Saturday, 24 November 2012

Living with MS - 24th November 2012

"The MS Society is hosting a meeting in Hammersmith today called 'Living with MS' (programme below). I am talking at the meeting and as usual I have only just completed my presentation."

"Apologies for not getting my presentation in before the Thursday deadline; as a result the attendees at the meeting won't have a print-out of my talk in their delegate packs. I have, however, uploaded it onto my fileshare site for you to download."

"My talk!"


  1. Prof G,

    Hats off to you fro the amount of your spare time which you give up to present at these events.

    I can't attend, but found that the slides were rather downbeat - highlighting the terminal phase and the early death of an MSer (you need to amend the date that Graeme Wilson passed away). If you want to scare the pants off newly diagnosed people you will have achieved this. I recall you saying that when you gave a similar presentation at MS Life a member of the audience started crying. I' not suggesting that we mask how bad this disease can be (and often is), but I'd hope that as we are nearly in 2013, that these presentations could be a little more hopeful (apologies if what you sya does this).

    I hadn't heard about the stem cell work for progressive MS and would be interested in what was said.

    1. Downbeat...look at all those studies we are doing on progressive MS. These are others in the MS world.

      If you aways want upbeat presentations, then we get accused as being liars etc.

      Without wanting to scare people, we are hopefully getting to the stage where you should consider drugs of high efficacy, higher risk as soon as possible, therefore information is the key to understanding your risk benefit profile

    2. Mouse,

      I don't always want upbeat presnetations, but I do (given all the research undertaken around the world) to see advances. If you get time, could you do a post on the neruo-protective drugs that are in trial i.e. by your team. I know that Lars Fugger's team is running a trial with Amiloride (sp?). I think Prof Kapoor's team are looking at another agent. Not sure what the Charcot trial will be testign in terms of affect on the disease.

      PS I am grateful for all the work done by Team G. I'm sure good things will come in the future (ust want it to be the near future).

    3. The idea for Prof Kappors trial came from our work, so did the lumbar puncture trial of Prof G, the CUPID trial was based on our idea from 2003, but the trial design was wrong, we have data on alot of others, some better than others, but until the trial design is worked out it does matter what we find. Look at Prof Gs talk there is alot more in there.

    4. How can you ask to put an upbeat spin on Wilson's story? He was diagnosed in 2004 and passed away very suddenly last year. He did everything in his power to overcome MS, from DMTs to CCSVI, but he still didn't make it. I used to love his blog. He never really talked much about his illness, more the things that happened to him in life such as friends, love and family. He was so much more than his ill health. Such a shame, really.

    5. Prof G was sad about his passing also and we know the date on his slides were wrong 2011

  2. Actually we were all quite cross with Prof G for announcing his U turn on progression (cos people always shoot the messenger of bad news) but I have come to the conclusion that he needs to announce the bleak news loud and clear because that's the only way forward. I have come to believe that a big chunk of this disease is neurodegenerative and neurologists/researchers as well as the general public need to rethink! Many have become complacent with all the new drugs for RRMS ignoring progression which is so much harder to tackle but we have seen what comes of this - disabled people despite years of so called effective treatments.

    As an aside - Graeme seemed such a nice guy, such a loss!

  3. "Actually we were all quite cross with Prof G for announcing his U turn on progression".

    Prof G is going to make another post with bullet points on this so that he can clearly explain his views are, as is was not clear.

    The question is about progression and RRMS. Are they different. We know that because current DMT have not stopped progression when used in progressive MSers. In animals they are different processes.

    So question is are they
    (a) two independent effects (neurodegeneration) and relapsing disease and whether treatment of relapsing disease have no effect on neurodegeneration.
    (b) Inflammation associated with relapsing disease causes the neurodegeneration
    (c) Inflammation associated with relapsing disease can shape the neurodegenerative course if used early but they can be still be two different processes driving disease

    I think Prof G was saying that he was rejecting (b) but was he rejecting(c)also, maybe but was he saying treating relapses is a bad idea...... definitely not.

  4. It's a) and that's the point: right now science looks a bit to me like renovating a big mansion. All the current DMTs are like putting new fancy wallpaper without (having taken)/taking into account that the wall underneath is crumbling into dust. But I still appreciate G's and yours efforts Mouse - maybe you will succeed and my mansion won't go bust in the end.....

  5. Having Listened to Prof G, I would say (c) is still on his cards. I know (a) is not wholey correct, look through prof G's talk to slide 52 and there is the answer

  6. Slide 52 - yes, when I looked at it the first time I also thought to myself: okay so we found a way to reduce neurodegeneration if natalizumab reduces axon damage=less brain atrophy=less disability. The interesting question would be if the patients were with advanced disease or CIS? So maybe there is hope to at least slow brain atrophy with the hard stuff? That would be enough for me, I don't believe in stopping the disease with the current drugs. You'll stop it when you find the cause, not before or to use my renovation analogy: the walls stop crumbling when you get rid of the woodworm eating away at the foundations.

  7. On slide 14 it says that in terms of response to DMDs, there are

    20% responders
    40% partial responders
    40% non-responders

    Is this just for the CRAB drugs or is it for all the MS drugs so far? Do the stronger drugs (Tysabri, Gilenya, etc.) have better response rates? Were there non-responders in the Alemtuzumab trials?

  8. I believe it is the interferons.

    I dont know about stronger DMT


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