Young MSers pay a very high price for having MS. #MSResearch #MSBlog
“It looks as if the developing brain tolerates MS very poorly, with the brunt of the disability being related to poor cognitive outcomes. Why is this? I suspect it because the brains of children with MS are not fully developed, have very little cognitive reserve and hence tolerate MS very poorly. At least in adult-onset MS the brain has had time to develop and expand and has some buffer, at least early on, against the ravages of MS. This study suggests that we need to treat pediatric-onset MS as aggressively as adult-onset MS. The problem with the latter approach is that all the high-efficacy DMTs are not licensed for use in children. Despite this many pediatric MSologists go out of their way to get their patients onto highly-effective treatments. My concern is that many countries expect children to cycle through the less effective 1st-line therapies before accessing the more effective treatments. The question I ask is at what price? On the other side of the coin is the developing immune system; we need to understand the effects of the more effective DMTs on the developing immune system to be able to assess the risk:benefits of these drugs for children. There are no quick and easy answers and extrapolating from adults is not entirely appropriate.”
“It must be tough for the parents of young MSers, so many question and so few answers. Being a parent myself and knowing how much we invest in our children emotionally, it must be very, very hard having a child with MS. Studies like the one below, and my comments above, must make your anxiety levels soar.”
Epub: Hosseini et al. Age of Onset as a Moderator of Cognitive Decline in Pediatric-Onset Multiple Sclerosis. J Int Neuropsychol Soc. 2014 Jul 17:1-9.
Background: Cognitive impairment is often reported in pediatric-onset MS.
Objectives & Methods: Using serial cognitive data from 35 individuals with pediatric-onset MS, this study examined how age at disease-onset and proxies of cognitive reserve may impact cognitive maturation over the course of childhood and adolescence. Neuropsychological evaluations were conducted at baseline and up to four more assessments. Of the 35 participants, 7 completed only one assessment, 5 completed two assessments, 13 completed three assessments, 10 completed four or more assessments. Growth curve modeling was used to assess longitudinal trajectories on the Trail Making Test-Part B (TMT-B) and the Symbol Digit Modalities (SDMT; oral version) and to examine how age at disease onset, baseline Full Scale IQ, and social status may moderate rate of change on these measures.
Results: Mean number of evaluations completed per patient was 2.8. Younger age at disease onset was associated with a greater likelihood of cognitive decline on both the TMT-B (p=.001) and SDMT (p=.005). Baseline IQ and parental social status did not moderate any of the cognitive trajectories.
Conclusions: Findings suggest that younger age at disease-onset increases the vulnerability for disrupted performance on measures of information processing, visual scanning, perceptual/motor speed, and working memory. Proxies of cognitive reserve did not protect against the progression of decline on these measures. Young MSers should be advised to seek follow-up cognitive evaluation to assess cognitive maturation and to screen for the potential late emergence of cognitive deficits.