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Multiple sclerosis

2007 Schools Wikipedia Selection. Related subjects: Health and medicine

   CAPTION: Multiple Sclerosis
   Classifications and external resources

   MRI image showing a bright spot where multiple sclerosis has damaged
   myelin in the brain
   ICD- 10 G 35.
   ICD- 9  340

   Multiple sclerosis (abbreviated MS, also known as disseminated
   sclerosis) is a chronic, inflammatory disease that affects the central
   nervous system (CNS). MS can cause a variety of symptoms, including
   changes in sensation, visual problems, muscle weakness, depression,
   difficulties with coordination and speech, severe fatigue, and pain.
   Although many patients lead full and rewarding lives, MS can cause
   impaired mobility and disability in more severe cases.

   Multiple sclerosis affects neurons, the cells of the brain and spinal
   cord that carry information, create thought and perception, and allow
   the brain to control the body. Surrounding and protecting some of these
   neurons is a fatty layer known as the myelin sheath, which helps
   neurons carry electrical signals. MS causes gradual destruction of
   myelin ( demyelination) and transection of neuron axons in patches
   throughout the brain and spinal cord. The name multiple sclerosis
   refers to the multiple scars (or scleroses) on the myelin sheaths. This
   scarring causes symptoms which vary widely depending upon which signals
   are interrupted. It is thought that MS results from attacks by an
   individual's immune system on the nervous system and is therefore
   categorized as an autoimmune disease.

   Multiple sclerosis may take several different forms, with new symptoms
   occurring either in discrete attacks or slowly accruing over time.
   Between attacks, symptoms may resolve completely, but permanent
   neurologic problems often persist. Although much is known about how MS
   causes damage, its exact cause remains unknown. MS currently does not
   have a cure, though several treatments are available which may slow the
   appearance of new symptoms. MS primarily affects adults, with an age of
   onset typically between 20 and 40 years, and is more common in women
   than in men.

Common symptoms

   Individuals with multiple sclerosis may experience a wide variety of
   symptoms. The initial attacks are often transient, mild (or
   asymptomatic), and self-limited. They often do not prompt a health care
   visit and sometimes are only identified in retrospect once the
   diagnosis has been made based on further attacks. The most common
   initial symptoms reported are: changes in sensation in the arms, legs
   or face (33%), complete or partial vision loss ( optic neuritis) (16%),
   weakness (13%), double vision (7%), unsteadiness when walking (5%), and
   balance problems (3%). Fifteen percent of individuals have multiple
   symptoms when they first seek medical attention. Most people find their
   initial MS symptoms occur over a period of hours to weeks. For some
   people the initial MS attack is preceded by infection, trauma or
   strenuous physical effort.

   Other symptoms and physical findings common in multiple sclerosis are
   flickering eye movements ( nystagmus), speech difficulties, tremor,
   clumsiness of the hands, abnormal muscle spasms, and bladder and bowel
   difficulties. Cognitive impairments are also common, such as difficulty
   performing multiple tasks at once, difficulty following detailed
   instructions, loss of short term memory, emotional instability, and
   fatigue. Emotional symptoms are common and can be the normal response
   to having a debilitating disease or the result of damage to the nerves
   that generate and control emotions. The most common condition, clinical
   depression, is a product of both causes. Feelings such as anger,
   anxiety, frustration, and hopelessness are also common, and suicide is
   a very real threat. People with MS may also experience a range of acute
   and chronic pain syndromes.

   Three clinical entities warrant further discussion because affected
   individuals are often eventually diagnosed with MS. (However, MS is
   only one of several potential causes for these entities.)

   Optic neuritis
          Individuals typically experience rapid onset of pain in one eye,
          followed by blurry vision in part or all of the visual field of
          that eye. This is a result of involvement of the optic nerve by
          MS. Only 10% to 50% of patients (depending on the population
          studied) with optic neuritis go on to develop MS. The blurred
          vision usually resolves within six months, but individuals are
          often left with less vivid colour vision (especially red) in the
          affected eye.

   Internuclear ophthalmoplegia
          Individuals usually notice binocular diplopia (double vision
          with both eyes open) when looking to one side. Internuclear
          ophthalmoplegia occurs when MS affects a part of the brain stem
          called the medial longitudinal fasciculus, which is responsible
          for communication between the two eyes. This results in the
          failure of the medial rectus muscle to contract appropriately,
          so that the eyes do not move equally (called disconjugate gaze).

   Transverse myelitis
          Individuals typically develop rapid onset of numbness, weakness,
          bowel or bladder dysfunction, and/or loss of muscle function,
          typically in the lower half of the body. This is the result of
          MS attacking the spinal cord. As many as 80% of individuals with
          transverse myelitis are left with lasting disabilities, even
          though there is usually some improvement during the first two
          years. MS can devastate lives or it can be a life changing
          experience.

Diagnosis

   Multiple sclerosis is difficult to diagnose in its early stages. In
   fact, definite diagnosis of MS cannot be made until there is evidence
   of at least two anatomically separate demyelinating events occurring at
   least thirty days apart. The McDonald criteria represent international
   efforts to standardize the diagnosis of MS using clinical data,
   laboratory data, and radiologic data.
     * Clinical data alone may be sufficient for a diagnosis of MS. If an
       individual has suffered two separate episodes of neurologic
       symptoms characteristic of MS, and the individual also has
       consistent abnormalities on physical examination, a diagnosis of MS
       can be made with no further testing. Since some people with MS seek
       medical attention after only one attack, other testing may hasten
       the diagnosis and allow earlier initiation of therapy.
     * Magnetic resonance imaging (MRI) of the brain and spine is often
       used to evaluate individuals with suspected MS. MRI shows areas of
       demyelination as bright lesions on T2-weighted images or FLAIR
       (fluid attenuated inversion recovery) sequences. Gadolinium
       contrast is used to demonstrate active plaques on T1-weighted
       images. Because MRI can reveal lesions which occurred previously
       but produced no clinical symptoms, it can provide the evidence of
       chronicity needed for a definite diagnosis of MS.
     * Testing of cerebrospinal fluid (CSF) can provide evidence of
       chronic inflammation of the central nervous system. The CSF is
       tested for oligoclonal bands, which are immunoglobulins found in
       85% to 95% of people with definite MS (but also found in people
       with other diseases). Combined with MRI and clinical data, the
       presence of oligoclonal bands can help make a definite diagnosis of
       MS. Lumbar puncture is the procedure used to collect a sample of
       CSF.
     * The brain of a person with MS often responds less actively to
       stimulation of the optic nerve and sensory nerves. These brain
       responses can be examined using Visual evoked potentials (VEPs) and
       somatosensory evoked potentials (SEPs). Decreased activity on
       either test can reveal demyelination which may be otherwise
       asymptomatic. Along with other data, these exams can help find the
       widespread nerve involvement required for a definite diagnosis of
       MS.

   Another test which may become important in the future is measurement of
   antibodies against myelin proteins such as myelin oligodendrocyte
   glycoprotein (MOG) and myelin basic protein (MBP). As of 2005, however,
   there is no established role for these tests in diagnosing MS.

   The signs and symptoms of MS can be similar to other medical problems,
   such as stroke, brain inflammation, infections such as Lyme disease
   (which can produce identical MRI lesions and CSF abnormalities),
   tumors, and other autoimmune problems, such as lupus. Additional
   testing may be needed to help distinguish MS from these other problems.

Disease course and clinical subtypes

   Graph representing the different types of multiple sclerosis
   Enlarge
   Graph representing the different types of multiple sclerosis

   The course of MS is difficult to predict, and the disease may at times
   either lie dormant or progress steadily. Several subtypes, or patterns
   of progression, have been described. Subtypes use the past course of
   the disease in an attempt to predict the future course. A person
   diagnosed with a particular subtype may, for unclear reasons, switch
   from one subtype to another over time. Subtypes are important not only
   for prognosis but also for therapeutic decisions. In 1996 the United
   States National Multiple Sclerosis Society standardized the following
   four subtype definitions:

   Relapsing-remitting
          Relapsing-remitting describes the initial course of 85% to 90%
          of individuals with MS. This subtype is characterized by
          unpredictable attacks ( relapses) followed by periods of months
          to years of relative quiet ( remission) with no new signs of
          disease activity. Deficits suffered during the attacks may
          either resolve or may be permanent. When deficits always resolve
          between attacks, this is referred to as " benign" MS.

   Secondary progressive
          Secondary progressive describes around 80% of those with initial
          relapsing-remitting MS, who then begin to have neurologic
          decline between their acute attacks without any definite periods
          of remission. This decline may include new neurologic symptoms,
          worsening cognitive function, or other deficits. Secondary
          progressive is the most common type of MS and causes the
          greatest amount of disability.

   Primary progressive
          Primary progressive describes the approximately 10% of
          individuals who never have remission after their initial MS
          symptoms. Decline occurs continuously without clear attacks. The
          primary progressive subtype tends to affect people who are older
          at disease onset.

   Progressive relapsing
          Progressive relapsing describes those individuals who, from the
          onset of their MS, have a steady neurologic decline but also
          suffer superimposed attacks.

Factors triggering a relapse

   Multiple sclerosis relapses are often unpredictable and can occur
   without warning with no obvious inciting factors. Some attacks,
   however, are preceded by common triggers. In general, relapses occur
   more frequently during spring and summer than during autumn and winter.
   Infections, such as the common cold, influenza, and gastroenteritis,
   increase the risk for a relapse. Emotional and physical stress may also
   trigger an attack, as can severe illness of any kind. Statistically,
   there is no good evidence that either trauma or surgery trigger
   relapses. People with MS can participate in sports, but they should
   probably avoid extremely strenuous exertion, such as marathon running.
   Heat can transiently increase symptoms, which is known as Uhthoff's
   phenomenon. This is why some people with MS avoid saunas or even hot
   showers. However, heat is not an established trigger of relapses.

   Pregnancy can directly affect the susceptibility for relapse. The last
   three months of pregnancy offer a natural protection against relapses.
   However, during the first few months after delivery, the risk for a
   relapse is increased 20%–40%. Pregnancy does not seem to influence
   long-term disability. Children born to mothers with MS are not at
   increased risk for birth defects or other problems.

   Many potential triggers have been examined and found not to influence
   relapse rates in MS. Influenza vaccination is safe, does not trigger
   relapses, and can therefore be recommended for people with MS. There is
   also no evidence that hepatitis B, varicella, tetanus, or Bacille
   Calmette-Guerin (BCG - immunization for tuberculosis) increases the
   risk for relapse. In fact, recent studies have shown that the tetanus
   vaccine may actually have a protective effect against the development
   of MS.

Pathophysiology

   Although much is known about how multiple sclerosis causes damage, the
   reasons why multiple sclerosis occurs are not known.

How multiple sclerosis causes damage

   Multiple sclerosis is a disease in which the body's immune system
   attacks the myelin surrounding nerve cells. Myelin is a fatty substance
   which covers the axons of nerve cells and is important for proper nerve
   conduction. A special subset of white blood cells, called T cells,
   plays a key role in the development of MS. Under normal circumstances,
   these lymphocytes can distinguish between self and non-self. However,
   in a person with MS, these cells recognize healthy parts of the central
   nervous system as foreign and attack them as if they were an invading
   virus.

   In MS, certain T cells trigger inflammatory processes when they
   encounter myelin, stimulating other immune cells and soluble factors
   like cytokines and antibodies. Normally, there is a tight barrier
   between the blood and brain, called the blood-brain barrier, built up
   of endothelial cells lining the blood vessel walls. The inflammatory
   processes triggered by the T cells create leaks in the blood-brain
   barrier. These leaks, in turn, cause a number of other damaging effects
   such as swelling, activation of macrophages, and more activation of
   cytokines and other destructive proteins such as matrix
   metalloproteinases. The final result is destruction of myelin, called
   demyelination.

   Repair processes, called remyelination, also play an important role in
   MS. Remyelination is one of the reasons why, especially in early phases
   of the disease, symptoms tend to decrease or disappear temporarily.
   Nevertheless, nerve damage and irreversible loss of neurons occur early
   in MS. Often, the brain is able to compensate for some of this damage,
   due to an ability called neuroplasticity. MS symptoms develop as the
   cumulative result of multiple lesions in the brain and spinal cord.
   This is why symptoms can vary greatly between different individuals,
   depending on where their lesions occur.

   The oligodendrocytes that originally formed a myelin sheath cannot
   completely rebuild a destroyed myelin sheath. However, the brain can
   recruit stem cells, which migrate from other unknown regions of the
   brain, differentiate into mature oligodendrocytes, and rebuild the
   myelin sheath. These new myelin sheaths are often not as effective as
   the original ones. Repeated attacks lead to successively less effective
   remyelinations, until a scar-like plaque is built up around the damaged
   axons. Under laboratory conditions, stem cells are quite capable of
   differentiating and remyelinating axons; it is therefore suspected that
   inflammatory conditions or axonal damage somehow inhibit stem cell
   differentiation in the body.

Pathophysiology research

   Until recently, most of the data available came from post-mortem brain
   samples and animal models of the disease, such as the experimental
   autoimmune encephalomyelitis (EAE), an autoimmune disease that rodents
   can develop, and which is considered a possible animal model for
   multiple sclerosis.

   In 1998, the National Multiple Sclerosis Society and the Mayo Clinic
   launched " The Lesion Project" to describe MS lesions as accurately as
   possible and to develop an accurate model of the evolution of the
   disease. They have used brain biopsies apart from the post-mortem
   samples. Four different damage patterns have been identified in the
   scars of the brain tissue, but the meaning of this fact remains
   controversial. For some researchers it means that MS is a heterogeneous
   disease. Other teams maintain that the shape of the scars can change
   from one type to other and this could be a marker of the disease action
   time.

   The four patterns that were identified are:

   Pattern I
          The scar presents T-cells and macrophages around blood vessels,
          with preservation of oligodendrocytes, but no signs of
          complement system activation.

   Pattern II
          The scar presents T-cells and macrophages around blood vessels,
          with preservation of oligodendrocytes, as before, but also signs
          of complement system activation can be found.

   Pattern III
          The scars are diffuse with inflammation, distal
          oligodendrogliopathy and microglial activation. There is also
          loss of myelin associated glicoprotein (MAG). The scars do not
          surround the blood vessels, and in fact, a rim of preserved
          myelin appears around the vessels. There is evidence of partial
          remyelinization and oligodendrocyte apoptosis.

   Pattern IV
          The scar presents sharp borders and oligodendrocyte
          degeneration, with a rim of normal appearing white matter. There
          is a lack of oligodendrocytes in the centre of the scar. There
          is no complement activation or MAG loss.

Why multiple sclerosis occurs

   Although many risk factors for multiple sclerosis have been identified,
   no definitive cause has been found. MS likely occurs as a result of
   some combination of both environmental and genetic factors. Various
   theories try to combine the known data into plausible explanations.
   Although most accept an autoimmune explanation, several theories
   suggest that MS is an appropriate immune response to an underlying
   condition.

Environmental

   The most popular hypothesis is that a viral infection or retroviral
   reactivation primes a susceptible immune system for an abnormal
   reaction later in life. On a molecular level, this might occur if there
   is a structural similarity between the infectious virus and some
   component of the central nervous system, leading to eventual confusion
   in the immune system.

   Since MS seems to be more common in people who live farther from the
   equator, another theory proposes that decreased sunlight exposure and
   possibly decreased vitamin D production may help cause MS. This theory
   is bolstered by recent research into the biochemistry of vitamin D,
   which has shown that it is an important immune system regulator.

   Other theories, noting that MS is less common in children with
   siblings, suggest that less exposure to illness in childhood leads to
   an immune system which is not primed to fight infection and is thus
   more likely to attack the body. One explanation for this would be an
   imbalance between the Th1 type of helper T-cells, which fight
   infection, and the Th2 type, which are more active in allergy and more
   likely to attack the body.

   Other theories describe MS as an immune response to a chronic
   infection. The association of MS with the Epstein-Barr virus suggests a
   potential viral contribution in at least some individuals. Still others
   believe that MS may sometimes result from a chronic infection with
   spirochetal bacteria, a hypothesis supported by research in which
   cystic forms were isolated from the cerebrospinal fluid of all MS
   patients in a small study. When the cysts were cultured, propagating
   spirochetes emerged. Another bacterium that has been implicated in MS
   is Chlamydophila pneumoniae; it or its DNA has been found in the
   cerebrospinal fluid of MS patients by several research laboratories,
   with one study finding that the oligoclonal bands of 14 of the 17 MS
   patients studied consisted largely of antibodies to Chlamydophila
   antigens.

Genetic

   MS is not considered a hereditary disease. However, increasing
   scientific evidence suggests that genetics may play a role in
   determining a person's susceptibility to MS. Some populations, such as
   the Roma, Inuit, and Bantus, never get MS. The indigenous peoples of
   the Americas, and Asians have very low incidence rates. It is unclear
   whether this is due mostly to genetic or environmental factors.

   In the population at large, the chance of developing MS is less than a
   tenth of one percent. However, if one person in a family has MS, that
   person's first-degree relatives—parents, children, and siblings—have a
   one to three percent chance of getting the disease.

   For identical twins, the likelihood that the second twin may develop MS
   if the first twin does is about 30%; for fraternal twins (who do not
   inherit identical gene pools), the likelihood is closer to that for
   non-twin siblings, or about 4%. The fact that the rate for identical
   twins both developing MS is significantly less than 100% suggests that
   the disease is not entirely genetically controlled. Some (but
   definitely not all) of this effect may be due to shared exposure to
   something in the environment, or to the fact that some people with MS
   lesions remain essentially asymptomatic throughout their lives.

   Further indications that more than one gene is involved in MS
   susceptibility comes from studies of families in which more than one
   member has MS. Several research teams found that people with MS inherit
   certain regions on individual genes more frequently than people without
   MS. Of particular interest is the human leukocyte antigen (HLA) or
   major histocompatibility complex region on chromosome 6. HLAs are
   genetically determined proteins that influence the immune system.

   The HLA patterns of MS patients tend to be different from those of
   people without the disease. Investigations in northern Europe and
   America have detected three HLAs that are more prevalent in people with
   MS than in the general population. Studies of American MS patients have
   shown that people with MS also tend to exhibit these HLAs in
   combination-that is, they have more than one of the three HLAs-more
   frequently than the rest of the population. Furthermore, there is
   evidence that different combinations of the HLAs may correspond to
   variations in disease severity and progression.

   Studies of families with multiple cases of MS and research comparing
   genetic regions of humans to those of mice with EAE suggest that
   another area related to MS susceptibility may be located on chromosome
   5. Other regions on chromosomes 2, 3, 7, 11, 17, 19, and X have also
   been identified as possibly containing genes involved in the
   development of MS.

   These studies strengthen the theory that MS is the result of a number
   of factors rather than a single gene or other agent. Development of MS
   is likely to be influenced by the interactions of a number of genes,
   each of which (individually) has only a modest effect. Additional
   studies are needed to specifically pinpoint which genes are involved,
   determine their function, and learn how each gene's interactions with
   other genes and with the environment make an individual susceptible to
   MS.

Treatment

   There is no known definitive cure for multiple sclerosis. However,
   several types of therapy have proven to be helpful. Different therapies
   are used for patients experiencing acute attacks, for patients who have
   the relapsing-remitting subtype, for patients who have the progressive
   subtypes, for patients without a diagnosis of MS who have a
   demyelinating event, and for managing the various consequences of MS
   attacks. Treatment is aimed at returning function after an attack,
   preventing new attacks, and preventing disability.

   Currently only relapsing-remitting Multiple Sclerosis has FDA approved
   treatments. As of 2006 there are six Food and Drug Administration
   (FDA)-approved treatments for patients with relapsing-remitting MS.
   Three are interferons: Interferon beta-1a (Avonex and Rebif) or beta-1b
   (Betaseron [in Europe and Japan Betaferon]). The interferons are
   medications derived from human cytokines which help regulate the immune
   system. A fourth medication is glatiramer acetate (Copaxone), a mixture
   of polypeptides which may protect important myelin proteins by
   substituting itself as the target of immune system attack. The fifth
   medication, mitoxantrone is effective but is limited by cardiac
   toxicity. Finally, the sixth medication is Natalizumab (marketed as
   Tysabri).

   Currently there are no approved treatments for the progressive
   varieties, though several medicaments are being studied and are
   described at Therapies for Multiple Sclerosis

   Relapsing-remitting symptomatic attacks can be treated. Patients in the
   United States are typically given high doses of intravenous
   corticosteroids, such as methylprednisolone, to end the attack sooner
   and leave fewer lasting deficits.

Prognosis

   The future course of the disease (or prognosis) for people with
   multiple sclerosis depends on the subtype of the disease, the
   individual's sex and race, their age, their initial symptoms, and the
   degree of disability they experience. The life expectancy of people
   with MS is now nearly the same as that of unaffected people. This is
   mainly due to improved methods of limiting disability, such as physical
   therapy and speech therapy, and more successful treatment of common
   complications of disability, such as pneumonia and urinary tract
   infections.
     * Individuals with progressive subtypes of MS, particularly the
       primary progressive subtype, have a more rapid decline in function.
       In the primary progressive subtype, supportive equipment (such as a
       wheelchair or standing frame) is often needed after six to seven
       years. However, when the initial disease course is the
       relapsing-remitting subtype, the average time until such equipment
       is needed is twenty years. This means that many individuals with MS
       will never need a wheelchair.
     * The earlier in life MS occurs, the slower disability progresses.
       Individuals who are older than fifty when diagnosed are more likely
       to experience a chronic progressive course, with more rapid
       progression of disability. Those diagnosed before age 35 have the
       best prognosis. Females generally have a better prognosis than
       males. Although black individuals tend to develop MS less
       frequently, they are often older at the time of onset and may have
       a worse prognosis.
     * Initial MS symptoms of visual loss or sensory problems, such as
       numbness or tingling, are markers for a relatively good prognosis,
       whereas difficulty walking and weakness are markers for a
       relatively poor prognosis. Better outcomes are also associated with
       the presence of only a single symptom at onset, the rapid
       development of initial symptoms, and the rapid regression of
       initial symptoms.
     * The degree of disability varies among individuals with MS. In
       general, one of three individuals will still be able to work after
       15–20 years. Fifteen percent of people diagnosed with MS never have
       a second relapse, and these people have minimal or no disability
       after ten years. The degree of disability after five years
       correlates well with the degree of disability after fifteen years.
       This means that two-thirds of people with MS with low disability
       after five years will not get much worse during the next ten years.
       It should be noted that most of these outcomes were observed before
       the use of medications such as interferon, which can delay disease
       progression for several years.

   Currently there are no clinically established laboratory investigations
   available that can predict prognosis or response to treatment. However,
   several promising approaches have been proposed. These include
   measurement of the two antibodies anti-myelin oligodendrocyte
   glycoprotein and anti-myelin basic protein, and measurement of TRAIL (
   TNF-Related Apoptosis Inducing Ligand).

Epidemiology

   World map showing that risk for MS increases with greater distance from
   the equator
   Enlarge
   World map showing that risk for MS increases with greater distance from
   the equator

   In northern Europe, continental North America, and Australasia, about
   one of every 1000 citizens suffers from multiple sclerosis, whereas in
   the Arabian peninsula, Asia, and continental South America, the
   frequency is much lower. In sub-Saharan Africa, MS is extremely rare.
   With important exceptions, there is a north-to-south gradient in the
   northern hemisphere and a south-to-north gradient in the southern
   hemisphere, with MS being much less common in people living near the
   equator. Climate, diet, geomagnetism, toxins, sunlight exposure,
   genetic factors, and infectious diseases have all been discussed as
   possible reasons for these regional differences. Environmental factors
   during childhood may play an important role in the development of MS
   later in life. This idea is based on several studies of migrants
   showing that if migration occurs before the age of fifteen, the migrant
   acquires the new region's susceptibility to MS. If migration takes
   place after age fifteen, the migrant keeps the susceptibility of his
   home country. Additionally, smoking has been shown to be an independent
   risk factor for developing MS.

   MS occurs mainly in Caucasians. It is twenty-fold lower in the Inuit
   people of Canada than in other Canadians living in the same region. It
   is also rare in the Native American tribes of North America, the
   Australian Aborigines and the Māori of New Zealand. These few examples
   point out that genetic background plays an important role in the
   development of MS.

   As observed in many autoimmune disorders, MS is more common in females
   than males; the mean sex ratio is about two females for every male. In
   children (who rarely develop MS) the sex ratio may reach three females
   for each male. In people over age fifty, MS affects males and females
   equally. Onset of symptoms usually occurs between twenty to forty years
   of age, rarely before age fifteen or after age sixty.

   As previously discussed, there is a genetic component to MS. On average
   one of every 25 siblings of individuals with MS will also develop MS.
   Almost half of the identical twins of MS-affected individuals will
   develop MS, but only one of twenty fraternal twins. If one parent is
   affected by MS, each child has a risk of only about one in forty of
   developing MS later in life.

History

   A French neurologist named Jean-Martin Charcot (1825–93) was the first
   person to recognize multiple sclerosis as a distinct, separate disease
   in 1868. Summarizing previous reports and adding his own important
   clinical and pathological observations, Charcot called the disease
   sclerose en plaques. The three signs of MS now known as Charcot's triad
   are dysarthria (problems with speech), ataxia (problems with
   coordination), and tremor. Prior to Charcot, Robert Hooper (1773–1835),
   a British pathologist and practicing physician, Robert Carswell
   (1793–1857), a British professor of pathology, and Jean Cruveilhier
   (1791–1873), a French professor of pathologic anatomy, had described
   and illustrated many of the disease's clinical details.

   There are several historical accounts of people who probably had MS.
   Saint Lidwina of Schiedam (1380–1433), a Dutch nun, may have been the
   first identifiable MS patient. From the age of sixteen until her death
   at age 53, she suffered intermittent pain, weakness of the legs, and
   vision loss—symptoms typical of MS. Augustus Frederick d'Este
   (1794–1848), an illegitimate grandson of King George III of Great
   Britain, almost certainly suffered from MS. D'Este left a detailed
   diary describing his 22 years living with the disease. His symptoms
   began at age 28 with a sudden transient visual loss after the funeral
   of a friend. During the course of his disease he developed weakness of
   the legs, clumsiness of the hands, numbness, dizziness, bladder
   disturbances, and erectile dysfunction. In 1844, he began to use a
   wheelchair. Despite his illness, he kept an optimistic view of life.
   Another early account of MS was kept by the British diarist W. N. P.
   Barbellion, who maintained a detailed log of his diagnosis and struggle
   with MS. His diary was published in 1919 as The Journal of a
   Disappointed Man.

Multiple sclerosis in film and television

   The German propaganda film Ich klage an (1941) by Wolfgang Liebeneiner
   had the main character suffering from MS and wishing herself to be
   killed because she had become unable to do so by herself.

   British cellist Jacqueline du Pré died of MS in 1987 after a long
   struggle with the disease, which robbed her of her capacity to perform
   as she progressively lost sensitivity in her fingers, muscle
   coordination, and her hearing. This decline was portrayed in the 1998
   film, Hilary and Jackie. In "Duet For One," Julie Andrews plays a
   concert violinist who must sacrifice her career when she is diagnosed
   with MS.

   In the American television series The West Wing, the fictional United
   States President, Josiah "Jed" Bartlet, has the relapsing-remitting
   subtype of MS. The storylines have educated many viewers about the
   nature of MS and have helped to dispel some of the misconceptions about
   the disease.

   Another American TV series, Extreme Makeover: Home Edition, aired a
   two-part episode on February 12, 2006 that featured a new home for
   Carol Crawford-Smith of Blacksburg, Virginia, a former principal dancer
   with the Dance Theatre of Harlem who was diagnosed with MS in 2000. Ty
   Pennington and his team not only built her a new home, but also
   renovated her Blacksburg dance studio, "The Centre of Dance."

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