PURPOSE: To investigate the cause and clinical significance of arterial enhancement (AE) in contrast-enhanced T1-weighted MR examinations after acute cerebral ischemia. METHODS: Contrast MR examinations and conventional angiograms of 17 patients studied following an acute ischemic event or an internal carotid occlusion were retrospectively reviewed. MR and angiographic studies were performed within 1 day of each other. The presence of AE was correlated with both angiographic findings and patient clinical status. RESULTS: AE was not confined to patients with angiographic evidence of complete arterial occlusion. Only 64% of patients demonstrating AE had complete occlusion angiographically. Complete arterial occlusion did not always correlate with AE. In two of nine patients with complete occlusion, no AE was identified. In five of 10 patients with AE, angiographic slow flow was identified. In patients without AE, no angiographic slow flow was identified. In the 64% of patients with AE, significant symptoms were identified. Patients without AE were either asymptomatic or had mild symptoms at the time of the MR study. CONCLUSIONS: Our data support the hypothesis that arterial slowing is the cause of AE, which appears to be an indicator of decreased brain perfusion. Such MR findings may add important supplemental information to those provided by conventional angiography.
PURPOSE: To investigate the cause and clinical significance of arterial enhancement (AE) in contrast-enhanced T1-weighted MR examinations after acute cerebral ischemia. METHODS: Contrast MR examinations and conventional angiograms of 17 patients studied following an acute ischemic event or an internal carotid occlusion were retrospectively reviewed. MR and angiographic studies were performed within 1 day of each other. The presence of AE was correlated with both angiographic findings and patient clinical status. RESULTS:AE was not confined to patients with angiographic evidence of complete arterial occlusion. Only 64% of patients demonstrating AE had complete occlusion angiographically. Complete arterial occlusion did not always correlate with AE. In two of nine patients with complete occlusion, no AE was identified. In five of 10 patients with AE, angiographic slow flow was identified. In patients without AE, no angiographic slow flow was identified. In the 64% of patients with AE, significant symptoms were identified. Patients without AE were either asymptomatic or had mild symptoms at the time of the MR study. CONCLUSIONS: Our data support the hypothesis that arterial slowing is the cause of AE, which appears to be an indicator of decreased brain perfusion. Such MR findings may add important supplemental information to those provided by conventional angiography.
Authors: P Pantano; D Toni; F Caramia; A Falcou; M Fiorelli; C Argentino; L M Fantozzi; L Bozzao Journal: AJNR Am J Neuroradiol Date: 2001-02 Impact factor: 3.825
Authors: H Ishimaru; M Ochi; M Morikawa; H Takahata; Y Matsuoka; T Koshiishi; T Fujimoto; A Egawa; K Mitarai; T Murakami; M Uetani Journal: AJNR Am J Neuroradiol Date: 2007-05 Impact factor: 3.825