In the past two decades we have witnessed a remarkable growth in our understanding of multiple sclerosis, and we are now on the threshold of an era in which effective treatment seems possible. Though the aetiology of the disease is not yet fully understood, evidence for an interaction between an environmental factor (perhaps viral) with a genetic susceptibility factor has grown. Four new studies just published (Ebers et al. 1996; Haines et al. 1996; Kuokkanen et al. 1996; Sawcer et al. 1996) have confirmed that the latter implicates several chromosomes; again, the HLA region of the 6th chromosome emerges as the most important.

Much has been learned about cellular mechanisms involved in pathogenesis and repair, and the evolution of the lesion is now much better understood through the exploitation of magnetic resonance imaging (MRI) and spectroscopy. A secure early diagnosis can be made earlier in the course of the disease through the application of MRI, evoked potentials, and cerebrospinal fluid analysis.

Developments in MRI have produced powerful new tools for monitoring the effectiveness of treatment. As a result, putative therapeutic agents can be screened relatively quickly to see whether they have an influence on at least some aspects of the pathological process. One of the most encouraging developments has been the demonstration that a number of agentsmost notably the beta-interferons–reduce the frequency of acute pathological activity, and that this can be reflected in a modest decrease in relapse rate.