简介:目的探讨医院及家庭联合治疗大龄儿童弱视的临床效果。方法选择7~15岁的大龄儿童73例(113眼),采用医院及家庭联合实施弱视综合疗法对患儿进行治疗,并对临床资料进行总结、分析。结果113眼中有96眼有效,总有效率84.96%,其中基本痊愈61眼(53.98%)、进步35眼(30.97%)、无效17眼(15.93%)。17例无效眼中,屈光度超过±10.00D者6眼、斜视伴双眼无同视功能5眼、眼颤者1眼、散光超过4.00D者2眼、家庭不配合未坚持治疗者3眼。轻、中度弱视的疗效优于重度弱视;中心注视的疗效优于旁中心注视。结论医院及家庭联合治疗大龄儿童弱视能取得满意疗效,需要医务人员、家属和儿童的共同配合。只有充分调动弱视患儿成长环境中关系密切的群体力量,才能提高其治疗效果。因此对大龄儿童的弱视治疗,除科学、系统及规范的治疗外,还应积极地提高家庭支持度。
简介:AIM:Todescribethecharacteristicsofmodulationtransferfunction(MTF)ofanteriorcornealsurface,andobtainthethenormalreferencerangeofMTFatdifferentspatialfrequenciesandopticalzonesoftheanteriorcornealsurfaceinmyopes.·METHODS:Fourhundredeyesfrom200patientswereexaminedunderSIRIUScornealtopographysystem.PhoenisanalysissoftwarewasappliedtosimulatetheMTFcurvesofanteriorcornealsurfaceatverticalandhorizontalmeridiansatthe3,4,5,6,7mmopticalzonesofcornea.TheMTFvaluesatspatialfrequenciesof5,10,15,20,25,30,35,40,45,50,55and60cycles/degree(c/d)wereselected.·RESULTS:TheMTFcurveofanteriorcornealsurfacedecreasedrapidlyfromlowtointermediatefrequency(0-15cpd)atvariousopticalzonesofcornea,thevaluedecreasedto0slowlyathigherfrequency(>15cpd).Withtheincreaseoftheopticalzonesofcornea,MTFcurvedecreasedgradually.3)Intherangeof3mm-6mmopticalzonesofthecornea,theMTFvaluesmeasuredathorizontalmeridianweregreaterthanthecorrespondingvaluesathorizontalmeridianofeachspatialfrequency,thedifferencewasstatisticallysignificant(P<0.05).At7mmopticalzonesofcornea,theMTFvaluesmeasuredathorizontalmeridianwerelessthanthecorrespondingvaluesatverticalmeridianat10-60spatialfrequencies(cpd),andthedifferencewasstatisticallysignificantin25,30,35,40,45,50cpd(P<0.05).·CONCLUSION:MTFcanbeusedtodescribetheimagingqualityofopticalsystemsatanteriorcornealsurfaceobjectivelyindetail.
简介:AIM:ToidentifythegeneticdefectinaChinesefamilywithbilateralprogressivechildhoodposteriorcataract.METHODS:Atwo-generationfamilywasrecruitedinthisstudy.Familyhistoryandclinicaldatawererecorded.AllreportedcandidategenesassociatedwithcongenitalposteriorcataractwerescreenedbydirectDNAsequencing.·RESULTS:Allaffectedindividualspresentedposterioropacitiesinthelens.Directsequencingofthecandidategenesshowedaheterozygousc.2668C>TvariationinEPHA2gene,whichresultedinthereplacementofargininebycysteineatcodon890(p.R890C).Thismutationwasfoundintwoaffectedindividuals,butwasnotobservedin200normalcontrols.·CONCLUSION:Wereportanovelmutation(p.R890C)intheEPHA2receptortyrosinekinasegene.ThefindingexpandsthemutationspectrumofEPHA2inassociationwithposteriorcataract.