Dural sinus thrombosis has been hypothesized as a possible cause of dural arteriovenous fistulas (AVF's). The pathogenesis and evolution from thrombosis to actual development of an AVF are still unknown. To study dural fistula formation, a surgically induced venous hypertension model in rats was created by producing an arteriovenous shunt between the carotid artery and the external jugular vein. The external jugular vein beyond the anastomosis was ligated 2 to 3 months after surgery and angiography was performed to identify any new acquired AVF's. Forty-six male Sprague-Dawley rats, each weighing approximately 300 gm, were used for this study. In Group I, 22 rats underwent a common carotid artery anastomosis to the external jugular vein, which is the largest draining vein from the transverse sinus via the posterior facial vein, followed by proximal external jugular vein ligation. In Group II, 13 rats underwent the same surgical procedure, followed by contralateral posterior facial vein occlusion. Group III served as the control group, in which 11 rats underwent only unilateral external jugular vein occlusion with or without contralateral posterior facial vein occlusion. The shunts in Groups I and II were ligated at 2 to 3 months following surgery, and transfemoral angiography was performed immediately before and after occlusion. New acquired AVF's had developed in three rats (13.6%) in Group I, three rats (23.1%) in Group II, and no rats (0%) in Group III. One of these newly formed fistulas was located at the dural sinus, analogous to the human dural AVF. The other five were located in the subcutaneous tissue, including the face and neck. The dural AVF in the rat was present on follow-up angiography at 1 week after the bypass occlusion. It is concluded that chronic venous hypertension of 2 to 3 months' duration, without associated venous or sinus thrombosis, can induce new AVF's affecting the dural sinuses or the subcutaneous tissue.

The authors report three cases of arteriovenous malformations (AVM's) with aneurysms arising from the feeding artery; all were successfully treated with a new nonadhesive liquid embolic material, ethylene vinyl alcohol copolymer (EVAL). In two patients the AVM's were totally removed without difficulty, and in one the AVM was managed conservatively after embolization. No new neurological deficits appeared during or after embolization. After road-mapping techniques, EVAL was injected slowly until the feeding artery and aneurysm were completely obliterated. This embolic agent is easy to handle and is considered safe compared with other adhesive liquid embolic agents, such as isobutyl-2-cyanoacrylate or n-butyl cyanoacrylate. It is concluded that EVAL is an excellent agent for embolizing an AVM with a peripheral aneurysm on the feeding artery.

Stent placement is more effective than PTA for stenosis of the petrous or cavernous portion of the ICA from the viewpoint of initial and late gain in diameter.

The clinical results of carotid stenting for ICA pseudo-occlusion under embolic protection were fairly good from the viewpoints of periprocedural neurological morbidity, angiographic follow-up results, and stroke prevention. Carotid stenting can be considered an alternative to carotid endarterectomy in patients with ICA pseudo-occlusion.

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