Over the past decade, the use of MRI to study multiple sclerosis (MS) has lead to substantial advances in understanding the disease process. Disease activity as detected by new lesions on T2-weighted images or contrast-enhancing lesions on T1-weighted images have established that the level of activity seen on MRI is considerably greater than that seen clinically. Further, MRI has become an important and powerful tool for the assessment of the effect of new experimental therapies in MS. Recent work continues to focus on defining the natural history of the disease using MRI and in examining the effect of experimental treatments on disease activity as measured by MRI. Specifically, recent studies have focused on the following; 1. Defining the natural history of the MS lesion using both conventional imaging as well as advanced imaging techniques including magnetization transfer imaging, proton spectroscopy and measures of T1 hypointensities. 2. Defining the level of new disease activity seen in patients who are early in the relapsing remitting course of the disease? 3. Defining the long term effect of treatment with interferon beta 1b on disease activity as measured by MRI. 4. Examination of the effect of new therapies on disease activity in MS as measured by MRI. Serial studies of patients with early, relapsing-remitting MS using contrast enhanced MRI have shown that nearly two thirds of the patients have evidence of active new lesion formation. Recent studies in the NIB have examined the evolution of the MS lesion using imaging techniques that measure tissue destruction such as lesion load on T2-weighted images or T1 hypointensities, alterations in magnetization transfer ratios and alterations seen using proton spectroscopy. Findings have demonstrated that progression of disease as measured by overall burden of disease increases during the early phase of the disease. However, only a modest correlation can be found between the frequency of acute enhancing lesions and the level of accumulated disease burden suggesting that distinct mechanisms may contribute to lesion progression. In addition, some patients showing a marked reduction in new disease activity as measured by contrast enhancing lesions continue to have progression of disease as measured by T2 lesion load or T1 hypointensities. Recent results indicate that the extent of tissue damage varies in acute contrast enhancing lesions. Recent evidence has shown that the persistence of a lesion as a T1 hypointensities is related to the duration of contrast enhancement. Those lesions that enhance for longer than 2 months have a greater chance of developing into a persistent T1 hypointensity indicating tissue damage. This evidence indicates that qualitative differences exist in contrast enhancing lesions The results indicate that mechanisms of tissue destruction may be, in part distinguished from the events that initiate the lesion. Attention continues to focus on the value of MRI as a predictor of future clinical course and disability. A major effort has been made over the past year to reevaluate all patients seen by the NIB between 8 and 5 years previously. Results of these efforts indicate that the magnitude of disease as seen on MRI early in the disease course does have some ability to predict the level of clinical disease. Consistent with the studies of T1 hypointensities, the results of the follow-up study indicate that while contrast enhancing lesions are related to clinical disease early in the disease course, measures that reflect destruction such as T1 hypointensities correlate with clinical disability at follow-up. Findings derived from this retrospective evaluation should have substantial influence on our understanding of MRI as a possible surrogate for clinical disability.
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