Catastrophic hyperemic states are known complications after the treatment of certain types of intracranial arteriovenous malformations (AVMs). A case is presented in which a large AVM was preoperatively embolized and later resected. There was clear intra- and postoperative evidence of edema and hemorrhage, which resulted in a fatal outcome. Regional cerebral blood flow (rCBF) data from this patient obtained with single photon emission computed tomography (SPECT) both before and after embolization were compared with data from four patients with similar size supratentorial AVMs treated and studied in a similar protocol who did not develop perfusion breakthrough. Pretreatment hemispheric rCBF was significantly reduced in this patient's ipsilateral hemisphere (50 ml/100 g/min) compared to the control group mean (83 +/- 9.5 ml/100 g/min). A similar relative depression was found in the contralateral hemisphere. After therapeutic embolization, the ipsilateral rCBF increased by 33 ml/100 g/min and the contralateral hemispheric rCBF increased by 30 ml/100 g/min; this embolization-induced increase in rCBF was significantly higher than in the control group. Acetazolamide, known to increase rCBF in normal tissue by 35 +/- 3%, resulted in a 56% augmentation of ipsilateral hemispheric flow before embolization in the reported patient vs. a 22 +/- 10% increase for the control group. Postembolization, this hyperresponsiveness to acetazolamide remained unchanged. It is possible that these hemodynamic derangements may indicate a dissociation between the vasoconstrictive and vasodilatory reactivity in chronically hypoperfused territories adjacent to AVMs such that pharmacological or metabolic stimuli may induce further vasodilation, but sudden redistribution of large volumes of flow will not promote protective vasoconstriction.