This classification provides useful data for determination of the risk with each dural AVF and enables decision-making about the appropriate therapy.

The likelihood of rupture of unruptured intracranial aneurysms that were less than 10 mm in diameter was exceedingly low among patients in group 1 and was substantially higher among those in group 2. The risk of morbidity and mortality related to surgery greatly exceeded the 7.5-year risk of rupture among patients in group 1 with unruptured intracranial aneurysms smaller than 10 mm in diameter.

Embolization was used to reduce the size of brain arteriovenous malformations (AVMs) prior to radiosurgical treatment in 125 patients who were poor surgical candidates or had refused surgery. Of these patients, 81% had suffered hemorrhage, and 22.4% had undergone treatment at another institution. According to the Spetzler-Martin scale, the AVMs were Grade II in 9.6%, Grade III in 31.2%, Grade IV in 30.4%, and Grades V to VI in 28.8% of the cases. Most embolizations were performed using cyanoacrylate delivered by flow-guided microcatheters. Radiosurgery was performed using a linear accelerator in 62 patients treated by the authors, and 34 patients were treated at other institutions using various methods. Embolization produced total occlusion in 11.2% of AVMs and reduced 76% of AVMs enough to allow radiosurgery. Radiosurgery produced total occlusion in 65% of the partially embolized AVMs (79% when the residual nidus was < 2 cm in diameter). Embolizations resulted in a mortality rate of 1.6% and a morbidity rate of 12.8%. No complications were associated with radiosurgery. The hemorrhage rate for partially embolized AVMs was 3% per year. No patient with a completely occluded AVM experienced rehemorrhage. Angiographic follow-up review of AVMs embolized with cyanoacrylate demonstrated a 11.8% revascularization rate, occurring within 1 year. It is concluded that after partial embolization with cyanoacrylate, the risk of hemorrhage from the residual nidus is comparable to the natural history of AVMs and that the residual nidus can be irradiated with results almost as good as for a native AVM of the same size.

Objectives-A retrospective study was carried out on 13 patients with intracranial dural arteriovenous fistulas (DAVFs) who presented with isolated or associated signs of intracranial hypertension. Methods-Nine patients presented with symptoms of intracranial hypertension at the time of diagnosis. Ocular fundoscopy available in 12 patients showed bilateral papilloedema in eight and optic disk atrophy in four. Clinical evolution was particularly noticeable in five patients because of chronic (two patients) or acute (after lumbar shunting or puncture: three patients, one death) tonsillar herniation. Results-Two patients had a type I fistula (drainage into a sinus, with a normal antegrade flow direction). The remaining 11 had type II fistulas (drainage into a sinus, with abnormal retrograde venous drainage into sinuses or cortical veins).Stenosis or thrombosis of the sinus(es) distal to the fistula was present in five patients. The cerebral venous drainage was abnormal in all patients. Conclusion-Type II (and some type I) DAVFs may present as isolated intracranial hypertension mimicking benign intracranial hypertension. Normal cerebral angiography should be added as a fifth criterion of benign intracranial hypertension. The cerebral venous drainage pattern must be carefully studied by contralateral carotid and vertebral artery injections to correctly evaluate the impairment of the cerebral venous outflow. Lumbar CSF diversion (puncture or shunting) may induce acute tonsillar herniation and should be avoided absolutely. DAVF may induce intracranial hypertension, which has a poor long term prognosis and may lead to an important loss of visual acuity and chronic tonsillar herniation. Consequently, patients with intracranial hypertension must be treated, even agressively, to obliterate the fistula or at least to reduce the arterial flow and to restore a normal cerebral venous drainage. The endovascular treatment may associate arterial or transvenous embolisation and /or surgery. Patients in whom the fistula is not obliterated after an endovascular therapeutic procedure, need continous clinical and angiographical follow up.(J Neurol Neurosurg Psychiatry 1998;65:308-316)

The clinical and angiographic features of 46 vertebral arteriovenous fistulas (AVFs) seen during a 12-year period (45 patients) were reviewed. Fourteen patients were asymptomatic, with vertebral AVF discovered at routine clinical examination. Specific symptoms at presentation in the other patients were tinnitus (n = 21), vertigo (n = 6), neurologic deficit (n = 3), and pain (n = 2). Of the 46 AVFs, 19 (41%) were caused by trauma and 27 (59%) were spontaneous. The fistula was found at C-1 to C-2 in 21 (46%) cases, at C-2 to C-5 in five (11%), and below C-5 in 20 (44%). Thirty-four patients (35 vertebral AVFs) were treated with the endovascular technique. Embolization was performed with latex balloons filled with contrast medium in most cases. Endovascular therapy resulted in complete occlusion in 32 cases (91%) and partial occlusion in three (9%). The vertebral artery could not be preserved in three patients. Endovascular balloon treatment of vertebral AVFs is effective in occluding the shunt, avoids general anesthesia and surgical intervention, and results in minimal morbidity. Endovascular therapy is the treatment of choice for vertebral AVF.

• Numerous interventional techniques have been used to embolise brain arteriovenous malformations (AVMs). • This prospective multicentre study demonstrates the suitability of a liquid embolic agent. • The safety of treatment using Onyx is acceptable. • Such embolisation leads to complete AVM occlusion in 23.5 % of patients.

We review seven patients with intracranial dural arteriovenous fistulae (ICDAVF), each altering the initial type of venous drainage to one with a higher grading during long-term follow-up. Five were discovered due to symptoms of intracranial hypertension, two due to changes in tinnitus and one case following subarachnoid haemorrhage. In five cases, cortical venous drainage developed during the follow-up period. Three different mechanisms were observed: stenosis or thrombosis in the draining veins in 4 cases: increased arterial flow in 2; and the appearance o a new fistula site or extension of the initial shunt in 2. Type I and type II a fistulae which are not completely cured, require both close clinical observation and Doppler examinations in the follow-up period. Any charge in the clinical pictures indicates a repeat angiogram. Stenosis of the venous drain-age, forecasting later worsening in the venous outlet, requires more thorough angiographic follow-up.

Neurotoxicity from contrast media used in angiography is a rare complication from these procedures. The infrequency with which it is encountered makes it a diagnostic challenge. We present the case of a 51-year-old male who, 30 min after successful angiography for treatment of a right carotid-ophthalmic fusiform aneurysm with a stent, developed psychomotor agitation, disorientation, and progressive left faciobrachial hemiparesis (4/5). An emergency nonenhanced CT showed marked cortical enhancement and edema in the right cerebral hemisphere. Cortical enhancement is thought to be secondary to contrast extravasation due to disruption of the blood-brain barrier. Angiography was performed immediately, without any pathologic findings. After this procedure there was an increase in the left faciobrachial hemiparesis (3/5), right gaze deviation, Gerstmann syndrome, and left anosognosia and left homonymous hemianopsia. Endovenous dexamethasone and mannitol were initiated. Twenty-four hours later an MRI showed no signs of acute infarct, just gyriform signal increase in the right cerebral hemisphere on FLAIR and a decrease in the edema observed before. The patient had progressive improvement of his neurological deficit. A control MRI done 5 days later was normal. The patient recovered completely and was discharged. This rare entity should be kept in mind but diagnosed only when all other causes have been ruled out, because more important and frequent causes, such as acute infarct, must be excluded promptly.