Arteriovenous Malformation

      The arteriovenous (AV) malformation consists of a congenital abnormality of anomalous, dilated capillaries that result in shunting of blood from the arterial to venous side. AV malformations are by far the most common of the cerebrovascular malfor mations. One-half of patients present with seizures or a neurological deficit due to compression of normal brain or a steal phenomenon. The other half presents with hemorrhage. The hemorrhage is usually more benign than that due to a ruptured aneurysm. Ninety-five percent of AV malformations are in the supratentorial compartment, either in a lobar or deep location and 10% are in the infratentorial region. Dural supply is more commonly found with infra tentorial lesions although it is important to remember than any AV malformation adjacent to a dural surface can receive dural contributions.

      CT features of an AV malformation on plain scan include a high- absorption irregular mass with large feeding arteries and draining veins, focal areas of calcification and no surrounding edema or mass effect. The contrast scan shows serpiginous enhancement with prominent arteries and veins. Due to the rapidly flowing blood from these lesions, a flow void is observed on MR scan. As a result, the characteristic feeding arteries and draining veins can be imaged without any injection of contrast material. Endnote

      The best MRA sequences for depicting the anatomy of AV malformations are 3D TOF and PC methods. The TOF technique may not show the draining veins in their entirety due to saturation effects. Endnote Gd will improve venous visualization, but in general, PC is better for imaging the venous side. By using two different velocity-encoding factors, 80 and 20 cm/sec, arterial and venous phase images can be generated. High flow through these lesions often produce turbulence and some signal loss within the feeding arteries. Selective saturation pulses can be used to isolate arterial supply.

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      As mentioned earlier, flow voids from AV shunting help identify AV malformations on spin-echo MR scans. In fact, spin-echo imaging is probably more sensitive than MRA for detecting AV malformations. Moreover, MRA probably has a limited role in the initial diagnostic workup of AV malformations because a conventional angiogram is required anyway. The proper role for MRA will likely be to follow these lesions, to assess the affects of radiation therapy or embolization procedures, and to check for growth of partially resected lesions.

      One should suspect AV malformation as a cause of an intracerebral hemorrhage if the hemorrhage is lobar and away from the territory of the anterior communicating and middle cerebral arteries, and also in deep hemorrhages in younger, normotensive patients. It is important to remember that the hematoma may compress a small AV malformation. If the initial angiogram is negative, a follow-up study should be done one to two months later, after the hematoma and mass effect have resolved. AV malformations can thrombose either spontaneously or due to compression by the hematoma.  

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