This document discusses arteriovenous malformations (AVMs) of the brain. It begins by defining AVMs and describing their three types. It then discusses the epidemiology of AVMs, noting they are usually congenital but develop over time, and are typically diagnosed around age 31. Clinical presentations of AVMs include being asymptomatic, seizures, headaches, ischemic events, and hemorrhaging. The pathology section describes the components of an AVM including feeding arteries, nidus, draining veins. Location is typically supratentorial. Radiographic features on CT, MRI, MRA, and DSA are discussed. In summary, this document provides an overview of brain AVMs, including their definition, epidemiology, clinical

1. Radiological imaging of Brain Arteriovenous Malformations(AVM).
Dr/ ABD ALLAH NAZEER. MD.

2. Cerebral arteriovenous malformations (CAVM's) are a common form
of cerebral vascular malformation and are composed of a nidus of vessels
through which arteriovenous shunting occur. Three types are described:
parenchymal (pial) AVM
dural AVM
mixed AVM
Epidemiology
Although arteriovenous malformations are thought to represent a congenital
abnormality, they are thought to develop over time and are rarely found
incidentally in the very young. Having said this, a third of AVMs which are
diagnosed due to hemorrhage are identified before the age of 20 years of
age. Overall AVMs are diagnosed at a mean age of 31 years.
Overall AVMs are thought to occur in approximately 4% of the population, but
become symptomatic in only 12% of affected individuals. There is no gender
predilection.
Arteriovenous malformations tend to be solitary in the vast majority of cases
(>95%). When multiple, syndromic associations include
Wyburn-Mason syndrome
Osler-Weber-Rendu syndrome

3. Clinical presentation
CAVMs are the most common symptomatic vascular malformations. Possible
presentations include
incidental finding in asymptomatic patients: 15%
seizures: 20%
headaches
ischemic events due to vascular steal from normal brain
hemorrhage: 65%5, 2-3% per year
parenchymal
subarachnoid
intraventricular
Pathology
The origin of arteriovenous malformations remains uncertain, although they are
thought to be congenital and perhaps involves dysregulation of vascular
endothelium growth factor (VEGF).
AVMs comprise of a number of components
feeding arteries
nidus
shunting arterioles: the true culprit
interconnected venous loops
draining veins

4. The nidus is fed by one or more arteries and drained by one or more veins. The feeding
arteries are enlarged due to the increased flow and flow related arterial aneurysms are
encountered . Venous aneurysms are also seen. It may contain dystrophic calcification,
small amount of gliotic tissue and blood in different stages of evolution.
Location: supratentorial: ~85%
superficial (two-thirds)
deep (one-third)
infratentorial: ~15%
Incidence
solitary AVMs (98%)
multiple AVMs (2%)
associated with syndromes
Associated abnormalities
flow related angiopathy secondary to endothelial hyperplasia
flow related aneurysm
intranidal: located in the nidus
intrapedicular: located in the feeding vessel
remote aneurysm: hemodynamically unrelated to malformation
Classification and grading
AVMs can be divided into two types :
compact: nidus contains little if any neuronal tissue, which is non-functioning
diffuse: no well formed nidus is present, with functional neuronal tissue interspersed
amongst the anomalous vessels.

5. Radiographic features
CT: Diagnosis can be difficult on non contrast CT. The nidus is blood density and
therefore usually somewhat hyperdense compared to adjacent brain. Enlarged
draining veins may be seen.
Following contrast administration, and especially with CTA the diagnosis is usually
self evident with feeding arteries, nidus and draining veins visible. The exact
anatomy of feeding vessels and draining veins is often difficult to delineate, and
thus angiography remains necessary.
MRI:
Fast flow generates flow voids easily seen on T2 weighted images. Complications
including previous hemorrhage and adjacent edema may be evident.
MRA: phase contrast MR angiography is often useful to subtract the hematoma
components when an AVM complicated by an acute hemorrhage needs to be
imaged DSA - angiography
Remains the gold standard, able to exquisitely delineate the location and number
of feeding vessels and the pattern of drainage. Ideally angiography is performed
in a bi-plane system with a high rate of acquisition, as the shunts can be very
rapid.
On angiogram AVM appears as tightly packed mass of enlarged feeding arteries
that supply central nidus. One or more dilated veins drain the nidus and there is
abnormal opacification of veins occurs in arterial phase, represents shunting.

7. Superficial AVM with parietal hematoma.

8. CTA MIP images demonstrated an AVM in the parieto-temporal lobe surrounding the hematoma

9. AVM in the right temporal lobe (arrows). AVM in the left parietal lobe (arrow).

10. Superficial AVM with intra-cerebral hematoma.

11. Deep AVM.

12. Deep AVM.

13. An AVM in the midbrain and right thalamus (arrow).

14. Proliferative type of brain AVM.

16. Proliferative type of left ganglionic AVM.

17. Large right hemispheric vascular lesion .

20. Developmental VA of the brain stem.

21. Pial AVM.

22. Dural AVF with left occipital and intra-ventricular hemorrhage.

24. Moyamoya with peri-mesencephlic AVM and associated IV hemorrhage

25. Grade 3 thalamic AVM with intra-nidal aneurysm.

28. (a) T2 axial, (b) T2 coronal, (c) T1 sagittal and, (d) MR angiogram sequence of cerebral magnetic resonance
imaging reveals a left frontal well defined flow void of size 60 × 66 mm communicating with the superior
sagittal sinus through dilated cortical vein with feeder supply from left anterior cerebral artery.

29. 128 Multi slice cerebral computed tomographic angiography sagittal (a) and coronal (b)
view demonstrates a large left frontal arteriovenous fistula supplied by the distal left
anterior cerebral artery draining through a dilated cortical vein into the superior sagittal
sinus. A large variceal dilatation of the proximal venous end measuring nearly 6.5 cm in
diameter with wall calcification is shown in association with the arteriovenous fistula.

30. Thank You.