Abstract Body

Pediatric MS (i.e. disease onset before 18 years) shares many characteristics with adult-onset MS. However, children with MS have higher relapse and new MRI lesion rates than adults. They tend to have more severe relapses, with better recovery, but still develop disability at a younger age than adult-onset MS. Pediatric MS has the potential for irreversible central nervous system injury especially as it is still maturing.

Differential diagnoses include ADEM, NMO and MOG-associated disease, among others.

Very few drugs have been formally tested in that age group limiting the availability of safety and efficacy data. Treatment compliance in teenagers can be a particular problem. Discussing treatment options with teenagers and understanding their expectations and preferences may help pick a treatment that will have a better patient adherence. Over the past 10 years, physicians caring for patients with pediatric MS have increasingly used early intervention to limit disability progression and more aggressive treatment options. Interferons and glatiramer acetate have been the usual initial treatment choices for MS in children as open-label studies have shown they are safe. Other drugs such as natalizumab, fingolimod, fumaric acid, or rituximab/ocrelizumab are newer options. Limited information is available from retrospective studies regarding the safety and efficacy of these drugs in children except for fingolimod and teriflunomide that were studied in a randomized controlled trials in patients 10-17 years of age. Several ongoing trials are investigating the use of dimethyl fumarate and ocrelizumab in pediatric MS and will aid future treatment decisions including short-term safety information.

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Accurate clinical course descriptions (phenotypes) of multiple sclerosis (MS) have been considered important for diagnosis communication, for estimating prognosis, for the design of clinical trials, and for treatment decision. Descriptions published in 2014 were based on MS experts consensus leaded by the International Advisory Committee on Clinical Trials of MS. Phenotypes were entirely based on the clinical picture but imaging and biological correlates were missing. Disease courses were divided into Clinically isolated syndromes (CIS), relapsing remitting disease (RRMS) and progressive disease (PMS). Progressive MS merged progressive forms from onset (PPMS) and secondary progressive forms (SPMS) after an initial relapsing course. For RRMS and for PMS, modifiers incorporating disease activity and disease progression were included but it was acknowledge that no clear clinical, imaging, immunologic, or pathologic criteria were able to determine the transition point when RRMS converts to SPMS. In recent years, we have learned several important concepts: 1) that pathological mechanisms leading to progression are present from disease onset, with degree changing over time and differing between individuals 2) that clinical progression starts when compensatory mechanisms failed and we must differentiate the drivers of neurodegeneration from compensatory mechanisms; 3) that age is also a contributing and confounding factor to the clinical expression. Questions that arise include: When does progression begin?; What clinical measure(s) of progression apart from EDSS should we incorporate to detect early or silent progression?; What other tools are available to measure the processes that contribute to neurodegeneration? What are the implications for treatment selection?