Results: Exact: Elapsed time: 46 ms. All rights reserved.

Author:Megar Nikolmaran
Language:English (Spanish)
Published (Last):14 April 2007
PDF File Size:6.52 Mb
ePub File Size:20.72 Mb
Price:Free* [*Free Regsitration Required]

Multiple sclerosis MS is a demyelinating disease in which the insulating covers of nerve cells in the brain and spinal cord are damaged. While the cause is unclear, the underlying mechanism is thought to be either destruction by the immune system or failure of the myelin -producing cells.

There is no known cure for multiple sclerosis. Multiple sclerosis is the most common immune-mediated disorder affecting the central nervous system. A person with MS can have almost any neurological symptom or sign, with autonomic , visual, motor, and sensory problems being the most common.

The cause of MS is unknown; however, it is believed to occur as a result of some combination of genetic and environmental factors such as infectious agents. While there are a number of environmental risk factors and although some are partly modifiable, further research is needed to determine whether their elimination can prevent MS.

MS is more common in people who live farther from the equator , although exceptions exist. MS is more common in regions with northern European populations [5] and the geographic variation may simply reflect the global distribution of these high-risk populations.

A relationship between season of birth and MS lends support to this idea, with fewer people born in the northern hemisphere in November as compared to May being affected later in life. Environmental factors may play a role during childhood, with several studies finding that people who move to a different region of the world before the age of 15 acquire the new region's risk to MS.

If migration takes place after age 15, however, the person retains the risk of their home country. MS is not considered a hereditary disease; however, a number of genetic variations have been shown to increase the risk. Specific genes that have been linked with MS include differences in the human leukocyte antigen HLA system—a group of genes on chromosome 6 that serves as the major histocompatibility complex MHC.

Many microbes have been proposed as triggers of MS, but none have been confirmed. The hygiene hypothesis proposes that exposure to certain infectious agents early in life is protective, the disease is a response to a late encounter with such agents.

Only in a few cases and after many years does it cause demyelination. Evidence for a virus as a cause include the presence of oligoclonal bands in the brain and cerebrospinal fluid of most people with MS, the association of several viruses with human demyelination encephalomyelitis , and the occurrence of demyelination in animals caused by some viral infections. Individuals having never been infected by the Epstein—Barr virus are at a reduced risk of getting MS, whereas those infected as young adults are at a greater risk than those having had it at a younger age.

Smoking may be an independent risk factor for MS. This has led to the theory that uric acid is protective, although its exact importance remains unknown. The three main characteristics of MS are the formation of lesions in the central nervous system also called plaques , inflammation, and the destruction of myelin sheaths of neurons.

These features interact in a complex and not yet fully understood manner to produce the breakdown of nerve tissue and in turn the signs and symptoms of the disease. The name multiple sclerosis refers to the scars sclerae — better known as plaques or lesions that form in the nervous system. These lesions most commonly affect the white matter in the optic nerve , brain stem , basal ganglia , and spinal cord , or white matter tracts close to the lateral ventricles.

The peripheral nervous system is rarely involved. To be specific, MS involves the loss of oligodendrocytes , the cells responsible for creating and maintaining a fatty layer—known as the myelin sheath—which helps the neurons carry electrical signals action potentials. When the myelin is lost, a neuron can no longer effectively conduct electrical signals. Apart from demyelination, the other sign of the disease is inflammation.

Fitting with an immunological explanation, the inflammatory process is caused by T cells , a kind of lymphocyte that plays an important role in the body's defenses. The T cells recognize myelin as foreign and attack it, explaining why these cells are also called "autoreactive lymphocytes". The attack of myelin starts inflammatory processes, which triggers other immune cells and the release of soluble factors like cytokines and antibodies. A further breakdown of the blood-brain barrier, in turn, causes a number of other damaging effects such as swelling , activation of macrophages , and more activation of cytokines and other destructive proteins.

These factors could lead to or enhance the loss of myelin, or they may cause the axon to break down completely. The blood—brain barrier BBB is a part of the capillary system that prevents the entry of T cells into the central nervous system.

It may become permeable to these types of cells secondary to an infection by a virus or bacteria. After it repairs itself, typically once the infection has cleared, T cells may remain trapped inside the brain. Multiple sclerosis is typically diagnosed based on the presenting signs and symptoms, in combination with supporting medical imaging and laboratory testing.

Clinical data alone may be sufficient for a diagnosis of MS if an individual has had separate episodes of neurological symptoms characteristic of the disease.

The most commonly used diagnostic tools are neuroimaging , analysis of cerebrospinal fluid and evoked potentials. Magnetic resonance imaging of the brain and spine may show areas of demyelination lesions or plaques.

Gadolinium can be administered intravenously as a contrast agent to highlight active plaques and, by elimination, demonstrate the existence of historical lesions not associated with symptoms at the moment of the evaluation. These brain responses can be examined using visual - and sensory- evoked potentials. While the above criteria allow for a non-invasive diagnosis, and even though some state [5] that the only definitive proof is an autopsy or biopsy where lesions typical of MS are detected, [49] [53] currently, as of , there is no single test including biopsy that can provide a definitive diagnosis of this disease.

Several phenotypes commonly termed types , or patterns of progression, have been described. Phenotypes use the past course of the disease in an attempt to predict the future course.

They are important not only for prognosis but also for treatment decisions. Relapsing-remitting MS is characterized by unpredictable relapses followed by periods of months to years of relative quiet remission with no new signs of disease activity. In CIS, a person has an attack suggestive of demyelination, but does not fulfill the criteria for multiple sclerosis. It is similar to the age that secondary progressive usually begins in relapsing-remitting MS, around 40 years of age.

Atypical variants of MS have been described; these include tumefactive multiple sclerosis , Balo concentric sclerosis , Schilder's diffuse sclerosis , and Marburg multiple sclerosis. There is debate on whether they are MS variants or different diseases. Multiple sclerosis behaves differently in children, taking more time to reach the progressive stage.

Although there is no known cure for multiple sclerosis, several therapies have proven helpful. The primary aims of therapy are returning function after an attack, preventing new attacks, and preventing disability. Starting medications is generally recommended in people after the first attack when more than two lesions are seen on MRI.

As with any medical treatment, medications used in the management of MS have several adverse effects. Alternative treatments are pursued by some people, despite the shortage of supporting evidence. During symptomatic attacks, administration of high doses of intravenous corticosteroids , such as methylprednisolone , is the usual therapy, [5] with oral corticosteroids seeming to have a similar efficacy and safety profile.

As of , multiple disease-modifying medications are approved by regulatory agencies for relapsing-remitting multiple sclerosis RRMS. They are interferon beta-1a , interferon beta-1b , [70] glatiramer acetate , mitoxantrone , natalizumab , [71] fingolimod , [72] teriflunomide , [73] [74] dimethyl fumarate , [75] [76] alemtuzumab , [77] [78] ocrelizumab , [79] [80] siponimod , [80] [81] [82] cladribine , [80] [83] and ozanimod.

Their cost effectiveness as of is unclear. In RRMS they are modestly effective at decreasing the number of attacks. Treatment of clinically isolated syndrome CIS with interferons decreases the chance of progressing to clinical MS.

As of , rituximab was widely used off-label to treat RRMS. The relative effectiveness of different treatments is unclear, as most have only been compared to placebo or a small number of other therapies. As of , review of 9 immunomodulators and immunosuppressants found no evidence of any being effective in preventing disability progression in people with progressive MS.

As of , rituximab has been widely used off-label to treat progressive primary MS. As of [update] , only one medication, mitoxantrone, has been approved for secondary progressive MS. In , ocrelizumab was approved in the United States for the treatment of primary progressive multiple sclerosis in adults. In , siponimod and cladribine were approved in the United States for the treatment of secondary progressive multiple sclerosis. The disease-modifying treatments have several adverse effects.

Fingolimod may give rise to hypertension and slowed heart rate , macular edema , elevated liver enzymes or a reduction in lymphocyte levels.

Both medications and neurorehabilitation have been shown to improve some symptoms, though neither changes the course of the disease. A multidisciplinary approach is important for improving quality of life; however, it is difficult to specify a 'core team' as many health services may be needed at different points in time. The expected future course of the disease depends on the subtype of the disease; the individual's sex, age, and initial symptoms; and the degree of disability the person has.

The average life expectancy is 30 years from the start of the disease, which is 5 to 10 years less than that of unaffected people. MS is the most common autoimmune disorder of the central nervous system. Rates of MS appear to be increasing; this, however, may be explained simply by better diagnosis. MS usually appears in adults in their late twenties or early thirties but it can rarely start in childhood and after 50 years of age.

Robert Carswell — , a British professor of pathology , and Jean Cruveilhier — , a French professor of pathologic anatomy, described and illustrated many of the disease's clinical details, but did not identify it as a separate disease. The French neurologist Jean-Martin Charcot — was the first person to recognize multiple sclerosis as a distinct disease in The first attempt to establish a set of diagnostic criteria was also due to Charcot in He published what now is known as the "Charcot Triad", consisting in nystagmus , intention tremor , and telegraphic speech scanning speech [] Charcot also observed cognition changes, describing his patients as having a "marked enfeeblement of the memory" and "conceptions that formed slowly".

Diagnosis was based on Charcot triad and clinical observation until Schumacher made the first attempt to standardize criteria in by introducing some fundamental requirements: Dissemination of the lesions in time DIT and space DIS , and that "signs and symptoms cannot be explained better by another disease process".

During the 20th century, theories about the cause and pathogenesis were developed and effective treatments began to appear in the s. There are several historical accounts of people who probably had MS and lived before or shortly after the disease was described by Charcot.

A young woman called Halldora who lived in Iceland around suddenly lost her vision and mobility but, after praying to the saints, recovered them seven days after. Saint Lidwina of Schiedam — , a Dutch nun , may be one of the first clearly identifiable people with MS. From the age of 16 until her death at 53, she had intermittent pain, weakness of the legs, and vision loss—symptoms typical of MS.

D'Este left a detailed diary describing his 22 years living with the disease. His diary began in and ended in , although it remained unknown until His symptoms began at age 28 with a sudden transient visual loss amaurosis fugax after the funeral of a friend.

During his disease, he developed weakness of the legs, clumsiness of the hands, numbness, dizziness, bladder disturbances, and erectile dysfunction. In , he began to use a wheelchair. Despite his illness, he kept an optimistic view of life. Barbellion , nom-de-plume of Bruce Frederick Cummings — , who maintained a detailed log of his diagnosis and struggle. There is ongoing research looking for more effective, convenient, and tolerable treatments for relapsing-remitting MS; creation of therapies for the progressive subtypes; neuroprotection strategies; and effective symptomatic treatments.

During the s and s, there has been approval of several oral drugs that are expected to gain in popularity and frequency of use.


Multiple sclerosis



MS hastalığı nedir? MS hastalığı belirtileri ve tedavi yöntemi…


Related Articles