Angiographic and clinical data from 155 patients with carotid cavernous fistulae were retrospectively reviewed to determine angiographic features associated with increased risk of morbidity and mortality. These features included presence of a pseudoaneurysm, large varix of the cavernous sinus, venous drainage to cortical veins, and thrombosis of venous outflow pathways distant from the fistula. Clinical signs and symptoms that characterized a hazardous carotid cavernous fistula included increased intracranial pressure, rapidly progressive proptosis, diminished visual acuity, hemorrhage, and transient ischemic attacks. Cortical venous drainage from the carotid cavernous fistula is secondary to occlusion or absence of the normal venous outflow pathways and is associated with signs and symptoms of increased intracranial pressure and an increased risk of intraparenchymal hemorrhage. Angiographic demonstration of a cavernous sinus varix, with extension of the sinus into the subarachnoid space, is associated with an increased risk of fatal subarachnoid hemorrhage. Identification of these high-risk features provides a basis for making decisions about treatment.

InterventionalNeuroradiology Section, 505 Pamassus Ave., L-352, San Francisco, CA 941 43. Address reprint requests to A. T. Higashida.

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.

Sixteen patients with dissecting aneurysms or pseudoaneurysms of the vertebral artery, 12 involving the intradural vertebral artery and four occurring in the extradural segment, were treated by endovascular occlusion of the dissection site. Patients with vertebral fistulas were excluded from this study. The dissection was caused by trauma in three patients (two iatrogenic) and in the remaining 13 no obvious etiology was disclosed. Nine patients presented with subarachnoid hemorrhage (SAH), two of whom had severe cardiac disturbances secondary to the bleed. The nontraumatic dissections occurred in seven women and six men, with a mean age on discovery of 48 years. Fifteen patients were treated with endovascular occlusion of the parent artery at or just proximal to the dissection site. One patient had occlusion of a traumatic pseudoaneurysm with preservation of the parent artery. Four patients required transluminal angioplasty because of severe vasospasm produced by the presenting hemorrhage, and all benefited from this procedure with improved arterial flow documented by transcranial Doppler ultrasonography and arteriography. In 15 patients angiography disclosed complete cure of the dissection. One patient with a long dissection of extracranial origin extending intracranially had proximal occlusion of the dissection site. Follow-up angiography demonstrated healing of the vertebral artery dissection but persistent filling of the artery above the balloons, which underscores the need for embolic occlusion near the dissection site. No hemorrhages recurred. One patient had a second SAH at the time of therapy which was immediately controlled with balloons and coils. This patient and one other had minor neurological worsening resulting from the procedure (mild Wallenberg syndrome in one and minor ataxia in the second). Symptomatic vertebral artery dissections involving the intradural and extradural segments can be effectively managed by endovascular techniques. Balloon test occlusion and transluminal angioplasty can be useful adjuncts in the management of this disease.

Thirty symptomatic indirect carotid cavernous fistulas were treated between 1978 and 1986 with a variety of treatment modalities. Combined carotid artery and jugular vein compression resulted in a complete cure in seven of 23 patients (30%) and improvement in one additional patient. There were no complications from this treatment, which is performed by the patient on an outpatient basis. Patients in whom carotid jugular compression therapy failed or who demonstrated cortical venous drainage or visual decline were treated with intravascular embolization. Embolization resulted in complete cure in 17 of 22 (77%) and improvement in four of 22 (18%). One patient required surgical excision of the involved dura after embolization to achieve complete cure. There was one permanent complication (stroke), which resulted in mild weakness caused by clot formation on a catheter.