V Shahi1, J E Fugate2, D F Kallmes3, A A Rabinstein4. 1. From the Mayo Medical School (V.S.). 2. Departments of Neurology (J.E.F., A.A.R.) fugate.jennifer@mayo.edu. 3. Radiology (D.F.K.), Mayo Clinic, Rochester, Minnesota. 4. Departments of Neurology (J.E.F., A.A.R.).
Abstract
BACKGROUND AND PURPOSE: CT perfusion scans are often used in acute stroke evaluations. We aimed to assess the outcome of areas of basal ganglia hyperperfusion on CTP in patients with acute ischemic stroke. MATERIALS AND METHODS: We retrospectively reviewed the medical records and brain imaging of 139 patients presenting with acute stroke who underwent CTP for consideration of endovascular recanalization. Hyperperfusion was assessed qualitatively and defined as a matched region of increased cerebral blood flow and cerebral blood volume. CTA was used to locate arterial occlusion. Follow-up imaging was used to determine whether regions of hyperperfusion at baseline became infarcted or developed hemorrhage. Angiographic imaging was assessed to determine the presence or absence of early venous opacification. RESULTS: Six patients (4.3%) demonstrated hyperperfusion in the basal ganglia of the affected side (4 in the lenticular nucleus and 2 in the caudate). In all cases, the area of hyperperfusion ultimately proved to be infarcted. All patients had received intravenous thrombolysis before the CTP. CTA at the time of CTP showed middle or distal M1 occlusion but patency of the proximal M1 and A1 segments. Intracranial hemorrhage was noted in 2 of these 6 patients at follow-up. CONCLUSIONS: Acute basal ganglia hyperperfusion in patients with stroke may indicate nonviable parenchyma and risk of hemorrhagic conversion.
BACKGROUND AND PURPOSE: CT perfusion scans are often used in acute stroke evaluations. We aimed to assess the outcome of areas of basal ganglia hyperperfusion on CTP in patients with acute ischemic stroke. MATERIALS AND METHODS: We retrospectively reviewed the medical records and brain imaging of 139 patients presenting with acute stroke who underwent CTP for consideration of endovascular recanalization. Hyperperfusion was assessed qualitatively and defined as a matched region of increased cerebral blood flow and cerebral blood volume. CTA was used to locate arterial occlusion. Follow-up imaging was used to determine whether regions of hyperperfusion at baseline became infarcted or developed hemorrhage. Angiographic imaging was assessed to determine the presence or absence of early venous opacification. RESULTS: Six patients (4.3%) demonstrated hyperperfusion in the basal ganglia of the affected side (4 in the lenticular nucleus and 2 in the caudate). In all cases, the area of hyperperfusion ultimately proved to be infarcted. All patients had received intravenous thrombolysis before the CTP. CTA at the time of CTP showed middle or distal M1 occlusion but patency of the proximal M1 and A1 segments. Intracranial hemorrhage was noted in 2 of these 6 patients at follow-up. CONCLUSIONS: Acute basal ganglia hyperperfusion in patients with stroke may indicate nonviable parenchyma and risk of hemorrhagic conversion.
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