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It is generally believed that most T2-weighted (T2) lesions in the central white matter of patients with multiple sclerosis begin with a variable period of T1-weighted (T1) gadolinium (Gd) enhancement and that T1Gd-enhancing and T2lesions 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 T1Gd-enhancing and T2lesions are identical. We generated T1Gd-enhancing and T2lesion probability maps from 19 patients with relapsing-remitting multiple sclerosis. There was a significantly higher probability (P = 0.001) for T2lesions to be found in the central relative to the peripheral white matter (risk ratio 4.5), although the relative distribution of T1Gd-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 T1Gd-enhancing and new T2lesions 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 T2lesions following T1Gd enhancement. The relative distribution of T1Gd-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 T2lesion volume may arise from mechanisms other than those associated with early breakdown of the blood-brain barrier leading to T1Gd enhancement.

Original publication




Journal article



Publication Date





1261 - 1270