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Cerebral AVM
Cerebral AVM
Brain AVMs are congenital high flow
vascular malformation consisting of
an abnormal tangle of small vessels
(nidus) which directly connect brain
arteries to brain veins, without any
capillaries in-between.
85% are supratentorial
Clinical presentation
 hemorrhage 65%
 ischemic events due to vascular steal from
normal brain.
 Seizures 20%
 headaches
 incidental finding in asymptomatic patients
15%
Diagnosis
7
With increased availability of MRI and CT scans,
many patients are found to have an AMV after
having a scan for an unrelated problem. Following
AVM diagnosis, patients are usually referred to
neurointerventional radiologist and/or
neurosurgeon, and undergo a diagnostic cerebral
angiogram.
Radiological diagnosis
The imaging features of a brain AVM are
(a) the presence of a nidus embedded within the brain
parenchyma, identified at either cross-sectional imaging (CT,MR)
or conventional angiography.
(b) early venous drainage, which is best seen on dynamic studies,
the standard of reference being conventional catheter
angiography.
Radiological diagnosis
 The nidus containing numerous serpentine vessels that appear
hyperdense in CT and flow void on MRI, there are usually
changes in the adjacent brain including gliosis, dystrophic
calcification, and blood products.
 AVM replaces rather than displaces brain, it causes minimal
mass effect.
Imaging findings
10
If a nidus is present, two subtypes of abnormal networks of vessels can be
encountered.
The typical type is the glomerular or compact type nidus, which consists of
abnormal vessels without any interspersed normal brain tissue .
The more rarely seen second type is the so-called diffuse or proliferative type
nidus, in which normal brain parenchyma is interspersed throughout the
tangle of vessels.
If this finding is present, proliferative angiopathy or cerebrofacial
arteriovenous metameric syndrome (CAMS) must be included in the
differential diagnosis and can be distinguished from a true brain AVM on the
basis of the absence of early venous drainage seen in proliferative angiopathy
and the classic location and association with facial AVMs seen in CAMS.
Imaging findings
11
Many vascular lesions can manifest with abnormal vessels in the brain
at imaging and must be differentiated from one another due to their
different natural histories and the various treatment strategies. For
example, classic brain AVMs and pial arteriovenous fistulas (AVFs)
should be managed according to the risk associated with the disease
versus treatment-related risk, DVAs are normal variants that never
require treatment.
Imaging of Brain AVMs:
What the Clinician Needs to Know
 Previous hemorrhage.
 Intranidal aneurysm.
 Venous stenosis.
 Deep venous drainage.
 Single venous drainage.
 Deep or posterior fossa location.
Risk of future hemorrhage:
19
The most important clue to the diagnosis of CAMS is the
presence of multiple AVMs in both the brain parenchyma and
the facial region. The brain AVMs have a characteristic
distribution, consisting of diffuse or proliferative type nidus
with supply from multiple small perforator collateral vessels
with rather slow arteriovenous shunting into the veins, which
makes these AVMs extremely difficult to treat.
Cerebrofacial Arteriovenous
Metameric Syndrome
Cerebrofacial Arteriovenous Metameric
Syndrome
21
The typical MR imaging and CT findings include a proliferative
type nidus in which normal brain parenchyma is interspersed
between the abnormal vessels. Often, an entire lobe or even
brain hemisphere is affected.
The lack of clear early venous drainage on dynamic images is
the key to differentiating this disease from classic brain AVM.
Proliferative angiopathy
Proliferative angiopathy
23
Developmental Venous Anomalies
Although they are not classified as
AVMs, DVAs may manifest at cross-
sectional imaging with an
intraparenchymal tangle of vessels
and represent extreme variants of
the normal transcerebral venous
system.
Apart from conservative management, there are three treatment options for
brain AVMs: surgery, endovascular embolization, or radiosurgery.
Surgery can provide a rapid cure in suitable cases (smaller and cortical-
based brain AVMs)
Endovascular embolization is another treatment option that can be used to
quickly eliminate angiographic risk factors. however, the cure rate with
embolization alone is relatively low .
Radiosurgery has a high cure rate with relatively low complication rates.
However, its major limitation is that radiation is slow to take effect; it may be
up to 2 years before any shrinkage of the brain AVM is seen.
Conservative management is typically used when the risk posed by treatment
is too high, such as in large brain AVMs or in asymptomatic patients who are
believed to have a low risk of future hemorrhage.
TREATMENT
The Spetzler-Martin (AVM) grading
system
size of nidus
small (<3 cm) = 1
medium (3-6 cm) = 2
large (>6 cm) = 3
venous drainage
superficial veins only = 0
deep veins = 1
eloquence of adjacent brain
non-eloquent = 0
eloquent = 1
eloquent brain
sensorimotor, language, visual cortex, hypothalamus, thalamus, brain
stem, cerebellar nuclei, or regions immediately adjacent to these
structures
non-eloquent brain
frontal lobe, temporal lobe, cerebellar hemispheres
Embolization
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cerebral AVM

  • 2. Cerebral AVM Brain AVMs are congenital high flow vascular malformation consisting of an abnormal tangle of small vessels (nidus) which directly connect brain arteries to brain veins, without any capillaries in-between. 85% are supratentorial
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  • 6. Clinical presentation  hemorrhage 65%  ischemic events due to vascular steal from normal brain.  Seizures 20%  headaches  incidental finding in asymptomatic patients 15%
  • 7. Diagnosis 7 With increased availability of MRI and CT scans, many patients are found to have an AMV after having a scan for an unrelated problem. Following AVM diagnosis, patients are usually referred to neurointerventional radiologist and/or neurosurgeon, and undergo a diagnostic cerebral angiogram.
  • 8. Radiological diagnosis The imaging features of a brain AVM are (a) the presence of a nidus embedded within the brain parenchyma, identified at either cross-sectional imaging (CT,MR) or conventional angiography. (b) early venous drainage, which is best seen on dynamic studies, the standard of reference being conventional catheter angiography.
  • 9. Radiological diagnosis  The nidus containing numerous serpentine vessels that appear hyperdense in CT and flow void on MRI, there are usually changes in the adjacent brain including gliosis, dystrophic calcification, and blood products.  AVM replaces rather than displaces brain, it causes minimal mass effect.
  • 10. Imaging findings 10 If a nidus is present, two subtypes of abnormal networks of vessels can be encountered. The typical type is the glomerular or compact type nidus, which consists of abnormal vessels without any interspersed normal brain tissue . The more rarely seen second type is the so-called diffuse or proliferative type nidus, in which normal brain parenchyma is interspersed throughout the tangle of vessels. If this finding is present, proliferative angiopathy or cerebrofacial arteriovenous metameric syndrome (CAMS) must be included in the differential diagnosis and can be distinguished from a true brain AVM on the basis of the absence of early venous drainage seen in proliferative angiopathy and the classic location and association with facial AVMs seen in CAMS.
  • 11. Imaging findings 11 Many vascular lesions can manifest with abnormal vessels in the brain at imaging and must be differentiated from one another due to their different natural histories and the various treatment strategies. For example, classic brain AVMs and pial arteriovenous fistulas (AVFs) should be managed according to the risk associated with the disease versus treatment-related risk, DVAs are normal variants that never require treatment.
  • 12. Imaging of Brain AVMs: What the Clinician Needs to Know  Previous hemorrhage.  Intranidal aneurysm.  Venous stenosis.  Deep venous drainage.  Single venous drainage.  Deep or posterior fossa location. Risk of future hemorrhage:
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  • 19. 19 The most important clue to the diagnosis of CAMS is the presence of multiple AVMs in both the brain parenchyma and the facial region. The brain AVMs have a characteristic distribution, consisting of diffuse or proliferative type nidus with supply from multiple small perforator collateral vessels with rather slow arteriovenous shunting into the veins, which makes these AVMs extremely difficult to treat. Cerebrofacial Arteriovenous Metameric Syndrome
  • 21. 21 The typical MR imaging and CT findings include a proliferative type nidus in which normal brain parenchyma is interspersed between the abnormal vessels. Often, an entire lobe or even brain hemisphere is affected. The lack of clear early venous drainage on dynamic images is the key to differentiating this disease from classic brain AVM. Proliferative angiopathy
  • 23. 23 Developmental Venous Anomalies Although they are not classified as AVMs, DVAs may manifest at cross- sectional imaging with an intraparenchymal tangle of vessels and represent extreme variants of the normal transcerebral venous system.
  • 24. Apart from conservative management, there are three treatment options for brain AVMs: surgery, endovascular embolization, or radiosurgery. Surgery can provide a rapid cure in suitable cases (smaller and cortical- based brain AVMs) Endovascular embolization is another treatment option that can be used to quickly eliminate angiographic risk factors. however, the cure rate with embolization alone is relatively low . Radiosurgery has a high cure rate with relatively low complication rates. However, its major limitation is that radiation is slow to take effect; it may be up to 2 years before any shrinkage of the brain AVM is seen. Conservative management is typically used when the risk posed by treatment is too high, such as in large brain AVMs or in asymptomatic patients who are believed to have a low risk of future hemorrhage. TREATMENT
  • 25. The Spetzler-Martin (AVM) grading system size of nidus small (<3 cm) = 1 medium (3-6 cm) = 2 large (>6 cm) = 3 venous drainage superficial veins only = 0 deep veins = 1 eloquence of adjacent brain non-eloquent = 0 eloquent = 1 eloquent brain sensorimotor, language, visual cortex, hypothalamus, thalamus, brain stem, cerebellar nuclei, or regions immediately adjacent to these structures non-eloquent brain frontal lobe, temporal lobe, cerebellar hemispheres