Walsh & Hoyt: Pathogenesis

Dural CCFs usually become symptomatic spontaneously. The pathogenesis of these fistulas is controversial. Newton and Hoyt speculated that spontaneous dural CCFs form after rupture of one or more of the thin-walled dural arteries that normally traverse the cavernous sinus. After rupture, extensive preformed dural arterial anastomoses not directly involved in the fistula may dilate and contribute collateral blood supply, resulting in an angiographic appearance indistinguishable from a congenital vascular malformation. Indeed, sequential arteriography demonstrates that the feeder vessels of dural CCFs change with time as the vessels spontaneously open and close. Although the theory of Newton and Hoyt is favored by some investigators, it fails to explain why spontaneous dural CCFs are more common in elderly women than in men. A second theory for the origin of dural CCFs was espoused by Houser et al., who suggested that most of these lesions develop in response to spontaneous venous thrombosis in the cavernous sinus in an attempt to provide a pathway for collateral venous outflow. This theory is favored by most investigators because it also explains the pathogenesis of arteriovenous fistulas that develop in the sigmoid and other dural sinuses.