Our opportunities in MS therapy have changed and improved significantly over the last 20 years. In the 90s of the last century, the goal of administering MS drugs was to delay the natural course of the disease.
With the use of interferons and glatiramer acetate, it was possible to suppress outbreaks and significantly delay the progression of disability compared to the natural course. Although such a delay was an improvement, it was not satisfactory as many patients still had to accept a progression of the disease, albeit in a milder form (see Figure 1).
The new therapy concepts in the 2000s have made significant progress. I am referring primarily to consistent early therapy and the application of an escalation concept. But the availability of new drugs has also enabled us to stabilize the course of the disease in a large number of patients (see Figure 2).
But expectations have continued to rise. We have seen through developments in the field of monoclonal antibodies that it is possible to not only stabilize the course of the disease with these new drugs, but even to achieve improvements (see Figure 3). This is the case with the use of natalizumab (Tysabri) – we can already practically understand this in our outpatient clinics.
The studies on the active ingredient alemtuzumab (Lemtrada) even show in the prospective analysis of the data that a certain percentage of patients achieve an improvement in their clinical condition. The recently reported evaluation of the study data from Lemtrada over 4 years has shown that more than 70% of patients show stable or even improved courses through administration.
Therapeutic innovation has thus significantly increased the possibilities of therapy. However, the promises of effectiveness of the new therapies must be weighed against a not insignificant risk of therapy.
This risk associated with therapy often leads to drugs not being used by doctors and patients, or being used too late. In discussions about side effects, it is often forgotten that there is also a significant risk associated with the course of MS. It will be the task of the next few years to identify individual risk factors and thus make the administration of effective drugs safer.
In the future, the question will be whether it will be possible to restore functions and repair nerve cells. This could possibly be equated with a cure for the disease (Figure 4). We must firmly aim for this goal in the coming years – even if it is still a vision. However, interesting approaches are already emerging. For example, the anti-Lingo antibody (see www.amsel.de and www.dmsg.de from January) has shown that neuroregeneration can be achieved in acute optic neuritis.
Currently, new active substances such as alemtuzumab and natalizumab already make neurological improvement possible for a significant clientele of MS patients when used in a targeted manner. Therefore, we should use them whenever necessary to take advantage of the possibilities of modern therapy.
