Multiple Sclerosis is the most common condition that destroys myelin in the central nervous system. The immune system attacks the protective sheath (myelin) that covers nerve fibers and causes communication problems between the brain and the rest of the body. It is mostly seen between the ages of 20 and 40, making it the leading disabling neurologic disease for young people.
Myelin is the proteolipid membrane that surrounds nerve axons to improve their ability to conduct electrical action potentials. When myelin is stripped away from the axon, the underlying membrane does not contain a high enough concentration of sodium, potassium, and other ionic channels to permit a sufficient flow of ions to cause depolarization. The loss of myelin makes it impossible to depolarize the membrane to conduct an action potential, so the nerve is rendered useless.The demyelination is largely an inflammatory process. Lymphocytes, macrophages, and other immunocompetent cells accumulate around venules focally in the central nervous system and exit into the brain, attacking and destroying the local myelin, in what appears to be an autoimmune process.
The most common symptoms of MS are pyramidal weakness, visual loss, sensory loss, brain stem dysfunction, cerebellar ataxia and sphincter disturbances. The diagnosis of MS are made with clinical criteria, MRI, cerebrospinal fluid analysis and evoked potentials.
MS usually follows one of a few distinctive patterns, classified largely on the timing of the symptoms. Individuals without overt clinical symptoms but with MRI features highly suggestive of MS can be identified as having a radiologically isolated syndrome (RIS). The first step of management is to exclude other differential diagnosis. Persons with RIS are at risk of developing MS but they do not suffer from MS yet. We follow these persons without treatment. A clinically isolated syndrome (CIS) is the first presentation of signs and symptoms that show characteristics of inflammatory demyelination that could be MS but is only a single monophasic event (not disseminated in time). An example of a CIS would be an episode of either optic neuritis or transverse myelitis or another single isolated event. If such patients have abnormal magnetic resonance imaging (MRI) showing other (asymptomatic) lesions characteristic of MS, it is highly likely that a CIS is actually the initial attack of MS. Relapsing–remitting MS is the most common pattern, accounting for about 80% of all MS. Patients have the sudden onset of neurologic symptoms that usually last several weeks and then resolve, often leaving few or no deficits. There is no progression of disease between attacks. Some patients develop symptoms slowly and gradually, progressive over 6 to 12 months or more. If this gradual worsening develops after an initial relapsing–remitting disease course, it is referred to as secondary progressive MS. Approximately 10% to 15% of all MS patients never experience a CIS or a relapse but rather have chronic progressive symptoms from the onset. This is referred to as primary progressive MS.
A few factors may portend a good prognosis. Early age of onset (first symptoms before age 40), sensory symptoms at onset (as opposed to weakness, ataxia, or other motor abnormalities), a relapsing–remitting course (vs a primary progressive symptom at onset) and female gender are good prognostic factors.
MS treatment involves acute attack and disease-modifying measures. A number of studies have suggested superiority of steroids over placebo for alleviating relapses of MS. Symptoms resolve more quickly, although it is not clear if treatment of attacks ultimately prevents disability or mitigates the final outcome of the disease. There is no cure for Multiple Sclerosis, but several drugs have been approved as long-term maintenance therapy to reduce the rate of attacks in relapsing–remitting MS. Immunomodulatory therapies for MS are interferon ß-1a (Avonex® and Rebif®), interferon ß-1b (Betaferon®), Glatiramer asetat (Copaxone®), Teriflunomid (Aubagio®), Dimetil fumarat (Tecfidera®),Natalizumab (Tysabri®), Fingolimod (Fingya®), Okrelizumab (Ocrevus®)and Alemtuzumab (Lemtrada®).In this drugs Teriflunomid (Aubagio®), Dimetil fumarat (Tecfidera®) and Fingolimod (Fingya®) are pills.
Management of neurologic deficits is an important part of the treatment of MS. The most disabling symptoms reported by patients are fatigue, motor deficits, and sphincter disturbance.
We do not know the exact answer to this question. MS is more common the farther one moves away from the equator. It is more common in women than men. It primarily strikes people of northern European ancestry and is almost unknown in other racial groups. There is no direct genetic transition. The risk of developing disease in persons who have MS in close relatives is 3%.
No. It is enough to eat plenty of vegetables, fruits, fish, grilled meat and chicken and not to eat processed food. Only during the treatment of cortisone salt, sugar, flour, fat should be avoided.
Patients whose disease are under control can of course have children. Studies have shown that the likelihood of exacerbation during pregnancy has decreased, but the risk of attack increased especially in the first 3 months after pregnancy. Multiple Sclerosis patients can breastfeed their children. However, since the drugs pass into milk during the breastfeeding period, disease-preventive treatments cannot be applied. Therefore, the treatment should be restarted as soon as possible after a short period of breastfeeding.