The treatment options available for patients with MS have changed considerably in the past two decades and, in all likelihood, will continue to change as time goes on. Large numbers of studies and trials have been performed in RRMS with the aim of modifying the disease process. From these emerged the most widely used disease-modifying therapies (DMTs) of β-interferon (βIFN) and glatiramer acetate (GA) with their well-known effect of reducing relapse rates by approximately one-third [31–34]. Other DMTs have been tested and, of these, monoclonal antibody therapies such as natalizumab and alemtuzumab have been shown to dramatically reduce relapse rates in RRMS, albeit at the expense of increasing the risk of serious drug-related side effects [35, 36]. Even more recently, the development of oral agents with better efficacies than βIFN or GA provides a further class of DMTs for use in RRMS [37].

Regarding progressive MS, however, options for disease modification are much more limited. The hope that drugs used to reduce relapse frequency might be effective in established progressive disease has, largely, proven to be unfounded. The likely reasons for this and a review of DMT drug trials relating to progressive MS are presented in Chap. 9. Despite these trial failures, the evidence gleaned from them has, in association with epidemiological, pathological, and MRI evidence, been hugely informative in determining pathophysiological mechanisms in progressive disease and has set the scene for a new generation of therapies specifically targeting disease processes occurring in progressive MS. These issues, along with general descriptions of progressive MS, will be discussed in detail throughout this book.