Wednesday, 14 May 2014

Redefining relapses: blurring the boundary between clinical and MRI monitoring

Is it time to rethink our definition of a relapse? #MSBlog #MSResearch


"I gave a talk today at a meeting that is focusing on the commissioning of MS services in England. I was discussing the future of MS treatments and made a case for “Saving Brain” with the aim of preventing or reducing end-organ damage in MSers. To do this we need to go beyond the current definition of NEDA (no evident disease activity) and target the base of the “MS iceberg” and try and normalise brain atrophy rates and spinal fluid neurofilament levels. I know that this target may seem unreasonable when some MSers in the country are have difficulty getting simple walking aids or have difficulty accessing their local or regional neurological services for an assessment for DMTs. Am I pushing the bubble too far? Do we have enough evidence that normalising brain atrophy rates makes a difference?"



"One suggestion I made was that we need to challenge the older NICE guidance on not being able to escalate DMTs on MRI criteria alone. To escalate from platform, or 1st-line, DMTs you need to have clinical attacks. However, the new NICE guidance allows alemtuzumab to be prescribed to MSers with active MS defined either clinically or on MRI. The latest guidelines therefore recognise that clinical attacks and MRI activity mean the same thing; i.e. that MS is active. I therefore propose that we stop referring to new T2-lesions, or gadolinium-enhancing T1-lesions, as MRI activity and call them subclinical, or asymptomatic, relapses. If we accept this definition it will change the way we classify MS and our approach to its management; for example we can change the meaning of current NICE guidance’s when they refer to relapses. We would also have to offer PPMSers who have active MRIs DMTs. What do you think?"

3 comments:

  1. Hi Gavin,

    Here on this blog and during the MS Life conference in April 2014 you basically make a case for "hit hard and early" with more effective treatment like alemtuzumab. You also say that for those already on 1st line DMTs (like Copaxone) it's important to keep track of both clinical and MRI activity and, if any activity is observed, quickly switch to, let's say, alemtuzumab. However, patients could stick to 1st line DMT, if there's no MRI or clinical activity.

    On the other hand, in this and some other posts you show that, although focal activity may not be observed through MRI, so called diffuse inflammation (which cannot normally be seen on MRI or otherwise) may be ongoing, and it leads to brain loss and atrophia and ultimately results in cognitive and other impairments.

    Is it indeed the case that 1st line treatments like Copaxone, although in some cases effective for keeping relapses at bay, do NOT prevent diffuse inflammations?

    If it's the case, would it be advisable for someone who's willing to live with potential risks/side effects of alemtuzumab to switch for it from something like Copaxone EVEN IF there's no MRI activity and no progression of clinical symptoms?

    Would really appreciate your response. Thanks a lot for your time and help.

    Misha

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  2. Prof G,

    My question above might have been lost among other posts on your blog. I beg your pardon for being persistent here, but I'd really appreciate if you or MD could make a brief comment on the above. I consider going through alemtuzumab therapy, and your expert opinion would be of immense help in arriving at the decision. Once again, thanks a lot for your time and help.

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  3. It would be good to add 'pseudo relapses' to the MS iceberg. A sperate layer.

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