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What is Multiple Sclerosis
Multiple sclerosis is a chronic, often disabling disease of the
central nervous system. Symptoms may be mild such as numbness
in the limbs or severe -- paralysis or loss of vision.
Most people with
MS are diagnosed between the ages of 20 and 40 but the
unpredictable physical and emotional effects can be lifelong.
The progress, severity and specific symptoms of MS in any one
person cannot yet be predicted, but advances in research and
treatment are giving hope to those affected by the disease.
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Symptoms
The symptoms of
MS are highly variable, depending on the areas of the central
nervous system that have been affected. Not only do the
symptoms vary from one person to another, but from day to day
for any given individual.
Symptoms
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- weakness of one or more extremities
- paralysis of one or more extremities
- tremor of one or more extremities
- muscle spasticity (uncontrollable spasm of
muscle groups)
- muscle atrophy
- movement, dysfunctional
- slowly progressive
- beginning in the legs
- numbness, decreased or abnormal sensation in
any area
- tingling
- facial pain
- pain in an extremity
- may start suddenly
- loss of vision -- usually affects one eye at
a time
- double vision
- eye discomfort
- rapid eye movements, uncontrollable
- eye symptoms worsen on movement of the eyes
- decreased coordination
- loss of balance
- decreased ability to control small or
intricate movements
- walking/gait abnormalities
- muscle spasms (especially in the legs)
- dizziness
- vertigo
- urinary hesitancy, difficult to begin
urinating
- strong urge to urinate (urinary urgency)
- frequent need to urinate
- incontinence(leakage of urine, loss of
control over urination)
- decreased memory
- decreased spontaneity
- decreased judgment
- loss of ability to think abstractly
- loss of ability to generalize
- depression
- decreased attention span
- slurred speech
- difficulty speaking or understanding speech
- fatigue, tired easily
Additional symptoms that may be associated with
this disease:
- constipation
- hearing loss
- positive Babinski’s reflex
Note: Symptoms may vary with each attack. They may
last days to months, then reduce or disappear,
then recur periodically. Fever can trigger or
worsen attacks, as can hot baths, sun exposure,
and stress.
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Signs and tests
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Symptoms of MS may mimic many other neurologic
disorders. A history of at least two attacks separate
by a period of reduced or no symptoms may indicate the
pattern of attack/remission seen in MS. If there are
observable decreases in any functions of the
central nervous system (such as abnormal
reflexes), the diagnosis of MS may be suspected.
Examination by the health care provider may show focal
neurologic deficits (localized decreases in function)
This may include decreased or abnormal sensation,
decreased ability to move a part of the body, speech
or vision changes, or other loss of neurologic
functions. The type of
neurologic deficit may indicate, to some extent,
the location of the damage to the nerves.
Eye examination may show abnormal pupil responses,
changes in the
visual fields or eye movements,
nystagmus (rapid eye movements) triggered by
movement of the eye,
decreased visual acuity, or abnormal findings on a
fundoscopy (an examination of the internal structures
of the eye).
Tests that indicate or confirm multiple sclerosis
include:
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Causes of MS
Many people with MS ask if their disease is caused by a virus or
other infectious agent. Much research has focused on trying to
answer this question.
It is tempting to speculate on a viral cause for MS because viruses
are known to cause demyelinating disease in animals and humans.
Demyelination (destruction of myelin—the fatty sheath the surrounds
and insulates nerve fibers in the central nervous system), causes
nerve impulses to be slowed or halted and produces the symptoms of
MS.
Data from epidemiological studies—those that analyze variations in
geographical, socioeconomic, genetic, and other factors—suggest that
exposure to an infectious agent may be involved in causing MS. Some
viruses are known to have a long latency period between time of
infection and appearance of clinical symptoms, as is thought to be
the case in multiple sclerosis.
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No Definitive Evidence to Link Any One Virus to MS
Although many different viruses have been suggested to cause MS,
there has not yet been definitive evidence linking any one virus to
the autoimmune reaction that is believed to be the process
responsible for the demyelination seen in MS. At one time or
another, canine distemper virus, measles virus, herpes virus
(HHV-6), rubella (or German measles) virus, HTLV-1 virus, and others
have been reported to be associated with MS. With the possible
exception of HHV-6, later studies have not substantiated these
reports, and there is no proof that any of them causes MS.
Increased antibodies to many different viruses have been found in
the sera and cerebrospinal fluid of people with MS. This may not
necessarily represent disease-causing infection by these viruses. It
is more is likely to be the result of non-specific immune
activation. The role of a virus as a causative or triggering agent
of MS remains speculative.
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MS is not Contagious
Currently, there is no evidence at all to suggest that MS is
infectious or contagious. The role of a virus or viruses, if there
is one, affects only people with a genetic predisposition to develop
MS.
Source of information:
National MS Society
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Genetics of multiple sclerosis:
linkage and association studies
Multiple sclerosis (MS) is a demyelinating autoimmune disease of the
central nervous system caused by an interplay of environmental and
genetic factors. The only genetic region that has been clearly
demonstrated by linkage and association studies to contribute to MS
genetic susceptibility is the human leukocyte antigen (HLA) system.
The majority of HLA population studies in MS have focused on
Caucasians of Northern European descent, where the predisposition to
disease has been consistently associated with the class II
DRB1*1501-DQA1*0102-DQB1*0602 haplotype. A positive association with
DR4 was detected in Sardinians and in other Mediterranean
populations. Moreover DR1, DR7, DR11 have been found to be
protective in several populations. Systematic searches aimed at
identifying non-HLA susceptibility genes were undertaken in several
populations by means of linkage studies with microsatellite markers
distributed across the whole genome. The conclusion of these studies
was that there is no major MS locus, and genetic susceptibility to
the disease is most likely explained by the presence of different
genes each conferring a small contribution to the overall familial
aggregation. The involvement of several candidate genes was tested
by association studies, utilising either a population-based (case
control) or a family-based (transmission disequilibrium test)
approach. Candidate genes were selected mainly on the basis of their
involvement in the autoimmune pathogenesis and include
immunorelevant molecules such as cytokines, cytokine receptors,
immunoglobulin, T cell receptor subunits and myelin antigens. With
the notable exception of HLA, association studies met only modest
success. This failure may result from the small size of the tested
samples and the small number of markers considered for each gene.
New tools for large scale screening are needed to identify genetic
determinants with a low phenotypic effect. Large collaborative
studies are planned to screen several thousands of patients with MS
with several thousands of genetic markers. The tests are
increasingly based on the DNA pooling procedure.
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