Tuesday, 12 July 2016

ResearchSpeak & BrainHealth: predicting MS outcomes at 10 years

Do you know how much neuronal, or cognitive, reserve you have? Would you be interested in finding out? #ResearchSpeak #BrainHealth #MSBlog #MSResearch

"The following observational study in the DMT era looks as predictors of disability at 10 years. The observation that secondary progression was the strongest predictor of severe disability is farcical; this is a classic tautology. To be diagnosed with SPMS in the modern era you really nee to have progressive disability; it is part of the definition. In addition, as we don't have any DMTs that have been shown to reliably slow down the progression in SPMS is another reason behind this observation. In short, progression begets progression."

"I note that complete recovery from neurological symptoms predicted a good outcome; I interpret this as being an indication that these MSers still had reserve capacity that protected them over the intermediate term, i.e. the next 10 years. In comparison those with cognitive impairment and depression, possible indicators of loss of cortical reserve, did worse."

"I note that in this cohort OCBs and pregnancy were not predictors of outcome. This is interesting and suggests that in the era of DMTs these factors are not that important. However, as only 5% of the cohort were OCB-ve this study was really not powered to see an impact of OCBs, or more importantly and lack of OCBs, on outcome. If I had MS I would want to know if I had OCBs or not. Why? As I have said many time before we have evidence that OCBs are pathogenic and hence I would want to take this information into account when making a decision about treatment. Similarly, if I was OCB-ve I would simply question my diagnosis and ask is there a small chance that I don't have MS. I predict that when we find the cause of MS, people who are consistently OCB-ve will turn out to have another disease."

"Do you know how much neuronal, or cognitive, reserve you have? Would you be interested in finding out? Protecting reserve capacity is one the core aims of our 'Brain Health: Time Matters' treatment philosophy. You need this reserve when you get older to protect you from age-related cognitive impairment. If you haven't read our policy document I would urge you do so; we have now produced a shorter version for people with MS."


Bsteh G, Ehling R, Lutterotti A, Hegen H, Di Pauli F, Auer M, Deisenhammer F, Reindl M, Berger T. Long Term Clinical Prognostic Factors in Relapsing-Remitting Multiple Sclerosis: Insights from a 10-Year Observational Study. PLoS One. 2016 Jul 8;11(7):e0158978

Background: Multiple sclerosis (MS) has a highly heterogenic course making prediction of long term outcome very difficult.


Objective: The objective was to evaluate current and identify additional clinical factors that are linked to long term outcome of relapsing-remitting MS assessed by disability status 10 years after disease onset.

Methods: This observational study included 793 patients with relapsing-remitting MS. Clinical factors hypothesized to influence long term outcome measured by EDSS scores 10 years after disease onset were analysed by Kaplan-Meier-estimates. Multinomial logistic regression models regarding mild (EDSS ≤2.5), moderate (EDSS 3.0–5.5) or severe (EDSS ≥6.0) disability were calculated to correct for confounders.

Results: Secondary progression was the strongest predictor of severe disability (Hazard ratio [HR] 503.8, 95% confidence interval [CI] 160.0–1580.1); p<0.001). Complete remission of neurological symptoms at onset reduced the risk of moderate disability (HR 0.42; CI 0.23–0.77; p = 0.005), while depression (HR 3.59; CI 1.14–11.24; p = 0.028) and cognitive dysfunction (HR 4.64; CI 1.11–19.50; p = 0.036) 10 years after disease onset were associated with severe disability. Oligoclonal bands and pregnancy were not correlated with disability.

Conclusion: We were able to identify clinically apparent chronic depression and cognitive dysfunction to be associated with adverse long term outcome in MS and to confirm that pregnancy has no negative impact. Additionally, we emphasize the positive predictive value of complete remission of initial symptoms.



5 comments:

  1. Where is the evidence that OCBs are pathogenic? If this is so, why are they seen in other diseases and not just MS? Are OCBs not simply a marker of general inflammation in the brain?

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    1. http://multiple-sclerosis-research.blogspot.com/2014/07/is-ocb-negative-ms-different-disease.html

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    2. Where is evidence?.. There are many papers where these have been injected in animal brains and damage/symptoms have occurred. As the OCBs in MS the same or different to other conditions

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  2. I had an attack in 2005, then again in 2008. My ocbs were negative in 2010 and 2014. No ms DX as didn't satisfy McDonald criteria. In 2016 ocbs finally positive and got the ms DX. So maybe ocbs don't show up early in disease

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  3. What is the exact definition of "complete remission of initial symptoms"? Do old symptoms that only reappear as part of Uhthoff's phenomenon count?

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