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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. Accessed September 10, 2018.


  • Multiple sclerosis (MS) is an inflammatory disease of the central nervous system (CNS) characterized by demyelination and axonal damage.

  • Two main characteristics of the disease

    • Multiple neurologic symptoms accruing over time

    • Characteristic plaques or sclerosed areas


  • 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


  • 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%.


  • Infiltration of peripheral immune cells into the CNS and promote neurodegeneration by stripping of the myelin sheath surrounding CNS axons.

    • Demyelination causes axonal damage, which correlates with disability.

      • Damage should be visualized as hypointense lesions, or “black holes,” on T1-weighted MRI.

  • T cells recognize and become activated against myelin.

    • Activated T cells release inflammatory cytokines and activate other immune cells.

  • 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.


  • Sex (female > male)

  • Geographical location

  • Genetic factors

  • Low vitamin D3 levels

  • Smoking

  • Infections


  • Primary symptoms/signs

    • Direct consequence of conduction disturbances produced by demyelination and axonal damage, and reflect the area of the CNS that is damaged.

      • Visual complaints/optic neuritis

      • Gait problems and falls

      • Paresthesias

      • Pain

      • Spasticity

      • Weakness

      • Ataxia

      • Speech difficulty

      • Psychological changes

      • Cognitive changes

      • Fatigue

      • Bowel/bladder dysfunction

      • Sexual dysfunction

      • Tremor

  • Secondary symptoms

    • Complications resulting from primary symptoms

      • Recurrent UTIs

      • Urinary calculi

      • Decubiti and osteomyelitis

      • Osteoporosis

      • Respiratory infections

      • Poor nutrition

      • Depression

  • Tertiary symptoms

    • Relate to the effect of the disease on the patient’s everyday life

      • Financial problems

      • Personal/social problems

      • Vocational problems

      • Emotional problems


  • Clinically isolated syndrome (CIS)

    • First clinical presentation of ...

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