What Is It?
Multiple sclerosis (MS) is a chronic, autoimmune, degenerative disorder affecting the central nervous system (CNS), which is made up of the brain, spinal cord, and optic nerves. "Chronic" means that it develops slowly over time; "autoimmune" means that the body's immune system becomes confused about some part of the body it is designed to protect. It attacks that part of the body as if it were a foreign invader. MS affects a person's ability to move, to feel, and to control his or her body functions. A fatty tissue called myelin coats protects the nerve fibers in the CNS. When the myelin sheath is damaged or destroyed in the CNS, either by inflammation, stroke, immune disorders, metabolic disorders, or nutritional deficiencies, scar tissue, or sclerosis, may form in multiple areas of the nerve fibers. As a result, the ability of the nerves to conduct electrical impulses from the brain to the rest of the body is impaired, and a wide variety of symptoms may appear.
Description:
Nerve messages consist of electrical impulses that travel through the body by means of nerve cells. Nerve cells are also called neurons. Neurons are covered by a thin layer of tissue known as myelin sheath that acts as an insulator. It prevents the electrical currents that pass through neurons from leaking away. MS occurs when the myelin sheath that surrounds neurons in the brain and spinal cord is destroyed. The loss of myelin sheath causes electrical impulses to pass through neurons more slowly. Over time, scar tissue forms around the damaged myelin sheath. This scar tissue, called plaque, also reduces the neurons' ability to function normally. Damage to myelin sheath can cause a variety of symptoms (Gale 2007). A person may lose the ability to use his or her senses, such as touch and vision. Loss of muscular control also occurs because movement of muscles is controlled by nerves. A person with MS may have problems with balance, strength, and coordination. MS affects more than 250,000 people in the United States. Most people experience their first symptoms between the ages of twenty and forty. Symptoms rarely begin before the age of fifteen or after sixty. Women are twice as likely to get MS as men, especially in their early years. MS is more common among some ethnic groups than others. For example, the disease is more common in North America and northern Europe than in other parts of the world. MS is very rare among Asians, Indians of North and South America, and Eskimos (2007).
The four forms of MS are relapsing-remitting, primary-progressive, secondary-progressive, and progressive-relapsing. Each of these patterns may be mild, moderate, or severe. At initial diagnosis, the most common form of MS is relapsing-remitting, occurring in approximately 85% of those with the disease. Individuals with this form of MS experience clearly defined flare-ups (also called relapses, attacks, or exacerbations). There are episodes of acute worsening neurological function, followed by partial or complete periods of recovery (remission) that are free of disease progression. The primary-progressive form of MS is relatively rare, occurring in approximately 10% of patients. People with this type of MS experience a slow but nearly continuous worsening of their disease from the time of disease onset, and have no clear relapses or remissions. There are, however, variations in rates of progression over time, occasional plateaus, and temporary minor improvements. About 50% of people with relapsing-remitting MS develop secondary-progressive MS within 10 years of their initial diagnosis and before the introduction of disease-modifying drugs (2010). Long-term data are not yet available to demonstrate if this form of MS is significantly delayed by treatment. People with secondary-progressive MS experience an initial period of relapsing-remitting disease, followed by a steadily worsening disease course that may or may not be accompanied by occasional flare-ups, minor remissions, or plateaus. The progressive-relapsing form of MS is relatively rare, occurring in approximately 5% of patients. People with this form of MS experience a steadily worsening disease from the onset, but also have clear acute relapses, with or without recovery. As opposed to relapsing-remitting MS, the disease continues to progress between periods of relapse.
Symptoms:
Multiple sclerosis symptoms often progress gradually and vary in intensity and predictability because different areas of myelin are attacked in each person. Each attack produces different symptoms, and new areas of the nervous system are affected. There is usually an increasing progression of symptoms, with episodes lasting days, weeks, or months, alternating with disease-free periods of remission. The disease may progress, however, without any periods of remission. Multiple sclerosis can develop in one of three patterns. The most common pattern is called relapsing-remitting. In this pattern, symptoms appear and then disappear. A person may feel fine for a while and then experience the symptoms of MS for a period of twenty-four hours or more (2007). Then the symptoms disappear again for a span of time. That span may be as long as a year or more at the beginning of the disease. But the span grows shorter as the person becomes older. This pattern is especially common in younger people with MS. Primary progressive is a second pattern in which the disease simply gets worse over time. A person may have brief periods when the disease does not get worse, but these are rare. The primary progressive pattern is more common in older people. The secondary progressive pattern is a combination of the first two patterns. A patient first goes through a period of relapsing and remitting. Eventually, however, the disease just continues to get worse, as in the primary progressive pattern. Some common symptoms include:
Description:
Nerve messages consist of electrical impulses that travel through the body by means of nerve cells. Nerve cells are also called neurons. Neurons are covered by a thin layer of tissue known as myelin sheath that acts as an insulator. It prevents the electrical currents that pass through neurons from leaking away. MS occurs when the myelin sheath that surrounds neurons in the brain and spinal cord is destroyed. The loss of myelin sheath causes electrical impulses to pass through neurons more slowly. Over time, scar tissue forms around the damaged myelin sheath. This scar tissue, called plaque, also reduces the neurons' ability to function normally. Damage to myelin sheath can cause a variety of symptoms (Gale 2007). A person may lose the ability to use his or her senses, such as touch and vision. Loss of muscular control also occurs because movement of muscles is controlled by nerves. A person with MS may have problems with balance, strength, and coordination. MS affects more than 250,000 people in the United States. Most people experience their first symptoms between the ages of twenty and forty. Symptoms rarely begin before the age of fifteen or after sixty. Women are twice as likely to get MS as men, especially in their early years. MS is more common among some ethnic groups than others. For example, the disease is more common in North America and northern Europe than in other parts of the world. MS is very rare among Asians, Indians of North and South America, and Eskimos (2007).
The four forms of MS are relapsing-remitting, primary-progressive, secondary-progressive, and progressive-relapsing. Each of these patterns may be mild, moderate, or severe. At initial diagnosis, the most common form of MS is relapsing-remitting, occurring in approximately 85% of those with the disease. Individuals with this form of MS experience clearly defined flare-ups (also called relapses, attacks, or exacerbations). There are episodes of acute worsening neurological function, followed by partial or complete periods of recovery (remission) that are free of disease progression. The primary-progressive form of MS is relatively rare, occurring in approximately 10% of patients. People with this type of MS experience a slow but nearly continuous worsening of their disease from the time of disease onset, and have no clear relapses or remissions. There are, however, variations in rates of progression over time, occasional plateaus, and temporary minor improvements. About 50% of people with relapsing-remitting MS develop secondary-progressive MS within 10 years of their initial diagnosis and before the introduction of disease-modifying drugs (2010). Long-term data are not yet available to demonstrate if this form of MS is significantly delayed by treatment. People with secondary-progressive MS experience an initial period of relapsing-remitting disease, followed by a steadily worsening disease course that may or may not be accompanied by occasional flare-ups, minor remissions, or plateaus. The progressive-relapsing form of MS is relatively rare, occurring in approximately 5% of patients. People with this form of MS experience a steadily worsening disease from the onset, but also have clear acute relapses, with or without recovery. As opposed to relapsing-remitting MS, the disease continues to progress between periods of relapse.
Symptoms:
Multiple sclerosis symptoms often progress gradually and vary in intensity and predictability because different areas of myelin are attacked in each person. Each attack produces different symptoms, and new areas of the nervous system are affected. There is usually an increasing progression of symptoms, with episodes lasting days, weeks, or months, alternating with disease-free periods of remission. The disease may progress, however, without any periods of remission. Multiple sclerosis can develop in one of three patterns. The most common pattern is called relapsing-remitting. In this pattern, symptoms appear and then disappear. A person may feel fine for a while and then experience the symptoms of MS for a period of twenty-four hours or more (2007). Then the symptoms disappear again for a span of time. That span may be as long as a year or more at the beginning of the disease. But the span grows shorter as the person becomes older. This pattern is especially common in younger people with MS. Primary progressive is a second pattern in which the disease simply gets worse over time. A person may have brief periods when the disease does not get worse, but these are rare. The primary progressive pattern is more common in older people. The secondary progressive pattern is a combination of the first two patterns. A patient first goes through a period of relapsing and remitting. Eventually, however, the disease just continues to get worse, as in the primary progressive pattern. Some common symptoms include:
- Muscle weakness, causing difficulty in walking
- Loss of coordination or balance
- Numbness, feelings of "pins and needles," or other abnormal sensations
- Problems with vision, including blurred or double vision
- Fatigue
- Pain
- Tremors (shaking)
- Loss of bladder or bowl control
Upper right is a magnified view of the spinal cord showing individual nerve fibers. Lower right is a magnified view of an axon within one of the nerve fibers which is covered with a protective myelin sheath (grey). In MS, patches of the myelin sheath are destroyed; these patches are known as plaques (black). The affected nerve fibers cannot conduct nerve impulses properly, so body functions such as movement and sensation are lost (Gale 2011).
What Causes It?
As I mentioned earlier, multiple sclerosis is an autoimmune disease in which the immune system begins to attack myelin sheath. It "decides" that the myelin sheath is a foreign substance that threatens the body and must be destroyed. Researchers do not know why this happens. As myelin sheath is destroyed, neurons no longer function normally. Brain neurons cannot receive and process information from the outside world. Neurons in the brain and the spinal cord cannot send messages to other parts of the body. Normal muscular functions, such as standing, walking, lifting, and turning, become difficult or impossible. The progress of MS seems to depend on the appearance of new plaques. These plaques slow down nerve messages and worsen the symptoms of the disease. Scientists do not understand how, where, and why plaques develop. For that reason, they cannot predict how the disease will progress in any one person over time (2007). Finding the reason for a body's autoimmune reaction to myelin sheath is a major field of research. So far, no final answer has been found. Some possible factors leading to this condition are a person's heredity or their genes, environmental factors, viruses, or a combination of these factors. The reason that heredity is considered a possible factor is that MS seems do run in some families. A person who has a family member with MS is more likely to develop the disease than someone whose family has no history of MS. In addition, the tendency of some ethnic groups to contract or get the disease suggests a hereditary factor.
Genetically, MS is a complex disease that is neither strictly dominant, recessive, nor sex-linked. Discovering the genes involved in MS requires careful scanning of the entire genome (the entire genetic composition of an organism) of patients and their relatives to identify small chromosomal regions linked to the disease. Once they are discovered, these genomic segments are examined in detail to determine the specific location (locus) and characteristics of the MS-associated genes. Studies have identified approximately 60 genomic regions that may be involved in MS, with 13 common regions harboring disease susceptibility, supporting the view that multiple genes are involved in this disorder. Seven of those were recently confirmed. This study, in combination with results from teams in Canada, Finland, and England, generated the first MS genetic map. These studies have sparked a global effort to search for the cause of MS susceptibility. A second-generation genome screen is near completion. Further work is needed to identify the complete list of MS loci (locations) and to map the complete set of MS-associated genes. Getting down to the cellular level, the HLA-DRB1 gene on chromosome 6p21 is the strongest genetic factor identified as influencing MS susceptibility. The association of MS with HLA genes, specifically the DRB1∗1501 allele, has been a consistent finding across nearly all populations, according to Dr. Stephen Hauser and Dr. Jorge Oksenberg (2006). The HLA-DRB1 gene plays a central role in the immune system by presenting peptides derived from extracellular proteins. More than 100 diseases have been associated with different alleles of HLA genes. In general, HLA genes have many possible variations, allowing each person's immune system to react to a wide range of foreign invaders. Some HLA genes have hundreds of identified versions (alleles), each of which is given a particular number.
Genetically, MS is a complex disease that is neither strictly dominant, recessive, nor sex-linked. Discovering the genes involved in MS requires careful scanning of the entire genome (the entire genetic composition of an organism) of patients and their relatives to identify small chromosomal regions linked to the disease. Once they are discovered, these genomic segments are examined in detail to determine the specific location (locus) and characteristics of the MS-associated genes. Studies have identified approximately 60 genomic regions that may be involved in MS, with 13 common regions harboring disease susceptibility, supporting the view that multiple genes are involved in this disorder. Seven of those were recently confirmed. This study, in combination with results from teams in Canada, Finland, and England, generated the first MS genetic map. These studies have sparked a global effort to search for the cause of MS susceptibility. A second-generation genome screen is near completion. Further work is needed to identify the complete list of MS loci (locations) and to map the complete set of MS-associated genes. Getting down to the cellular level, the HLA-DRB1 gene on chromosome 6p21 is the strongest genetic factor identified as influencing MS susceptibility. The association of MS with HLA genes, specifically the DRB1∗1501 allele, has been a consistent finding across nearly all populations, according to Dr. Stephen Hauser and Dr. Jorge Oksenberg (2006). The HLA-DRB1 gene plays a central role in the immune system by presenting peptides derived from extracellular proteins. More than 100 diseases have been associated with different alleles of HLA genes. In general, HLA genes have many possible variations, allowing each person's immune system to react to a wide range of foreign invaders. Some HLA genes have hundreds of identified versions (alleles), each of which is given a particular number.
Lane Phalen, author of The New Book Lover's Guide and a multiple sclerosis sufferer, with her service dog. The dog helps her with daily activities that have become difficult because of MS such as standing up by herself and walking around (Gale 2010).
How Do We Fix It?
Treatment:There is no cure for MS. Nevertheless, there are numerous drug and nondrug therapies available to manage and treat the symptoms of the disease. It is standard practice to wait until a person has experienced two or more MS attacks before initiating drug treatment. Studies indicate that initiating treatment in the early stages of the disease may lesson damage to the CNS and potentially slow disease progression. The type of treatment a patient receives is based on a wide variety of factors, including the course and severity of disease. Six disease-modifying drugs have been approved by the U.S. Food and Drug Administration (FDA) for use in people with MS. The drugs approved for relapsing-remitting MS include interferon beta-1a (Avonex, Rebif), interferon beta-1b (Betaseron), and glatiramer acetate (Copaxone) (2010). These drugs, which are injected either under the skin or into the muscle, reduce the number and severity of attacks, and some may slow the onset of disability. Interferons are naturally occurring proteins that fight invading viruses. Although the mechanism of action of these drugs is not fully understood in MS, the drugs appear to protect the CNS from the body’s attack of its own immune system. Glatiramer acetate is a synthetic compound made from substances found in myelin sheath, and is thought to help alter the body’s immune system.
Moreover, physical therapy is important in treating MS. It helps the patient strengthen and retrain affected muscles, maintain range of motion to prevent muscle stiffening, learn to use assistive devices such as canes and walkers, and learn safer and more energy-efficient ways of moving and sitting. A program of physical therapy usually includes exercise and stretching. These activities can be taught and practiced at home. Swimming is often recommended. It provides a way for a patient to get exercise without becoming overheated. Treatment programs usually include occupational therapy as well. People with MS are taught how to deal with daily activities, such as dressing, feeding, and washing. The occupational therapist can make suggestions for arranging the home and work environment so that an MS patient can function more safely and efficiently (2010). Spasticity can be treated with drugs as well. Baclofen and Diazepam are given by mouth, while botulin toxin (Botox) is given by injection. These drugs can help relieve the pain caused by spasticity. Back pain can be treated with over-the-counter pain relievers, such as aspirin or acetaminophen (Tylenol), or with physical therapy.
Theoretical Cure:
Theoretically speaking, along with drugs and vitamins, there may as well be a way to “cure” multiple sclerosis. It has been theorized by a few that a cause of MS is due to the buildup of iron in the main blood passages in the brain. This theory led me to hypothesize this: iron builds up in the brain, blocking and damaging these crucial blood vessels. As the vessels rupture, they allow both the iron itself, and immune cells from the bloodstream, to cross the blood-brain barrier into the cerebro-spinal fluid. Once the immune cells have direct access to the immune system, they begin to attack the myelin sheathing of the cerebral nerves, and thus multiple sclerosis develops. Only a theory, of course, a possible way of getting rid of this disease may be to clear the passages within the brain with some sort of a mechanism, for example, a catheter that would pass air to de-clog the passages. Other than this, there is always genetic engineering in which you would have to take out the infected gene, in this case the HLA-DRB1 gene, and replace it with a well, functioning one so that this gene wouldn’t cause multiple sclerosis.
Moreover, physical therapy is important in treating MS. It helps the patient strengthen and retrain affected muscles, maintain range of motion to prevent muscle stiffening, learn to use assistive devices such as canes and walkers, and learn safer and more energy-efficient ways of moving and sitting. A program of physical therapy usually includes exercise and stretching. These activities can be taught and practiced at home. Swimming is often recommended. It provides a way for a patient to get exercise without becoming overheated. Treatment programs usually include occupational therapy as well. People with MS are taught how to deal with daily activities, such as dressing, feeding, and washing. The occupational therapist can make suggestions for arranging the home and work environment so that an MS patient can function more safely and efficiently (2010). Spasticity can be treated with drugs as well. Baclofen and Diazepam are given by mouth, while botulin toxin (Botox) is given by injection. These drugs can help relieve the pain caused by spasticity. Back pain can be treated with over-the-counter pain relievers, such as aspirin or acetaminophen (Tylenol), or with physical therapy.
Theoretical Cure:
Theoretically speaking, along with drugs and vitamins, there may as well be a way to “cure” multiple sclerosis. It has been theorized by a few that a cause of MS is due to the buildup of iron in the main blood passages in the brain. This theory led me to hypothesize this: iron builds up in the brain, blocking and damaging these crucial blood vessels. As the vessels rupture, they allow both the iron itself, and immune cells from the bloodstream, to cross the blood-brain barrier into the cerebro-spinal fluid. Once the immune cells have direct access to the immune system, they begin to attack the myelin sheathing of the cerebral nerves, and thus multiple sclerosis develops. Only a theory, of course, a possible way of getting rid of this disease may be to clear the passages within the brain with some sort of a mechanism, for example, a catheter that would pass air to de-clog the passages. Other than this, there is always genetic engineering in which you would have to take out the infected gene, in this case the HLA-DRB1 gene, and replace it with a well, functioning one so that this gene wouldn’t cause multiple sclerosis.