Redefining relapses: blurring the boundary between clinical and MRI monitoring

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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?”


About the author

Prof G

Professor of Neurology, Barts & The London. MS & Preventive Neurology thinker, blogger, runner, vegetable gardener, husband, father, cook and wine & food lover.

3 comments

  • 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

  • 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.

By Prof G

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