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Treat patients with radiologically isolated syndrome when the MRI brain scan shows dissemination in time: Commentary

Although an infrequent presentation, patients with the radiologically isolated syndrome (RIS) will be seen by every neurologist, who will perhaps manage about ten of these patients in their professional career. The injunction of Dennis Bourdette that we must exclude MRI mimics, is an important first step in the assessment of the problem. The RIS label means that we are dealing with asymptomatic patients with typical demyelinating pathology as observed by the MRI; most of them should have cerebrospinal fluid (CSF) examined for oligoclonal banding. So, if we find truly asymptomatic patients who satisfy MRI criteria for dissemination in space and who have evidence of dissemination in time, either by serial MRI scans or by a single scan demonstrating both non-enhancing T2 lesions and gadolinium enhancing lesions, what do we do? Commentator slips into anecdotage. Ten to 15 years ago I observed these patients without prescribing diseasemodifying therapy; I remember two who developed a dementing illness and died from intercurrent infection. Yes, I know that anecdotes have the least standing as evidence base but there is the distinct advantage of the long view. Most acute multiple sclerosis lesions (at least 90%) are asymptomatic. The weighting of symptomatic disease (an episode of optic neuritis) as being more relevant or trustworthy as evidence of disease activity than a typical asymptomatic gadolinium-enhancing lesion in the corpus callosum makes no scientific sense to this commentator. Thus patients with RIS, because of their luck in avoiding symptomatic lesions, are condemned to no therapy. What proponents for non-therapeutic intervention in RIS are saying is ‘Don’t trust the MRI scan’. Given the infrequent occurrence of RIS and the need for prolonged follow-up, it is highly unlikely that any randomized controlled trial could be performed even in an international context. There will be safe oral therapy available for demyelinating disease in the near future. I think we will have to be pragmatic about our management of these patients on an individual basis and I would advocate treating RIS patients with typical new T2 or gadoliniumenhancing lesions on serial MRI scans. The recent revision of the McDonald Criteria was conservative in its approach: ‘in the absence of supportive research findings, the Panel concluded that a firm diagnosis of MS based on incidental findings on MRI alone, even with additional supportive findings on evoked potentials or typical CSF findings in the absence of MS-relevant clinical symptoms, is problematic.’1 It does seem that the consensus opinion as to therapy of RIS is with Dennis Bourdette, but further analyses of longitudinal cohorts2–4 and the guidelines suggested by David Brassat and Christine LeBrun-Frenay might help the decision process.