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ARTERIOVENOUS MALFORMATIONS
AVM: a TLA for the CNS CEREBRAL ARTERIOVENOUS MALFORMATIONS
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Incidence 0.52% at autopsy Slight male preponderance (1.09 to 1.94)
Congenital lesions (although rarely familial)
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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
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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
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Pathology & Pathophysiology
absence of normal capillary system
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Pathology & Pathophysiology
absence of normal capillary system usual function displaced
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Pathology & Pathophysiology
absence of normal capillary system usual function displaced asymptomatic at birth
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Pathology & Pathophysiology
absence of normal capillary system usual function displaced asymptomatic at birth vessels change with time may develop aneurysms
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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
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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
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Clinical presentation
95% have symptoms by age of 70 years
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Clinical presentation
95% have symptoms by age of 70 years peak presentation second to fourth decade
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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
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Clinical presentation
factors contributing to symptoms vessel walls, flow and pressures
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Clinical presentation
factors contributing to symptoms vessel walls, flow and pressures enlargement and encroachment
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Clinical presentation
factors contributing to symptoms vessel walls, flow and pressures enlargement and encroachment dural sinuses
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Clinical presentation
factors contributing to symptoms vessel walls, flow and pressures enlargement and encroachment dural sinuses ischaemia
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Clinical presentation
factors contributing to symptoms vessel walls, flow and pressures enlargement and encroachment dural sinuses ischaemia cardiac output
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Clinical presentation
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Hemorrhage AVM Aneurysm rupture not a function of size
rupture related to aneurysm size
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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
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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
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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%
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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%)
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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
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Hemorrhage - AVM Nonetheless, risk of major, incapacitating, or fatal hemorrhage in untreated lesion is 40 to 50%
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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
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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
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Treatment Options Surgical Resection
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Treatment Options Surgical Resection Endovascular Embolisation
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Treatment Options Surgical Resection Endovascular Embolisation
Stereotatic Radiosurgery
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Treatment Options Surgical Resection Endovascular Embolisation
Stereotatic Radiosurgery Multimodal Therapy
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Treatment Options Surgical Resection Endovascular Embolisation
Stereotatic Radiosurgery Multimodal Therapy Conservative Management
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Normal Perfusion Pressure Breakthrough Theory
R.F. Spetzler et al
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Normal perfusion pressure breakthrough theory
Loss of autoregulation and carbon dioxide reactivity in presence of large arteriovenous malformation.
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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
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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
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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
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Mathematical Models Arterial inflow
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Mathematical Models Arterial inflow Nidus
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Mathematical Models Arterial inflow Nidus Venous Outflow
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Anaesthesia Technique
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