**6. Conclusion**

According to previous theories concerning the mechanism of DAVF, it is very important to consider the occlusive pathway and hypertension of the affected sinus. However, previous theories did not indicate an initiation of this pathological situation which can explain both sinus and non-sinus type DAVF and the promoting factors to develop the extension of DAVF. We propose a new theory: the inflammatory vascular network at the penetration site of emissary veins may induce local shunt formation. Subsequent occlusion of the affected EV completes the usual figure of DAVF, and, the sinus (venous) occlusive pathway and arterial recruitment are important steps in the maturation of the DAVF. Previous mechanistic hypotheses focusing on sinus hypertension and sinus thromboses cannot explain the pathogenesis of non-sinus type of DAVF. Although the etiology of DAVF may be concerned by the thrombo-occlusive change of sinus, and our theory is only a speculation without the base of experimental study, it may enable to understanding the common etiology of the two (sinus & non-sinus) types of DAVF, and is not contradictory to the previous sinus-oriented theory. Pathological proof of the initial stage of DAVF will be mandatory.

Abbreviations: DAVF: dural arteriovenous fistula, EV: emissary vein, CS: cavernous sinus, SSS: superior sagittal sinus, TS: transvers sinus, SS: sigmoid sinus, ACC: anterior condylor confluence, CCJ: craniocervical junction
