presentation1.pptx, radiological imaging of brain av malformation

Radiological imaging of Brain Arteriovenous Malformations(AVM).

Dr/ ABD ALLAH NAZEER. MD.

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) AVMdural AVMmixed AVMEpidemiologyAlthough 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 includeWyburn-Mason syndromeOsler-Weber-Rendu syndrome

Clinical presentationCAVMs are the most common symptomatic vascular malformations. Possible presentations includeincidental finding in asymptomatic patients: 15% seizures: 20%headachesischemic events due to vascular steal from normal brainhemorrhage: 65%5, 2-3% per year

parenchymalsubarachnoidintraventricular

PathologyThe 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 arteriesnidus

shunting arterioles: the true culpritinterconnected venous loops

draining veins

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%Incidencesolitary AVMs (98%)multiple AVMs (2%)

associated with syndromesAssociated abnormalitiesflow related angiopathy secondary to endothelial hyperplasiaflow related aneurysm

intranidal: located in the nidusintrapedicular: located in the feeding vessel

remote aneurysm: hemodynamically unrelated to malformationClassification and gradingAVMs can be divided into two types :compact: nidus contains little if any neuronal tissue, which is non-functioningdiffuse: no well formed nidus is present, with functional neuronal tissue interspersed amongst the anomalous vessels.

Radiographic featuresCT: 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 - angiographyRemains 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.

Superficial AVM with parietal hematoma.

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

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

Superficial AVM with intra-cerebral hematoma.

Deep AVM.

Deep AVM.

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

Proliferative type of brain AVM.

Proliferative type of left ganglionic AVM.

Large right hemispheric vascular lesion .

Developmental VA of the brain stem.

Pial AVM.

Dural AVF with left occipital and intra-ventricular hemorrhage.

Moyamoya with peri-mesencephlic AVM and associated IV hemorrhage

Grade 3 thalamic AVM with intra-nidal aneurysm.

(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.

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.

Thank You.