Demyelination Case Study

It is also unclear if it is the brain injury itself that causes the result and if it is the same for healthy people.

Changes in the brain will be that some parts are not getting the blood supply which then leads to dead tissue causing a form of disability depending on the area of the brain affected.

They can cause blood to seep out of the brain and accumulate around it, resulting in increased pressure in the brain. This build up of pressure within the brain can cause altered brain function (1).

memory loss, brain damage, breathing problems, reduced blood flow to the brain as well as a

and affects your central nervous system. When that happen your central body system shut down,

There is no cure for Multiple Sclerosis (Mayo Clinic, 2017). Most treatment is focused on improving quality of life by treating symptoms and slowing its progression. There are a few drugs to help slow progression, most of which are for relapsing-remitting MS (Mayo Clinic, 2017). In March of this year, the FDA approved the first drug for primary-progressive MS (FDA, 2017), called ocrelizumab, which slows the advancement of disability (Mayo Clinic, 2017). Ocrelizumab may cause infusion related reactions, such as hives, shortness of breath, fever, etc, and may lead to an upper respiratory tract infection (FDA, 2017). Acute relapses are treated with corticosteroids to reduce nerve inflammation, a traditional and approved method of treatment. (NIH, 2013). To treat symptoms, those with MS may go to physical therapy to help strengthen muscles and manage gait problems (Mayo Clinic, 2017). They may also use muscle relaxers to treat extremely painful

MS is characterized by the destruction of myelin, inflammation in the CNS and the formation of lesions in the CNS.

Multiple Sclerosis, commonly known as MS is an autoimmune disease of the central nervous system. Scientists have been studying MS since the 19th century. In MS, the body’s immune system produces cells and antibodies that attack myelin in your brain which is essential for the nerves in your brain and spinal cord to conduct electricity to perform its function. The attack on myelin results in vison loss, paralysis, numbness, muscle weakness, difficulty walking, stiffness, spasms, and bladder and bowel problems. MS has varying degrees of severity and affects people between the ages of 20-50, mostly women. Although there are treatments, there is no cause and cure yet.

Individuals suffering from MS face continually worsening symptoms leading to progressing disability and early mortality. There is currently no cure and current treatments have negative impacts on the life of the individual receiving the treatment. The story of the discovery and understanding of the disease spans to almost two centuries of medical research and still there is much to understand. Autoimmune disorders are becoming more common in our society and it is crucial to understand the cause of these diseases and to develop better treatments. In the two centuries of research, the life expectancy of an individual with MS has increased dramatically. Upon diagnosis in the late 1800's and early 1900's individuals had an average life span of 10 years but today, due to advances in medical technologies, individuals with MS may live 30 years or more. More research is required to understand how to better treat this disease or prevent the initial autoimmune response from

Multiple sclerosis (MS) is a demyelinating disease which affects nerves in the brain and spinal cord which results problems in muscle movement, balance and vision. The nerve fiber in the brain and spinal cord are surrounded by layer of protein called myelin which help to protects the nerve and helps electrical signals from the brain travel to the rest of the body. In case of multiple sclerosis the tissue which is affected is myelin sheaths. During multiple sclerosis something goes wrong with immune system and immune system starts attacking myelin sheaths as they recognize them as foreigner bodies. During macrophage myelin sheaths is engulf and they are presented as foreign bodies to the T-lymphocytes cell which produce antibodies and destroy

human MS. In this model, the injection of BM-MSCs improvedthe clinical course and promoted peripheral T cell tolerance tomyelin proteins, thus reducing the migration of pathogenic T cellsto the CNS (Morando et al., 2012; Bai et al., 2009; Gerdoni et al.,2007; Zhang et al., 2005). In this model setting, the therapeuticeffects of MSCs were not likely attributable to graft- or host-driven remyelination, but rather were mediated by an immunemodulatory mechanism guarding the CNS from immune-mediatedinsult (Morando et al., 2012; Rafei et al., 2009). Similarly, BM-MSCs have been reported to have been successfully used in animalmodels of acute disorders, such as stroke or spinal cord injury,while they are disappointingly unable to remedy the neurologicaldeficits when chronic neural damage occurs. These observationssuggest that the immunosuppressive nature of BM-MSCs, whichis substantially increased by inflammatory cues, allows them tomodulate immune response and inhibit inflammation (Uccelli et al.,2011).These findings pose the question of whether the reported ben-eficial effects of BM-MSCs in immune models such as EAE are dueto suppression of the peripheral immune response that damagesmyelin or due to immune-independent mechanisms of action, suchas the direct replacement of the dying cells, oligo/neuroprotection,and/or enhancing endogenous repair. This question is furtherhighlighted by a recent study conducted in a non-immune toxinmodel in which intravenously injected BM-MSCs did

These interruptions of the nerve impulses can cause a whole list of symptoms such as fatigue, numbness, or vision problems. (National Multiple Sclerosis Society, 2017) In general, there are four types of Multiple Sclerosis: Clinically Isolated Syndrome, Relapsing Remitting Multiple Sclerosis, Primary Progressive Multiple Sclerosis, and Secondary Progressive Multiple Sclerosis. Clinically Isolated Syndrome, or CIS, is characterized by 24 hour minimum episode of inflammation and demyelination in the CNS. Those who have suffered from this do not necessarily go on to fully develop Multiple

Multiple Sclerosis, an autoimmune disorder of the central nervous system, was first discovered in 1868 by Jean-Martin Charcot.1,2 He defined it by its “clinical and pathological characteristics: paralysis and the cardinal symptoms of intention tremor, scanning speech, and nystagmus, later termed Charcot’s triad.”2 In Physical Rehabilitation, O’Sullivan, Schmitz, and Fulk defined multiple sclerosis as “a chronic disease of the central nervous system characterized by inflammation, selective demyelination, and gliosis of neurons of the brain and spinal cord.”2 This results in disruptions in the conduction of nerve impulses.2 The National Multiple Sclerosis Society states that more than 2.3 million people are affected by MS worldwide.1 There is no cure for Multiple Sclerosis, but several treatments can be given to help reduce complications and expand the individual’s lifespan. This paper will discuss the anatomy of a neuron, predisposing factors and causes of MS, the disease course of MS, common signs and symptoms, how to diagnose and evaluate for MS, psychological effects of the disease on the patient and his/her family, possible treatment options, cost association with treatment and disability, and special needs and resources in the community to assist patients with MS.

MS is traditionally described as clinical symptoms or signs of two CNS lesions separated in time and space that are not caused by other CNS disease. Due to the absence of a specific immune-based assay, the diagnosis of MS continues to be predicated on the clinical history and neurological examination; that is, finding multiple lesions in time and space in the CNS. Magnetic resonance imaging (MRI) remains the most important diagnostic tool for allowing the early and more precise diagnosis of the disease. Revised diagnostic criteria classify individuals in the categories of MS into either not multiple sclerosis or possible MS based on evidence from MRI (McDonald, 2001).

Scientists who research the epidemiology of autoimmune diseases have experienced many complications in their work. In a field where one plus one rarely equals two, researchers have been work fervently to determine which cell types are responsible for, or at least involved in, autoimmune dysfunction. The main subject of study by Esposito et al. is the deleterious effects of chronic activation of proinflammatory cytokines. To this end, this team has sought to characterize and quantify the cells found in various loci in mice plagued with relapsing-remitting experimental autoimmune encephalomyelitis (RR-EAE), an induce murine model of human multiple sclerosis (MS). Another question of paramount importance is how to elucidate the mechanisms of these cells and their specific cell markers. For example, are certain cells present only in the target organ? Or did these cells migrate to that location? Or were there sequential stages of differentiation that occurred? Or is it a combination of the aforementioned postulates?