Monday, 2 June 2014

EFNS-ENS Istanbul: Biomarkers in MS

As promised by presentation from today's talk at the EFNS-ENS meeting in Istanbul. #MSBlog #MSResearch

NEDA is simply not good enough; we need to target the whole disease. #MSBlog #MSResearch

"I note my post yesterday on an MSer with NEDA and progressive brain atrophy generated some heated debate, with some of you promoting self-management by taking unlicensed neuroprotective drugs. I would caution against this; until we know the risk-benefit ratio of these drugs it is hard to make a call. The following is my talk I have just given at the EFNS-ENS meeting when I bring all these topics together and try and build in the early highly-active treatment paradigm stating that we need to also target end-organ damage and reduce brain atrophy and normalise CSF neurofilament levels."



"What do you think of the pyramid in this presentation to illustrate the MS iceberg? I was having difficulty using the iceberg in its previous form."


CoI: multiple

9 comments:

  1. Prof G,

    Thanks for sharing your presentations etc. Perhaps your real calling was as a graphic designer.

    I knew you would caution against taking unlicensed neuro-protective drugs. Unfortunately, your honesty (which I'm grateful for) is a factor. When I was diagnosed my neuro told me not to worry as MS was an inflammatory disease which come and goes. This blog has opened my eyes to how bad MS is (one of your last slides summarises this). Knowing that the disease causes brain atrophy (with a nice picture alongside a healthy brain) doesn't help me sleep well at night. Then we are exposed to results of early trials of neuroprotective agents e.g, simvastin. The hope which this generates is then quashed by the usual larger trials required (and in simvastin's case, the likelihood of no further trial). So I and others are left in no-man's land. We have a grim life- shortening disease, but little chance in the next decade of getting access to drugs that can reduce brain atrophy. The prospect of reparative drugs are still science fiction. Faced with this dilemma I will seek access to the drugs such as simvastin - what else can I do? Can you really blame me. I've been forced down this path as I have no other option apart from waiting while my brain reduces further and disability accrues. How long would you wait?

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  2. Some of the comments I read yesterday scared me. It read like a battalion of MSers willing to cut their nose off to spite their face. Where is the responsibility here?

    There is such desperation on display here on this blog. They will do absolutely anything that somebody suggests to 'cure' their MS. But there is no cure, is there? I think we lose sight of this.

    So many insidious beings are out there wanting to exploit our fears for money. MSers have a responsibility to see the wood for the trees. We need to be smart, not reckless lemmings. This blog needs to stop provoking us into worrying about time being brain, especially when the new DMTs may not benefit most current MSers. Let's be responsible.

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    Replies
    1. Nobody makes much money out of statins. They don't cause PML, Grave's disease, ITP or Goodpastures. They aren't completely safe and their use in MS isn't proven - if their use in SPMS is still not completely proven, it's much less clear what their benefit or harm is in RRMS.

      They are however available over the counter in places like Spain, and people can get their own liver function tests checked privately. I wouldn't necessarily call people taking a statin lemmings or irresponsible - it's their body and there are much worse things they could be doing to it. There are millions of people who are much older than the average person with MS who are on a statin and they aren't dying or falling off a cliff because of them.

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  3. Prof G

    I love biomarkers - glad you do too. Neurofilaments should be de rigeur in MS diagnostics - please keep on pressing the community to make that happen.

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  4. I agree with the first comment - I have been diagnosed with spms for two years now and have been waiting for the SMART trial to start. Meanwhile, simvastatin showed good results in phase 2 clinical trials. The question of a 'cure' isn't helpful. MS is a complex disease and I would like the freedom to try various ideas to see what helps. I'm taking simvastatin in the hope that this may be neuroprotective. I wish medical grade cannabis were available in the UK as I know this could reduce tremor. I have a tremor in my right hand so I can't write but maybe I could find some cannabinoid that would help. (BTW, what is a neurofilament?) I hate that, in general, medics have no sense of urgency about addressing the progress of this disease. I realize though that this blog is great as it raises issues in an honest way.

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    1. What is neurofilament.

      It is a protein in nerves that is released when they get damaged and can be measured in fluids such as spinal fluid and blood.

      Search on neurofilaments in the blog search function there are many posts on this and how it may be used in trials including PROXIMUS trial which has started to recruit

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  5. "What do you think of the pyramid"

    I prefer the pyramid to the iceberg, but neither really show enough of what is going on inside my CNS.
    In the average world outside of London, I don't know of many people who get MRI's done after initial diagnosis. I know I am getting clinically worse, but would like to know what is going on inside my CNS. If I did know, I might be able to ask my neuro more questions!

    So maybe a rectangle might help me more.
    On the left hand side the clinical symptoms such as relapses/walking stick/urinary incontinence /walking stick/wheelchair/etc are listed.
    Using bars in the centre section of the rectangle, use bio-markers such as
    MRI scans/brain atrophy/neuro-filaments/CSF results/etc.
    Each different bio-marker is represented by a different bar in the rectangle.
    Perhaps two different rectangles side by side, one showing the effect of early DMT, the other showing the old world of no DMT.

    It sounds as if brain atrophy starts very early on, and continues throughout. For other bio-markers, they may start at different points in MS. Would the clinical outcomes on the left hand side of the rectangle correspond to the internal CNS events in either rectangle? Perhaps they would? But hopefully the DMT rectangle would incorporate a longer timescale from beginning to wheelchair.

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  6. Prof. Gio.


    What is the reply about slide # 43 Natalizumab , prevent the atrophy or not? .
    what do you think about result.
    thanks.

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    Replies
    1. Year 1 there is pseudoatrophy because the drug is anti-inflammatory the oedema (swelling) is lost making it look like the drug is causing the spine to shrink and in year 1-2 the placebo arm shows more atrophy than treated. The net result over two years not much difference but in reality it is slowing atrophy lok at year 3 and one would suspect placebo to shrink by 0.4 and the nataluzimab to shrink by 0.2 so now 0-3 data would be -1.2 pacebo verses -1.0 tysabri

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