脑动静脉畸形大学ppt课件

脑动静脉畸形大学课件脑动静脉畸形大学课件脑动静脉畸形大学课件脑动静脉畸形大学课件1Incidencen0.52%at autopsynSlight male preponderance(1.09 to 1.94)nCongenital lesions(although rarely familial)Incidence0.52%at autopsy2EmbryologynFirst 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 systemEmbryologyFirst half of third 3EmbryologynFirst half of third week of gestationepiblastic cells migrate to form mesodermmesodermal 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&transcerebral circneventually connect arterial and venous systems by around the twelfth week EmbryologyFirst half of third 4Pathology&Pathophysiologynabsence of normal capillary systemPathology&Pathophysiologyabs5Pathology&Pathophysiologynabsence of normal capillary systemnusual function displacedPathology&Pathophysiologyabs6Pathology&Pathophysiologynabsence of normal capillary systemnusual function displacednasymptomatic at birthPathology&Pathophysiologyabs7Pathology&Pathophysiologynabsence of normal capillary systemnusual function displacednasymptomatic at birthnvessels change with timenmay develop aneurysmsPathology&Pathophysiologyabs8parenchymal changes within and around the lesionPathology&Pathophysiologynabsence of normal capillary systemnusual function displacednasymptomatic at birthnvessels change with timenmay develop aneurysmsparenchymal changes within and9parenchymal changes within and around the lesionsite frequency is proportional to brain volumePathology&Pathophysiologynabsence of normal capillary systemnusual function displacednasymptomatic at birthnvessels change with timenmay develop aneurysmsparenchymal changes within and10Clinical presentationn95%have symptoms by age of 70 yearsClinical presentation95%have 11Clinical presentationn95%have symptoms by age of 70 yearsnpeak presentation second to fourth decadeClinical presentation95%have 12Clinical presentationn95%have symptoms by age of 70 yearsnpeak presentation second to fourth decadehigh output failure,neonate,vein of Galenhydrocephalus,first decadeheadache,hemorrhage,seizures,2nd&3rdClinical presentation95%have 13Clinical presentationnfactors contributing to symptomsvessel walls,flow and pressuresClinical presentationfactors c14Clinical presentationnfactors contributing to symptomsvessel walls,flow and pressuresenlargement and encroachmentClinical presentationfactors c15Clinical presentationnfactors contributing to symptomsvessel walls,flow and pressuresenlargement and encroachmentdural sinusesClinical presentationfactors c16Clinical presentationnfactors contributing to symptomsvessel walls,flow and pressuresenlargement and encroachmentdural sinusesischaemiaClinical presentationfactors c17Clinical presentationnfactors contributing to symptomsvessel walls,flow and pressuresenlargement and encroachmentdural sinusesischaemiacardiac outputClinical presentationfactors c18Clinical presentationClinical presentation19HemorrhagenAVMrupture not a function of sizenAneurysmrupture related to aneurysm sizeHemorrhageAVMAneurysm20HemorrhagenAVMrupture not a function of sizeno marked increase with exercise,pregnancy,traumanAneurysmrupture related to aneurysm sizeincrease with trauma exercise,end pregnancyHemorrhageAVMAneurysm21HemorrhagenAVMrupture not a function of sizeno marked increase with exercise,pregnancy,traumaarteriovenous,therefore less severenAneurysmrupture related to aneurysm sizeincrease with trauma exercise,end pregnancyarterial,therefore more severeHemorrhageAVMAneurysm22HemorrhagenAVMrupture 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 severemortality 30-50%HemorrhageAVMAneurysm23HemorrhagenAVMrupture 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 more severemortality 30-50%higher rebleed mortality rate(13%)HemorrhageAVMAneurysm24HemorrhagenAVMrupture 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 sizeincrease with trauma exercise,end pregnancyarterial,therefore more severemortality 30-50%higher rebleed mortality rate(13%)vasospasm commonHemorrhageAVMAneurysm25Hemorrhage-AVMnNonetheless,risk of major,incapacitating,or fatal hemorrhage in untreated lesion is 40 to 50%Hemorrhage-AVMNonetheless,r26Hemorrhage-AVMnNonetheless,risk of major,incapacitating,or 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 Hemorrhage-AVMNonetheless,r27Spetzler&Martin Grading SystemCriteriaScoreSize of Nidus Small(6cm)3Eloquence of Adjacent Brain No0Yes1Deep Vascular Component No0Yes1Spetzler&Martin Grading Syst28Treatment OptionsHSurgical ResectionTreatment OptionsSurgical Rese29Treatment OptionsHSurgical ResectionHEndovascular EmbolisationTreatment OptionsSurgical Rese30Treatment OptionsHSurgical ResectionHEndovascular EmbolisationHStereotatic RadiosurgeryTreatment OptionsSurgical Rese31Treatment OptionsHSurgical ResectionHEndovascular EmbolisationHStereotatic RadiosurgeryHMultimodal TherapyTreatment OptionsSurgical Rese32Treatment OptionsHSurgical ResectionHEndovascular EmbolisationHStereotatic RadiosurgeryHMultimodal TherapyHConservative ManagementTreatment OptionsSurgical Rese33Normal Perfusion Pressure Breakthrough TheoryR.F.Spetzler et alNormal Perfusion Pressure Brea34Normal perfusion pressure breakthrough theoryLoss of autoregulation and carbon dioxide reactivity in presence of large arteriovenous malformation.Normal perfusion pressure brea35Normal 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 AVMNormal perfusion pressure brea36Normal 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 maximally dilated vessels which have lost their normal control mechanismsNormal perfusion pressure brea37Normal 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 maximally dilated vessels which have lost their normal control mechanismsResults in loss of protection of the capillary bed,with edema and hemorrhageNormal perfusion pressure brea38Arterial inflowMathematical ModelsArterial inflowMathematical Mo39Arterial inflowNidusMathematical ModelsArterial inflowMathematical Mo40Arterial inflowNidusVenous OutflowMathematical ModelsArterial inflowMathematical Mo41Anaesthesia TechniqueAnaesthesia Technique42谢谢观赏谢谢观赏谢谢观赏43谢谢谢谢44