstandardizedfourthcentralmomentofthewaterdisplacementdistribution.ItisadimensionlessmeasurethatquantifiesthedeviationofthewaterdiffusiondisplacementprofilefromtheGaussiandistributionofunrestricteddiffusion,providingameasureofthedegreeofdiffusionhindranceorrestriction.fourthcentralmoment:四阶中心距,主要用来衡量随机分布变量旳分布在均值附近旳陡峭程度SincethedeviationfromGaussianbehaviorisgovernedbythecomplexityofthetissuewithinwhichthewaterisdiffusing,thisexcessdiffusionalkurtosiscanberegardedasameasureofatissue’sdegreeofstructure.OtheradvantagesofDKIDKIprovidesahigher-orderdescriptionofrestrictedwaterdiffusionprocessbya2nd-order3Ddiffusivitytensor(DTasinconventionalDTI)togetherwitha4th-order3Dkurtosistensor(KT).ConditionsThemethodisbasedonthesametypeofpulsesequencesemployedforconventionaldiffusion-weightedimaging(DWI),buttherequiredbvaluesaresomewhatlargerthanthoseusuallyusedtomeasurediffusioncoefficients.Inthebrain,bvaluesofabout2023s/mm2aresufficient.Atleast15non-collinearandnon-coplanardirectionsarerequiredtoconstructKT.DKIvsq-spaceimagingtechniquesDKIhasacloserelationshiptoq-spaceimagingtechniques.q-spaceimagingmethodshaveindeedrecentlybeenemployedtoestimatediffusionalkurtosis.Theprincipaldifferencebetweenthemisthatq-spaceimagingseekstoestimatethefulldiffusiondisplacementprobabilitydistributionratherthanjustthekurtosis.Asaconsequence,q-spaceimagingismoredemandingintermsofimagingtimeandgradientstrengths.MeasuringthediffusionalkurtosisrequiresonlymodestincreasesinbvaluesAndDKIislessdemandingintermsofhardwarerequirementsandpostprocessingeffort.Kurtosistensor(KT)derivedparametersMK(meankurtosis):MKisameasureoftheoverallkurtosis.Itdoesnothaveanydirectionalspecificity.MK旳大小取决于感爱好区内组织旳构造复杂程度,构造越复杂非正态分布水分子扩散受限越明显,MK也即越大K∥(Axialkurtosis)andK⊥(Radialkurtosis)
:canbedefinedasthekurtosisparallelandperpendiculartotheprinciplediffusioneigenvector(e1)K⊥越大表白在该方向非正态分布水分子扩散受限越明显,反之则表白扩散受限越弱FAK(fractionalanisotropyofkurtosis)SimilartoFAinDTI,theanisotropyofdirectionalkurtosiscanbeconvenientlydefinedasFAK
KA越小即表达越趋于各向同性扩散;若组织构造越紧密越规则,KA越大DKIparametricmapsDKIparametricmapsTypicalDKI-derivedparametricmapsfromasinglesliceofa)invivo,b)formalin-fixedadultratbrainsandc)anormalhumansubject(male,44yearsold).Axialdiffusivity(λ//),radialdiffusivity(λ⊥),meandiffusivity(MD),axialkurtosis(K//),radialkurtosis(K⊥),meankurtosis(MK),fractionalanisotropy(FA),directionallyencodedcolourFA(DEC-FA)andfractionalanisotropyofkurtosis(FAK)mapsarecomputedfromDKImodel.DKIparametricmapsFor(a),rawDWIswereacquiredbySEEPIwithTR/TE = 3000/30.3 ms,δ/Δ = 5/17 ms,slicethickness = 1 mm,FOV = 30 × 30 mm2,datamatrix = 128 × 128(zerofilledto256 × 256),NEX = 4,6b-values(0.0,0.5,1.0,1.5,2.0and2.5 ms/µm2)andalong30directionsusing7TscannerDKIparametricmapsFor(b),rawDWIswereacquiredwiththesameparametersasthoseforinvivoexceptTE = 34.3 ms,δ = 9 msandb-valuesof0.0,1.0,2.0,3.0,4.0and5.0 ms/µm2.Alargerb-valuerangewasusedinexvivoexperimentduetothegenerallylowerdiffusivities.DKIparametricmaps
For(c),rawDWIswereacquiredbySEEPIwithTR/TE = 2300/109 ms,slicethickness = 2 mm,FOV = 256 × 256 mm2,datamatrix = 128 × 128,NEX = 2,6b-values(0.0,0.5,1.0,1.5,2.0and2.5 ms/µm2)andalong30directionsusinga3TSiemensscannerDKIparametricmaps
HigherMKisfoundinWM,indicatingagenerallyhigherdegreeofdiffusioncomplexityandrestrictionintheWMstructures.ItcanbeseenfromthedirectionalkurtosismapsthatsuchhighMKinWMismainlycontributedbyK⊥.ThissuggeststheexistenceofheterogeneityandrestricteddiffusioninaxonalstructuresBothMKandK⊥
exhibitstrongcontrastbetweenWMandGMstructures.DKIparametricmapsBothMKandK⊥
exhibitstrongcontrastbetweenWMandGMstructures.PositivemeananddirectionalkurtosesareobservedinbothWMandGM,indicatingfasterDWsignaldecayatlowerb-valuesandrestricteddiffusionenvironmentinbothWMandGMunderinvivoandformalin-fixedconditions.DKIshowsageneraldecreaseindiffusivityandincreaseinkurtosisinWMandGMofthefixedbrainsThebreakdownsofneurofilamentsandmicrotubulescausedbyfixativesarebelievedtoproducemorediffusionbarriersandhenceleadtotheλ//
decreaseandK//
increase.Otherfixationeffectssuchastissueshrinkage,decreaseinmembranepermeability,increaseinaxonalpackingdensityandreductionofextracellularspaceinparenchymaalsolikelycontributetothesignificantλ⊥decreaseandK⊥
increase.Directionalkurtosisanalysisoffixedexperimentalautoimmuneencephalitis(EAE)spinalcordTheinflammatoryneurodegenerativediseaseEAE
ischaracterizedbybothaxonallossanddemyelinationInrecentDKIstudies,therearepromisingresultsofusingMKtodetectchangesinnormalorpathologicalneuraltissue
However,asanaverageofkurtosesalongallthediffusiondirections,MKcanlosesensitivityandspecificityinprobingdirectionalchangesofpathologicaltissueEAEspinalcordK//
isfoundtobesignificantlyincreasedandλ//
decreasedinthelesionareaλ//
reductionislikelyduetocytoskeletalperturbationordebrisformationwhentheaxonalstructuresbreakdownInaddition,λ⊥
increaseswhereasK⊥
decreaseslikelybecauseofthedemyelinationandaxonallossthatalsoleadtolessdiffusionrestrictioninradialdirection.EAEspinalcordThedirectionallyaveragedMDandMKarefoundtobelesssensitivetoEAEpathologyduetotheoppositetrendsofdiffusivityandkurtosischangesinaxialandradialdirection.MonitoringpostnatalbrainmaturationbyconventionalDTI
CC:corpuscallosum(胼胝体);EC:externalcapsule(外囊);CP:cerebralpeduncle(大脑脚);AC:anteriorcommissure;(前联合)CT:cerebralcortex(脑皮质);HP:hippocampus(海马);CPu:caudateputamen(新纹状体)MonitoringpostnatalbrainmaturationbyconventionalDTI
Thesensitivityofλ//
indetectingratbrainWMmaturationisgenerallyobservedtobethehighestatlowb-value
Atrelativelylowb-values,theapparentdiffusivityisprimarilycontributedfromthefastwaterdiffusionactivitiesinextracellularspacethatdependonbothcellularmicrostructureandmembranepermeability.
Theuseoflowb-valuecanbestdetectthesechanges.Thehighλ//
sensitivityatlowb-valueobservedinthecurrentstudysuggeststhealterationsofthesefastwaterdiffusionactivitiesalongaxonaldirectionduringbrainmaturation.
Suchalterationsmayresultfromtheincreaseinpackingdensityoffiberbundlesandaxons,axonaldiameterincrease,changesinneurofibrils,andincreasedcomplexityofextracellularmatrix.MonitoringpostnatalbrainmaturationbyconventionalDTI
Whereasthatofλ⟂
isthehighestathighb-valueThediffusionchangesprobedinWMusinghighb-valuesareascribedmoretotheslowwatermoleculediffusionparticularlyalongtheradialdirectionwhentraversingthemembranesandmyelinsheathsThehighsensitivityofλ⟂
athighb-valueindetectingbrainmaturationshowninthefigurelikelyreflectstheseWMmicrostructuralchanges,includingmyelinationandaxonaldensityanddiameterchangesduringpostnatalbraindevelopment.MonitoringpostnatalbrainmaturationbyconventionalDTIFAquantitationisalsoaffectedbytheb-valueanditsabilityindetectingbrainmaturationalchangesvariesamongdifferentstructures.MonitoringpostnatalbrainmaturationbyDKIFigure7ashowsthatthesensitivityoffittingallthemulti-b-valueDWIstoDTImodelisgenerallysimilartothatofemployingamediumb-value(b = 1.5 ms/µm2)showninFigure6InFigure7b,thegeneralandcontinualkurtosisincreasewithageisobserved,indicatingthatmorediffusionrestrictionoccursduringbrainmaturationinbothWMandGMstructures.TheDKI-deriveddiffusivityandkurtosisindicesarehighlysensitivetobraindevelopmentalchanges.MonitoringpostnatalbrainmaturationbyDKI
Bothλ//
andK//
ofWMarefoundtoincreaseswithage,whichmayarisefromvariousbiologicaleventsduringearlypostnatalbrainmaturation.TheincreaseofdiffusivitycanbecausedbyaxoplasmicflowduringthemyelinationperiodneuronallossandaxonalpruningthatshortenstheaxonlengthcanleadtoanincreaseofrestrictionMonitoringpostnatalbrainmaturationbyDKITheincreaseofK⊥
inWMislikelyascribedtothemyelinationandmodificationofaxonalstructuresthatincreasesrestrictionintheradialdirection.
DKIanalysisalsorevealsthatdiffusionrestrictionintherelativelyisotropicGMincreaseswithage.ThismayreflectthemoredenselypackedstructuresandthedendriticarchitecturalmodificationinGMDTIVSDKIinmonitoringpostnatalbrainmaturation
WhenthereisalargeK,theestimateddiffusivityinconventionalDTIshowsalargediscrepancywiththediffusivityestimatedinDKIapproach.AsKinallthestructuresispositive,DTI-deriveddiffusivi
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