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Source: Bainbridge JL, Miravalle A, Wong P. Multiple sclerosis. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey L, eds. Pharmacotherapy: A Pathophysiologic Approach. 10th ed. New York, NY: McGraw-Hill; 2017. https://accesspharmacy.mhmedical.com/content.aspx?bookid=1861§ionid=146062622. Accessed September 10, 2018.
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Affects approximately 2.3 million people worldwide
Usually diagnosed between the ages of 15 and 45; peak incidence occurs in the fourth decade
Women are afflicted more than men by a ratio of 2:1
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Exact cause of MS is still unknown, but disease is thought to develop in genetically susceptible individuals that are exposed to random events and environmental factors.
Genetic variation accounts for approximately 30% of the overall disease risk.
Nongenetic factors have a proportionately larger contribution than genetic factors to immunological heterogeneity.
Certain viral or bacterial infections may also participate in the pathogenesis of MS by initiating or activating autoreactive immune cells.
The familial recurrence rate of MS is approximately 5%, with siblings being the most commonly reported relationship, and a concordance rate among monozygotic twins of approximately 25%.
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Infiltration of peripheral immune cells into the CNS and promote neurodegeneration by stripping of the myelin sheath surrounding CNS axons.
T cells recognize and become activated against myelin.
Loss of myelin slows and disrupts signal transmission.
MS lesions are heterogeneous.
Acute lesions show demyelination and axonal destruction with lymphocytic activity consistent with an inflammatory state.
Chronic lesions display less inflammatory lymphocytes with active remyelination.
Repeated damage leads to axonal destruction and permanent loss of function.
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Sex (female > male)
Geographical location
Genetic factors
Low vitamin D3 levels
Smoking
Infections
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CLINICAL PRESENTATION
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Primary symptoms/signs
Secondary symptoms
Tertiary symptoms
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