Dural arteriovenous malformation in the posterior fossa.

Abstract

Arteriovenous malformations that involve the dura of the posterior fossa are rare, and they are therefore seldom considered in the differential diagnosis of posterior fossa lesions. Such malformations may involve the tentorium and the dura that covers the remainder of the posterior fossa. Their presence and extent can be evaluated accurately only by angiography. The purpose of this report is to present the clinical and angiographic features of 16 patients with dural arteriovenous malformations of the posterior fossa. These patients were studied either at the University of California Medical Center at San Francisco or Los Angeles or at the Karolinska Hospital in Stockholm, Sweden. Clinical Features The clinical features of the 9 males and 7 females are summarized in Table I. The ages ranged from one to sixty-eight years. In 11 patients a pulse-synchronous bruit was audible either at the vertex or over the mastoid region. Of these patients, 7 complained of hearing a pulsatile buzzing sound. Both the bruit and the subjective buzzing sound could usually be stopped or markedly diminished by compression of the carotid artery. The arteriovenous malformation was manifested externally in 5 patients. These external findings included dilated scalp and facial veins in 2 patients, pulsatile masses behind the ear in 2 others, and an enlarged head in the fifth. In addition, 2 of these patients had unilateral proptosis. Neurologic abnormalities were observed in 8 patients. Three complained of headaches, and 1 gave a history of convulsions. Visual complaints, visual field defects, or both were noted in 3 patients and papilledema in another 3. Motor and sensory deficits were present in 3 patients. Subarachnoid hemorrhage was a presenting sign in only 2. An asymptomatic small dural arteriovenous malformation was an incidental finding in 1 patient studied because of suspected cerebrovascular insufficiency. Roentgen Findings Plain roentgenograms of the skull showed evidence of increased vascular markings in 5 patients (Cases I, IV–VI, and IX) and localized bony thinning in one of these (Case IV). The angiographic features are summarized in Table II. In each patient we noted enlargement of one or more of the meningeal arteries that supplied the arteriovenous malformation. Enlarged tentorial branches of the internal carotid artery supplied a portion of the malformation in 11 patients (Figs. 1, A-C, 2, A, 3, A, and 4, A and B). The posterior branches of the middle meningeal artery were involved in 9 patients. In 2 of these, both the right and left middle meningeal arteries were enlarged (Figs. 1, D and E, and 2, B and D). Hypertrophy of the meningeal branches of the occipital artery was noted in 13 patients (Figs. 3, B, 5, A and C, and 6, A) and enlargement of the posterior meningeal branches of the vertebral artery in 5 (Fig. 1, F).