Recently there have been considerable advances made in the treatment of mul
tiple sclerosis. For the first time since its initial clinical description
in the 1800s, there are now available several medications which unequivocal
ly exert favourable clinical effects through the lowering of the biological
activity of die human illness. The therapeutic efficacy of IFN-beta prepar
ations seems particularly well established in this regard on the basis of f
ive large, independent, trials of this agent. These: trials have demonstrat
ed remarkably consistent reductions in both attack rates and disability lev
els using a combination of clinical and magnetic resonance imaging outcome
measures. The therapeutic benefit of glatiramer acetate also has been well
established, although there is less available data on this agent than there
is for interferon. It is important to recognise, however, that, although t
hese agents represent an important first step in the management of patients
with multiple sclerosis, they are only partial therapies. In order to actu
ally cure the illness or even to substantially improve patient outcome pie
need considerably better agents than we have currently. Nevertheless, it is
likely that, with improved knowledge of the role that interferon beta play
s in the pathogenesis of multiple sclerosis and with better understanding o
f the mechanism by which glatiramer acetate exerts its therapeutic: effect,
greatly improved therapeutic agents will be available in the future. In ad
dition, it seems likely that, in the future (by analogy to the experience i
n oncology), we will begin utilising combinations of therapies in order to
better control it the biological activity of this debilitating disease. Suc
h combination therapy well almost certainly include combinations of partial
ly effective agents as well as combinations of these agents with other medi
cations (e.g., the immunosuppressive drugs) which, by themselves, have only
been demonstrated tu exert marginal clinical benefits on the course of ill
ness. Moreover, it also seems likely that, increasingly, therapeutic strate
gies that enhance or promote myelin repair will become a major focus of cli
nical research in this area.