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It is generally believed that most T 2 -weighted (T 2 ) lesions in the central white matter of patients with multiple sclerosis begin with a variable period of T 1 -weighted (T 1 ) gadolinium (Gd) enhancement and that T 1 Gd-enhancing and T 2 lesions represent stages of a single pathological process. Lesion probability maps can be used to test this hypothesis by providing a quantitative description of the spatial distribution of these two types of lesions across a patient population. The simplest prediction of this hypothesis mould be that the spatial distributions of T 1 Gd-enhancing and T 2 lesions are identical. We generated T 1 Gd-enhancing and T 2 lesion probability maps from 19 patients with relapsing-remitting multiple sclerosis. There was a significantly higher probability (P = 0.001) for T 2 lesions to be found in the central relative to the peripheral white matter (risk ratio 4.5), although the relative distribution o f T 1 Gd-enhancing lesions was not significantly different (P = 0.7) between central and peripheral white matter regions (risk ratio 0.6). Longitudinal data on the same population were used to demonstrate a similar distribution asymmetry between new T 1 Gd-enhancing and new T 2 lesions that developed over the course of 1 year. Alternative hypotheses to explain this observation were tested. We found no spatial difference in the likelihood of development of persistent T 2 lesions following T 1 Gd enhancement. The relative distribution of T 1 Gd-enhancing lesions was shown to be independent of the dose of Gd contrast agent and the frequency of scanning. Our findings suggest that a proportion of the periventricular T 2 lesion volume may arise from mechanisms other than those associated with early breakdown of the blood-brain barrier leading to T 1 Gd enhancement.

Original publication

DOI

10.1093/brain/122.7.1261

Type

Journal article

Journal

Brain

Publication Date

01/07/1999

Volume

122

Pages

1261 - 1270