Cortisone for MR Changes?

I have often written about the role of MRI. In reality, I often experience a distinction problem between clinical stimulus and failure symptoms (= MS relapse) and changes in the MRI (new lesions).

In a clinical relapse, a patient develops clinical symptoms relatively suddenly due to MS – e.g. a visual disturbance, numbness and weakness of the legs, balance disorders etc. In such a case, it is plausible to offer a cortisone shock therapy – although this is not a panacea and the scientific benefit is controversially discussed, but in many patients there is (felt) a faster regression of the relapse symptoms. Therefore, there are no objections to the administration of cortisone during a clinical relapse. Although I sometimes think that this measure is used a bit too generously – because a steroid pulse therapy is not completely free of side effects and therefore the indication should be well checked. On the other hand, our guidelines state that any clinical relapse symptoms that the patient finds disturbing should also be treated.

On the other hand, the administration of cortisone in a symptom-free MS patient, due to new (contrast medium-absorbing) MR lesions in the MRI, does not make sense. Of course, such a finding is anything but good, because new foci in the MRI are an indication of inadequate disease control and therefore one should reconsider the previous immunotherapy in any case – but a cortisone shock? In such a situation, little will be achieved with this – because if there are no complaints, there is also nothing to “treat” and in the worst case, only side effects are provoked by the high-dose steroid therapy. Cortisone administration also has no long-term effects on the course of the disease, as long-term observations have shown very well, and is therefore dispensable in this situation.

Accordingly, referrals for plasma exchange treatment (see „Blood washing“ at MS), even if many acute inflammatory foci are shown in the MRI, are not useful if the person concerned has no clinical symptoms. Of course, in such a case, one must reconsider the long-term immunotherapy, but there is no indication for the use of relapse therapy or escalation therapy of the acute MS relapse (= plasma exchange).

In summary, it can be said that a cortisone treatment serves to treat symptoms that have been triggered by an acute clinical relapse – the treatment of a contrast medium-absorbing lesion in the MRI with cortisone is not necessary. However, such a lesion should always prompt reconsideration of the current MS therapy – because the goal of immunotherapy is to suppress any disease activity.
At this point it should also be said again that the value of a contrast medium-absorbing lesion is ultimately no different from that of a new non-contrast medium-absorbing lesion. The contrast medium uptake only indicates that a lesion has occurred within the last approx. 4 – 6 weeks.

By the way, this is also an argument against treatment based solely on MRI images. Many inflammatory changes are not noticed at all, but only later appear as so-called new T2 lesions during an MRI check – and these patients have also managed well without cortisone therapy in the meantime. So much for the distinction between clinical relapses and so-called subclinical disease activity in MRI.

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