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Multiple sclerosis (MS) is a chronic disease of the CNS and was described as early as the fourteenth century. Early attempts at treatment included primarily symptomatic therapies, but in the 1960s and 1970s the focus of research shifted to disease-modifying therapy (DMT). The first of these therapies to be approved by the FDA was interferon-beta1b (IFN-β1b) in 1993. Since that time there has been a significant expansion of research aimed at modifying the MS disease process.
The present-day management of MS patients requires an understanding of an evolving therapeutic paradigm. In this paradigm, the efficacy, mechanisms of action, and effects of the available therapies intersect and are relevant to clinical practice. The efficacy of four of the DMTs—IFN-β1b SC, IFN-β1a SC and IM formulations, and glatiramer acetate SC—is well established, with some studies having over a decade of follow-up data.1–3 The practicing clinician should understand the differences in the administration and mechanisms of action of the DMTs and how these differences impact the clinical effects.4–6 The clinical effect of neutralizing antibodies (NAbs) and the risk for serious adverse effects of some DMTs (e.g., progressive multifocal leukoencephalopathy with natalizumab) are also factors that must be considered in …
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