ABSTRACT
Our understanding of the pathophysiology of multiple sclerosis (MS) still remains incomplete. Currently evolving concepts support the view that MS is autoimmune in nature. There is little indication that MS is based on a disturbance of the immune system per se implying that this disease more likely does not result from an intrinsic disorder of immune regulation or control, but rather from a normal response to an inappropriate antigen.1 The definition of such antigens remains elusive. Although the possibility that MS might be caused by a virus or any other infectious agent cannot be excluded, evidence for such an agent consistently being linked to MS is not available. Provocative recent work suggests that individual patients may have fundamentally distinct pathologies that persist throughout their illness.2 If true, it will be important to have technical possibilities at hand that will define these pathological patterns and, ultimately, guide more specific therapy.
