Significance of 'Arterial Enhancement' in Acute Ischemic Stroke: Evaluation with Gadolinium-enhanced MR imaging and Angiography.
- Author:
Byung Chul LEE
1
;
Kyung Ho YU
;
Ki Hal KWON
;
Sung Min KIM
;
Sang Yoon KIM
;
Ik Won KANG
Author Information
1. Department of Neurology, Hallym University College of Medicine, Korea.
- Publication Type:Original Article
- MeSH:
Angiography*;
Angiography, Digital Subtraction;
Arteries;
Brain Ischemia;
Collateral Circulation;
Constriction, Pathologic;
Contrast Media;
Gadolinium;
Hemodynamics;
Humans;
Magnetic Resonance Imaging*;
Research Personnel;
Stroke*
- From:Journal of the Korean Neurological Association
1995;13(4):795-805
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Although the patterns of arterial enhancement (AE) in gadolinium (Gd) enhanced MR imaging have been reported in patients with cerebral ischemia, the significance of AE has not been well established. The purpose of the study was to investigate the mechanisms and significance of AE in Gd-enhanced MR imaging. In particular, we tried to relate MR findings of AE to the hemodynamic alterations after acute cerebral ischemia. Twelve patients with acute ischemic stroke limited to the supratentorial region were subjected to this study. In all patients, MR imaging and Gd enhancement were performed using the 1. 0 T superconductive MR scanner by spin-echo sequence. Digital subtraction angiography was followed within 24hr of MR examination. MR images and angiograms were reviewed separately by two blinded investigators, giving special attention to the presence of AE, vascular abnormalities and degree of collateral circulation. The AE on Gd-enhanced MR imaging was noted in 7 of 12 patients with acute ischemic stroke(4, cortical; 2, striatocapsular; 1, lacunar). All these 7 patients had angiographic findings of stenosis or complete occlusion on the proximal portions of major intracranial arteries with prompt collateral circulations. Other five patients not showing (2, cortical; 3, lacunar) had complete occlusion of major arteries with poor collateral or normal angiographic findings. The AE is caused by slower arterial flow, which can be identified in cerebral angiograms demonstrating delayed opacification of contrast agents. The findings of AE may be regarded as equivalent to an angiographic findings of stenosis of the proximal artery or complete occlusion with excellent collateral circulation. Therefore, we conclude that the AE might reflect the underlying vascular abnormalities and may help to estimate, the hemodynamic alterations in patients with acute ischemic stroke.
