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 categories: disease modifying agents and symptomatic medications. Where pharmacological agents are used to manage pain in patients (Solaro & Uccelli, 2010). Meletis and Zabriskie (2007) present a natural approach to MS suggesting that vitamins, anti-oxidants and diet provide benefits for patients suffering from the disease.
The cause of MS is still unknown (Chastain, Duncan, Rodgers & Miller, 2011), however, the demyelination of axons within the brain is the foundation in which acts as the catalyst for neurological deficits affecting the transmission of signals by the nerve cells within the CNS therefore affecting other systemic functions (Haines, Inglese & Casaccia, 2011). As MS is an autoimmune disease, this results with the differentiation of self and non-self being hindered whereby cells attack the myelin of an axon as if it were a foreign body causing demyelination and axonal damage (Boppana, Huang, Ito & Dhib-Jalbut, 2011).
Demyelination is a result of the formation of lesions on the myelin sheath as well as the breakdown of the blood brain barrier [BBB] (Boppanna, Huang, Ito & Dhib-Jalbut, 2011) and inflammation of the CNS is the primary cause of damage in MS (Loma & Heyman, 2011). Chastain, Duncan, Rodgers and Miller (2011) suggest that antigen-presenting cells are necessary for the pathogenesis of MS. Inflammation in MS is mediated by a coordinated attack by T-cells, monocytes and B-cells against the CNS tissue (Boppanna, Huang, Ito & Dhib-Jalbut, 2011). Antigen presenting cells [APC’s] encounter myelin, which is presented to CD4+ naïve T cells in the lymph nodes (Chastain, Duncan, Rodgers & Miller, 2011) and differentiate naïve T cells into effector T-helper cells [Th1], influenced by the proteins, Interluken-12 [Il-12], producing pro-inflammatory cytokines (Boppanna, Huang, Ito & Dhib-Jalbut, 2011). Interluken-1 [Il-1] and interluken-23 [Il-23] promote the development of a T cell lineage, Th17 cells, which is a...
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