Multiple sclerosis

Multiple sclerosis ( MS), also known as disseminated sclerosis or encephalomyelitis disseminata is an inflammatory disease in which the fatty myelin sheaths around the axons of the brain and spinal cord are damaged, leading to demyelination and scarring as well as a broad spectrum of signs and symptoms. Disease onset usually occurs in young adults, and it is more common in women.
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Multiple sclerosis is an autoimmune disease that affects the brain and spinal cord (central nervous system).


An autoimmune disorder is a condition that occurs when the immune system mistakenly attacks and destroys healthy body tissue. There are more than 80 different types of autoimmune disorders.

Causes, incidence, and risk factors

Multiple sclerosis (MS) affects women more than men. The disorder is most commonly diagnosed between ages 20 and 40, but can be seen at any age.

MS is caused by damage to the myelin sheath, the protective covering that surrounds nerve cells. When this nerve covering is damaged, nerve impulses are slowed down or stopped.

The nerve damage is caused by inflammation. Inflammation occurs when the body's own immune cells attack the nervous system. Repeated episodes of inflammation can occur along any area of the brain, optic nerve, and spinal cord.

Researchers are not sure what triggers the inflammation. The most common theories point to a virus or genetic defect, or a combination of both. Geographic studies indicate there may be an environmental factor involved.

People with a family history of MS and those who live in a geographical area where MS is more common have a slightly higher risk of the disease.

Symptoms

Symptoms vary, because the location and severity of each attack can be different. Episodes can last for days, weeks, or months. These episodes alternate with periods of reduced or no symptoms (remissions).

Fever, hot baths, sun exposure, and stress can trigger or worsen attacks.

It is common for the disease to return (relapse). However, the disease may continue to get worse without periods of remission.

Because nerves in any part of the brain or spinal cord may be damaged, patients with multiple sclerosis can have symptoms in many parts of the body.

Muscle symptoms:

• Loss of balance
• Muscle spasms
• Numbness or abnormal sensation in any area
• Problems moving arms or legs
• Problems walking
• Problems with coordination and making small movements
• Tremor in one or more arms or legs
• Weakness in one or more arms or legs

Bowel and bladder symptoms:

• Constipation and stool leakage
• Difficulty beginning to urinate
• Frequent need to urinate
• Strong urge to urinate
• Urine leakage (incontinence)

Eye symptoms:

• Double vision
• Eye discomfort
• Uncontrollable rapid eye movements
• Vision loss (usually affects one eye at a time)

Numbness, tingling, or pain

• Facial pain
• Painful muscle spasms
• Tingling, crawling, or burning feeling in the arms and legs

Other brain and nerve symptoms:

• Decreased attention span, poor judgment, and memory loss
• Difficulty reasoning and solving problems
• Depression or feelings of sadness
• Dizziness and balance problems
• Hearing loss

Sexual symptoms:

• Problems with erections
• Problems with vaginal lubrication

Speech and swallowing symptoms:

• Slurred or difficult-to-understand speech
• Trouble chewing and swallowing

Fatigue is a common and bothersome symptoms as MS progresses. It is often worse in the late afternoon.

TREATMENT:

Dalfampridine is a broad spectrum potassium channel blocker. In animal studies, dalfampridine has been shown to increase conduction of action potentials in demyelinated axons through inhibition of potassium channels.

Fingolimod is metabolized by sphingosine kinase to the active metabolite, fingolimod-phosphate. Fingolimod-phosphate is a sphingosine 1-phosphate receptor modulator, and binds with high affinity to sphingosine 1-phosphate receptors 1, 3, 4, and 5. Fingolimod-phosphate blocks the capacity of lymphocytes to egress from lymph nodes, reducing the number of lymphocytes in peripheral blood. The mechanism by which fingolimod exerts therapeutic effects in multiple sclerosis is unknown, but may involve reduction of lymphocyte migration into the central nervous system.

Glatiramer acetate is an immunomodulator believed to induce glatiramer acetate-specific suppressor T cells to inhibit the autoimmune response to myelin in the treatment of multiple sclerosis (MS).

Interferons, produced in response to viral infections and other biological agents, exert their effects through suppression of cell proliferation, increased phagocytic activity of macrophages and cytotoxicity of lymphocytes, and inhibition of viral replication in virus-infected cells. The binding of interferons to specific cell surface receptors induces the expression of interferon-induced gene products and markers (eg, neopterin, 2,5-oligoadenylate synthetase, ß2-microglobulin, and IL-10) that may be involved in some of these immunomodulatory effects. Beta interferons exert additional effects: interferon beta-1a inhibits the release of proinflammatory cytokines (eg, IFN-gamma , IL-1, IL-6, TNF-α, and TNF-β); interferon beta-1b suppresses T lymphocyte proliferation and inhibits their movement into the CNS, promotes suppressor T-cell activity, reduces antigen presentation, and decreases the synthesis of pro-inflammatory cytokines.

Natalizumab binds to the α4-subunit of α4β1 and α4β7 integrins expressed on the surface of all leukocytes except neutrophils, and inhibits the α4-mediated adhesion of leukocytes to their counter-receptor(s). The clinical effect of natalizumab in multiple sclerosis may be secondary to blockade of the molecular interaction of α4β1-integrin expressed by inflammatory cells with VCAM-1 on vascular endothelial cells, and with CS-1 and/or osteopontin expressed by parenchymal cells in the brain.