Spatial mapping of T<inf>2</inf>and gadolinium-enhancing T<inf>1</inf>lesion volumes in multiple sclerosis: Evidence for distinct mechanisms of lesion genesis?
Lee MA., Smith S., Palace J., Narayanan S., Silver N., Minicucci L., Filippi M., Miller DH., Arnold DL., Matthews PM.
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 of 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.