Multiple sclerosis [MS] is a chronic, autoimmune, inflammatory, neurodegenerative condition of the central nervous system [CNS] (Boppanna, Huang, Ito & Dhib-Jalbut, 2011) characterized by demyelination and axonal loss (Chastain, Duncan, Rodgers & Miller, 2011). MS expresses itself in 4 forms: relapsing remitting MS [RRMS], secondary progressive MS [SPMS], primary progressive MS [PPMS], and progressive relapsing MS [PRMS] (Boppanna, Huang, Ito & Dhib-Jalbut, 2011). MS affects 0.1 per cent of the world’s population (Chastain, Duncan, Rodgers & Miller, 2011), occurring 2- and 2.5-fold more frequently in women than in men, having an incidence range of post-pubertal teenagers to adults in their 50’s (Calabresi, 2011). The exact cause of MS is unknown (Boppanna, Huang, Ito & Dhib-Jalbut, 2011; Chastain, Duncan, Rodgers & Miller, 2011). Boppanna, Huang, Ito and Dhib-Jalbut (2011) suggest that MS is a result of an immunological response against the CNS as well as genetic factors. Owens, Gilden, Burgoon, Yu and Bennet (2011) suggest that a virus or virus-triggered immunopathology causes MS. Vitamin D deficiency is also regarded as a cause for MS as Vitamin D is an immune regulator (Burton, Kimball, Vieth, Bar-Or, Dosche, Chung, Gagne, D’Souza, Ursell & Connor, 2010). Signs and symptoms of MS vary, based on the location of lesions, and may change throughout the duration of the disease (Schapiro, 2005). Sensory abnormalities, optic neuritis, motor symptoms, organ dysfunction, systemic symptoms, etc., are some aspects of the body in which may be affected by MS and are a result of debilitating transmission of an action potential from nerve cells from the brain to the spinal chord due to the demyelination of the axon (Calabresi, 2011). MS is an incurable disease (Boppanna, Huang, Ito & Dhib-Jalbut, 2011). According to Kargiotis, Paschali, Messinis and Papathanaspolous (2010), treatment options for MS are divided into two
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