Silent Spinal lesions may evetually take their toll

Zecca C, Disanto G, Sormani MP, Riccitelli GC, Cianfoni A, Delgrande F, Pravatà E, Gobbi C.Relevance of asymptomatic spinal MRI lesions in patients with multiple sclerosis.Mult Scler. 2015 Oct 12. pii: 1352458515599246. [Epub ahead of print]

BACKGROUND:The impact of new asymptomatic spinal cord lesions (a-SL) in multiple sclerosis (MS) course is poorly characterized.
OBJECTIVE:The objective of this research paper is to assess the prognostic value of a-SL in predicting MS course.
METHODS:Relapsing-remitting MS patients who received serial MRI (brain and spinal) at baseline (t1) and within 12 to 36 months (t2) during clinical stability, and had a follow-up (t2-t3) ⩾24 months were included. Relapses and disability progression were evaluated between t2 and t3.
RESULTS:Of 413 consecutive screened MS patients, 103 patients (65 females, median age 43 years) were included. After a median t1-t2 interval of 17 (IQR 13-26) months, 25.2% and 43.7% patients had ⩾1 new a-SL (a-SL+) and asymptomatic brain lesions (a-BL+), respectively. Relapse risk between t2 and t3 (median interval: 42 (IQR 32-57.5) months) was significantly increased in a-SL+ and/or a-BL+ vs a-BL- and a-SL- (HR = 2.31, 95% CI = 1.13-4.72, p = 0.02). No differences in the risk of disability progression were found in a-SL+ and/or a-BL+ vs a-SL- and a-BL-.
CONCLUSION: a-SL occur in one-quarter of clinically stable RRMS, and combined with a-BL contribute significantly in predicting future disease course.

As many as 85% of brain lesions are silent and likewise silent spinal cord lesions develop but with time these create more and more damage in nerve tracts and are best not to have them.

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  • Agree completely with you MD – definitely best not to have them – or any lesions at all for that matter. Please tell me where to send mine back to – am happy to pay the postage costs to return them to Sender……………..

  • A logical question might be back towards the Lumbar Puncture debate since many researchers feel many MRI's in use do not have the resolution to necessarily detect activity and said MRI's are often read by a radiologist and thus open to interpretation and/or error.

    If someone's MRI shows up essentially clear that'd be a good time to do a lumbar puncture and see if proteins are in the CSF suggesting myelin breakdown.

    While an uncomfortable procedure to be sure I have yet to read any study towards that end.

    Patients seemingly clear of flare-up's having lumbar puncture to see if things really are stable.

    • What active DMT does one take if they have PPMS?

      This post is both ridiculous and dumbfounded. There are forms of MS that are untreatable. You should know that, MD.

    • Agree completely again with you MD re "Take an active DMT..what ever that may be" but that only applies if you have RRMS (which I do recognise that this study is referring to). Maybe I'd be in better shape now if my MS had been diagnosed years earlier as my brain and spinal lesions were not totally asymptomatic, but no GP was actually listening when I told them about the bits of me that were not working as they should be. What's more, I even told two GPs that I was concerned that it could be MS and thought that my "problems" ought to be checked out. One of them thought that Myasthenia Gravis was a possibility, but didn't refer me on to a specialist. As a patient there's not much you can do if the Docs are not listening.

    • I could say find another Doctor so they refer you to a MS specialist, but I know you will have to fight because if you read ProfGs post last week they are being paid not to refer and as they are the budget holder they are the gate keeper and the ferry.

      I had severe mvement pain in my shoulder and was pretty sure the pain was not in my shoulder but it was a referred pain coming from a problem in my neck. One of neurologists said get refered to Barts by my GP we can dosome electrophysiology and pinpoin the damage however the GP would not refer because of the costand said it was a frozen shoulder….laughable diagnosis. I knew the treatment was going to be physiotherapy if the problem was neck or shoulder but at least I got to see a physiolotherapists who also instantly said frozen shoulder my arse:-) and gave me some excersises that the neurologist at work had already given me.

    • Clearly what is needed is a simple blood test to determine if you have RRMS. All of the new therapies for RRMS are different variations of immunosuppresants, and now it is just a race to see which one shuts down relapse rate the quickest in a 2 year trial. If we had a blood test, the splitting hairs on relapse rate wouldn't matter anymore (and really has now bearing on long-term outcome).

      So for the academics, you say you can't do a phase 3 trial for RRMS because it costs too much. Why not put your efforts into a blood test? Surely this would not have the hurdles that are required to get a drug through trial testing.

    • Whist a blood test to detect neurofilament (a marker of nerve degeneration) would be very useful to determine how effective stopping new lesions can reduce nerve damage), there's no way a blood test could replace MRI as a detector of active inflammatory lesions in the CNS.

    • Maybe not a blood test to indicate active inflammation but a blood test to tell if you are susceptible to getting ms. MS seems to be a combination of genes and environment, but if the genetic component can be firmly established it may shorten the time to get a patient in the hands of an MS specialist instead of relying on a GP.

  • I am wondering more and more these days about whether I have had silent lesions/relapses in the past and that my MS only became noticeable when I developed a significant spinal lesion. I just do not believe in PPMS any more, in terms of it being a distinct condition from RRMS going on to SPMS.

    • I agree PPMS is part of the spectrum and the progression shows itself sooner, but there will have been attacks that current DMTs will deal with however, because lower limb progression is not stopped they deem it not cost effective, this does not mean it is of no use.

    • So attacks typical of RRMS can occur in PPMS which would respond to "normal" DMTs such as beta interferon? These attacks don't require some "fancy" anti-inflammatory like Ocrelizumab? That is what I seem to be waking up to…

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