The 32-year-old engineer was diagnosed with MS at the age of 25. From my perspective, everything initially went quite smoothly: The diagnosis was made directly after the first event and an immunotherapy was initiated. Back then, after detailed clarification, he had chosen an interferon and hardly suffered from compatibility problems. According to his own statements, he carried out the therapy “very regularly”.Until 2012, he didn’t notice anything about the disease. His regular MRI check-ups were stable, in the first few years even a slight reduction of lesion load was shown. However, since mid-2012 he reports the reappearance of relapses. These were rather mild – mostly it was sensory disturbances, which completely receded after a cortisone administration by the family doctor. But the events can definitely be classified as MS relapses. Also in the MRI, an increase in lesion load can be traced since 2013 – in the last MRI, which he presented to me during the presentation, two new lesions with contrast agent uptake were also detectable. Clinically, however, there were no complaints – even the neurological examination showed a normal result.
In view of this development, I advised the patient and his wife in a detailed conversation to switch to a preparation that is indicated for higher active MS (i.e., Fingolimod/Alemtuzumab/Natalizumab). This surprised my patient and he said a sentence that I hear quite often: “Every now and then a relapse, is that so bad? – I feel good.”
I understand his point of view – he perceives the sensitive relapses as not very stressful and so far cannot determine any negative effects of the disease. In fact, he feels good, he has no complaints and therefore no interest in changing the medication and switching to an unknown preparation with potentially more problematic side effects.
On the other hand, we know that relapses and continued disease activity in the CNS contribute to disability progression in the long term and that relapses recede completely less often with longer-lasting disease.
Therefore, I try to bring my idea of “therapy goals in MS” closer to the patient. I think it is fundamentally important to formulate clear goals and expectations for a therapy. In my view, this patient should be able to expect from a therapy that relapses and MRI activity are prevented and this leads to stability of the disease at all levels. In technical jargon we call this state “no evidence of disease activity”, abbreviated NEDA, which means “no indication of any disease activity”. This was obviously not achieved with his preparation recently, which is why I would recommend a change in therapy to achieve this goal again. I think, especially because the interferon therapy is associated with some inconvenience for the patient, it is his good right to expect a maximum therapeutic result – ideally the complete suppression of disease activity – i.e., NEDA. If this is not the case, he probably does not have the optimal therapy.
Of course, the concept of NEDA is not uncontroversial. Critics claim that a complete suppression of disease activity cannot be achieved with the current means and consider the formulation of such a goal as not honest.
But I believe that it is basically no mistake to formulate a clear, albeit ambitious therapy goal, which we can certainly achieve individually through the new drugs. It also facilitates communication when doctor and patient pursue a clear goal. Therefore, I try – whenever possible – to align therapeutic strategies with this goal.
On the patient’s side, I often hear the concern that one might “shoot off the powder too early” – then one would have nothing more “in the backhand”. But I believe that the currently very active development of MS drugs does not require us to save anything at all. I rather assume that we will have more and more effective drugs at our disposal with which we can achieve our therapy goals. For this reason, it is always the right time when one sees the necessity to optimize a therapy.
I am curious to see how my patient decides…
