DKI-(弥散峰度成像)-英文简介课件

DiffusionalKurtosisImaging

DKIContents

DWI(diffusionweightedimaging)DTI(diffusiontensorimaging)DKI(diffusionkurtosisimaging)DWI原理MR图像的信号组织T1、T2驰豫时间、H1的密度、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的差异

均质介质中可以水分子的自由运动为各向同性，即在各个方向上的弥散强度大小一致，弥散张量D描述为球形，沿磁共振的三个主坐标的特征值为

λ1=λ2=λ3在脑白质中由于髓鞘的阻挡，水分子的弥散被限制在与纤维走行一致的方向上，具有较高的各向异性，此时弥散张量可表示为椭球形，其特征值λ1>λ2>λ3，最大特征值对应的方向与经过该体素的纤维束走行平行defectsofDTIConventionalDTIfailstofullyutilizetheMRdiffusionmeasurementsthatareinherenttotissuemicrostructure.

DTIcomputesapparentdiffusivitybasedontheassumptionthatdiffusionweighted(DW)MRsignalhasamonoexponentialdependenceonthediffusionfactor(b-value).DTIimplicitlyassumesthatwatermoleculediffusionoccursinafreeandunrestrictedenvironmentwithaGaussiandistributionofdiffusiondisplacement.defectsofDTI

Inbiologicaltissue,complexcellularmicrostructuresmakewaterdiffusionahighlyhinderedorrestrictedprocess.

Non-monoexponentialdecaysareexperimentallyobservedinbothwhitematterandgraymatter.Moreover,thesimplifieddescriptionofthediffusionprocessinvivobya2nd-order3DdiffusivitytensorpreventsDTIfrombeingtrulyeffectiveincharacterizingrelativelyisotropictissuesuchasGM.EveninWM,theDTImodelcanfailifthetissuecontainssubstantialcrossingordivergingfibers.

defectsofDTIAsaresult,DTIquantitationisb-valuedependentandDTIfailstofullyutilizethediffusionmeasurementsthatareinherenttotissuemicrostructure.OtheradvantagesofDKIMeankurtosis(MK),theaverageapparentkurtosisalongalldiffusiongradientencodingdirections,hasbeenmeasuredanddemonstratedtoofferanimprovedsensitivityindetectingdevelopmentalandpathologicalchangesinneuraltissuesascomparedtoconventionalDTI.Inaddition,directionalkurtosisanalysishasbeenformulatedtorevealdirectionallyspecificinformation,suchasthewaterdiffusionkurtosesalongthedirectionparallelorperpendiculartotheprinciplewaterdiffusiondirectionasdeterminedbythe2nd-orderdiffusiontensorConditionsThemethodisbasedonthesametypeofpulsesequencesemployedforconventionaldiffusion-weightedimaging(DWI),buttherequiredbvaluesaresomewhatlargerthanthoseusuallyusedtomeasurediffusioncoefficients.Inthebrain,bvaluesofabout2000s/mm2aresufficient.Atleast15non-collinearandnon-coplanardirectionsarerequiredtoconstructKT.Kurtosistensor(KT)derivedparametersMK(meankurtosis):MKisameasureoftheoverallkurtosis.Itdoesnothaveanydirectionalspecificity.MK的大小取决于感兴趣区内组织的结构复杂程度，结构越复杂非正态分布水分子扩散受限越显著，MK也即越大K∥(Axialkurtosis)andK⊥(Radialkurtosis)

:canbedefinedasthekurtosisparallelandperpendiculartotheprinciplediffusioneigenvector(e1)K⊥越大表明在该方向非正态分布水分子扩散受限越明显，反之则表明扩散受限越弱FAK(fractionalanisotropyofkurtosis)SimilartoFAinDTI,theanisotropyofdirectionalkurtosiscanbeconvenientlydefinedasFAK

KA越小即表示越趋于各向同性扩散;若组织结构越紧密越规则，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

HigherMKisfoundinWM,indicatingagenerallyhigherdegreeofdiffusioncomplexityandrestrictionintheWMstructures.ItcanbeseenfromthedirectionalkurtosismapsthatsuchhighMKinWMismainlycontributedbyK⊥.ThissuggeststheexistenceofheterogeneityandrestricteddiffusioninaxonalstructuresBothMKandK⊥

exhibitstrongcontrastbetweenWMandGMstructures.DKIparametricmapsBothMKandK⊥

exhibitstrongcontrastbetweenWMandGMstructures.PositivemeananddirectionalkurtosesareobservedinbothWMandGM,indicatingfasterDWsignaldecayatlowerb-valuesandrestricteddiffusionenvironmentinbothWMandGMunderinvivoandformalin-fixedconditions.Directionalkurtosisanalysisoffixedexperimentalautoimmuneencephalitis(EAE)spinalcordTheinflammatoryneurodegenerativediseaseEAE

ischaracterizedbybothaxonallossanddemyelinationInrecentDKIstudies,therearepromisingresultsofusingMKtodetectchangesinnormalorpathologicalneuraltissue

However,asanaverageofkurtosesalongallthediffusiondirections,MKcanlosesensitivityandspecificityinprobingdirectionalchangesofpathologicaltissueEAEspinalcordK//

isfoundtobesignificantlyincreasedandλ//

decreasedinthelesionareaλ//

reductionislikelyduetocytoskeletalperturbationordebrisformationwhentheaxonalstructuresbreakdownInaddition,λ⊥

increaseswhereasK⊥

decreaseslikelybecauseofthedemyelinationandaxonallossthatalsoleadtolessdiffusionrestrictioninradialdirection.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.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-deriveddiffusivitiesaregenerallylowerthanthosebyDKI.Therelativelyhighsensitivityoftheλ⊥

inmonoexponentialDTImodelismainlyaresultofincreasingK⊥

withage(whilethechangesofλ⊥

inDKIaremoderate).DTIVSDKIinmonitoringpostnatalbrain