Multiple Sclerosis: A Therapeutic Overview

Mark H. J. Litzinger, BSc, BSc Pharm, RPh; Monica Litzinger, BSc, BSc Pharm, RPh

Disclosures

US Pharmacist. 2009;34(1):HS3-HS9. 

In This Article

Epidemiology and Pathophysiology

According to the National Multiple Sclerosis Society, there are almost 400,000 diagnosed cases in the United States, yet the numbers may be higher due to patients having mild symptoms and seeking no treatment.[6] Typically, MS begins early in adulthood, with the onset of symptoms at age 28 years and diagnosis at 33 years. Women are two times more likely to be diagnosed with MS. Caucasians have the highest incidence of MS, whereas persons of Japanese decent have the lowest. Geographical mapping has shown concentrated areas of increased risk for the development of MS. However, no concrete data have been shown as to why certain regions have a higher incidence of MS, although genetic susceptibility and ethnic migratory patterns are likely involved.

Although the pathogenesis of MS is still unknown, viral and autoimmune hypotheses lead the numerous theories as to its cause.[7] These hypotheses include immune system malfunction, environmental factors, genetics, susceptible blood-brain barrier (BBB), diet, vitamin deficiencies, and allergic reactions.[7] The common thread in all hypotheses is the resulting inflammatory response and sclerosis of the neuron. T-cells (CD4+ or CD8+) can produce inflammatory demyelination of the CNS,[8] and myelin specific CD8+ T-cells are more abundant in patients with relapsing-remitting MS (RRMS).[7] MS is also thought to be mediated by helper T-cells type 1 that produce interferon-gamma and other pro inflammatory cytokines.[9]

During a relapse, patients with MS experience an inflammatory response in which the myelin of the nerve cell gets stripped, otherwise known as demyelination.[10,11] The inflammation also damages the axonal membrane, thus inhibiting the action potential along the nerve from the brain to the spinal cord. In addition, the inflammatory response damages the oligodendrocytes, which are the myelin-producing cells within the CNS. Researchers are now asking whether oligodendrocyte death causes inflammation, or if inflammation causes oligodendrocyte death. MS remission is characterized by a reduction in the inflammatory response and subsequent healing. The demyelinated axon increases sodium channels, which are integral in sending the action potential down the neuron. Since the CNS is a "plastic" organ, it can develop new neuronal pathways around the damaged neurons; however, this is not a speedy process. Oligodendrocytes sponsor remyelination, although axons do not function as well theoretically, and patients may not notice they have had a relapse. However, remyelination may not take place, resulting in a dysfunctional nerve, and the function of the underlying axon may become permanently lost. This lost myelin can be replaced with scar tissue, hence the name multiple (many) sclerosis (scar-forming).

There are four types of MS: RRMS, secondary progressive MS (SPMS), primary progressive MS (PPMS), and progressive-relapsing MS (PRMS) (Figure 1).[12] Approximately 80% of patients with MS have RRMS, which is characterized by episodes of symptoms (relapse) followed by the absence of symptoms (remission). Symptoms may evolve over days and disappear, although this varies between patients, and relapse appears approximately every two years. SPMS occurs as a result of RRMS developing into a progressive state. In this case, the patient previously would have been diagnosed with RRMS, but is now presenting with fewer relapses, with continual progression of neurologic symptoms. PPMS occurs when the patient's symptoms steadily increase proportional with time, and there are no episodes of relapse or remission. This form of MS has short periods where symptoms stabilize or improve slightly. The rarest form of MS is PRMS, which is expressed as gradual worsening with superimposed relapse/remission episodes.

Figure 1.

The four types of multiple sclerosis.
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