TIME-COURSE OF LESION DEVELOPMENT IN PATIENTS WITH ACUTE STROKE - SERIAL DIFFUSION-WEIGHTED AND HEMODYNAMIC-WEIGHTED MAGNETIC-RESONANCE-IMAGING

Citation
Lh. Schwamm et al., TIME-COURSE OF LESION DEVELOPMENT IN PATIENTS WITH ACUTE STROKE - SERIAL DIFFUSION-WEIGHTED AND HEMODYNAMIC-WEIGHTED MAGNETIC-RESONANCE-IMAGING, Stroke, 29(11), 1998, pp. 2268-2276
Citations number
27
Categorie Soggetti
Peripheal Vascular Diseas","Clinical Neurology
Journal title
StrokeACNP
ISSN journal
00392499
Volume
29
Issue
11
Year of publication
1998
Pages
2268 - 2276
Database
ISI
SICI code
0039-2499(1998)29:11<2268:TOLDIP>2.0.ZU;2-Q
Abstract
Background and Purpose-We sought to characterize the evolution of acut e ischemic stroke by MRI and its relationship to patients' neurologica l outcome. Methods-Fourteen patients with acute ischemic stroke underw ent MRI within 13 hours of symptom onset (mean, 7.4+/-3 hours) and und erwent repeated imaging and concurrent neurological examination at 8, 24, 36, and 48 hours and 7 days and >42 days after first imaging. Resu lts-Diffusion-weighted imaging (DWI) lesion volumes increased between the first and second scans in 10 of 14 patients; scans with maximum DW I lesion volume occurred at a mean of 70.4 hours. Initial DWI lesion v olume correlated with the largest T2 lesion volume (r=0.97; P<0.001). Final lesion volume was smaller than maximum lesion volume in 12 of 14 patients. There was positive correlation between the follow-up Nation al Institutes of Health Stroke Scale score and the initial DWI lesion volume (r=0.67; P=0.01) and maximum T2 lesion volume (r=0.77; P<0.01) and negative correlation with initial mean apparent diffusion coeffici ent ratio (ADCr) (r=-0.64; P<0.05). The ADCr was 0.73 at initial imagi ng and fell between the initial and second scans in 10 of 14 patients. Mean ADCr did not rise above normal until 42 days after stroke onset (P<0.001). Conclusions-Serial MRT demonstrates the dynamic nature of p rogressive ischemic injury in acute stroke patients developing over ho urs to days, and it suggests that both primary and secondary pathophys iological precesses can be valuable targets for neuroprotective interv entions.