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Pharmacology for Nurses

11.3 Introduction to Multiple Sclerosis

Pharmacology for Nurses11.3 Introduction to Multiple Sclerosis

Learning Outcomes

By the end of this section, you should be able to:

  • 11.3.1 Describe the pathophysiology of multiple sclerosis.
  • 11.3.2 Identify the clinical manifestations related to multiple sclerosis.
  • 11.3.3 Identify the etiology and diagnostic studies related to multiple sclerosis.

Multiple sclerosis (MS) is a debilitating, inflammatory, immune-mediated condition. According to the National Multiple Sclerosis Society (2023), studies have confirmed that nearly 1 million people are living with MS in the United States. This disease is characterized by a progressive and irreversible demyelination and axonal degeneration of the brain, spinal cord, and optic nerves. Myelin is a protective sheath that acts as an insulator of the electrical signal (see Figure 11.4). It allows rapid conduction of a nerve impulse down the axon. Degeneration of the myelin sheath results in the inability of nerves to conduct electrical impulses. As the myelin deteriorates, oligodendrocytes repair the damage but also form scar tissue called gliotic plaques. These plaques will begin to interfere with electrical impulses traveling through the axon. Over time, the myelin cannot regenerate and nerves eventually wither away. Typically, the client experiences remissions and exacerbations throughout the progression. Sensory and motor deficits become worse as the client ages. The disease is progressive and affects nerves in both the CNS and peripheral nervous system (PNS) (Capriotti, 2020).

Two diagrams show an undamaged nerve cell and a nerve cell with multiple sclerosis. In the undamaged cell, myelin covers the axon and allows the muscle to contract. In the nerve cell with multiple sclerosis, the myelin is damaged and exposes parts of the axion. This results in a muscle being unable to contract.
Figure 11.4 MS causes the protective myelin sheath and axons to degenerate, which negatively affects the transmission of nerve impulses and affects muscle contraction. (attribution: Copyright Rice University, OpenStax, under CC BY 4.0 license)

Special Considerations

Age, Sex, Race/Ethnicity, and Location

  • MS often presents in adults between the ages of 20 and 40 years.
  • It more commonly affects females.
  • It is seen more frequently in White clients than in Hispanic or Black clients.
  • MS more commonly affects individuals who live farther away from the equator.

(Source: Multiple Sclerosis Foundation, 2018)


MS is an autoimmune disorder that occurs when there is a malfunction of the immune system and the body mistakenly attacks its own tissue. In this case, it attacks the myelin sheath of the CNS. The exact cause of MS has not yet been fully determined; however, it is believed a combination of factors are involved. Risk factors include viral infections that theoretically mimic the components of the myelin sheath. The virus most associated with MS is the Epstein-Barr virus, which causes infectious mononucleosis. Other potential risk factors include geographic location, exposure to heavy metals, cigarette smoking (contributes to inflammation), lack of sunlight exposure, and deficient vitamin D levels. It is believed that vitamin D can lower the risk of developing autoimmune disorders because it plays a role in immune function and regulation. Moreover, obesity is a risk factor because it contributes to long-term inflammation. Likewise, family history is shown to contribute to a person’s risk of developing MS. Current research suggests there are numerous genetic variants, most of them correlating with the immune system. Some researchers believe the immune system attacks the CNS because it is simply destroying unhealthy brain cells (National Institute of Neurological Disorders and Stroke, 2023a).


Autoreactive lymphocytes mediate the destruction in MS. T-lymphocytes are sensitized and reactive to protein on the myelin sheath. These overactive immune cells cause inflammation, which begins to damage the myelin. The damage occurs in diffuse patches throughout the CNS. The damage mainly affects the white matter and results in lesions, which are called plaques because they are easily visible on imaging studies. Over time, hardened scar tissue develops at the lesion site, which disrupts the transmission of nerve signals. The scar tissue can slow or even stop nerve impulses altogether. Overall, signals are unable to communicate with the brain to receive information about what the body should do in situations. Other immune involvement includes B lymphocytes, macrophages, and immunoglobulins (IgG and IgM) as well as T-helper and T-regulator cells. The immune cells are believed to release various cytokines, such as interleukins. The blood–brain barrier becomes disrupted and oligodendrocytes, along with axons, are destroyed. The oligodendrocytes that have not been affected are incapable of adequately proliferating; therefore, they are ineffective in repairing the myelin. As the disease progresses, the cerebral cortex of the brain atrophies and scar tissue begins to develop (Capriotti, 2020).


Diagnosis is sometimes delayed because there is no definitive test for MS, and many early clinical manifestations are subtle and correlate with other diagnoses. The first steps toward a diagnosis are a thorough medical history and full neurological examination. An MRI test with contrast is the most sensitive method available to identify areas of demyelination. The response of the CNS to peripheral sensory stimuli can be determined using evoked potential testing—tests that measure electrical activity in response to certain stimuli—for various pathways (visual, auditory, and sensory). Another diagnostic tool is the evaluation of the cerebrospinal fluid (CSF) obtained from a lumbar puncture. Clients with MS have high protein levels, oligoclonal bands (OCBs), IgG/IgM, and T and B lymphocytes in their CSF. Blood tests may be obtained to rule out other conditions that mimic MS or to check for risk factors, such as a vitamin D level (Capriotti, 2020).

Clinical Manifestations

The course of MS is unpredictable. Signs and symptoms vary depending on severity and the specific nerves affected by the plaque. Some clients will have very little disability, whereas others experience a steady decline with increasing disability. Fever, sun exposure, and stress can trigger exacerbations. Characteristic manifestations include:

  • Sensory deficits in extremities and face (numbness and tingling sensation, itching, coldness, paralysis)
    • Some clients experience Lhermitte sign, an electrical shock–like sensation that runs down the back and into the limbs. This mainly occurs when the client bends their head forward.
  • Visual changes (diplopia, nystagmus, unilateral vision loss, abnormal gaze, and pain with eye movement)
    • The most common and earliest symptoms are associated with the eyes.
  • Motor spasticity, weakness, ataxia, and hyperactive reflexes
  • Elimination issues (urgency, incontinence, urinary retention, constipation)
  • Cognitive and mental changes (fatigue, reduced attention span, poor judgment, loss of recent memory, difficulty with abstract reasoning and solving problems—depression and anxiety are very common)
  • Sexual dysfunction (decreased libido, erectile disorder, reduced genital sensation)
  • Brainstem problems (dysarthria, dysphagia, weak cough)
  • Pain (neuropathic pain in extremities, painful muscle spasms)

The most common form of MS is the relapsing-remitting form, which consists of brief episodes of several weeks to 3 months. These episodes are followed by a complete or almost complete return to baseline. The primary-progressive form does not have any remissions or exacerbations. The onset of this form is around age 40. Those with relapsing-remitting form may go on to develop secondary-progressive deterioration that leads to disabilities (Capriotti, 2020; National Institute of Neurological Disorders and Stroke, 2023a). Refer to Table 11.13 for descriptions of the various forms of MS.

Form of MS Description
Clinically isolated syndrome (CIS) Refers to the first episode of MS. Neurological symptoms caused by demyelination and inflammation lasting for at least 24 hours. MRI displays findings consistent with MS.
Relapsing remitting (RRMS) Characterized by clearly defined acute attacks with full recovery. The symptoms experienced are varied and occur every 1–3 years.
Primary progressive (PPMS) Characterized by progression of disability from the onset. There may or may not be occasional plateaus and temporary minor improvements.
Secondary progressive (SPMS) Begins with an initial relapsing-remitting disease course, followed by progression of disability with occasional relapses and minor remissions and plateaus.
Table 11.13 Disease Courses of Multiple Sclerosis (source: Capriotti, 2020)

Pharmacologic Management

There is currently no cure for MS; however, the use of drugs has made a significant difference in the lives of those with MS. Most of the drugs target specific symptoms, reduce relapse rates, and delay progression. In the most common form (relapsing-remitting), early initiation of medications is highly recommended. Several drug classifications are used that work through different mechanisms: corticosteroids can reduce inflammation and speed recovery during acute exacerbations; beta interferons can slow damage; and disease-modifying agents and immunomodulators suppress the immune system to prevent the antibodies from attacking their own cells. Additionally, various components of the immune system are specifically targeted by medications. Some drugs reduce the number of T cells circulating in the periphery; others destroy target B cells or deplete B and T cells; still others prevent leukocyte mobilization to injured tissue. Drugs, such as antispasmodics, antidepressants, and antiepileptics, are prescribed to control symptoms.

Nonpharmacologic Management

Plasmapheresis (removal of abnormal antibodies) can be done for those who do not respond well to drugs. Significant nonpharmacologic management should involve teaching the client coping mechanisms, ensuring support systems are in place, and emphasizing proper nutrition and sufficient rest; the client should be encouraged to incorporate exercise into their daily routine. These actions can promote overall health, which can help the client better deal with symptoms of relapse as well as maintain their quality of life. Finally, physical therapy and occupational therapy can help to maximize functioning in various ways (National Institute of Neurological Disorders and Stroke, 2023a).

Clinical Tip

Treating an Acute Relapse

A short course of a high-dose intravenous (IV) glucocorticoid (e.g., 500–1000 mg of methylprednisolone daily for 3–5 days) is the preferred treatment for an acute episode. These drugs suppress inflammation and can reduce the severity and duration of an attack. When used short-term, these drugs are safe except for a possible elevation of blood glucose levels. In contrast, long-term use (e.g., over 3 weeks) can cause multiple adverse effects in numerous areas of the body, including adrenal insufficiency leading to fluid and electrolyte imbalances, osteoporosis, high risk for infections, myopathy, and psychological disturbances (agitation, anxiety, or irritability).

Acute relapse may also be treated with IV gamma globulin. This option is especially beneficial for clients who are unable to tolerant or respond adequately to glucocorticoids.


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