ClinicSpeak: smouldering MS

How big a problem is smouldering MS? #MSBlog #MSResearch #ClinicSpeak

"I had a meeting a week ago with a group of science policy makers and writers who want to develop a document to inform MS-related health policy. Someone in the meeting asked me ‘how big a problem is smouldering MS?’. This is a very good question. Although I can’t answer the question I hypothesise that it is a much bigger problem than we realise."



"The uninitiated may ask what is smouldering MS? Smouldering MS simply refers to MS that is clinically silent, but remains active pathologically. Think of smouldering MS as the shredder running on slow. Smouldering MS gradually uses up all your reserve capacity of the brain and spinal cord that you require to adapt to the damage caused by MS. Once this reserve capacity is gone progressive MS becomes clinically apparent. When this occurs it is too late to reverse the process and the moment too late to restore function through repair. “


“Can we monitor smouldering MS? Yes, we can by using biomarkers of disease activity that are more sensitive than our current clinical read-outs (relapses and disease progression or EDSS). MRI is one biomarker that is capable of finding disease activity that is not clinically apparent. However, routine clinical MRI is not good enough; we know it is missing most if not all of the disease activity in the gray matter and it is also missing a large quantity of disease activity in the white matter. This is why we need to find a way of incorporating brain atrophy measurements into clinical practice. At the moment the technique is too variable to be used on an individual MSer level, but it can be used to study populations of MSers. It is quite clear when you study populations of MSers that brain atrophy is a tractable problem in MS. The brain of the average MSer is shrinking at twice the rate of normal and it is now clear that brain atrophy is associated with poor clinical outcomes. Why would anyone want to be losing brain at a rate above normal? It is also becoming evident that only the highly active treatments have a consistent impact on brain atrophy; i.e. from fingolimod upwards. All the low and intermediate efficacy drugs don’t have an impact on brain atrophy at a population level. Herein lays the problem. These drugs all slow the shredder down and reduce clinical disease activity, but are they switching off the disease? These drugs may switch-off the shredder in some MSers but the majority of MSers on these drugs will have their disease converted to smouldering MS.”

“If I was a public health doctor and treating a population of MSers I would want them all to be on highly-effective DMTs. I would want the population to do well. This is why individualised care pathway makes a mockery of the science; if we are simply converting clinically active MS, into smouldering MS, with low efficacy DMTs we are doing the field, and many MSers, a disservice. What we should be doing is switching off the shredder in as many MSers as possible and improving the outcome for everyone. Any thoughts?”


CoI: multiple

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