In terms of a realized predetermination of events of injury and of reconstituted remyelination within multiple sclerosis plaques, it is perhaps reasonable to consider demyelination as an endresult of various pathways of primarily developmental nature.  In such a context remyelination rather than demyelination would characterize a disease process that is diffusely inflammatory in white matter but that is morphologically and pathologically definable as multifocal lesions of plaque type.  It is further to be determined whether the blood brain barrier hyperpermeability constitutes a recharacterized series of pathways that transform interface reactivity with regard to T lymphocyte entry and reentry within a context of variable cytokine and chemokine effect.  A strictly heterogeneous process of epitope spreading akin to possible viral transfer dynamics would implicate primary or secondary progression of a multiple sclerosis process both in established genesis and subsequent amplification.  Inflammatory progression would evolve in terms particularly of a lack of growth factors that predetermine outcome of demyelination both as systems of injury to the axon and as a central process of neurodegeneration.