Multiple sclerosis is a chronic, inflammatory, immune-mediated disease of the central nervous system. Current evidence indicates that a complex genetic trait associated with environmental factors probably triggers MS. The hypothesis is that the inflammatory response starts when CNS protein-specific CD4+ T cells become activated in the periphery, cross the blood/brain barrier, and induce CNS autoimmunity. A disturbed balance between cells that induce or cause demyelination and regulatory T cells capable of suppressing these auto-reactive T cells underlie MS pathogenesis. Inflammation and oxidative stress are major causes of tissue damage in the CNS. Diagnostic criteria include paraclinical laboratory assessments emphasizing the principle of lesions disseminated in time and space. Cerebrospinal fluid analysis remains mandatory in order to support the diagnosis and differentiate MS from other diseases. Disease modifying therapies (DMT) are available for MS patients like recombinant Interferon β (IFN-β) and Glatiramer Acetate (GA) that present similar clinical outcomes showing reduction in patient’s annual number of relapses, MRI T2 lesion load reduction and delay of disability. Recently, a monoclonal humanized antibody, Natalizumab, was re-launched showing a larger reduction in annual number of relapses and MRI lesions in the CNS. Besides, Fingolimod (FTY720) was also introduced as the first oral drug with similar effects. Corticosteroids are the first line therapy for acute MS exacerbations. The parenteral use of Cyclophosphamide, Mitoxantrone and Cladribine may benefit some patients with aggressive disease. Oral immunosuppressive drugs (azathioprine, mycophenolatemofetil and methotrexate) have also been reserved for patients whose disease progression cannot be controlled by DMTs.
Keywords: CSF study, genetics of MS, immunology of MS, multiple sclerosis, MS treatment, MS diagnosis, white matter pathology, brain cortical atrophy, CSF oligoclonal bands, CNS demyelinating disease, EAE model, low vitamin D level, MRI brainT2 lesions, reactive oxygen species, Th17 cells, EDSS scale, neurodegeneration, HLA-related susceptibility, relapsing, secondary progressive phase.