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Presentation1.pptx, radiological imaging of brain av malformation.
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
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Presentation1.pptx, radiological imaging of brain av malformation.
- 1. Radiological imaging ofBrain 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 arethe 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 isfed 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: Diagnosiscan 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 withparietal hematoma.
- 8. CTA MIP imagesdemonstrated an AVM in the parieto-temporal lobe surrounding the hematoma
- 9. AVM in theright temporal lobe (arrows). AVM in the left parietal lobe (arrow).
- 10. Superficial AVM withintra-cerebral hematoma.
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- 13. An AVM inthe midbrain and right thalamus (arrow).
- 14. Proliferative type ofbrain AVM.
- 16. Proliferative type ofleft ganglionic AVM.
- 17. Large right hemisphericvascular lesion .
- 20. Developmental VA ofthe brain stem.
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- 22. Dural AVF withleft occipital and intra-ventricular hemorrhage.
- 24. Moyamoya with peri-mesencephlicAVM and associated IV hemorrhage
- 25. Grade 3 thalamicAVM 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 slicecerebral 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.
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