‘Steal’ Is an Unestablished Mechanism for the Clinical Presentation of Cerebral Arteriovenous Malformations

Abstract

Background and Purpose Focal neurological deficits (FNDs) in patients with arteriovenous malformations (AVMs) have been widely attributed to the phenomenon of “cerebral steal.” The incidence of focal deficits was investigated in a large prospective sample. Methods Using data from patient history and examination, CT or MRI, and transcranial Doppler sonography, we studied 152 consecutive, prospective AVM patients for evidence of FNDs unrelated to a hemorrhagic event. Feeding mean arterial pressure was measured during superselective angiography. Results Two (1.3%) of 152 patients met the criteria for a progressive FND. Nonprogressive FNDs were seen in 11 (7.2%) patients (stable in 4.6%, reversible in 2.6%). The median observation time period was 17 months (range, 1 to 60 months). There were no differences in transcranial Doppler mean velocities in feeding arteries in FND versus non-FND groups (118±44 versus 112±37 cm/s, P >.05) or pulsatility indexes (0.53±0.20 versus 0.55±0.15, P >.05). Feeding artery pressure was similar in FND (n=10) and non-FND (n=96) groups (39±16 versus 39±16 mm Hg at a systemic pressure of 82±18 versus 75±14 mm Hg, NS). Conclusions Nonhemorrhagic focal neurological syndromes in AVM patients are infrequent. Progressive deficits are especially rare. There was no relation between feeding artery pressure or flow velocities and FND. There does not appear to be sufficient evidence to assign steal as an operative pathophysiological mechanism in the vast majority of AVM patients.