The specific cause of MS is not fully understood.Symptoms are caused by an abnormal inflammatory attack on the nerves of the brain or spinal cord. This inflammatory response may be triggered by genetic, environmental, and viral factors that initiate demyelination.
Demyelination is associated with an abnormalimmune system response that causes a type of white blood cell (called T cells) to attack myelin. Damage to the myelin then leads to sclerosis of nerve fibers in the central nervous system (CNS). The CNS has the ability to repair some of the damage but may not be able to achieve complete restoration. Exacerbations and remissions (common in multiple sclerosis) result from the intermittent damage and restoration.
MS is not considered a hereditary disease. However, a number of generic variations have been shown to
increase the risk of developing the disease.
The risk of acquiring MS is higher in relatives of a person with the disease
than in the general population, especially in the case of siblings, parents, and children. The
disease has an overall familial recurrence rate of 20%. In the
case of monozygotic twins, concordance
occurs only in about 35% of cases, while it goes down to around 5% in the case
of siblings and even lower in half-siblings. This indicates susceptibility is
partly polygenically driven.
It seems to be more common in some ethnic groups than others.
Apart from familial studies, specific genes have been linked with MS. Differences in the human
leukocyte antigen (HLA) system—a group of genes in chromosome6 that serves as the major histocompatibility
complex (MHC) in humans—increase the probability of suffering MS. The
most consistent finding is the association between multiple sclerosis and
alleles of the MHC defined as DR15
and DQ6. Other
loci have shown a protective effect, such as HLA-C554
Different environmental factors, both of infectious and non infectious origin
have been proposed as risk factors for MS. Although some are partly modifiable,
only further research—especially clinical trials—will reveal whether their
elimination can help prevent MS.
MS is more common in people who live farther from the equator, although many
Decreased sunlight exposure has been linked with a higher risk of MS.
Decreased vitamin D production
and intake has been the main biological mechanism used to explain the higher
risk among those less exposed to sun.
Severe stress may also be a risk factor although
evidence is weak.Smoking has also been
shown to be an independent risk factor for developing MS.
Association with occupational exposures and toxins—mainly solvents—has been evaluated, but no clear conclusions
have been reached.Vaccinations were also
considered as causal factors for the disease; however, most studies show no
association between MS and vaccines.
Several other possible risk factors, such as diet and hormone intake, have been investigated;
however, more evidence is needed to confirm or refute their relation with the
Gout occurs less than would statistically
be expected in people with MS, and low levels of uric acid have been found in MS patients as compared
to normal individuals. This led to the theory that uric acid protects against
MS, although its exact importance remains unknown.
Many microbes have been proposed as potential infectious triggers of MS, but
none has been substantiated.
Genetic susceptibility can explain some of the geographic and epidemiological
variations in MS incidence, like the high incidence of the disease among some
families or the risk decline with genetic distance, but does not account for
other phenomena, such as the changes in risk that occur with migration at an
early age. An
explanation for this epidemiological finding could be that some kind of
infection, produced by a widespread microbe rather than a rare pathogen, is the
origin of the disease.
Different hypotheses have elaborated on the mechanism by which this may occur.
hypothesis proposes that exposure to several infectious agents early in life
is protective against MS, the disease being a response to a later encounter with
such agents. The
prevalence hypothesis proposes that the disease is due to a pathogen more common in regions of high
MS prevalence. This pathogen is very common, causing in most individuals an asymptomatic persistent
infection. Only in a few cases, and after many years since the original
infection, does it cause demyelination. The
hygiene hypothesis has received more support than the prevalence hypothesis.
Evidence for viruses as a cause includes the presence of oligoclonal bands
in the brain and cerebrospinal fluid of most patients, the association of
several viruses with human demyelination encephalomyelitis, and induction of
demyelination in animals through viral infection.Human herpes viruses are a candidate group
of viruses linked to MS. Individuals who have never been infected by the Epstein-Barr
virus have a reduced risk of having the disease, and those infected as young
adults have a greater risk than those who had it at a younger age.
Although some consider that this goes against the hygiene hypothesis, since the
non-infected have probably experienced a more hygienic upbringing, others
believe that there is no contradiction since it is a first encounter at a later
moment with the causative virus that is the trigger for the disease. Other
diseases that have also been related with MS are measles, mumps
A higher incidence of MS in certain geographical areas, such as the northern United States, suggests thatenvironmental factorsmay be involved, but none have been confirmed.
A specific viral risk factor has not been indentified, but exposure to a virusthat causes demyelination (especially prior to adolescence) may be a risk factor.
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