Endovascular Treatment of Cranial Arteriovenous Malformations and Dural Arteriovenous Fistulas

Pial arteriovenous malformations (AVMs) and dural arteriovenous fistulas (DAVFs) are high-flow vascular lesions with abnormal communications between the arterial and venous system. AVMs are congenital lesions, whereas DAVFs are considered acquired lesions. Both can cause significant morbidity and mortality if they rupture and result in intracranial hemorrhage. The primary goal of treatment is to eliminate the risk of bleeding or at least decrease it. Because the epidemiology, clinical presentation, and classification of AVMs and DAVFs have been covered in previous articles in this issue, the authors only briefly touch on these subjects as they relate to endovascular treatment.

Endovascular therapy for AVMs

When considering the treatment of an AVM, it is useful to distinguish between those that have hemorrhaged from those that have not. The annual risk of AVM rupture ranges between 2% and 4% ; however, the risk of repeat hemorrhage increases to between 7% and 17% during the first year following the initial event. It is because of this increased risk that prompt treatment of ruptured AVMs is recommended.

The main determinant for the role of endovascular therapy is the location of the AVM with regard to tissue eloquence. If a lesion is within eloquent tissue, the role of endovascular therapy may be limited because the risk of stroke may be unacceptable. For superficial lesions near the motor cortex or deep lesions near the corona radiata or the internal capsule, the intraoperative monitoring of somatosensory-evoked potentials and muscle motor–evoked potentials in combination with pharmacologic provocative testing with amobarbital (Amytal) and lidocaine can increase the safety of such procedures.

For unruptured AVMs, it is important to properly select patients in whom therapy is indicated. Initial evaluation of patients with an unruptured AVM should attempt to determine if the patients’ clinical symptoms are related to the AVM. AVMs with high-flow shunts may present in childhood with signs of cardiac insufficiency or developmental delay. Venous congestion may also be present secondary to stenosis of the outflow vein or increased vascular resistance secondary to a long draining vein and may result in dementia. Venous varices have been associated with seizures. The supplying arteries and draining veins of an AVM should be further evaluated for anatomic features that may predispose patients to intracranial hemorrhage ( Fig. 1 ) (ie, intranidal aneurysms, venous ectasias, venous stenosis, and exclusive deep venous drainage).

The angioarchitecture of the AVM must also be evaluated to determine whether endovascular therapy is technically feasible. On the arterial side, the number and size of the feeding vessels will determine the feasibility of endovascular treatment. Catheterization of a large number of small, minimally dilated feeding vessels is more technically demanding than the treatment of a single, large feeding artery. Feeding arteries may be further categorized as direct arterial feeders that end in the AVM and indirect feeders that supply the normal cortex with small branches to the AVM, so-called en passant vessels. The treatment of direct feeding vessels is relatively safe because the injection of liquid embolic agents with the catheter tip distal to the arterial branches supplying normal brain tissue can usually be achieved. If there is reflux of the embolic material around the catheter tip, it is usually inconsequential. If there is not sufficient purchase of the catheter tip into an indirect feeding vessel, reflux of embolic material into the parent vessel may occur with distal embolization into normal brain tissue with catastrophic consequences, (ie, stroke).

The connection between the feeding arteries and the draining veins should be evaluated to determine the nature of the connection, nidal or fistulous, and the number of compartments in the AVM. This evalutaion may be difficult if the AVM is large and there is rapid shunting. The venous outflow should be scrutinized for features that increase the risk of endovascular therapy. Multiple draining veins have a decreased risk as compared with a single vein with a stenosis. Embolization of the outflow vein without treatment of the feeding arteries may lead to a sudden increase in pressure within the AVM with subsequent rupture and catastrophic results. By studying the angioarchitectue on the AVM, one can begin to understand the underlying pathophysiology and appropriately select patients for treatment.

Complete cure of an AVM by endovascular means is only possible in approximately 20% of cases. Those AVMs that exhibit an angioarchitecture favorable for complete cure are those that are small and have a single feeding artery and a single compartment. As the size of the AVM nidus increases, the success of embolization as a single mode of treatment decreases and the risk of complication increases. In these cases, partial targeted embolization becomes a much more reasonable option. Partial targeted embolization may be used alone or in conjunction with surgery or radiosurgery ( Fig. 2 ). In the case of radiosurgery, the periphery of the AVM may be the target of embolization with the goal of reducing the size of the AVM to limit the area and, thus, the radiation dose required to treat the residual AVM and to secure focal weak areas within the AVM while the AVM undergoes complete occlusion. When combined with microsurgery, the goal is to secure those regions that will be more difficult for surgical access, which are the deep feeding vessels that are more difficult for the surgeon to directly visualize and control. Because no two AVMs are the same, every patient requires a tailored, team approach that takes into account the specifics of each case.