The authors tested the hypothesis that cerebral blood flow (CBF) would increase after acute and relatively brief internal carotid artery (ICA) test occlusion, and examined the relationship of the postdeflation CBF to the development of neurologic symptoms. In 16 patients undergoing ICA test occlusion with deliberate hypotension, the authors measured intracarotid 133Xe CBF at baseline, occlusion, and deflation. Four patients developed neurologic symptoms during occlusion. As positive controls, 11 other patients received intracarotid verapamil or papaverine before deflation as part of another protocol. Balloon occlusion was 23.1 ± 10.5 minutes (mean ± standard deviation) in duration. At 1.3 ± 1.6 minutes after balloon deflation, there was a trend (12 ± 31%) for CBF to increase (48 ± 9 mL/100 g/min versus 53 ± 17 mL/100 g/min, P = .15), and a 16 ± 27% decrease in cerebrovascular resistance (CVR; 2.1 ± 0.6 mm Hg/100 g/min/mL versus 1.7 ± 0.6 mm Hg/100 g/min/mL, P = .03) compared with baseline values. By comparison, patients who received a intracarotid dilator demonstrated a 53 ± 55% increase in CBF (48 ± 10 mL/100/min versus 70 ± 23 mL/100 g/min, P = .007) and a 33 ± 31% decrease in CVR (2.2 ± 0.6 mm Hg/100 g/min/mL versus 1.4 ± 0.6 mm Hg/100 g/min/mL, P = .0007) compared with baseline. Analysis of variance and regression analysis showed no other relationships between postocclusion CBF and balloon occlusion duration, distal internal carotid occlusion ("stump") pressure, or the development of neurologic symptoms. Acute, temporary interruption of ICA blood flow resulted in minimal postocclusive changes in cerebrovascular hemodynamics, even in those patients who developed neurologic symptoms during the period of test occlusion.