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Standardized descriptions published in 1996 based on a survey of international MS experts provided purely clinical phenotypes based on data and consensus at that time, but imaging and biological correlates were lacking. Increased understanding of MS and its pathology, coupled with general concern that the original descriptors may not adequately reflect more recently identified clinical aspects of the disease, prompted a re-examination of MS disease phenotypes by the International Advisory Committee on Clinical Trials of MS. [...] In 2011, the Committee (now jointly sponsored by NMSS and The European Committee for Treatment and Research in MS) and other experts (The MS Phenotype Group) re-examined MS phenotypes, exploring clinical, imaging, and biomarker advances through working groups and literature searches. In October 2012, we convened to review the 1996 clinical course descriptions and determine if sufficient progress and new insights were available to recommend changes. ...
The MS Phenotype Group has reconsidered prior MS disease course descriptors, some 16 years after their original publication. We recommend the following: ...
As of October 2017, the US Food and Drug Administration has approved 15 medications for modifying the course of MS: 5 preparations of interferon [!] beta; 2 preparations of glatiramer acetate; the monoclonal antibodies [!] natalizumab, alemtuzumab, daclizumab, and ocrelizumab (the first B-cell targeted therapy); the chemotherapy [!] mitoxantrone; and the small-molecule [mRNA!] oral agents fingolimod, dimethyl fumarate*, and teriflunomide. Dalfampridine* has been approved as a symptomatic therapy to improve walking speed. [start]It is beyond the scope of this article to discuss the relative benefits, risks, modes of action, and routes of administration of these various medications (though some targets are depicted in Figure 4), except to say that all are approved for relapsing-remitting MS and reduce, to various extents, the likelihood of developing new white matter lesions, clinical relapses, and stepwise accumulation of disability.[end]
At the same time, a renewed focus on lesion development and repair - more broadly conceived to include lesions in white matter, gray matter, and leptomeninges - should ultimately unify lines of research, particularly on the side of fluid and imaging biomarkers and clinical outcomes, which have sometimes strayed too far from the causative biology.
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