脑动静脉畸形大学课件.ppt

1、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Incidencen0.52%at autopsynSlight male preponderance(1.09 to 1.94)nCongenital lesions(although rarely familial)I n c i d e n c e 0.5 2%a t a u t o p s yEmbryologynFirst half of third week of gestationepiblastic cells migrate to form mesodermmesodermal cells differentiate

2、 to arterial and venous vessels on the surface of the embryonic nervous systemE mb r y o l o g y F i r s t h a l f o f t h i r d EmbryologynFirst half of third week of gestationepiblastic cells migrate to form mesodermmesodermal cells differentaite to arterial and venous vessels on the surface of th

3、e 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

4、 week E mb r y o l o g y F i r s t h a l f o f t h i r d Pathology&Pathophysiologynabsence of normal capillary systemP a t h o l o g y&P a t h o p h y s i o l o g y a b sPathology&Pathophysiologynabsence of normal capillary systemnusual function displacedP a t h o l o g y&P a t h o p h y s i o l o g

5、 y a b sPathology&Pathophysiologynabsence of normal capillary systemnusual function displacednasymptomatic at birthP a t h o l o g y&P a t h o p h y s i o l o g y a b sPathology&Pathophysiologynabsence of normal capillary systemnusual function displacednasymptomatic at birthnvessels change with time

6、nmay develop aneurysmsP a t h o l o g y&P a t h o p h y s i o l o g y a b sparenchymal changes within and around the lesionPathology&Pathophysiologynabsence of normal capillary systemnusual function displacednasymptomatic at birthnvessels change with timenmay develop aneurysmsp a r e n c h y ma l c

7、h a n g e s w i t h i n a n dparenchymal 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 aneurysmsp a r e n c h y ma l c

8、h a n g e s w i t h i n a n dClinical presentationn95%have symptoms by age of 70 yearsC l i n i c a l p r e s e n t a t i o n 9 5%h a v e Clinical presentationn95%have symptoms by age of 70 yearsnpeak presentation second to fourth decadeC l i n i c a l p r e s e n t a t i o n 9 5%h a v e Clinical pr

9、esentationn95%have symptoms by age of 70 yearsnpeak presentation second to fourth decadehigh output failure,neonate,vein of Galenhydrocephalus,first decadeheadache,hemorrhage,seizures,2nd&3rdC l i n i c a l p r e s e n t a t i o n 9 5%h a v e Clinical presentationnfactors contributing to symptomsves

10、sel walls,flow and pressuresC l i n i c a l p r e s e n t a t i o n f a c t o r s cClinical presentationnfactors contributing to symptomsvessel walls,flow and pressuresenlargement and encroachmentC l i n i c a l p r e s e n t a t i o n f a c t o r s cClinical presentationnfactors contributing to sym

11、ptomsvessel walls,flow and pressuresenlargement and encroachmentdural sinusesC l i n i c a l p r e s e n t a t i o n f a c t o r s cClinical presentationnfactors contributing to symptomsvessel walls,flow and pressuresenlargement and encroachmentdural sinusesischaemiaC l i n i c a l p r e s e n t a t

12、 i o n f a c t o r s cClinical presentationnfactors contributing to symptomsvessel walls,flow and pressuresenlargement and encroachmentdural sinusesischaemiacardiac outputC l i n i c a l p r e s e n t a t i o n f a c t o r s cClinical presentationDeficits10%Headaches10%Seizures30%Hemorrhage50%C l i

13、n i c a l p r e s e n t a t i o nHemorrhagenAVMrupture not a function of sizenAneurysmrupture related to aneurysm sizeH e mo r r h a g e A V MA n e u r y s mHemorrhagenAVMrupture not a function of sizeno marked increase with exercise,pregnancy,traumanAneurysmrupture related to aneurysm sizeincrease

14、with trauma exercise,end pregnancyH e mo r r h a g e A V MA n e u r y s mHemorrhagenAVMrupture not a function of sizeno marked increase with exercise,pregnancy,traumaarteriovenous,therefore less severenAneurysmrupture related to aneurysm sizeincrease with trauma exercise,end pregnancyarterial,theref

15、ore more severeH e mo r r h a g e A V MA n e u r y s mHemorrhagenAVMrupture 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,there

16、fore more severemortality 30-50%H e mo r r h a g e A V MA n e u r y s mHemorrhagenAVMrupture 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

17、 with trauma exercise,end pregnancyarterial,therefore more severemortality 30-50%higher rebleed mortality rate(13%)H e mo r r h a g e A V MA n e u r y s mHemorrhagenAVMrupture not a function of sizeno marked increase with exercise,pregnancy,traumaarteriovenous,therefore less severemortality 6 to 13.

18、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 commonH e mo r r h a g e A V MA n e u r y s mHemorrhage-AVMnNonetheless,risk o

19、f major,incapacitating,or fatal hemorrhage in untreated lesion is 40 to 50%H e mo r r h a g e -A V MN o n e t h e l e s s,rHemorrhage-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 yea

20、r 6-18%,reducing to 3%again thereafternPediatric prognosis worse than adult H e mo r r h a g e -A V MN o n e t h e l e s s,rSpetzler&Martin Grading SystemCriteriaScoreSize of Nidus Small(6cm)3Eloquence of Adjacent Brain No0Yes1Deep Vascular Component No0Yes1S p e t z l e r&Ma r t i n G r a d i n g S

21、 y s tTreatment OptionsHSurgical ResectionT r e a t me n t O p t i o n s S u r g i c a l R e s eTreatment OptionsHSurgical ResectionHEndovascular EmbolisationT r e a t me n t O p t i o n s S u r g i c a l R e s eTreatment OptionsHSurgical ResectionHEndovascular EmbolisationHStereotatic RadiosurgeryT

22、 r e a t me n t O p t i o n s S u r g i c a l R e s eTreatment OptionsHSurgical ResectionHEndovascular EmbolisationHStereotatic RadiosurgeryHMultimodal TherapyT r e a t me n t O p t i o n s S u r g i c a l R e s eTreatment OptionsHSurgical ResectionHEndovascular EmbolisationHStereotatic Radiosurgery

23、HMultimodal TherapyHConservative ManagementT r e a t me n t O p t i o n s S u r g i c a l R e s eNormal Perfusion Pressure Breakthrough TheoryR.F.Spetzler et alN o r ma l P e r f u s i o n P r e s s u r e B r e aNormal perfusion pressure breakthrough theoryLoss of autoregulation and carbon dioxide r

24、eactivity in presence of large arteriovenous malformation.N o r ma l p e r f u s i o n p r e s s u r e b r e aNormal perfusion pressure breakthrough theoryLoss of autoregulation and carbon dioxide reactivity in presence of large arteriovenous malformation.Normal hemispheric vessels are chronically m

25、aximally dilated to attempt to divert flow from the AVMN o r ma l p e r f u s i o n p r e s s u r e b r e aNormal perfusion pressure breakthrough theoryLoss of autoregulation and carbon dioxide reactivity in presence of large arteriovenous malformation.Normal hemispheric vessels are chronically maxi

26、mally 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 mechanismsN o r ma l p e r f u s i o n p r e s s u r e b r e aNormal perfusion pressure breakthrough theoryLoss of autoregulation and c

27、arbon 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 mechanismsResul

28、ts in loss of protection of the capillary bed,with edema and hemorrhageN o r ma l p e r f u s i o n p r e s s u r e b r e aArterial inflowMathematical ModelsA r t e r i a l i n f l o w Ma t h e ma t i c a l MoArterial inflowNidusMathematical ModelsA r t e r i a l i n f l o w Ma t h e ma t i c a l MoArterial inflowNidusVenous OutflowMathematical ModelsA r t e r i a l i n f l o w Ma t h e ma t i c a l MoAnaesthesia TechniqueA n a e s t h e s i a T e c h n i q u e谢谢观赏谢谢