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Multiple Sclerosis
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Contrast-enhanced MRI lesions during treatment with interferonß-1b predict increase in T1 black hole volume in patients with relapsing-remitting multiple sclerosis

K Morgen

National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA, Department of Neurology, Justus-Liebig-Universität, and Bender Institute of Neuroimaging, Giessen, Germany, Katrin.Morgen{at}neuro.med.uni-giessen.de

A LT Crawford

National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Division of Hematologic Malignancies, Baltimore, MD, USA

R D Stone

National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA

R Martin

National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA

N D Richert

National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA

J A Frank

Experimental Neuroimaging Section, Laboratory of Diagnostic Radiology Research, National Institutes of Health, Bethesda, MD, USA

H F McFarland

National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA

T1 black holes (BH) have been found to represent focal areas of substantial central nervous system tissue damage in multiple sclerosis (MS) patients. We examined the development of T1 BH over a three-year period of treatment with interferon (IFN)ß-1b in a group of 20 patients with relapsing-remitting MS. The number of contrast-enhancing lesions (CEL) after one year of treatment predicted a change in the T1 BH volume in the following two years. In patients without CEL, the T1 BH volume remained stable, whereas it increased in patients with CEL. The occurrence of CEL in patients treated with IFNß may indicate a heightened risk of accumulating T1 BH.

Key Words: black holes • contrast-enhancing lesions • IFNß-1b • relapsing-remitting MS

Multiple Sclerosis, Vol. 11, No. 2, 146-148 (2005)
DOI: 10.1191/1352458505ms1147oa


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