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Neurology 2000;55:185-192
© 2000 American Academy of Neurology


Articles

A longitudinal study of T1 hypointense lesions in relapsing MS

MSCRG trial of interferon ß-1a

J. H. Simon, MD, PhD, J. Lull, L. D. Jacobs, MD, R. A. Rudick, MD, D. L. Cookfair, PhD, R. M. Herndon, MD, J. R. Richert, MD, A. M. Salazar, MD, J. Sheeder, BA, D. Miller, PhD, K. McCabe, MD, A. Serra, MD, M. K. Campion, MS, J. S. Fischer, PhD, D. E. Goodkin, MD, N. Simonian, MD, M. Lajaunie, MD, K. Wende, PhD, A. Martens-Davidson, MS, R. P. Kinkel, MD, F. E. Munschauer, III, MD and the Multiple Sclerosis Collaborative Research Group (MSCRG)*

From the Department of Radiology–MRI (Drs. Simon, Miller, McCabe, Serra, and Lajaunie, and J. Sheeder), University of Colorado Health Sciences Center, Denver; Biogen, Inc. (J. Lull, M.K. Campion, and Dr. Simonian), Cambridge, MA; William C. Baird Multiple Sclerosis Research Center (Drs. Jacobs and Munschauer), Millard Fillmore Health System, and the MSCRG Data Management and Statistical Center (Drs. Cookfair and Wende, and A. Martens-Davidson), Department of Neurology (Drs. Jacobs and Munschauer), The Buffalo General Hospital, Buffalo, NY; the Mellen Center for Multiple Sclerosis Treatment and Research (Drs. Rudick, Fischer, and Kinkel), Cleveland Clinic Foundation, OH; the Department of Neurology (Dr. Herndon), Good Samaritan Hospital and Medical Center, Portland, OR; the Department of Neurology (Dr. Richert), Georgetown University Medical Center, Washington, DC; the Department of Neurology (Dr. Salazar), Walter Reed Army Medical Center, Washington, DC; and the UCSF/Mount Zion Multiple Sclerosis Center (Dr. Goodkin), San Francisco, CA.

Address correspondence and reprint requests to Dr. Jack H. Simon, University of Colorado Health Sciences Center, 4200 East Ninth Avenue, Campus Box A034, Denver, CO 80262; e-mail: Jack.Simon{at}uchsc.edu

BACKGROUND: T1 hypointense lesions (T1 black holes) are focal areas of relatively severe CNS tissue damage detected by MRI in patients with MS.

OBJECTIVE: To determine the natural history of T1 hypointense lesions in relapsing MS and the utility of T1 hypointense lesions as outcome measures in MS clinical trials.

METHODS: MR studies were from the Multiple Sclerosis Collaborative Research Group trial. Longitudinal results are reported in 80 placebo- and 80 interferon ß-1a (IFNß-1a)–treated patients with mild to moderate disability relapsing-remitting MS.

RESULTS: There was a small but significant correlation between T1 hypointense lesion volume and disability at baseline and on trial (r = 0.22, r = 0.28). In placebo patients there was a 29.2% increase in the mean volume of T1 hypointense lesions (median 124.5 mm3) over 2 years (p < 0.001 for change from baseline), as compared to an 11.8% increase (median 40 mm3) in the IFNß-1a–treated patients (change from baseline not significant). These treatment group comparisons did not quite reach significance. The most significant contributor to change in T1 hypointense lesions was the baseline number of enhancing lesions (model r2 = 0.554). Placebo patients with more active disease, defined by enhancing lesions at baseline, were the only group to show a significant increase in T1 hypointense lesion volume from baseline.

CONCLUSION: The development of T1 hypointense lesions is strongly influenced by prior inflammatory disease activity, as indicated by enhancing lesions. These results suggest that treatment with once weekly IM IFNß-1a (30 mcg) slows the 2-year accumulation of these lesions in the brain.




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