Mechanism of the formation of dural arteriovenous fistula: the role of the emissary vein.

摘要: Dural arteriovenous fistula (DAVF) can be separated into two types: DAVF which drains through an affected sinus (sinus type) and with direct reflux to the cortical vein (non-sinus type). The present report attempted clarify mechanism of formation development focusing on emissary (EV) hypothesis. First, inflammation occurs at penetrating point EV dura due idiopathic or secondary causes. Local inflammatory reactions induce vessel dilatation neovascularization, subsequently create (AV) connections arteriole level. Although communicating dural arteries might play a role as draining routes first, they start degrade compression enlarged hemodynamic shift drainage pathway least resistance. Following occlusion veins may form, resulting in clinically detectable DAVF. AV shunt then expands surrounding associated recruitment feeders from distant sites induced by expression angiogenetic factors balance. In type DAVF, is progressively compartmentalized finally occludes thrombogenesis activated coagulopathy hypertrophy wall. This progression results mature, aggressive impairments. Previous mechanistic hypotheses hypertension thromboses cannot explain pathogenesis non-sinus etiology concerned thrombo-occlusive change sinus, unique theory presented this enable understanding common both types