Thursday, 18 September 2014

MS Day: Progression

Today Ben Turner talks about Progression
Dr Ben Turner: Q & A

How can a neurologist see a transition from RRMS to SPMS in a patient if they don’t give you MRI scan?
I cannot predict SPMS from the MRI scan, it’s a clinical diagnosis. It’s often a retrospective question as we look at the patient over the last 6-12 months and realise that the patient has gradually changed, but haven’t had a relapse. Now this raises a very hard point to notice who is entering that progressive phase, and that’s why maybe this work about neuro-filaments may be promising. If we can have a test when we think we are not sure, let’s do lumbar puncture and measure neuro- filaments and that would suggest a patient is entering a progressive phase, than if we have an effective treatment for a progressive phase, we can treat it. We always struggled to do lumbar punctures, if we just find a treatment for a progressive phase, we just probably want to start it quite early on anyway. So don’t worry about not having MRI scan, if you have symptoms and a good communication with your neurologist, then hopefully it will be picked up on that.

If I have RRMS does it guarantee that I will definitely develop SPMS?
The key word in MS is heterogeneity. Reviewing statistics, we would say if you have RRMS at 10-15 years you have 50% chance of converting, 20 years you have 80% chance. There is nothing absolute in biology, but yes overtime you have high likelihood of developing SPMS. It can be very subtle, very gradual, and very variable.
I have been put on Tysabri, and on one of your slides it says that you treat SPMS with it. My neurologist has never termed my MS as SPMS and never discussed that I have entered SPMS stage even that I asked, is he doing this preventatively?
Well there is a trial on SPMS for Natalizumab. So we do not know the answer whether it does stop the progression. We had quite few patients on Natalizumab for many years and unfortunately we have seen some patients continue to progress. So like any treatment it is not perfect. Hopefully we can see in the study that it slows it down. I admit neurologists try to avoid the diagnosis of SPMS, because it is not good news and as there is no clear treatment. We don’t know many things, but hopefully with the new treatments we should be more honest and discuss it and be more alert to it.

4 comments:

  1. The independence of inflammation from neuro-degeneration in the French and British Columbia studies is still under debate? Since betaseron and copaxone have been in use for over 20 years is there any data that patients have delayed their MS progression (i.e. clinical progression not radiological) from untreated patient population?

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    1. Inflammation is part of neurodegeneraton you just have to look in the brains of progressive MSers but there are different types of inflammation and some aspects may not link to progression.

      Q2 Look on blog there are posts on this

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  2. I'm happy with either of these explanations of the disease:
    (i) nerves begin to die off an inflammatory cells pile in to the CNS to clear up the debris - MS primary neuro-degeneative disease; or
    (ii) inflammatory cells pile into the CNS (mistakenly or after a virus) and cause damage to myein which leads to death of nerve cells - MS primary inflammatory disease.

    The idea than inflamamtion and neurodegeneration is independent is proposterous. What thhis suggests is that we are really unlucky as we get two different diseases!

    The recently published long-term Alemtuzumab follow-up showed that many patients had remained stable years after being treated (same for BMT).

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    Replies
    1. "The idea than inflamamtion and neurodegeneration is independent is proposterous".

      I agree but i know where dr Turner was coming from but there are different types of inflammation and some parts do not seem to control progression

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