Multiple sclerosis is a chronic inflammatory disease of the nervous system
in which a T-cell-mediated inflammatory process is associated with destruct
ion of myelin sheaths. Although demyelination is the primary event, axons a
re also destroyed in the lesions, and the loss of axons correlates with per
manent functional deficit. Here, we discuss evidence that demyelination and
axonal destruction follow different pathogenetic pathways in subgroups of
patients. This might, at least in part, explain the heterogeneity in geneti
c susceptibility, clinical presentation and response to treatment observed
between individuals.