Influence of 3 Stigmas of Small Vessel Disease on FLAIR Change in Acute Ischemic Stroke: Case-Control Study.
- Author:
Dohoung KIM
1
;
Jihoon KANG
;
Nayoung KIM
;
Won Young NOH
;
Min Uk JANG
;
Beom Joon KIM
;
Moon Ku HAN
;
Cheolkyu JUNG
;
Byung Se CHOI
;
Jae Hyoung KIM
;
Hee Joon BAE
Author Information
1. Department of Neurology, Seoul National University Bundang Hospital Stroke Center, Seoul National University College of Medicine, Seongnam, Korea. braindoc@snu.ac.kr
- Publication Type:Original Article
- Keywords:
Acute stroke;
Fluid attenuated inversion recovery;
Small-vessel disease
- MeSH:
Angiography;
Biomarkers;
Case-Control Studies;
Cerebral Arteries;
Glycosaminoglycans;
Humans;
Male;
Prospective Studies;
Stroke
- From:Journal of the Korean Neurological Association
2013;31(3):165-172
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Attempts have been made to use the signal changes of fluid-attenuated inversion recovery (FLAIR) MRI as "a tissue clock," defined as a surrogate marker of the tissue damage resulting from acute ischemic stroke. The evolution of FLAIR signals after stroke onset has never been fully explained solely by time. The aim of this study was to determine whether cerebral small-vessel disease (SVD) affects FLAIR changes following acute ischemic stroke. METHODS: Based on data from a prospective stroke registry, consecutive patients who were hospitalized to the stroke center within 12 hours of stroke onset between January 2004 and May 2011 and had occlusion of the major cerebral arteries in the anterior circulation, as evidenced by MR angiography, were enrolled. Cases with FLAIR changes and controls without FLAIR changes were matched according to the time elapsed from stroke onset to MR study. RESULTS: Among the 130 patients who met the eligibility criteria, 62 (47.7%) had FLAIR changes. The time interval between stroke onset and MR study differed significantly between those with and without FLAIR changes (5.2 hours vs. 3.0 hours). FLAIR changes were more common among males and smokers. Comparisons between cases and controls matched on a one-to-one basis did not reveal any difference in the three signs of cerebral SVD: white-matter hyperintensities, lacunae, and cerebral microbleeds. CONCLUSIONS: This study failed to find any data supporting the hypothesis that cerebral SVD affects FLAIR changes after acute ischemic stroke.
