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1、脑动静脉畸形-大学课件(1)EmbryologynFirst half of third week of gestationepiblastic cells migrate to form mesodermmesodermal cells differentiate to arterial and venous vessels on the surface of the embryonic nervous systemEmbryologynFirst half of third week of gestationepiblastic cells migrate to form mesoderm
2、mesodermal cells differentaite to arterial and venous vessels on the surface of the embryonic nervous systemnSeventh gestational weekvessels sprout branches&penetrate developing brainreach the gray-white interface,either loop back to pial surface or traverse entire neural tube,thus epicerebral&trans
3、cerebral circneventually connect arterial and venous systems by around the twelfth week Pathology&Pathophysiologynabsence of normal capillary systemPathology&Pathophysiologynabsence of normal capillary systemnusual function displacedPathology&Pathophysiologynabsence of normal capillary systemnusual
4、function displacednasymptomatic at birthPathology&Pathophysiologynabsence of normal capillary systemnusual function displacednasymptomatic at birthnvessels change with timenmay develop aneurysmsnparenchymal changes within and around the lesionPathology&Pathophysiologynabsence of normal capillary sys
5、temnusual function displacednasymptomatic at birthnvessels change with timenmay develop aneurysmsnparenchymal changes within and around the lesionnsite frequency is proportional to brain volumePathology&Pathophysiologynabsence of normal capillary systemnusual function displacednasymptomatic at birth
6、nvessels change with timenmay develop aneurysmsClinical presentationn95%have symptoms by age of 70 yearsClinical presentationn95%have symptoms by age of 70 yearsnpeak presentation second to fourth decadeClinical presentationn95%have symptoms by age of 70 yearsnpeak presentation second to fourth deca
7、dehigh output failure,neonate,vein of Galenhydrocephalus,first decadeheadache,hemorrhage,seizures,2nd&3rdClinical presentationnfactors contributing to symptomsvessel walls,flow and pressuresClinical presentationnfactors contributing to symptomsvessel walls,flow and pressuresenlargement and encroachm
8、entClinical presentationnfactors contributing to symptomsvessel walls,flow and pressuresenlargement and encroachmentdural sinusesClinical presentationnfactors contributing to symptomsvessel walls,flow and pressuresenlargement and encroachmentdural sinusesischaemiaClinical presentationnfactors contri
9、buting to symptomsvessel walls,flow and pressuresenlargement and encroachmentdural sinusesischaemiacardiac outputClinical presentationHemorrhagenAVMrupture not a function of sizenAneurysmrupture related to aneurysm sizeHemorrhagenAVMrupture not a function of sizeno marked increase with exercise,preg
10、nancy,traumanAneurysmrupture related to aneurysm sizeincrease with trauma exercise,end pregnancyHemorrhagenAVMrupture not a function of sizeno marked increase with exercise,pregnancy,traumaarteriovenous,therefore less severenAneurysmrupture related to aneurysm sizeincrease with trauma exercise,end p
11、regnancyarterial,therefore more severeHemorrhagenAVMrupture not a function of sizeno marked increase with exercise,pregnancy,traumaarteriovenous,therefore less severemortality 6 to 13.6%nAneurysmrupture related to aneurysm sizeincrease with trauma exercise,end pregnancyarterial,therefore more severe
12、mortality 30-50%HemorrhagenAVMrupture not a function of sizeno marked increase with exercise,pregnancy,traumaarteriovenous,therefore less severemortality 6 to 13.6%lower rebleed mortality rate(1%)nAneurysmrupture related to aneurysm sizeincrease with trauma exercise,end pregnancyarterial,therefore m
13、ore severemortality 30-50%higher rebleed mortality rate(13%)HemorrhagenAVMrupture not a function of sizeno marked increase with exercise,pregnancy,traumaarteriovenous,therefore less severemortality 6 to 13.6%lower rebleed mortality rate(1%)vasospasm rarenAneurysmrupture related to aneurysm sizeincre
14、ase with trauma exercise,end pregnancyarterial,therefore more severemortality 30-50%higher rebleed mortality rate(13%)vasospasm commonHemorrhage-AVMnNonetheless,risk of major,incapacitating,or fatal hemorrhage in untreated lesion is 40 to 50%Hemorrhage-AVMnNonetheless,risk of major,incapacitating,or
15、 fatal hemorrhage in untreated lesion is 40 to 50%nYearly risk of initial hemorrhage 3%nRebleed in first subsequent year 6-18%,reducing to 3%again thereafternPediatric prognosis worse than adult Spetzler&Martin Grading SystemCriteriaScoreSize of Nidus Small(6cm)3Eloquence of Adjacent Brain No0Yes1De
16、ep Vascular Component No0Yes1Treatment OptionsHSurgical ResectionTreatment OptionsHSurgical ResectionHEndovascular EmbolisationTreatment OptionsHSurgical ResectionHEndovascular EmbolisationHStereotatic RadiosurgeryTreatment OptionsHSurgical ResectionHEndovascular EmbolisationHStereotatic Radiosurger
17、yHMultimodal TherapyTreatment OptionsHSurgical ResectionHEndovascular EmbolisationHStereotatic RadiosurgeryHMultimodal TherapyHConservative ManagementNormal Perfusion Pressure Breakthrough TheoryR.F.Spetzler et alNormal perfusion pressure breakthrough theoryLoss of autoregulation and carbon dioxide
18、reactivity in presence of large arteriovenous malformation.Normal perfusion pressure breakthrough theoryLoss of autoregulation and carbon dioxide reactivity in presence of large arteriovenous malformation.Normal hemispheric vessels are chronically maximally dilated to attempt to divert flow from the
19、 AVMNormal perfusion pressure breakthrough theoryLoss of autoregulation and carbon dioxide reactivity in presence of large arteriovenous malformation.Normal hemispheric vessels are chronically maximally dilated to attempt to divert flow from the AVMObliteration of the AVM diverts all flow to these m
20、aximally dilated vessels which have lost their normal control mechanismsNormal perfusion pressure breakthrough theoryLoss of autoregulation and carbon dioxide reactivity in presence of large arteriovenous malformation.Normal hemispheric vessels are chronically maximally dilated to attempt to divert
21、flow from the AVMObliteration of the AVM diverts all flow to these maximally dilated vessels which have lost their normal control mechanismsResults in loss of protection of the capillary bed,with edema and hemorrhagenArterial inflowMathematical ModelsnArterial inflownNidusMathematical ModelsnArterial inflownNidusnVenous OutflowMathematical ModelsAnaesthesia Technique此此课课件下件下载载可自行可自行编辑编辑修改，修改，仅仅供参考！供参考！感感谢谢您的支持，我您的支持，我们们努力做得更好！努力做得更好！谢谢谢谢