Peer-Review ReportMultimodality Treatment of Intracranial Dural Arteriovenous Fistulas in the Onyx Era: a Single Center Experience
Introduction
Dural arteriovenous fistulas (DAVFs) are abnormal arteriovenous connections between an arterial feeder and a dural venous sinus or leptomeningeal vein with the nidus located within the dural leaflets. They account for 10% to 15% of all intracranial arteriovenous malformations (44). Although their etiology is not clearly understood, DAVFs have been found in association with venous thrombosis, intracranial surgery, tumor, puerperium, and trauma; (53) and some of these lesions are congenital (21). Depending on their location and the venous drainage pattern, the clinical manifestations range from asymptomatic to various signs and symptoms such as headaches, tinnitus, bruit, neurologic deficits, venous hypertensive encephalopathy with cognitive dysfunction, and intracranial hemorrhage (3, 33).
The venous drainage pattern is the most important predictor of the clinical behavior, and DAVFs with cortical venous reflux (CVR) exhibit a much higher incidence of hemorrhage or venous infarction. The annual mortality rate for DAVFs with CVR may be as high as 10.4%, whereas the annual risk for hemorrhage or nonhemorrhagic neurologic deficits during follow-up are 8.1% and 6.9%, respectively, resulting in an annual event rate of 15% (64). In addition, rebleeding rates may be as high as 35% during the first 2 weeks after the initial hemorrhage (18). Thus, these formidable lesions need careful evaluation to determine the best therapeutic option.
Many treatment approaches to these lesions have been proposed (4, 12, 19, 22, 23, 28, 51). With the advent of Onyx (ev3, Irvine, CA), most intracranial DAVFs can be successfully managed with endovascular techniques. Transarterial access to these lesions through their supply from the external carotid artery (ECA) branches, which can be safely embolized, is more often used with Onyx. Their location close to dural venous sinuses also facilitates access and occlusion through the sinus. The combination of transarterial and transvenous embolization results in higher obliteration rates than previously reported in series with only transvenous embolization. However, surgery is still required in certain subsets of patients with 1) complex anatomic features, 2) in case of failure of both transarterial and transvenous embolization, or 3) in lesions for which direct endovascular access is not possible (28). Radiosurgery is mainly used for palliation of type I fistulas or if other modalities fail.
In this study we reviewed our experience with a consecutive series of 32 patients subjected to a multimodality approach for intracranial DAVF treatment. On the basis of our initial experience with Onyx and insights into the management of a variety of complex DAVFs, we propose our current algorithm and detailed consideration of the surgical, radiosurgical, and endovascular treatment options for DAVFs at various locations in the present Onyx era.
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Patients
The study was approved by the institutional review board at the University of Washington, Harborview Medical Center (Seattle, WA) and conducted in compliance with Health Insurance Portability and Accountability Act regulations. All symptomatic intracranial DAVFs were evaluated and treated by a neurovascular team (LNS, BG, LJK, DKH, and GWB). The team determined whether patients were candidates for preoperative embolization and potential endovascular cure. If a fistula was not amenable to
Anatomic and Angiographic Features
Thirteen lesions (41%) were classified as Borden type III, another 13 lesions (41%) as Borden type II, and 6 lesions (18%) as Borden type I. Seven of the type II fistulas were dural cavernous sinus fistula (DCFs) in patients who presented with visual symptoms and had no hemorrhage. Ten DAVFs (31%) were located at the transverse/sigmoid sinus region, 7 (22%) were located at the tentorial region, 3 (9%) were located at the falcine/superior sagittal sinus region, 7 (22%) were DCFs 3 (9%) were in
Etiology, Clinical Features, and DAVF Location
The pathogenesis of DAVFs is controversial, with a congenital and an acquired etiology having been proposed (34). Lasjaunias et al. (34) proposed that a primary structural weakness of the dura coincides with a trigger factor and results in the formation of a DAVF. The common predisposing factor appears to be venous sinus thrombosis, with the body compensating for this by attempts at recanalization (32). In our series, sinus occlusion was observed in two patients. There were 3 patients with
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