I recently wrote on the topic of cortisone for MRI changes. The comments on the blog were so interesting that I wanted to pick them up and comment on them again.
One note read: “There are also neurologists who don’t even look at the CD (with the MRI images), the examination of the patient on site is more important, so why an MRI?”
Practicing neurologists must see a large number of patients with very different diseases every day – they really have little time. Reading a CD with an MRI into the computer takes a lot of time, many practices also do not have the appropriate infrastructure to compare the current images with the previous ones. In principle, this is the task of the radiologist, who is paid quite decently for his findings. Therefore, many neurological colleagues actually refrain from a personal view of the MRI images and rely solely on the radiological report text. I find this suboptimal and always make my own picture of the pictures, but unlike many practicing colleagues, I have more time and a better infrastructure (radiology in the house). To improve this, the health insurance companies would have to acknowledge that the care of an MS patient is time-consuming and also compensate for this time. But that’s just by the way.
The clinical examination on site is of course also important, but only in combination with the MRI does the picture become complete. The MRI is much more sensitive in the detection of subclinical inflammation and therefore a very essential addition to the personal examination. Only in the interplay of the different information can a competent therapy decision be made.
Another comment was exactly the opposite: “Oh and what about the relapses that supposedly do not exist because no contrast-enhancing lesion is found in the MRI? Today, only images are treated in many clinics.”
As already mentioned– it is neither useful to treat only the MRI images nor to completely ignore the information from the MRI. The more information and aspects I consider, the more differentiated is my knowledge of the patient and the individual course of the disease. This in turn increases the quality of the therapy decision. And by the way, of course you can have a clinical relapse without seeing a contrast-enhancing lesion in the MRI – the MRI (especially with the widely used devices with low field strength in the outpatient area) is always only an approximation of reality.
And then there was the comment: “I was always told that inflammation also damages the myelin without symptoms. Shouldn’t cortisone stop this?”
That is indeed a smart question. Cortisone shortens the symptoms of a clinical relapse – it is therefore given during a relapse as symptomatic therapy to reduce the patient’s suffering under the relapse symptoms. But if there are no symptoms, I personally lack the basis for treatment. Cortisone has not been able to show that it has a long-term effect on the disease – only the immunotherapeutics could do that. So it makes much more sense to me to think about a more potent immunological long-term therapy when new MRI lesions appear.
