Epub ahead of print: Sämann et al. Brain Volume and Diffusion Markers as Predictors of Disability and Short-Term Disease Evolution in Multiple Sclerosis. AJNR Am J Neuroradiol. 2012 Mar 1.
“This study shows that an MRI marker of structural integrity can predict disability progression in MS’ers in the future. This implies that MS’ers with damage are more likely to progress in the future; i.e. damage be-gets damage. This supports many other clinical and MRI studies in MS. MS’ers who already have acquired damage, clinically or sub-clinically on MRI, are the ones who will progress more in the future.”
BACKGROUND AND PURPOSE: MRI markers of neuronal and axonal damage in MS have emerged as critical long-term predictors of MS-related disability. Here the researchers investigated the potential of whole-brain diffusivity (” a big term for a marker of structural integrity of the brain”) and brain volume (“a gross marker of nerve cell bulk”) for the prediction of disability and short- to medium-term clinical evolution.
MATERIALS AND METHODS: 54 patients with MS (87% under immunomodulatory therapy, baseline and follow-up at a median of 12 months).
RESULTS: At both time points, ADC (diffusivity) histogram analysis provided robust predictors of the MS functional composite scores (R-squared = 0.58, P < .001)*, incorporated cognition and fine-motor skill subscores, and EDSS scores.
CONCLUSIONS: Diffusion histogram analysis provided stable surrogates of disability in MS and proved sensitive for monitoring disease progression during a median of 12 months. Advanced neuroaxonal pathology at baseline was indicative of an increased risk for sustained progression during a median of 12 months, independent of intercurrent relapses.
MATERIALS AND METHODS: 54 patients with MS (87% under immunomodulatory therapy, baseline and follow-up at a median of 12 months).
RESULTS: At both time points, ADC (diffusivity) histogram analysis provided robust predictors of the MS functional composite scores (R-squared = 0.58, P < .001)*, incorporated cognition and fine-motor skill subscores, and EDSS scores.
* “R-squared of 0.58 means that 58% of the change of the MSFC can be explained by the changes in the ADC histogram; this is a very impressive correlation. As a doubting Thomas I would need to see this study reproduced.”
CONCLUSIONS: Diffusion histogram analysis provided stable surrogates of disability in MS and proved sensitive for monitoring disease progression during a median of 12 months. Advanced neuroaxonal pathology at baseline was indicative of an increased risk for sustained progression during a median of 12 months, independent of intercurrent relapses.
Fairly depressing, then!
Re "MS'ers with damage are more likely to progress in the future; i.e. damage be-gets damage"You mean that damage itself is capable of inflicting more damage, right?There is another possible explanation, though: the destructive forces, whatever their nature, are more powerful when there is more damage. The latter is an indirect measure of the severity of the former. In other words the amount of damage depicts the current strength of the causative agent. What do you think?
Can radiologists look at old MRI films to do this analysis or does it require a change in how they do the scan?
Re: "You mean that damage itself is capable of inflicting more damage, right?"No, all that I am saying is that damage predicts more damage. In other words it is a marker of a process. This is what happens clinically, the best predictor of disease progression is progression of disability in the last 6 to 12 months. MS'ers who are stable are more likely to remain stable.I am discussing association not causation. I which we have the answer to what causes progression.
Re: "Can radiologists look at old MRI films to do this analysis or does it require a change in how they do the scan?"At a gross level they can say that there is atrophy or not. They are not good at picking-up subtle changes that occur early on the in course of the disease. By the time radiologists report atrophy it is gross atrophy!
Re: "Fairly depressing, then!"Unfortunately, this is the reality. We all need to realise that MS is a bad disease and treat it as such. These observations and others tell me that if we want to have an impact on the long-term course of MS we need to treat it aggressively as early on as possible or we need to try and prevent the disease. The rationale of waiting for damage to occur and to then try and repair it is flawed; firstly we have little data regarding repair particularly in established MS. We have some data in early MS that with intensive suppression of inflammation a minority of MS'ers improve with MRI metrics that suggest repair. The latter is unlikely to be due to the drugs, but more likely to spontaneous repair mechanisms. Why repair fails as MS advances is an unanswered question; and is something a large number of groups are working on.
Re – "The rationale of waiting for damage to occur and to then try and repair it is flawed; firstly we have little data regarding repair particularly in established MS."Well that just sucks Prof G. I have PPMS and that means the disease didn't even give me a chance. The progression is slow at the start and then buids up. By the time a GP refers an individual to see a neurologist much of the damage is done and continues to be done.I would suggest MS research is what is flawed and continues to fail us. It's just a bunch of highly paid people sat on their jobs.No wonder some eople with progressive MS pare going to Dignitas. Neurology has completely failed us and continues to do so.
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Re: Re: "Neurology has completely failed us and continues to do so."It is not for lack of trying; if we had something that modified the course of progressive MS we would give it to you. It is not for lack of trying; to date all the trials in progressive MS have been negative. I am simply being honest, which is why you need to question any "unrealistic" claims of efficacy or cures in progressive MS. I would rather disappoint you with the "evidence" than make "false claims" and seduce you with "quackery"!