In contrast with the situation just a few years ago, the most widely accept
ed model for the pathogenesis of FMS now invokes CNS mechanisms like nocice
ption and allodynia rather than pathologically painful muscles. The levels
of platelet serotonin and CSF substance P appear to be abnormal in directio
ns that could logically amplify pain perception. The extent to which these
mechanisms are unique to FMS will be critical in determining the direction
that future research should take. Certainly, a better understanding of the
cause of FMS could represent an important step toward the development of mo
re effective therapy.