INTRODUCTION: We retrospectively evaluated computed tomography angiography (CTA) and perfusion imaging (CTP) of patients with aneurysmal subarachnoid hemorrhage (SAH) for any correlation between degree of vasospasm and perfusion deficit. MATERIALS AND METHODS: Sequentially performed CTP and CTA of 41 patients at least at the third day of postbleeding were reviewed for vasospasm and perfusion deficit throughout the anterior and middle cerebral arteries and corresponding territories. Vasospasm was noted comparing the contralateral normal ones or extradural components of the vessel itself and graded to negative, mild, moderate, and severe as luminal narrowing none, <25%, between 25% and 50%, and >or=50%, respectively. CTP abnormality was noted using cerebral blood flow and volume and mean transit time maps. RESULTS: Of 41 patients, 20 had no vasospasm; 15 had mild to moderate and six had severe vasospasm. Three of 20 patients with no vasospasm (15%), four of 15 patients with mild to moderate vasospasm (26%), and five of six patients with severe vasospasm (83%) had perfusion abnormality. Perfusion abnormalities noted were ischemia, infarction, and hyperperfusion. Perfusion abnormality without vasospasm was observed in the watershed areas and adjacent to sulcal clots. CONCLUSION: In SAH patients, if there is a macrovascular vasospasm with luminal narrowing >or=50%, there is a high likelihood (83%) of perfusion abnormality in the territory of the vasospastic vessel. There may also be perfusion abnormality without macrovascular vasospasm in the watershed areas or in the vicinity of sulcal clots.
INTRODUCTION: We retrospectively evaluated computed tomography angiography (CTA) and perfusion imaging (CTP) of patients with aneurysmal subarachnoid hemorrhage (SAH) for any correlation between degree of vasospasm and perfusion deficit. MATERIALS AND METHODS: Sequentially performed CTP and CTA of 41 patients at least at the third day of postbleeding were reviewed for vasospasm and perfusion deficit throughout the anterior and middle cerebral arteries and corresponding territories. Vasospasm was noted comparing the contralateral normal ones or extradural components of the vessel itself and graded to negative, mild, moderate, and severe as luminal narrowing none, <25%, between 25% and 50%, and >or=50%, respectively. CTP abnormality was noted using cerebral blood flow and volume and mean transit time maps. RESULTS: Of 41 patients, 20 had no vasospasm; 15 had mild to moderate and six had severe vasospasm. Three of 20 patients with no vasospasm (15%), four of 15 patients with mild to moderate vasospasm (26%), and five of six patients with severe vasospasm (83%) had perfusion abnormality. Perfusion abnormalities noted were ischemia, infarction, and hyperperfusion. Perfusion abnormality without vasospasm was observed in the watershed areas and adjacent to sulcal clots. CONCLUSION: In SAHpatients, if there is a macrovascular vasospasm with luminal narrowing >or=50%, there is a high likelihood (83%) of perfusion abnormality in the territory of the vasospastic vessel. There may also be perfusion abnormality without macrovascular vasospasm in the watershed areas or in the vicinity of sulcal clots.
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