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Chapter 31: Multiple Sclerosis

Sarah Rajkovic; Jacquelyn L. Bainbridge

LEARNING OBJECTIVES

LEARNING OBJECTIVES

Upon completion of the chapter, the reader will be able to:

  1. Identify risk factors for multiple sclerosis (MS).

  2. Distinguish between phenotypes of MS based on patient presentation and disease course.

  3. Compare and contrast choice of disease-modifying therapies (DMT) for a given patient.

  4. Determine appropriate symptomatic treatment options for a given patient.

  5. Develop a monitoring plan for a patient initiated on a specific DMT.

INTRODUCTION

Multiple sclerosis (MS) is an inflammatory disease of the central nervous system (CNS) characterized by myelin destruction and axonal damage. Multiple describes the numerous CNS lesions that accrue over time, and sclerosis refers to the demyelination of lesions, also called plaques.

EPIDEMIOLOGY AND ETIOLOGY

Epidemiology

MS is the most common progressive neurologic disease, affecting approximately 2.3 million people worldwide.1 Diagnosis usually occurs between 20 and 50 years of age, impacting at least twice as many women as men.1 People of northern European ancestry are more likely to develop MS and the geographical risk increases with increasing distance (north or south) from the equator.2

Etiology

The cause of MS is unknown, but may be due to a combination of genetic, environmental, immunologic, or infectious factors. Genetic risks may explain up to 35% of cases.2 Environmental theories involve infectious exposures (eg, Epstein–Barr Virus), decreased patient or maternal vitamin D serum concentrations, tobacco use, residence at high latitude, and childhood obesity.2,3

PATHOPHYSIOLOGY

While the causative agent of MS is unclear, the result is the development of an autoimmune disorder with areas of CNS inflammation and degeneration.

Inflammation

An unknown antigen presented by the major histocompatibility complex (MHC) class II molecules causes T cells to become autoreactive (Figure 31–1). Autoreactive T cells enter lymphatic tissues to expand. Upon a signal involving sphingosine-1-phosphate, T cells reenter the circulation.4 Once activated, T cells cause blood–brain barrier breakdown and enter the CNS. These T cells come into contact with antigen-presenting cells (APCs) and proliferate and differentiate. Th1 cells secrete cytokines that enhance macrophage and microglial cells that attack myelin.4

FIGURE 31–1.

Autoimmune theory of the pathogenesis of multiple sclerosis (MS). In MS, the immunogenic cells tend to be more myelin reactive, and these T cells produce cytokines mimicking a Th1-mediated proinflammatory reaction. T-helper cells (CD4+) appear to be key initiators of myelin destruction in MS. These autoreactive CD4+ cells, especially of the T-helper cell type 1 (Th1) subtype, are activated in the periphery, perhaps following a viral infection. The activation of T and B cells requires two signals. The first signal is the interaction between MHC and APC (macrophage, dendritic cell, and B cell). The second signal consists of ...

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