说明分析教案0210

fMRIpost-stimulusundershootsinvisualcortexareneuronalinKarenJMullinger1,2,MatthewCherukara1,SusanTFrancis1,andStephenD1SPMIC,SchoolofPhysicsandAstronomy,UniversityofNottingham,Nottingham,Nottinghamshire,UnitedKingdom,2BUIC,SchoolofPsychology,UniversityofBirmingham,Birmingham,WestMidlands,UnitedKingdomIntroduction:Thepost-stimulusundershootisawellrecognisedcomponentofthe response[1].However,theBOLDresponseoriginatesfromacomplexinctionbetweencerebralbloodflow(CBF),cerebralbloodvolume(CBV)andthemetabolicrateofoxygenconsumption(CMRO2),makingthephysiologicaloriginofthepost-stimulusundershootunclear.InarecenthumanEEG-fMRIstudy[2],wehaveprovidedevidencethatthepost-stimulusBOLDundershootis,atleastinpart,neuronalinorigin.Thisworkshowedthat

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post-stimulusevent-relatedsynchronisation(PERS)powerofEEGactivityinthe8-13Hz(alpha/mu)frequencybandwascorrelatedwiththenaturalvariabilityintheamplitudeofthepost-stimulusBOLDandCBFundershootsinthesensorimotorcortex.Here,werecordEEG-fMRIresponsestoflickeringandstaticcheckerboardvisualstimulipreviouslyshowntodrivedifferencesinthepost-stimulusBOLDundershoot(flicker=strongundershoot,

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TimeFigure1:GroupEEGalphapower(A),BOLD(B)andCBF(C)responsesfromcontralalV1totheflicker(green)andstatic(purple)visualstimuli.Significantdifferences(pairedT-tests)intheresponseamplitudesbetweenflickerandstaticstimuliatcertaintime-pointsaredenotedby**=p<0.001,*=p<0.05.Hypothesis:Previouslyobservedpost-stimulusEEG-fMRIcorrelations[2]canbeelicitedinothersensorymodalities;adifferenceinthemeanpost-stimulusBOLDundershootbetweenflickerandstaticstimuliwillbeassociatedwithacorrespondingdifferenceinPERSalphapower,whilstcorrelationsbetweenthenaturaltrial-by-trialvariabilityofPERSalphapowerandBOLDpost-stimulusundershootwillalsobeobserved.Ifproventhiswouldprovidenewevidencethatpost-stimulusundershootsareneuronalinoriginthroughoutthebrain.Methods:fMRIandEEGdatawereacquiredsimultaneouslyusingaPhilipsAchieva3TMRscanneranda64-channelEEGsystem(BrainProducts).AFAIRDABS[2]sequencewasusedtosimultaneouslyacquirebackgroundsuppressedASLandBOLDdatafromprimaryvisualcortex(V1)(TR=2.6s,TE=9.2/40.2ms[ASL/BOLD],labeldelay=1400ms,3x3x5mm3voxels,12slices,212mmFOV,SENSEfactor2.3,backgroundsuppressionatTIBGS1/TIBGS2=339ms/560ms).Datawereacquiredon14subjects(age=27±6yrs)whofixatedonacentrallydisyedcrossthroughoutwhilstpassivelyviewingstatic(100%contrast)andflicker(3Hz,33%contrast)left-hemifieldcheckerboardstimuli.StimulusintensitieswerematchedtoinducecomparableprimaryBOLDresponseamplitudes[3].Datawererecordedover4runswith8pseudo-randomisedtrialsofeachstimulusperrun(10s/30sstimulation/rest)anda98.8srestperiodatthestartofeachruntomeasurefMRIbaselinesignal.ysis:1subjectwacludedfromfurtherysisbecausetheyfellasleep.Intheremaining13subjectsEEGandfMRIdatawerepre-processedusingconventionalmethodsinBrainVisionyzer2andFSL[2].EEG:Pre-processeddatawerefiltered8-13Hz.Aregularised,scalarbeamformerwasusedtolocalisethealpharesponsetovisualstimuli[2,4].VirtualelectrodetimecoursesofelectricalactivitywereextractedfromthepeakpseudoT-statlocationincontralalV1(active/passivewindow:0-9.5s/30-39.5s)derivedusingallstimuluspresentations.Averageresponsesforthestaticandflickerstimuliwerefound.Fortheaverageresponsesandindividualtrialsinthetwostimulusconditions,themeanstimulusresponse(0-9.5s),PERS(10.5-20s),andcontrol(35-39.5s)windowalphapowervalueswerecalculated.Foreachsubjectandstimuluscondition,trialsweresortedintolower(0-25%),median(37.5-62.5%)andupper(75-100%)quartilesbasedon:stimulusresponse,PERS,orcontrolwindowalphapower[2].fMRI:GLMysis(FEAT6.01)identifiedsignificantpositiveandnegativeresponsesofBOLDandCBFsignalscombinedacrossbothvisualstimuli.Thegroup-levelconjunctionofBOLDandCBFresponsestobothstimuliwasusedtodefinesubjectspecific,cubicregionsofinterest(ROIs,3x3x3voxels).Thesewerecentredonthesubject’speakvoxelinthepositive(contralal)andnegative(ipsilal)V1BOLDregions[2].BOLDandCBFsingle-trialhaemodynamicresponses(HRs)wereextractedforeachtrial;allowingdirectcomparisonbetweenCBFandBOLDresponsesandstimulusconditions.HRswereconvertedtopercentagechangerelativetotheinitialbaselineperrun.HRsweresortedintoquartilesaccordingtoeitherthePERS,stimulusresponseorcontrolwindowalphapowerseparayforthestaticandflickerstimuliandtheagedoversubjects.Results:EEG:Figure1Ashowstheaveragealphapowerresponsestobothstimuli.Pairedstudentt-testsrevealedsignificantlyhigheralphapowerinflicker(green)thanstatic(purple)trialsduringthePERS(p<0.001)windowbutnosignificantdifferenceinthestimulusorcontrolwindows.NosignificantcorrelationbetweenPERSalphapowerandeitherstimulusresponseorcontrolwindowalphapowerwasobserved.fMRI:TheprimaryBOLD/CBFsignalresponse(at~10s)tovisualstimulationwaspositiveontralalV1(Fig.2pink)andnegativeinipsilalV1(Fig.2green).ThegroupaveragecontralalBOLDandCBFresponses(Figure1B&C)bothshowedsignificantlylargerundershootsforflickerthanstaticstimuli,agreeingwith[3].InbothpositiveandnegativeBOLD/CBFregions,thepost-stimulusundershootamplitudewasnegativelycorrelatedwithPERSalphapower(Fig.2).Foreachtimepoint,aone-wayRMANOVAwasusedtotestforsignificantdifferenceinHRamplitudweenPERSalphapowerquartiles.Intheundershootperiod,asignificanteffectofPERSpowerwasobservedontralalV1BOLD(18.5-25sflicker&16.7-24.5sstatic)andCBF(17.9-22.5sflicker&20-22.5sstatic)amplitudes(Fig2A,C,E&G).ForipsilalV1(Fig2B,D,F&H),asignificantdifferenceinundershootbetweenquartileswasonlyobservedforthenegativeBOLDtimecoursefortheflickeringstimulus(20.4-24.5s)(Fig2B).NosignificantsortingeffectontheprimaryfMRIresponseswasobservedforeitherstimulus.NosignificanteffectsonBOLDorCBFresponseswerefoundwhensortingaccordingtoeitherstimulusorcontrolalphapower.Discussion:Here,weprovidefurtherevidencethattheBOLDpost-stimulusundershoot(>17s)islinkedtopost-stimuluschangesinelectricaloscillatoryactivity(10-20s)inhumans.Weadvancepreviousworkintwoways.Firstly,byshowingthatcorrelationsbetweennaturalvariabilityinpost-stimulusEEGandfMRIresponsesseeninsensorimotorcortex[2]extendtothevisualsystem;trialswithhigherpost-stimulusalphapowerexhibitedmorenegativeBOLD/CBFundershootsinbothpositiveandnegativeBOLDregions,agreeingwith[2].ThelackofrelationshipbetweenfMRIundershootandeitherstimulusorcontrolalphapower,providesfurtherevidencethatourfindingsspecificallyreflectcorrelationofthepost-stimulusneuronalandfMRIsignals.Secondly,byshowingaconcurrentsignificantdifferenceinthemeanpost-stimulusalpha,BOLDandCBFresponsesinthecontralalhemispherebetweenflickerandstaticstimuli,withhigherPERSalphapowerandlargerundershootsobservedfortheflickerstimulus,complementing[3].SealphaERSiscommonlybelievedtoreflectinhibitoryneuronalactivity[5],wehypothesizethatachangeinthebalanceofexcitatory/inhibitoryactivityoccursuponterminationofstimulationcausingachangeMRO2.Wesuggestthislonglastingchangeinneuronalactivitymaybeamechanismbywhichthebrainreturnstoarestingstate.Giventhegrowingevidencethatpost-stimulusundershootsareneuronalinorigin,andrelativelyslowresponses,futureworkwillfurtherinvestigatethefunctionalroleofthesebrainresponses.Proc.Intl.Soc.Mag.Reson.Med.23 fMRIKarenJMullinger1,2、MatthewCherukara1、 Mayhew21SPMIC，物理与天文学学院，诺丁汉大学，诺丁汉，诺丁汉郡，英国，2BUIC，翰大学心理学院，翰，西兹，英国简介：刺激后下冲是公认的大胆的回应[1]。然而，BOLD反应源于脑血流EEG-fMRI[2BOLD关同步(PERS)功率与刺激后BOLD和CBF下冲幅度的自然变异相关。感觉运动皮层。在这里，我们记录了对闪烁和静态棋盘视觉刺激的EEG-fMRI反应，先前显示这些刺激会驱动刺激后BOLD下冲的差异（闪烁=强下冲，静态=无下冲[3]），以进一步研究刺激后下冲。EEG-fMRI[2]BOLDPERSαPERSα方法：使用PhilipsAchieva3TMR扫描仪和64通道EEG系统（BrainProducts）同时采集fMRIEEGFAIRDABS[2(V1)ASLBOLD数据（TR=2.6s，TE=9.2/40.2ms[ASL/BOLD]，标签延迟=1400ms，3x3x5mm3体素，12个切片，212mmFOV，SENSE因子2.3，TIBGS1/TIBGS2=339ms/560ms的背景抑制）。数据采集自14名受试者（年龄=27±6），他们始终注视着中央显示的十字，同时被动地观看静态（100%度）和闪烁（3Hz，33%对比度）左半视野棋盘刺激。刺激强度相匹配以诱导可比较的初级BOLD反应幅度[3]。数据记录在4次运行中，每次运行每次刺激进行8次伪随机试验（10秒/30秒刺激/休息），每次运行开始时有98.8秒的休息时间来测量fMRI基线信号。分析：113像数据使用BrainVisionyzer2和FSL中的常规方法进行预处理[2]。EEG：预处理数据经8-13Hzalpha[2,4]。电活动的V1T（：0-9.5秒/30-39.5秒）中提取的。发现了静态和闪烁刺激的平均反应。对于两种刺激条件下的αPERSalpha2ofMRI：GLM分析(FEAT6.01)确定了两种视觉刺激中BOLD和CBF信号组合的显着阳性和阴BOLDCBF（ROI，3x3x3体素）。这些以受试者在正（对侧）和负（同侧）V1BOLD区域的峰值体素为中心[2]。为每个试验提取BOLD和