Two types of complications of radiation occur at a combined rate of approximately 2 to 4 percent. The first is delayed radiation necrosis, which is predictable based on the radiation dose, and the second is venous congestion that occurs several weeks or months after treatment. The latter is indicative of the desired effect of thrombosis of the malformation. Both may cause local symptoms for weeks or months. Radiation necrosis may be reduced by the administration of corticosteroids but the vascular problem generally is not helped.
The treatment of AVMs by endovascular techniques is increasingly being used but has not been fully evaluated. Nearly every AVM has several feeding arteries, some not reachable by a catheter, and some part of the AVM may remain after treatment. In most series, 25 percent or more of AVMs, mostly of small and medium size, have been completely obliterated, with a mortality rate below 3 percent and morbidity of 5 to 7 percent, both of which compare favorably with surgical outcomes. These techniques are particularly suited to lesions of a combined AVM and an aneurysm on the feeding vessel.
In the past several years, combined therapy that begins with endovascular reduction of the lesion and is followed by either surgery or radiation has been viewed favorably. Using this approach, more than 90 percent of lesions can be obliterated with a very low rebleeding rate over several years. It is clear that the plan for each patient must be individualized based on the size, location, nature of feeding vessels, the presence of other vascular lesions (aneurysm or additional AVM), and the age of the patient. Another strategy for otherwise untreatable grade IV and V lesions has been to stage radiosurgery in order to reduce parts of the lesions sequentially as described by Sirin and colleagues. Even then, there will be differences of opinion based on local resources and experience.
Finally, if the primary problem is recurrent seizure, eliminating the malformation often achieves reduction or cessation of seizures in a high proportion of cases but some observational series suggest otherwise. In the interval, antiepileptic drugs are required and may be needed for a period of years after obliteration.
These curious vascular abnormalities, occurring in both the cranial and spinal dura, have different presentations at each site. The spinal form, more common in general experience, is discussed with other diseases of the spinal cord in Chap. 42. The cranial type is being detected with increasing frequency as refinements continue to be made in imaging of the cerebral vessels, but its incidence and pathogenesis are not fully known. The defining features are radiologic—a nidus of abnormal arteries and veins with arteriovenous shunting contained entirely within the leaflets of the dura. The lesion is usually fed by dural arterial vessels derived from the internal cranial circulation and often, more prolifically, from the external cranial circulation (external carotid artery and muscular branches of the vertebral artery). Venous drainage of these lesions is often complex and is largely directed to the dural venous sinuses (Fig. 33-31). The rapid transit of injected angiographic dye through dural fistulas accounts for the early opacification of the draining venous structures. In the case of high-flow connections, this may not be seen unless images are taken almost immediately after the injection. A number of potential feeding vessels must be individually opacified to demonstrate all the conduits into the lesion. On CT and MRI, the fistula is sometimes detected as a thickening or enhancement of a region of dura, generally close to a large dural venous sinus. In other cases, the dilated draining vessels may be seen only with the injection of dye or gadolinium. Probably, many are not detected by either of these techniques.
Several classification systems have been developed that are based on the nature and direction of the drainage of the lesion. There are some associations between the nature of these drainage patters, as summarized by the classification systems, and clinical presentation.