What is Emes (MS) Disease? Emes (MS) Disease Treatment Methods

What is Emes (MS) Disease?

Today, we often hear the name of Emes (MS), the disease known as Multiple Sclerosis in the medical language. So what is Emes (MS) disease? What are the symptoms of Emes disease? What does Emes disease mean? What causes Emes disease? Will Emes kill the disease? How long is the life of Emes patients? Is there a cure for Emes disease? Here we researched and answered all these questions for you.

WHAT IS EMES (MS) DISEASE?

MS is a chronic disease of the central nervous system originating from the immune system, in which permanent demyelinated plaques are formed with gliotic scar associated with varying degrees of axon loss as a result of repeated inflammatory demyelination.

The central nervous system, the region affected by the disease, controls the information received from the sensory organs of the person and processes it in the brain. This information is provided by electrical impulses transmitted by nerve cells. When looking at the nerve cell, the cell body consists of the dendrite, axon and myelin sheath consisting of the fatty structure on the axon. Electrical impulses received from the sense organs enter the nerve cell from the dendrite side and come to the axon. Thanks to the myelin sheath in the axon, these impulses are accelerated and pass to the other nerve cell via synapses. The neuron myelin allows an electrical impulse to be transmitted faster than 100 meters per second. If the myelin sheath surrounding the neurons is destroyed or damaged, the nerve impulses slow down, are transmitted to the wrong units or become completely non-transmissible.

The clinical classification of the disease is largely based on the course of the disease and there are 4 types in general. These;

Relapsing-Remitting MS (NIMS)
Secondary-Progressive MS (IIMS)
Primary Progressive MS (BIMS)
Progressive-Relapsing MS (INMS)

Although MS disease has been categorized and subtypes defined, the course and symptoms of the disease are quite heterogeneous. Although approximately 85% of the diseases are the most common form of the NIMS type, how to actually diagnose the different symptoms and classify them as one type is a really significant challenge. Because this classification has important effects on understanding different pathophysiological mechanisms and targeting treatment.

What Causes Emes (MS) Disease?

Although the cause of MS is not known exactly, it is accepted as a "complex character" triggered by environmental factors in genetically sensitive / susceptible individuals. The complexity of the genetic component has been demonstrated by familial studies and recent genome studies. Although MS is not a hereditary disease, the visibility of MS cases in the same family reveals a strong interaction with genetic components. MS in first-degree relatives of patients with MS significantly reduced the risk of risk seen in the normal population (absolute risk 2-5%) is higher by 10-50 times the risk of monozygotic twins is about a third of a percent. Thanks to whole genome linkage analysis studies, MSSeveral gene loci thought to be associated with The human leukocyte antigen complex (HLA), which encodes genes associated with immune functions, identified in the early 1970s, is the first genetic risk factor found. Recent studies show that the HLA class II extension DRB1 * 1501 haplotype poses a very strong genetic risk for MS . Recently, interleukin 2 receptor alpha gene (IL2RA) and interleukin 7 receptor alpha gene (IL7RA) alleles have also been identified as risk factors. Additionally, a number of non-MHC genes / loci associated with MS susceptibility have been identified.

In all recent genome-linked analysis studies , 135 potential MS- related loci were determined by screening 161,311 autosomal variants by performing genotyping sequence analysis in 14,498 MS patients and 24,091 healthy control samples (Beecham et al.2013 ). Most of these genes (CXCR5, IL2Ra, IL7R, IL12RB1, IL22Ra2, IL12A, IL12B, IRF8, TNFRSF1A, TNFRSF14 and TNFSF14, CD37, CD40, CD58, CD80, CD86, CLECL1, CBLB, GPR65, MALT1, RGSAG1, TYK2) supports that MS is immune mediated as it is associated with the immune system.

Despite all these, many genetic factors underlying the susceptibility to MS are still unclear. Moreover, genetic predisposition is not the sole cause of MS risk factors , it is known that environmental factors also play a role. It has been suggested that environmental factors such as viral infections, smoking and vitamin D deficiency are important in the pathogenesis of MS. The strong connection between vitamin D deficiency and Epstein-Barr virus infection with the occurrence of MS has been demonstrated by studies. Smoking is emerging as another important environmental risk factor for MS susceptibility . As with other risk factors, smoking can affect susceptibility to MS in connection with other genetic and environmental factors.

Although the cause is not fully known, most evidence supports autoimmune pathogenesis in disease formation. Recent studies of MSIt shows that myelin specific CD4 + T cells play a critical role in the initiation of the autoimmune response. Autoreactive T cells are deleted by the thymus during the establishment of central tolerance. However, this process is not perfect. From time to time, some autoreactive T cells are released into the peripheral system. In healthy individuals, this functioning is under control by peripheral tolerance mechanisms. However, these mechanisms are suppressed due to the suppression of the functions of regulatory T cells and / or the increased resistance of effector B and T cells. Thus, central nervous system (CNS) autoreactive T and B cells are activated in the peripheral system. Genetic and environmental factors, including the aforementioned infectious agents and components such as smoking, contribute to these events.

Activated CD8 + T cells differentiated CD4 + helper T1 (Th1) and Th17 cells, B cells and innate immune cells can infiltrate the CNS, causing inflammation and tissue damage. Immune cell infiltration from the periphery to the CNS can be through the direct passage of the blood-brain barrier in the cerebral blood vessels, through the subarachnoid space, or through the choroidplexus through the blood-cerebrospinal fluid (CSF) barrier. These cells accumulate in the perivascular spaces and enter the central nervous system (CNS) parenchyma. Together with activated CNS-resident microglia and astrocytes, these entering cells trigger oligodendrocyte (ODC) damage, demyelination, and neuroaxonal injury through mechanisms associated with direct cell contact and the action of soluble inflammatory and neurotoxic mediators.

Emes (MS) Disease Symptoms

Initial symptoms may include headache, loss of vision, diplopia, decreased vision in one or both eyes, imbalance or loss of strength in the arms and legs. In some cases, no symptoms may occur. Since the symptoms of the disease vary according to the area of involvement in the brain, there is a wide range of symptoms. Generally, symptoms can be listed as follows. Blurred or double vision, ataxia, Babinski's sign, nystagmus, clonus, clumsiness, dysarthria (speech disorder), mood disorders, fatigue, hemiparesis, paresthesia, frequent urination and incontinence, incoordination (coordination disorder), monoparesis Hyperactive deep tendon reflexes (such as kneecap reflex).

Treatment of Emes (MS) Disease

There is no known definitive reversible treatment for MS disease , there are lifelong treatment methods to increase the quality of life of the patient and prolong life. We can collect them under the following headings; Supportive therapy, relapse treatment, symptomatic therapy and rehabilitation therapy aimed at suppressing disease activity with neuroprotective methods. Among these treatments, interferon and its derivatives play an important role in treatment. Since interferon treatment suppresses the effect of the immune system on the CNS, it is possible to slow down or even stop the course of the disease if MS disease is initiated in the early stages. This is why early diagnosis of the disease is very important and intensive studies are ongoing for early diagnosis.