This Is MS Multiple Sclerosis Community: Knowledge & Support

In a highly controversial attack on the conventional approach to MS, published last November in the Journal of the Royal College of Physicians of Edinburgh, Professor Peter Behan, a neurologist at Glasgow University, claimed that the effectiveness of the most widely prescribed drug — beta interferon — was no better than a placebo. Last month two separate studies, one published in the BMJ and the other in The Lancet, raised questions about the effectiveness of beta interferon. While noting a modest effect in reducing the number of relapses, the reports concluded that there was no reliable data for its effect beyond a year, which is quite a problem for a drug treating a lifelong disease.

Behind this debate over drug effectiveness is an increasingly bitter argument about the origins of multiple sclerosis. It is a debate that has enormous implications, not only for the sort of research that should be done and how patients should be treated, but also for an ongoing legal argument involving millions of dollars about whether MS can be brought on by certain sorts of physical trauma, most significantly whiplash in a car crash. Under the autoimmune model such a link makes no sense, whereas if other causal factors are involved the trauma theory gains credence.

Professor Behan, who has testified in the courts to the possibility that trauma triggers a predisposition, outlined a range of criticisms of autoimmune theory in his paper. One involves the animal model used by researchers to study the disease. The model is created by injecting vaccine-like substances into the brains of mice, which cause them to have an autoimmune reaction that damages their myelin sheath.

But Professor Behan is not alone in his thinking. As well as the recent reviews of beta interferon, a paper due out later this month from Dr Massimo Filippi, of the Istituto Scientifico Universitario Ospedale San Raffaele in Milan, casts doubt on one of the basic assumptions of the autoimmune theory. Dr Filippi scanned the brains of patients with early symptoms of MS and found not only signs of extensive damage to neurones, but also that this was “largely independent of what inflammation can be detected”.

In other words, damage doesn’t develop gradually driven by autoimmune inflammation, but is both there at the beginning and not obviously linked with inflammation.

Which brings us to the key question: why do people get MS, if not because of a rogue immune system? We still do not know, but Professor Behan, Dr Filippi and others believe that it is worth looking elsewhere, possibly at metabolic change leading to neurodegeneration, which then might be slowed down or halted.

one of the side effects of copaxone is vasodilation. maybe that is how it helps.

I remember Coles's answer when he was asked about CCSVI. He just said: "we know MS is autoimmune because when we give patients immune suppressants they get better". This is far from an educated answer i d say. He forgot to mention that every single substance given to us MAY have a modest effect ONLY on out relapse rate and nothing more.