Abstract
Since 1981, when multiple sclerosis (MS) lesions were first visualized in vivo using MRI, understanding of MS disease processes has expanded dramatically. Serial postcontrast imaging shows that MS inflammatory activity is much more frequent than clinical relapses1 and that lesion evolution can take different paths.2 In clinical trials, reduction of new lesion formation predicts clinical efficacy of disease-modifying drugs.3 Despite these advances, key questions remain unanswered: What initiates development of an MS lesion? Which lesions represent severe irreversible tissue damage, and which are likely to remyelinate? What is the most sensitive way to detect new lesions?
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