Multiple sclerosis (MS) is an unpredictable disorder that can cause a variety of symptoms, which for many, can flare-up and then subside over the course of days, months, or even years. While MS is not contagious, its causes are not yet fully understood and researchers continue to search for answers.
MS is most frequently diagnosed in young adults, although individuals of any age may be diagnosed with this neurological condition. People who are not familiar with MS can easily be confused by its name and its unique symptoms. Particularly with today'
s approved treatments and wellness strategies, most individuals with MS are able to live a full and productive life, with much hope for the future.
If you are reading this information for the first time, you may know someone who was recently diagnosed, or perhaps you are experiencing the symptoms of MS but have not yet been diagnosed and want to learn more. While the symptoms vary greatly - from visual changes to numbness, and from bladder issues to fatigue or depression - many individuals may feel relieved to know that early in the disease course, these symptoms are often temporary for the majority of patients.
The fact that symptoms flare-up and subside for many people with multiple sclerosis (MS), combined with the wide variety and unpredictability of symptoms, has made MS a difficult disease to recognize, define, and treat - right from the start. Since the late 1300s, individuals with a progressive illness suggestive of MS have been observed. It wasn't until 1868 that the famous neurologist, Jean-Martin Charcot, lectured on the features of MS and gave it a name.
Jean-Martin Charcot was a french neurologist who defined and gave a name to multiple sclerosis in 1868.
Charcot was a French scientist, instructor, and physician who is claimed by some to be the founder of modern neurology. He lived during the 1800s and Sigmund Freud was among the famous students he inspired. In addition to the many neurological disorders that he defined and treated, he was also known for his treatment of hysteria with hypnotism, which he believed was hereditary and caused by weaknesses in one's neurological system.
Throughout the 1800s and 1900s, hundreds of therapies were tried, without success, in the treatment of multiple sclerosis. Deadly nightshade (a plant with poisonous fruit), arsenic, mercury, and the injection of malaria parasites, are just a few examples of the types of ineffective and even dangerous therapies that were once given to individuals with MS.
In 1951, cortisone (a steroid) was first used to treat MS relapses (also known as exacerbations, attacks, or symptom flare-ups). Cortisone was found to reduce the severity of the relapse and to shorten its duration, but it had no long-term effects on the disease.
The first drug proving to be effective in the long-term treatment of MS received approval in 1993. Ten long-term treatments are now approved for relapsing forms of MS, with many more on the way. These are also referred to as disease-modifying therapies (DMTs). While these medications do not cure MS, they do work to slow disease activity as well as reduce the severity and frequency of flare-ups. Additionally, these DMTs may delay disease progression, delay disability, and increase longevity.
Shown above is an illustration of two nerve cells. The normal one on the left has a healthy nerve fiber, or axon, protected by myelin (insulation covering the nerve), and is able to transmit signals at a very fast speed - similar to electricity traveling along an electrical cord. The ms nerve cell on the right shows damage to the myelin, and as a result, signals do not travel well along the nerve.
Multiple sclerosis (MS) is a disease of the central nervous system (CNS). The CNS consists of the brain, optic nerves and spinal cord. With MS, areas of the CNS become inflamed, damaging the protective covering (known as "myelin") that surrounds and insulates the nerves (known as "axons"). In addition to the myelin, over time, the axons and nerve cells (neurons) within the CNS may also become damaged.
The damage to the protective covering and also to the nerves disrupts the smooth flow of nerve impulses. As a result, messages from the brain and spinal cord going to other parts of the body may be delayed and have trouble reaching their destination - causing the symptoms of MS.
Shown above is an illustration of a nerve cell. The nerve fiber, or axon, when protected by healthy myelin, is able to transmit signals at a very fast speed - similar to electricity traveling along an electrical cord.
When the myelin becomes damaged (as shown in the top illustration), or the nerve itself becomes damaged, signals can no longer travel across the nerve fiber efficiently. As signals slow down or are lost, the body cannot respond appropriately - causing the symptoms of ms.
Areas of inflammation and damage are known as "lesions." The changes in size, number, and location of these lesions may determine the type and severity of symptoms. While individuals with relapsing forms of MS are believed to experience more inflammation than those with progressive forms of MS, lesions still occur for individuals with all forms of MS. However, the lesions in progressive forms of MS may be less active and expand more slowly.
In addition to symptoms, disease activity may be evaluated from changes in the size or number of lesions. Frequently, MS may be "clinically silent," showing no increase in symptoms, yet continuing to show signs of disease activity within the CNS. For individuals with relapsing forms of MS, early and continued treatment with a disease-modifying therapy (DMT) can often slow the "clinically silent" disease activity in the brain, reducing the size and number of active lesions. This is why most neurologists, as well as the American Academy of Neurology, recommend that individuals with relapsing forms of MS begin treatment as soon as possible after the diagnosis is established.
Additionally, areas of thick scar tissue may eventually form along the areas of permanently damaged myelin. These areas of scar tissue are referred to as "plaques." The term "multiple sclerosis" originates from the discovery of these hardened plaques. Multiple refers to "many;" sclerosis refers to "scars."
Lesions and plaques are viewed on a magnetic resonance imaging (MRI) scanner. This technology is used to help diagnose MS and evaluate its progress at various intervals.
Approximately 400,000 individuals have been diagnosed with MS in the United States and as many as two and a half million worldwide, with an estimated 10,000 new cases diagnosed in the United States annually. Most people with MS experience their first symptoms and are diagnosed between the ages of 15 and 50, although individuals of any age may be diagnosed with MS.
The estimate of individuals living in the United States with MS is more of an educated guess from experts in the field, versus an exact number of patients. MS organizations have been advocating for several years to create a national MS registry in the United States, but this has yet to become a reality.
In the meantime, the North American Research Committee on Multiple Sclerosis (NARCOMS) has an MS registry with an active database of more than 35,000 individuals with MS. The benefits of a national registry include the ability to learn about the rate of disease diagnosis, progression, and disability, as well as the success of treatments and the availability of services - to better meet the needs of the MS community. If you are interested in learning more or becoming a part of this registry, please visit narcoms.org.
The distribution of this disease is not totally random. On average, with relapsing forms of MS, women are three times more likely than men to develop this disorder. With the primary-progressive form, genders are more equally divided.
Geographically, people who live farther from the equator (in more temperate climates) have a higher risk of developing MS than people living in hotter areas near the equator, or in very cold areas near the north or south poles. Individuals living beyond the 40-degree mark north or south of the equator are far more likely to develop MS, and this is especially true for people in North America, Europe, and southern Australia.
MS is very rare in Inuit populations (sometimes referred to as Eskimos) living in the far north. Asia continues to have a lower incidence of MS. More prevalent among those of northern European or Scandinavian ancestry, Caucasians have a higher incidence than those of African heritage to develop MS.
In addition to the fact that a lower percentage of African-Americans are diagnosed with MS than White-Americans, other differences have been observed. According to recent studies, on average, African-Americans are slightly older at diagnosis, although these statistics can sometimes conflict. Analysis of NARCOMS data shows that a larger proportion of African-Americans have never seen a neurologist who specializes in MS.
African-Americans tend to have more symptoms at the time of diagnosis, which are usually limited to the optic nerves and spinal cord, and this is termed "opticospinal MS." This means that African-Americans may experience more problems with vision and mobility, versus other common MS symptoms. The disease course tends to be more progressive and responds less to disease-modifying therapies.
A recently published study, however, challenges the existing theories on the prevalence of MS according to race and ethnic background. Appearing in the May 7, 2013 issue of Neurology, the results of this study contradict theories that African-Americans are less prone to MS as compared to Caucasians. The study looked at data from the Kaiser Permanente Southern California health plan (with more than 3.5 million members) from January 1, 2008 to December 31, 2010.
During the timeframe mentioned, 496 individuals were diagnosed with MS. Approximately 70 percent of those diagnosed were women, most of whom were diagnosed with relapsing-remitting MS (RRMS). According to the published results, compared to Caucasians, African-Americans had a 47-percent increased risk of MS, while Hispanics had a 50-percent reduced risk and Asians had an 80-percent reduced risk. The risk of MS was highest for African-American women, whereas the risk of MS for African-American men was lower and about the same as the risk for Caucasian men.
The authors of this study suggest that limitations in earlier studies may have provided inaccurate figures as to the proportion of individuals diagnosed with MS within the different ethnic populations, along with other factors such as misdiagnosis and inadequate medical care. The authors present several possible theories for the results of this study, but in general, explain that their findings "indicate that MS risk is determined by complex interactions among race/ethnicity, sex, environmental factors, and likely genotype." More studies are needed to confirm the risk of MS among different ethnic populations.
With the help of NARCOMS data, research reveals that Latinos are usually diagnosed at a younger age than both African-American as well as White-American individuals. They tend to have fewer mobility and bladder/bowel problems compared to White-Americans, but may experience more depression. Additionally, research has indicated that fewer Latinos receive access to services to address mental health needs. The same is true for much-needed rehabilitation from specialists in MS, where fewer Latinos are able to access adequate services.
While MS is not contagious or hereditary, MS susceptibility is increased if a family member has MS. The average risk of developing MS in the United States is one in 1,000, or one tenth of one percent. For first-degree relatives (such as a child or sibling), the risk increases to three or four percent. This is not true for adopted children or half siblings (who do not share the same parent who has MS), whose risk is the same as unrelated individuals.
In situations where one identical twin has been diagnosed with MS, the other twin has a 31-percent risk of developing the disease. (If MS was strictly hereditary, when one identical twin has MS, the other identical twin would have a 100-percent risk of getting MS.) The risk for twins who are not identical is five percent - similar to that of other siblings.
Another factor linked to MS is cigarette smoking. Women who smoke are 1.6 times more likely to develop MS than women who are non-smokers. Individuals with MS who smoke also appear to be at a much greater risk of experiencing a more rapid progression of their disease.
Vitamin D as well as exposure to sunlight (both discussed under Possible Causes of MS), appear to reduce the risk of developing MS. The Nurses' Health Studies (I & II) found that women who were taking 400 IU or more of vitamin D daily had a lower risk of developing MS. Also, populations exposed to greater amounts of sunshine or ultraviolet radiation had lower rates of MS.
Parasites are another possible risk factor in the development of MS. Research has found that parasites can modulate the immune system and dampen its responses. People who have parasites are less likely to be diagnosed with MS, and as conditions in different countries become cleaner - with fewer parasites - the number of individuals being diagnosed is increasing in these parts of the world.
The most common types of MS are: relapsing-remitting MS (RRMS); secondary-progressive MS (SPMS); primary-progressive MS (PPMS); and progressive-relapsing MS (PRMS)
Uncommon types of MS include benign MS and fulminate MS
Prior to an MS diagnosis, individuals with "possible MS" may have clinically isolated syndrome (CIS) or radiologically isolated syndrome (RIS)
Multiple sclerosis (MS) affects each person differently.
The most common types of MS are:
Relapsing-Remitting MS (RRMS)
Secondary-Progressive MS (SPMS)
Primary-Progressive MS (PPMS)
Progressive-Relapsing MS (PRMS)
These charts appear in the publication, Primary Progressive Multiple Sclerosis: What You Need to Know, jointly published by MSAA and NMSS.
Initially, most people with MS experience symptom flare-ups, which are also known as relapses, exacerbations, or attacks. When someone experiences a relapse, he or she may be having new symptoms or an increase in existing symptoms. These usually persist for a short period of time (from a few days to a few months) and afterward may remain symptom-free for periods of months or years. This type of MS is referred to as relapsing-remitting MS (RRMS). Approximately 80 to 85 percent of MS patients are initially diagnosed with this form of the disease.
Over time, RRMS may advance to secondary-progressive MS (SPMS). This form of MS does not have the dramatic variations in symptoms that RRMS does, but rather has a slow, steady progression - with or without relapses. If relapses do occur, they usually do not fully remit.
Without treatment, approximately half of individuals with RRMS convert to SPMS within 10 years. However, with the introduction of long-term disease-modifying therapies (DMTs), fewer individuals advance to this latter form of the disease. Since 1993, a total of 10 DMTs have been approved for relapsing forms of MS and are available through prescription.
Individuals who are not initially diagnosed with RRMS may be experiencing a more steady progression of the disease from the onset. Approximately 10 percent of the MS population is diagnosed with primary-progressive MS (PPMS), where individuals experience a steady worsening of symptoms from the start, and do not have periodic relapses and remissions.
Approximately 5 percent of patients are initially diagnosed with progressive-relapsing MS (PRMS). This type of MS steadily worsens from the onset, but symptom flare-ups - with or without remissions - are also present.
Other types of MS exist, but these are uncommon. These include:
benign MS (with little or no change after 15 years; however, progression may occur at a later time)
fulminate MS (a rapidly progressive disease course with severe relapses within five years after diagnosis; also known as "malignant MS" or "Marburg MS")
burned-out MS (controversial term used to describe MS patients whose MS progression slows dramatically in later life)
Prior to an MS diagnosis, individuals with "possible MS" may often fall under the parameters of one of two syndromes. The first is clinically isolated syndrome (CIS), where someone may have experienced symptoms of MS for the first time, and an MRI may show evidence of MS, but a diagnosis cannot be confirmed at that time. The second syndrome is radiologically isolated syndrome (RIS), which is the term used when someone has an MRI performed for an unrelated reason, and shows evidence of MS on the MRI scan, but does not have any signs of MS symptoms. As with CIS, more evidence will be needed in the future to determine if someone with RIS may be diagnosed with MS.
Relapses, also referred to as exacerbations, attacks, flare-ups, episodes, or bouts, are initially experienced by most people diagnosed with multiple sclerosis (MS). Relapses occur with relapsing-remitting, progressive-relapsing, and sometimes secondary-progressive forms of MS. Relapses do not occur with primary-progressive MS, although patients may experience day-to-day fluctuations in how they feel.
During a relapse, inflammation is occurring along the nerves and the myelin, causing patients to have a temporary worsening or recurrence of existing symptoms and/or the appearance of new symptoms. This can range from a few days in duration to a few months, followed by a complete or partial recovery (remission). Acute physical symptoms and neurological signs must be present for at least 24 to 48 hours, without any signs of infection or fever, before the treating physician may consider this type of flare-up to be a true relapse.
A pseudoexacerbation is a temporary worsening of symptoms without actual myelin inflammation or damage, brought on by other influences. Examples include other illnesses or infection, exercise, a warm environment, depression, exhaustion, and stress. When symptoms flare, checking for a fever is important, since even a minor infection and slight increase in temperature can cause symptoms to appear.
Urinary tract infection (UTI) is the most common type of infection to cause a pseudoexacerbation. Additionally, people with "heat-sensitive" MS will experience a temporary increase in symptoms when their body temperature rises, often after exercise. Many heat-sensitive individuals may opt to avoid hot tubs, saunas, or other situations that can raise the body's temperature.
Relapses are usually treated with a high-dose course of powerful corticosteroids (a type of steroid) over a period of three to five days. These are given by intravenous (IV) infusion, administering the drug directly into the bloodstream for a quicker response. Administration may be performed at a hospital, infusion center, or sometimes at home. Some doctors prescribe oral steroids after the high-dose treatment, to ease the patient off of the medication. These are usually tapered over one to two weeks.
Another FDA-approved option is Acthar® Gel, which contains a highly purified form of the hormone adrenocorticotropin (ACTH). It is given once daily for two to three weeks and is injected either into the muscle or under the skin.
In a healthy body, nerve fibers (also referred to as "axons") have a protective, fatty-rich protein covering known as myelin. This covering insulates the nerve fibers, similar to the insulating rubber covering of an electric wire. Myelin allows for the smooth and uninterrupted flow of nerve impulses, which in turn, enables the body to send vital instructions from the brain to the different parts of the body.
These renderings of the inside of a blood vessel show normal red blood cells, along with immune-system cells that are designed to fight infection and disease. With ms, these cells of the immune system are thought to become misdirected and attack the body's own tissues - in this case, the nerves of the cns. In order to reach the cns, these immune-system cells must cross the blood-brain barrier - traveling through the blood vessel wall and into the brain and spinal cord.
With multiple sclerosis (MS), the body's own system of defense, known as the immune system, malfunctions. It sends disease-fighting cells into the central nervous system (CNS) that may destroy the body's own myelin. This occurs because the immune system is incorrectly identifying the myelin in the CNS as a foreign body. When the body's own immune system attacks its own tissue, this is referred to as an "autoimmune disease," and MS is believed to fall into this category. Examples of other autoimmune diseases include lupus and rheumatoid arthritis.
Lymphocytes are a type of white blood cell and play a strong role in the body's defense system. Another type of white blood cell is the macrophage, and this works to ingest and destroy foreign substances.
White blood cells circulate in the blood and are produced when the immune system perceives a foreign body and instructs the cells to eliminate it, thereby "protecting" the body. In order to reach the nerves within the CNS, the immune system cells and molecules must cross a protective barrier that surrounds the blood vessels. Known as the blood-brain barrier (BBB), this layer of cells is designed to prevent damaging cells and other substances in the blood (including those that could cause disease) from entering the brain, optic nerves, and spinal cord of the CNS.
With MS, damaging immune-system cells are able to break through the BBB and enter the CNS, where they begin their attack on the myelin. Once the damaging cells enter the CNS, macrophages and other lymphocytes begin their attack on the myelin. This creates inflammation along the nerves where the myelin is being damaged. Areas of activity are known as lesions (or plaques). Lesions vary in activity levels, ranging from very active (acute), to chronic, to inactive.
Shown above is a 3-D rendering of nerve cells; the axon and protective myelin can easily be seen extending out to the side of the cell body.
Remyelination is believed to occur in relapsing-remitting MS (RRMS) when a symptom flare-up subsides and goes into remission. The return of function is thought to result from not only myelin repair, but reduced inflammation as well. Eventually, the axon becomes exposed and damaged, and the myelin may no longer be repaired. With primary-progressive MS (PPMS) and other forms of progressive MS, the oligodendrocytes are unable to repair the myelin, and therefore symptoms do not remit.
Often, myelin that is damaged may be restored through a process called "remyelination," particularly early in the disease. Oligodendrocytes are cells that produce and maintain myelin. Over time, however, oligodendrocytes may be lost and unable to repair the damaged myelin.
Areas of damaged myelin become scarred and can no longer fully insulate the nerve - leaving unprotected areas, where the flow of nerve impulses is interrupted. This interruption in the communication between the brain and other parts of the body results in the symptoms experienced by individuals with MS.
Many possible causes for MS have been studied; a combination of factors appears to be involved
Slow-acting viruses, such as Epstein-Barr, could be involved
Researchers theorize that under certain conditions, MS may develop in genetically-susceptible individuals
Nutritional factors, such as fat intake and omega-3 fatty acids, may play a role in increasing or reducing one's risk of MS
Insufficient vitamin D and/or sunlight may also play a role
The reduction in parasites from different countries appears to be related to an increase in MS; individuals with parasites are less-likely to be diagnosed with MS
Smoking increases the risk of MS
CCSVI is a complex condition involving changes in blood flow from the brain back to the heart; some theorize this could be involved
Researchers have studied a variety of possible causes for multiple sclerosis (MS), and a combination of factors appears to be involved. A popular theory looks at commonly known slow-acting viruses (one that could remain dormant for many years), such as measles, herpes, human T-cell lymphoma, and Epstein-Barr. After being exposed to one of these viruses, some researchers theorize that MS may develop in genetically susceptible people.
In the absence of a solid understanding of the mechanisms that underlie MS, no compelling candidate genes for MS have been identified. For this reason, the list of genes that have been investigated for MS susceptibility is long and continually expanding. Genes have some role in susceptibility to MS, but the exact mechanisms remain unclear. Nevertheless, genetic studies in MS have clearly shown that the increased frequency of MS seen within families is a result of relatives sharing DNA (the molecule that carries our genetic information) and not from living together as a family in the same environment.
Researchers are working to identify genes that may increase one's susceptibility to MS, using a Karyotype (chart) to show the chromosomal makeup of an individual.
Some scientists are looking for a connection between MS and nutritional factors, including fat intake, as well as deficiencies in fish oil and vitamin D. The idea that a diet rich in saturated fat may increase one's risk of getting MS, as well as worsen his or her disease course, has been a popular theory for several decades.
Both Dr. Roy Swank and Dr. John McDougall have promoted diets with very low saturated fats for individuals with MS. Individuals with MS on the Swank Diet were followed for almost 50 years, and benefits such as fewer symptoms, greater mobility, and greater longevity were reported. However, incomplete follow-up and the lack of a control group to compare results prevent these claims from being considered as evidence-based medicine. Scientific clinical trials need to be conducted before any conclusions can be made. However, a nutritious diet - such as a heart-healthy diet - can control weight, blood sugar, and blood pressure, and is generally recommended.
In addition to food and supplements, vitamin D is also derived from sunlight, which may be involved in the development of MS. As noted in the section, Who Gets MS, populations living closer to the equator experience a lower incidence of MS. A popular theory is that those living closer to the equator are exposed to more sunlight and therefore are less likely to experience a vitamin D deficiency (studies suggest that low levels of vitamin D may increase one's risk of MS).
Also noted in the section, Who Gets MS, parasites are another possible risk factor in the development of MS. Research has found that parasites can modulate the immune system and dampen its responses. People who have parasites are less likely to be diagnosed with MS, and as conditions in different countries become cleaner - with fewer parasites - the number of individuals being diagnosed is increasing in these parts of the world.
Another factor linked to MS is cigarette smoking. Women who smoke are 1.6 times more likely to develop MS than women who are non-smokers. Individuals with MS who smoke also appear to be at a much greater risk of experiencing a more rapid progression of their disease.
Other potential causes continue to be investigated, some of which show promise, while others create much controversy within the MS community. Receiving a great amount of attention during recent years is the possible connection between chronic cerebrospinal venous insufficiency (CCSVI) and MS. CCSVI is a complex condition involving changes in blood flow from the brain back to the heart, which some researchers theorize could possibly lead to activation of the immune system, excess iron deposits, loss of myelin, and other nervous system damage.
While this theory has a large following, CCSVI also has a great amount of opposition. Despite the controversy, some patients have opted for risky treatments on their own, sometimes going to clinics outside of the country. A recent, large study in Italy did not support the link of CCSVI and MS. Numerous other CCSVI research projects are still in progress, including research in Europe and the United States. In May 2012, the United States Food and Drug Administration (FDA) issued a warning about experimental therapies aimed at treating chronic cerebrospinal venous insufficiency (CCSVI), informing healthcare professionals and patients about the resulting injuries and deaths that have occurred.
As with any unproven theory and treatment, interested patients are strongly encouraged to first talk with their doctor. If appropriate, individuals may seek to participate in an approved clinical trial. Without a tested and proven protocol for the diagnosis and treatment of CCSVI, individuals could be putting themselves at risk by undergoing a procedure in a non-research, "commercial" setting. Caution and skepticism is advised pertaining to research projects that have not been reviewed by the FDA, are not listed on clinicaltrials.gov, and charge "retail prices" or require travel to a foreign country for the procedure.
Diagnosing and evaluating MS disease activity is most reliably done by neurologists through a neurological history and examination. Tests that can indicate MS and rule out "MS mimickers" (other diseases that resemble MS but have other causes) are also performed.
Lesions (areas of inflammation and myelin damage in the brain and/or spine) may be viewed on a magnetic resonance imaging (MRI) scan. The MRI uses a computer, radiofrequency stimulator, and a large electromagnet to provide a picture of the brain and/or spine. While the picture looks a bit like an x-ray, please note that unlike an x-ray, the MRI does not expose the patient to any radiation.
An MRI image enables doctors to view lesions (areas of inflammation) and plaques (areas of scarring) as well as other changes in the CNS.
For those with multiple sclerosis (MS), the MRI is used to evaluate the size and location of lesions. Inflammation can be better evaluated with gadolinium (or contrast) enhancement - a type of dye given to the patient via injection prior to the procedure.
The MRI, particularly with gadolinium enhancement, allows doctors to measure disease activity within the central nervous system (brain, optic nerves, and spinal cord). Test results can help determine the effectiveness of a disease-modifying therapy (DMT), or to get an "inside view" of a patient's disease status.
Another tool that is sometimes used in the diagnosis of MS is a lumbar puncture (also known as a spinal tap). This is a procedure where a very thin needle is inserted at the base of the spine and a small amount of cerebrospinal fluid (CSF) is collected. CSF is the liquid that surrounds the brain and spinal cord. By collecting a small amount of this fluid, laboratory testing may be performed to evaluate cellular and chemical abnormalities. Since the introduction of the MRI, CSF analysis is used less often, but it may be helpful in supporting an MS diagnosis if the MRI results are inconclusive.
Evoked potential (EP) tests may also be used to help diagnose MS, if further support is needed. These measure the speed of the brain's response to visual, auditory (sound), or sensory (feeling) stimuli, using electrodes taped to the patient's head. Delayed responses can indicate possible damage to the nerve pathways.
Additional tools are available to measure disease activity. These are used mainly in clinical trials to help evaluate disease progression as well as changes in specific symptoms, such as fatigue, strength, mobility, vision, cognition, and others.
Through these universally accepted systems of measurement, physicians can record their patients' presenting condition and subsequent improvements, relapses, or disease progression. These systems are particularly valuable in clinical trials, which test the effectiveness and safety of experimental treatments for MS, prior to their approval by the United States Food and Drug Administration (FDA).
The most widely known scale among the MS community is the Kurtzke Expanded Disability Status Scale (EDSS). Dr. Kurtzke first introduced this system in 1955 as the Disability Status Scale (DSS). It used whole numbers from one to 10 to measure degree of disability, largely in terms of mobility.
To make the measurements more sensitive, Kurtzke later "expanded" the scale by adding half-points between the numbers. The EDSS is used in conjunction with Kurtzke's Functional System (FS). This measures the function of seven major systems in the CNS (plus a section for "other"), each relating to the different areas of functioning that can be affected by MS (such as movement, sensory, bowel and bladder, vision, cognition, etc.). These are each graded on a scale of zero (normal) to six (severe).
A newer measurement system designed to be even more sensitive is the MS Functional Composite (MSFC) scale. This measures lower extremity function with a Timed 25-Foot Walk, upper extremity function through the 9-Hole Peg Test (9-HPT), and cognitive function, using the Paced Auditory Serial Additions Test (PASAT).
At the present, approved long-term treatments are only available for individuals with relapsing forms of MS
10 disease-modifying therapies (DMTs) are now approved for relapsing forms of MS (as of March 2013)
DMTs may: reduce the number and severity of symptom flare-ups; delay disease progression; reduce the number of active lesions; and potentially extend one's lifespan
DMTs have reduced or delayed the number of individuals who advance from relapsing-remitting MS to secondary-progressive MS
At the present, approved treatments are only available for individuals with relapsing forms of multiple sclerosis (MS) - largely for those with RRMS. Research (including many clinical trials) is ongoing at a rigorous pace to find treatments that will also be effective for the progressive forms of MS. Fortunately, symptom-management strategies and comprehensive care plans with teams of doctors, nurses, and therapists, help to greatly improve the quality of life for individuals with MS - both with relapsing and progressive forms of MS.
Treatment with a long-term, disease-modifying therapy (DMT) is crucial for most patients with relapsing forms of MS, since disease activity and damage continues within the CNS even when no new symptoms are present. When a patient begins a treatment regimen early in his or her disease course, disease activity is slowed. This not only reduces the number and severity of symptom flare-ups, as well as delays the progression of the disease (and possibly delays any related disability), but also reduces the number of active lesions that appear on an MRI.
Additionally, a 21-year prospective study of individuals (with relapsing-remitting MS) who began therapy early in the disease found that they experienced a longer lifespan than those who did not begin treatment as early. Of those who didn't start treatment early, MS-related pulmonary infection was the most common cause of mortality over the 21-year period.
Tecfidera™ (dimethyl fumarate or DMF, formerly known as BG-12)
Getting early treatment and staying on one of the long-term DMTs for MS may also delay the rate of conversion from RRMS to secondary-progressive MS (SPMS). This form of MS that follows RRMS exhibits a steady worsening, with or without relapses (or flare-ups). If flare-ups do occur, they usually do not remit fully. As mentioned in the previous section, without treatment, approximately half of individuals with RRMS convert to SPMS within 10 years. However, with the introduction of 10 DMTs since the first treatment became available in 1993, those taking a DMT have reduced or delayed the conversion rate.
For more information on long-term treatments for MS and how to select the treatment that is right for you, please see MSAA's S.E.A.R.C.H.™ program.
Targets for multiple sclerosis (MS) treatments include the many components and functions of the immune system response. In general, treatments have been developed to block, reduce, or deplete those cells and other agents that promote inflammation and/or damage to the central nervous system (CNS).
Interrupting this chain of events also includes preventing the damaging cells from entering the CNS through the blood-brain barrier (BBB). Researchers approach this by developing methods to limit the number of immune-system cells circulating in the blood system, so they do not cross the BBB. Another approach is to interfere with the process that allows these immune-system cells to pass through to the CNS.
In addition to the treatments that are FDA-approved or in development to limit or slow the MS process, treatments are also being developed for neuroprotection and remyelination. Such strategies would protect the axons and myelin from further damage, and through repair of the myelin, could potentially return lost function for individuals with MS. The future looks bright as science continues to uncover more vital clues about the immune system and MS.
Introduction
History
The MS Process and Symptoms
Who Gets MS
Types of MS
Relapses
The Immune System and MS
Possible Causes of MS
Diagnosing MS and Evaluating Disease Activity
Additional Evaluative Tools
The Importance of Long-Term Treatment
The Future of MS Research and Treatments
Jean-Martin Charcot was a french neurologist who defined and gave a name to multiple sclerosis in 1868.
Shown above is an illustration of two nerve cells. The normal one on the left has a healthy nerve fiber, or axon, protected by myelin (insulation covering the nerve), and is able to transmit signals at a very fast speed - similar to electricity traveling along an electrical cord. The ms nerve cell on the right shows damage to the myelin, and as a result, signals do not travel well along the nerve.
Shown above is an illustration of a nerve cell. The nerve fiber, or axon, when protected by healthy myelin, is able to transmit signals at a very fast speed - similar to electricity traveling along an electrical cord.
When the myelin becomes damaged (as shown in the top illustration), or the nerve itself becomes damaged, signals can no longer travel across the nerve fiber efficiently. As signals slow down or are lost, the body cannot respond appropriately - causing the symptoms of ms.
Geographically, people who live farther from the equator (in more temperate climates) have a higher risk of developing MS than people living in hotter areas near the equator, or in very cold areas near the north or south poles. Individuals living beyond the 40-degree mark north or south of the equator are far more likely to develop MS, and this is especially true for people in North America, Europe, and southern Australia.
A pseudoexacerbation is a temporary worsening of symptoms without actual myelin inflammation or damage, brought on by other influences. Examples include other illnesses or infection, exercise, a warm environment, depression, exhaustion, and stress. When symptoms flare, checking for a fever is important, since even a minor infection and slight increase in temperature can cause symptoms to appear.
These renderings of the inside of a blood vessel show normal red blood cells, along with immune-system cells that are designed to fight infection and disease. With ms, these cells of the immune system are thought to become misdirected and attack the body's own tissues - in this case, the nerves of the cns. In order to reach the cns, these immune-system cells must cross the blood-brain barrier - traveling through the blood vessel wall and into the brain and spinal cord.
Shown above is a 3-D rendering of nerve cells; the axon and protective myelin can easily be seen extending out to the side of the cell body.
Researchers are working to identify genes that may increase one's susceptibility to MS, using a Karyotype (chart) to show the chromosomal makeup of an individual.
An MRI image enables doctors to view lesions (areas of inflammation) and plaques (areas of scarring) as well as other changes in the CNS.
The most widely known scale among the MS community is the Kurtzke Expanded Disability Status Scale (EDSS). Dr. Kurtzke first introduced this system in 1955 as the Disability Status Scale (DSS). It used whole numbers from one to 10 to measure degree of disability, largely in terms of mobility.
Treatment with a long-term, 
Interrupting this chain of events also includes preventing the damaging cells from entering the CNS through the blood-brain barrier (BBB). Researchers approach this by developing methods to limit the number of immune-system cells circulating in the blood system, so they do not cross the BBB. Another approach is to interfere with the process that allows these immune-system cells to pass through to the CNS.
