Considerations regarding pathogenesis of multiple sclerosis plaques would revolve around heterogeneous modes of involvement of a central venule in the ongoing progression of relapsing/remitting demyelination and of axonal loss. Neurodegeneration of the parent neuron appears pivotal as a demyelinating /remyelinating series of events borne out by the inflammatory nature of the lesions, the multiple sclerosis plaques.  Implied involvement of inflammatory and immune cell elements might help account for modes of progression of an ischemic lesion that targets the oligodendrocyte with loss of its myelin sheath around multiple independent segments of an integral axon.  Indeed, multiple sclerosis proves a neurodegenerative state that progresses as a demyelination of segmental axonal involvement and of individual oligodendrocytes around specific venules of supply.