Introduction

Multiple sclerosis (MS) is one of the most common neurological diseases in young adults. Prevalence is especially high in Central and North Europe, North America and Australia with around 100/100,000 inhabitants onset of the disease is mainly in the third and fourth decade of life (Beer and Kesselring, 1994; Hogancamp et al., 1997; Noseworthy et al., 2000; Compston and Coles, 2002). The aetiology is still unknown but a dysregulation of the immune system can be assumed probably initiating the disease process already in childhood in genetically susceptible individuals (Bachmann and Kesselring, 1998; Dyment et al., 2004). Based on this autoimmunity a chronic inflammatory process is set off, allowing immunological active T-cells and monocytes invading the central nervous system (CNS) through a disrupted blood–brain-barrier, thus initiating a cascade of immunological processes (activation of macrophages, microglia, production of immunomediators) and inflammatory reactions which lead to lesions of CNS pathways and finally to glial scaring (Lucchinetti et al., 2000; Noseworthy et al., 2000). The most prominent pathology in MS is demyelination. There is, however, an increasing evidence, that even in an early phase of the disease axonal loss may occur (Trapp et al., 1999; Lucchinetti et al., 2000). Depending on the kind, extent and localisation of such lesions, various functional deficits may occur. Clinically MS runs in two-thirds of the patients a primary relapsing–remitting course, the major number of these cases, however, turning into a secondary progressive course later on.