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December 1, 1996

Accumulation of hypointense lesions ("black holes") on T1 spin-echo MRI correlates with disease progression in multiple sclerosis

December 1996 issue
47 (6) 1469-1476

Abstract

MRI findings are increasingly used as outcome measures in therapeutic trials in MS.The discrepancy between the extent of the lesions on conventional T2 images and the clinical condition of the patient is one of the problems encountered in such studies. This clinical-radiological paradox prevents the use of MRI data as surrogate markers of disability in MS. A recent pilot study suggested a relationship between hypointense lesions on T1 MRI and disability. To assess in more detail the correlation of changes in hypointense lesion load on T1-weighted spin-echo MR images ("black holes") with changes in disability in MS, we studied 46 patients with clinically definite MS at baseline and after a median follow-up of 40 months. There was a significant correlation between baseline disability and hypointense lesion load (Spearman rank correlation coefficient [SRCC] = 0.46, p = 0.001). In secondary progressive patients, the rate of accumulation of these "black holes" was significantly related to progression rate (SRCC = 0.81, p < 0.0001). We speculate that the appearance of hypointense lesions is the MRI equivalent of a failure of remission. Overall, T1 lesion load measurements correlated better with clinical assessments than T2 lesion load measurements. Quantification of hypointense lesion load on T (1-weighted) spin-echo MRI helps to resolve the clinical-radiological paradox between disability and MRI and has the potential to be a surrogate marker of disability in MS.
NEUROLOGY 1996;47: 1469-1476

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Published In

Neurology®
Volume 47Number 6December 1996
Pages: 1469-1476
PubMed: 8960729

Publication History

Published online: December 1, 1996
Published in print: December 1996

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Authors

Affiliations & Disclosures

J. H.T.M. van Waesberghe, MD
M.A.A. van Walderveen, MD
From the Dutch MR Centre for MS Research (Drs. Truyen, van Waesberghe, Van Walderveen, Polman, and Barkhof) and Department of Neurology (Drs. Truyen, Van Oosten, and Polman), Free University Hospital, Amsterdam, The Netherlands; the Department of Neurology (Dr. Hommes), University Hospital St. Radboud, Nijmegen, The Netherlands; and the Department of Epidemiology and Biostatistics (Dr. Ader), Free University Amsterdam, The Netherlands.
Supported in part by a grant from the Dutch MS society ("Stichting Vrienden MS Research").
Received February 29, 1996. Accepted in final form April 11, 1996.
Address correspondence and reprint requests to Dr. F. Barkhof, Radiology Department, Free University Hospital Amsterdam, P.O. Box 7057, 1007 MB Amsterdam, The Netherlands.

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