Abstract

odern treatment of cerebral arteriovenous malformations (AVMs) has evolved in the era of preoperative M embolization and radiosurgical treatment into a multidisciplinary, patient-specific approach that carefully balances the natural history of the disease with the inherent risks of surgical, endovascular, or radiosurgical treatments. Despite excellent results of AVM obliteration, the postoperative course of these patients can be complicated by hyperemic events, which can result in cerebral edema and intracerebral hemorrhages (3). Whether hyperemia occurs secondary to reperfusion of previously hypoperfused areas owing to poor arterial autoregulation (normal perfusion pressure breakthrough) or active hyperemia (2, 8) or secondary to occlusion of venous outflow (occlusive or passive hyperemia (1)), it has a significant impact on the morbidity and mortality of these patients. As previously shown by several studies, larger, more complex AVMs are associated with higher rates of hyperemic complications (7), but the pathophysiology of these events is unclear, and a predictive tool to identify patients with higher risks of hyperemic complications could modify postoperative care and improve patient outcomes.

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