1. ARTERIOVENOUS MALFORMATIONS
AVM: a TLA for the CNS
CEREBRAL
ARTERIOVENOUS MALFORMATIONS

2. Incidence 0.52% at autopsy Slight male preponderance (1.09 to 1.94)
Congenital lesions (although rarely familial)

3. Embryology First half of third week of gestation
epiblastic cells migrate to form mesoderm
mesodermal cells differentiate to arterial and venous vessels on the surface of the embryonic nervous system

4. Embryology First half of third week of gestation
epiblastic cells migrate to form mesoderm
mesodermal cells differentaite to arterial and venous vessels on the surface of the embryonic nervous system
Seventh gestational week
vessels sprout branches & penetrate developing brain
reach the gray-white interface, either loop back to pial surface or traverse entire neural tube, thus epicerebral & transcerebral circ'n
eventually connect arterial and venous systems by around the twelfth week

5. Pathology & Pathophysiology
absence of normal capillary system

6. Pathology & Pathophysiology
absence of normal capillary system
usual function displaced

7. Pathology & Pathophysiology
absence of normal capillary system
usual function displaced
asymptomatic at birth

8. Pathology & Pathophysiology
absence of normal capillary system
usual function displaced
asymptomatic at birth
vessels change with time
may develop aneurysms

9. Pathology & Pathophysiology
absence of normal capillary system
usual function displaced
asymptomatic at birth
vessels change with time
may develop aneurysms
parenchymal changes within and around the lesion

10. Pathology & Pathophysiology
absence of normal capillary system
usual function displaced
asymptomatic at birth
vessels change with time
may develop aneurysms
parenchymal changes within and around the lesion
site frequency is proportional to brain volume

11. Clinical presentation
95% have symptoms by age of 70 years

12. Clinical presentation
95% have symptoms by age of 70 years
peak presentation second to fourth decade

13. Clinical presentation
95% have symptoms by age of 70 years
peak presentation second to fourth decade
high output failure, neonate, vein of Galen
hydrocephalus, first decade
headache, hemorrhage, seizures, 2nd & 3rd

14. Clinical presentation
factors contributing to symptoms
vessel walls, flow and pressures

15. Clinical presentation
factors contributing to symptoms
vessel walls, flow and pressures
enlargement and encroachment

16. Clinical presentation
factors contributing to symptoms
vessel walls, flow and pressures
enlargement and encroachment
dural sinuses

17. Clinical presentation
factors contributing to symptoms
vessel walls, flow and pressures
enlargement and encroachment
dural sinuses
ischaemia

18. Clinical presentation
factors contributing to symptoms
vessel walls, flow and pressures
enlargement and encroachment
dural sinuses
ischaemia
cardiac output

19. Clinical presentation

20. Hemorrhage AVM Aneurysm rupture not a function of size
rupture related to aneurysm size

21. Hemorrhage AVM Aneurysm rupture not a function of size
no marked increase with exercise, pregnancy, trauma
Aneurysm
rupture related to aneurysm size
increase with trauma exercise, end pregnancy

22. Hemorrhage AVM Aneurysm rupture not a function of size
no marked increase with exercise, pregnancy, trauma
arteriovenous, therefore less severe
Aneurysm
rupture related to aneurysm size
increase with trauma exercise, end pregnancy
arterial, therefore more severe

23. Hemorrhage AVM Aneurysm rupture not a function of size
no marked increase with exercise, pregnancy, trauma
arteriovenous, therefore less severe
mortality 6 to 13.6%
Aneurysm
rupture related to aneurysm size
increase with trauma exercise, end pregnancy
arterial, therefore more severe
mortality 30-50%

24. Hemorrhage AVM Aneurysm rupture not a function of size
no marked increase with exercise, pregnancy, trauma
arteriovenous, therefore less severe
mortality 6 to 13.6%
lower rebleed mortality rate (1%)
Aneurysm
rupture related to aneurysm size
increase with trauma exercise, end pregnancy
arterial, therefore more severe
mortality 30-50%
higher rebleed mortality rate (13%)

25. Hemorrhage AVM Aneurysm rupture not a function of size
no marked increase with exercise, pregnancy, trauma
arteriovenous, therefore less severe
mortality 6 to 13.6%
lower rebleed mortality rate (1%)
vasospasm rare
Aneurysm
rupture related to aneurysm size
increase with trauma exercise, end pregnancy
arterial, therefore more severe
mortality 30-50%
higher rebleed mortality rate (13%)
vasospasm common

26. Hemorrhage - AVM
Nonetheless, risk of major, incapacitating, or fatal hemorrhage in untreated lesion is 40 to 50%

27. Hemorrhage - AVM
Nonetheless, risk of major, incapacitating, or fatal hemorrhage in untreated lesion is 40 to 50%
Yearly risk of initial hemorrhage ~3%
Rebleed in first subsequent year 6-18%, reducing to ~3% again thereafter
Pediatric prognosis worse than adult

28. Spetzler & Martin Grading System
Criteria
Score
Size of Nidus
Spetzler & Martin Grading System
Small (<3cm) 1
Medium (3-6cm) 2
Large (>6cm) 3
Eloquence of Adjacent Brain No
Yes 1
Deep Vascular Component No
Yes 1

29. Treatment Options
Surgical Resection

30. Treatment Options
Surgical Resection
Endovascular Embolisation

31. Treatment Options Surgical Resection Endovascular Embolisation
Stereotatic Radiosurgery

32. Treatment Options Surgical Resection Endovascular Embolisation
Stereotatic Radiosurgery
Multimodal Therapy

33. Treatment Options Surgical Resection Endovascular Embolisation
Stereotatic Radiosurgery
Multimodal Therapy
Conservative Management

34. Normal Perfusion Pressure Breakthrough Theory
R.F. Spetzler et al

35. Normal perfusion pressure breakthrough theory
Loss of autoregulation and carbon dioxide reactivity in presence of large arteriovenous malformation.

36. Normal perfusion pressure breakthrough theory
Loss 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 AVM

37. Normal perfusion pressure breakthrough theory
Loss 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 AVM
Obliteration of the AVM diverts all flow to these maximally dilated vessels which have lost their normal control mechanisms

38. Normal perfusion pressure breakthrough theory
Loss 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 AVM
Obliteration of the AVM diverts all flow to these maximally dilated vessels which have lost their normal control mechanisms
Results in loss of protection of the capillary bed, with edema and hemorrhage

39. Mathematical Models
Arterial inflow

40. Mathematical Models
Arterial inflow
Nidus

41. Mathematical Models
Arterial inflow
Nidus
Venous Outflow

42. Anaesthesia Technique