Arteriovenous Malformations

The AVM nidus is a compact tangle of dys-plastic, thin-walled vessels of varied length connecting feeding arteries to draining veins. An AVM nidus can either be globular or conical in shape. Within the AVM nidus, arterial blood is shunted directly into draining veins without passage through a normal, high-resistance arte-riolar-capillary network. The amount of arteriovenous shunting varies among AVMs and is determined by nidal vessel impedance. There is usually little brain parenchyma within an AVM nidus. However, functional parenchyma may occasionally be found among the vessels of a diffuse nidus. Most intra-nidal parenchyma is densely sclerotic and stained with hemosiderin [9]. Fusiform or pseudo-aneurysms may be present on intra-nidal vessels. Although the weak, dysplastic nidal vessels are usually the source of AVM hemorrhage, concomitant aneurysms represent an independent risk factor for AVM hemorrhage [1].

Each AVM has a variable number of feeding arteries. Each arterial feeder may drain directly into a vein (an arteriovenous fistula), or connect through a mass of dysplastic vessels within the AVM nidus before draining into a vein. Vessels feeding an AVM are frequently histologically normal. However, chronically elevated blood flow may cause accelerated atherosclerosis [11] or flow-related aneurysm formation [1]. These flow-related aneurysms occur on the proximal intracranial vessels and are pathologically similar to saccular aneurysms. Veins draining an AVM are often large and dilated. In addition, direct arterial blood flow into draining veins may promote intimal hyperplasia and subsequently cause venous wall thickening and stenosis. Venous drainage can be directed into deep subependymal or superficial cortical venous systems.

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