Multiple Sclerosis Treatment Drugs and Side Effects
What Is Multiple Sclerosis?
Multiple sclerosis (MS) can be thought of as an inflammatory process involving different areas of the central nervous system (CNS) at various points in time.
What Causes This Disease?
The cause of multiple sclerosis is not known. Both environmental and genetic factors are thought to predispose a person to develop the disease.
Multiple sclerosis results in the destruction of the myelin that surrounds the nerves of the CNS. Myelin is a fatty substance that insulates the nerves and allows them to transmit information to and from the brain. If the myelin is damaged, the transmitted information is not only delayed but also may be misinterpreted by the brain. The myelin destruction, also known as demyelination, is thought to be caused by the body's immune cells entering the CNS. The disruption of the normal barrier to the entry of these cells, termed the blood-brain barrier, leads to local swelling (known as edema). Also damaged are the nerve cell bodies (termed neuronal loss) or their prolongations (termed axonal loss). A plaque (area of inflammation, demyelination, axonal loss, edema or scarring) represents a typical multiple sclerosis lesion, or area of injury.
What initially triggers the immune system attack is not known. Microglia are cells in the CNS that take up fragments of myelin and present these fragments to the immune cells. In healthy individuals, this presentation of myelin fragments is not thought to trigger the immune cells to attack the CNS. In people with multiple sclerosis, this presentation of myelin fragments may trigger an exaggerated response by immune cells that leads to the formation of plaques around the blood vessels in the CNS.
What Are the Signs and Symptoms?
Perhaps the most common symptom of MS is sensory disturbance, which manifests as tingling or numbness sensations, throughout the body.
Visual disturbances are also among the most common symptoms and:
- Blurred or hazy vision
- Color perception alteration
Vision loss may occur because of the development of optic neuritis (inflammation of the optic nerve). In a typical case of optic neuritis, the person with multiple sclerosis experiences ocular pain with eye movement.
Other common symptoms include:
- Loss of balance and fine motor skills
- Facial pain or weakness
- Vertigo (a spinning sensation)
- Limb weakness or paralysis
- Impaired control of bladder or bowel function
- Memory loss
Individuals with advanced disease lose the ability to walk and may become bedridden, requiring assistance with most activities.
Is There a Cure for MS?
No, currently there is no vaccine or treatment cure for multiple sclerosis.
What Drugs Treat the Symptoms?
Several medications are now available to decrease the number of attacks (periods of relapse) of multiple sclerosis or delay the progression of physical disability.
Your doctor or health care professional my prescribe medications and other therapies to treat general symptoms associated with the disease, such as depression, muscle spasms, fatigue, bladder problems, tremors (shakiness), poor coordination, and sexual dysfunction.
Interferons and glatiramer acetate (Capaxone)
Interferon beta-1a (Avonex, Rebif), interferon beta-1b (Betaseron), and glatiramer acetate (Copaxone), are examples of immune-modifying drugs used for MS.
Generally, these medications tend to decrease the frequency of attacks in patients with mild-to-moderate relapsing remitting MS (RRMS) by 18% to 33%. The rate of new lesions that appear on magnetic resonance imaging (MRI) is also reduced by approximately one-third. With the interferon drugs, the effectiveness is directly related to the dose (higher doses of IFN, if tolerated, are generally more effective). Whether the delay in the onset of new attacks by these drugs ultimately has a long-term impact on the disability associated with multiple sclerosis is controversial. However, clinical trials suggest that patients receiving early treatment have a beneficial impact on relapses and disability that may not be matched by patients in whom the treatment is delayed. Research regarding this continues.
The ability to respond to long-term interferon beta-1a and beta-1b may be limited, in some patients, by the development of persistent, high titer neutralizing antibodies. Patients treated with glatiramer also eventually develop antibodies, but these antibodies do not seem to limit glatiramer's activity.
Last Reviewed 9/11/2017
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