Medications are modestly effective at decreasing the number of attacks in RRMS and in reducing the accumulation of brain lesions, which is measured using gadolinium - enhanced magnetic resonance imaging (MRI).  Interferons and glatiramer acetate are roughly equivalent, reducing relapses by approximately 30% and their safe profile make them the first-line treatments.  Nevertheless, not all the patients are responsive to these therapies. It is known that 30% of MS patients are non-responsive to Beta interferon.  One of the factors related to non-respondance is the presence of high levels of interferon beta neutralizing antibodies . Interferon therapy, and specially interferon beta-1b, induces the production of neutralizing antibodies, usually in the second 6 months of treatment, in 5 to 30% of treated patients.   Moreover, a subset of RRMS patients with specially active MS, sometimes called "rapidly worsening MS" are normally non-responders to immunomodulators and are treated with either mitoxantrone or natalizumab. 
Intravenous steroids are safe and effective in treating acute exacerbations of MS. Its use is directed at the early halting or diminishing of the destructive inflammatory process in the central nervous system, so that neurologic disability doesn't accumulate. For an acute relapse, a course of intravenous corticosteroids is typically given (500 mg to 1 gram of methylprednisolone (Solu-Medrol) over 30 to 60 mins for 3 days). This course can be extended up to 5 days (or to even 10 days) if the attack continues to progress or is slow in improving. Intravenous methylprednisolone is also the usual primary treatment for optic neuritis. The somewhat rapid effect of steroid treatment is based partly by reduction of white matter edema, and somewhat by an alteration of immunological factors. It is unusual in practice to give more than 2 or 3 courses of steroids for the treatment of relapses.