Incidence and risk factors for symptomatic cerebral hyperperfusion after superficial temporal artery-middle cerebral artery anastomosis in patients with moyamoya disease

Background: Superficial temporal artery-middle cerebral artery anastomosis for moyamoya disease prevents cerebral ischemic attack by improving CBE, whereas recent evidence suggests that the temporary neurologic deterioration because of postoperative cerebral hyperfusion could occur despite its low-flow revascularization. The present study investigates the incidence and the risk factors for symptomatic hyperfusion after STA-MCA anastomosis in patients with moyamoya disease. Methods: We prospectively performed N-isopropyl-p-(sic) iodoamphetamine single-photon emission computed tomography 1 and 7 days after STA-MCA anastomosis on 80 hemispheres of 58 consecutive patients with moyamoya disease (approximately 2-62 years old, 34.4 years old in average). Mean follow-up period was 22.7 months. Symptomatic cerebral hyperperfusion was defined as the presence of the significant increase in CBF at the site of the anastomosis that is responsible for the apparent neurologic sign. Results: Twenty-one patients (22 sides, 27.5%) temporarily had symptomatic cerebral hyperfusion, who were subjected of intensive blood pressure control. Postoperative magnetic resonance imaging/angiography showed the thiek high signal of bypass without ischemic changes in all 21 patients. Adult-onset (P = .013) or hemorrhagic-onset patients (P = .027) had significantly higher risk for symptomatic hyperfusion. There was no difference in intraoperative temporary occlusion time between each group. No patients had permanent neurologic deficit because of hyperperfusion. Conclusion: The STA-MCA anastomosis is a safe and effective treatment of moyamoya disease, although adult-onset and/or hemorrhagic-onset patients had higher risk for symptomatic hyperperfusion. We recommend routine CBF measurement especially for these patients because the management of hyperperfusion is contradictory to that of ischemia. (c) 2009 Elsevier Inc. All rights reserved.