By definition, in PP patients disease progression is characterized by a progressive course without relapses or remissions from the onset of the disease [4] . PP patients tend to have lower inflammatory lesional activity, for which no immunological or genetic explanation has been identified yet. The scarce compar-ative neuropathological studies show a large overlap in lesional pathology, but indicate less inflammatory activity for PP, with still substantial axonal damage [5] . The general picture is that relapse onset and PP forms share substantial characteristics. In other words, it has remained a challenge to identify the biological parameters that determine a PP disease course.