Is stagnating flow in former feeding arteries an indication of cerebral hypoperfusion after resection of arteriovenous malformations?

Object. The authors' goal in this study was to challenge the proposed mecha nism of the occlusive hyperemia theory, in which it is asserted that stagna ting flow in the former feeding arteries of cerebral arteriovenous malforma tions (AVMs) leads to parenchymal hypoperfusion or ischemia, from which pos toperative edema and hemorrhage originate. Methods. Cortical oxygen saturation (SaO(2)) was measured in 52 patients by using microspectrophotometry in areas adjacent to AVMs before and after re section. The appearance of the former feeding arteries was categorized as n ormal (Group A); moderately stagnating (Group B); and excessively stagnatin g (Group C) on postoperative angiographic fast-film series. Patients and Sa O(2) values were pooled accordingly and compared using analysis of variance and Duncan tests (p < 0.05). Angiographic stagnation times in former feedi ng arteries were correlated in a linear regression/correlation analysis wit h SaO(2) data (p < 0.05). All values are given as the mean +/- standard dev iation. The average median postoperative SaO(2) in Group C (15 patients) was signif icantly higher than in Groups B (17 patients) and A (20 patients) (Group C, 75.2 +/- 8.5; Group B, 67.5 +/- 10.8; Group A, 67.1 +/- 12 %SaO(2)), as wa s the average postoperative increase in SaO(2) (Group C, 25.9 +/- 14.9; Gro up B, 14.6 +/- 14; Group A, 11.1 +/- 14 %SaO(2)). Angiographically confirme d stagnation times were also significantly longer in Group C than in Group B (Group C, 5.6 +/- 2.5; Group B, 1.3 +/- 0.6 seconds). A significant corre lation/regression analysis showed a clear trend toward higher postoperative SaO(2) levels with increasing stagnation time. Conclusions. Stagnating flow in former feeding arteries does not cause cort ical ischemia, but its presence on angiographic studies is usually indicati ve of hyperperfusion in the surrounding brain tissue after AVM resection. I n the context of the pathophysiology of AVMs extrapolations made from angio graphically visible shunt flow to blood flow in the surrounding brain tissu e must be regarded with caution.