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Multiple Sclerosis: Hyperintense Lesions in the Brain on Nonenhanced T1-weighted MR Images Evidenced as Areas of T1 Shortening¹

¹ From the Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, Mass (V.J.); Department of Radiology, University at Buffalo, State University of New York, Buffalo, NY (S.S.); and Departments of Neurology and Radiology, Center for Neurological Imaging, Partners Multiple Sclerosis Center, Brigham and Women's Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, HIM 730, Boston, MA 02115 (R.B.). Received July 14, 2005; revision requested September 21; revision received August 31, 2006; accepted October 5; final version accepted February 7, 2007. R.B. supported in part by research grants from the National Institutes of Health–National Institute of Neurological Disorders and Stroke (1 K23 NS42379-01), National Multiple Sclerosis Society (RG 3258A2/1, RG 3574A1), and National Science Foundation (DBI-0234895). Address correspondence to R.B. (e-mail: rbakshi{at}bwh.harvard.edu).

Purpose: To retrospectively document hyperintense lesions on nonenhanced T1-weighted magnetic resonance (MR) images in patients with multiple sclerosis (MS) and study their relationship to physical disability, disease course, and other MR markers of tissue damage (brain atrophy).

Materials and Methods: Institutional review board approval was obtained; informed consent was waived for this HIPAA-compliant study, with 145 patients with MS (mean age, 43 years). Patients had relapsing-remitting (RR) (n = 92) or secondary-progressive (SP) (n = 49) MS; clinical course was unknown in four. Mean Expanded Disability Status Scale (EDSS) score was 3.5. T1 lesions were compared with normal white matter on nonenhanced images and judged hyperintense. Spearman rank correlation, Wilcoxon rank sum, and Fisher exact probability tests and analysis of variance and analysis of covariance (ANCOVA) were employed.

Results: At least one T1 hyperintense lesion was found in 113 patients (total, 340 lesions). Two-thirds of lesions had hyperintense rim; others were uniformly hyperintense. Lesions were more common in patients with SP MS (P = .003, Wilcoxon test) and correlated with EDSS score (Spearman = 0.19, P = .04) and brain atrophy measures (total cortical atrophy, Spearman = 0.42, P < .001; third ventricular width, Spearman = 0.40, P < .001) but not disease duration (Spearman = 0.038, P = .69). Lesions were more likely multiple in the SP versus RR group (P < .001, Fisher test). After adjustment for disease course, T1 hyperintense lesions remained associated with brain atrophy (P .001, ANCOVA). No independent effect of imager type (ANCOVA F value = 1.4, P = .24) or spin-echo method (P = .67, Wilcoxon test) on number of lesions was detected. An effect of other MR protocol adjustments (analysis of variance F value = 5.6, P = .001) was unconfirmed after clinical characteristic adjustment (ANCOVA F value = 1.1, P = .35).

Conclusion: Hyperintense MS plaques on T1-weighted MR images are common and associated with brain atrophy, disability, and advancing disease; a hyperintense lesion may be a clinically relevant biomarker.

© RSNA, 2007