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This paradox arises from the inherent complexity of MS pathogenesis which we argue is driven by a convolution of relapsing/acute adaptive autoimmunity and chronic cytodegeneration (cyto-is used here rather than neuro-to underscore the point that myelin/oligodendrocytes are the likely primary targets of this process), including an elaborate innate immune response (Figure 1)
The difference between treated and untreated injury recovery often becomes apparent during this window
Patients who feel dramatically better and return to full training too soon before the tissue has actually repaired structurally are at elevated risk of re-injury
Menopause can also increase the activity of collagen-degrading enzymes
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