Monday, 23 September 2013

Benign MS may not be so Benign

Achtnichts L, Gonen O, Rigotti DJ, Babb JS, Naegelin Y, Penner IK, Bendtfeld K, Hirsch J, Amann M, Kappos L, Gass A. Global N-acetylaspartate concentration in benign and non-benign multiple sclerosis patients of long disease duration. Eur J Radiol. 2013 Sep 4. doi:pii: S0720-048X(13)00450-6. 10.1016/j.ejrad.2013.08.037

BACKGROUND AND OBJECTIVE:To examine whether clinically benign multiple sclerosis patients (BMS) show similar losses of their global N-acetylaspartate (NAA) neuronal marker relative to more clinically disabled patients of similar disease duration.
METHODS:  The whole-brain NAA concentration (WBNAA) was acquired with whole-head non-localizing proton MR spectroscopy. Fractional brain parenchymal volume (fBPV), T2 and T1 lesion loads, were obtained from the MRI in: (i) 24 BMS patients: 23.1±7.2 years disease duration, median Expanded Disability Status Scale (EDSS) score of 2.0 (range: 0-3); (ii) 26 non-benign MS patients (non-BMS), 24.5±7.4 years disease duration, median EDSS of 4.0 (range: 3.5-6.5); (iii) 15 healthy controls.
RESULTS: Controls' 12.4±2.3mM WBNAA was significantly higher than the BMS's and non-BMS's 10.5±2.4 and 9.9±2.1mM (both p<0.02), but the difference between the patients' groups was not (p>0.4). Likewise, the controls' 81.2±4.5% fBPV exceeded the BMS and non-BMS's 77.0±5.8% and 76.3±8.6% (p<0.03), which were also not different from one another (p>0.7). BMS patients' T1-hypointense lesion load, 2.1±2.2cm3, was not significantly different than the non-BMS's 4.1±5.4cm3 (p>0.08) and T2-hyperintense loads: 6.0±5.7cm3 and 8.7±7.8cm3, were also not different (p>0.1).
CONCLUSIONS: 
WBNAA differentiates normal controls from MS patients but does not distinguish BMS from more disabled MS patients of similar disease duration. Nevertheless, all MS patients who remain RR for 15+ years suffered WBNAA loss similar to the average RR MS population at fourfold shorter disease duration suggesting relative global neuronal sparing or leveling-off of the neurodegeneration rate.

NAA is found in nerves and provides an estimate in nerve content. This is reduced in MSers, whether benign or not compared to healthy controls. So should we do nothing in this group of people or give them a treatment option?

5 comments:

  1. This study is flawed as not enough patients used in this research. How is benign MS identified? Why would anyone want to have a toxic treatment, suffer the side effects, with so little evidence? Maybe. some will. Very costly.

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    1. Thats fine if they do not want to go onto a DMD. Just don't come back 20 years later and start complaining when they are progressing that none of the treatments work and that big pharma is keeping them sick.

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  2. This study is compatible with almost all studies on benign MS; if you follow up the cohort almost all will become disabled given sufficient time. MS is a life-long disease and needs a life-long perspective. This is why we are now shifting our view to keeping the brain as healthy as possible to allow MSers to age well. Brain Health is my new mantra!

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    1. Prof G, Do you advocate neuroprotective drugs for patients with benign MS? I guess drugs targeting relapses makes no sense for this patient population.

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    2. People with benign MS have relapses and MRI activity or they tend to come back years later with SPMS. I think if we monitor MSer more closely clinically and with MRI we may pick-up their disease activity sooner. We already know that over half of benign MSers have cognitive impairment went tested formerly with neuropsychometry. In addition, they as likely to suffer fatigue and depression as MSer with non-benign disease.

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