ABSTRACT
Although the aetiology of multiple sclerosis (MS) remains unknown, it is widely accepted that MS is a T-cell mediated autoimmune disease. However, a poor response to immunosuppressive therapies, clinical heterogeneity and the poor correlation between inflammation and disease progression suggest that inflammation may play a dual role in MS. On the one hand inflammation mediates oligodendrocyte and neuroaxonal toxicity, while on the other it provides trophic support, which aids axonal recovery and remyelination. This may explain why the strategy of broad-spectrum immunosuppression, which reduces clinical relapses and magnetic resonance imaging (MRI) activity, has little impact on the development of disability. By removing the inflammatory component, which is responsible for relapses, the underlying neurodegenerative process may be exposed, i.e. converting relapsing-remitting MS (RRMS) into non-relapsing progressive MS. To investigate the complex role that inflammation plays in the pathogenesis of MS we need to be able to monitor the pathogenic processes involved in tissue destruction and repair. This chapter reviews the key pathogenic processes, the principles of immunological and biochemical monitoring and putative cerebrospinal fluid (CSF) markers of tissue destruction and repair in MS.
