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MULTIPLE SCLEROSIS

Multiple Sclerosis

Multiple sclerosis is a Chronic neurological condition that causes disability and limit participation in young adults. Many of the patients of Multiple Sclerosis are of the ages of twenty to fifty, although it is possible for one to get the disease at an early as of two years and elder age of seventy-five years. Some medical practitioners think it is an autoimmune disease, but others disagree because they do not know any specific immune target of the disease. For this reason, they categorize it as an immune-mediated disease. This disease cannot spread from one person to the other, and for the reason it falls under the group of non-communicable diseases. Health practitioners do not regard Multiple Sclerosis as a fatal ailment since many of the patients learn to live with it and manage a normal life span (Sandra and Hans, 2012).

To glean how multiple sclerosis spreads and damages the brain, axon, cells and body, it is essential to study the basic structure of the central nervous. The central nervous comprises of the brain and spinal cord. The Central nervous system is full of nerve cells (neurons). These are the brain cells. The brain looks like a net work of cables rounded up to form a ball like structure. These cables like structures are the neurons (brain cells). Brain cells are different in diverse parts of central nervous system. The axon is an elongated strand comprising soma and myelin sheaths. The axon looks like a necklace of sausage like structures threaded together. Since it is part of the neurons in the brain white matter, tissue it is among the cells prone to Multiple sclerosis attacks. The soma has thin branch like protruding growing from it (dendrites). The axon of one neuron connects to dendrites of other neurons through a synapse (special connection of neurons). Signals travel through axon and pass to other neurons through neurotransmitters (chemical signals) moving across the special connection of nerves. The axon has a coating of a fatty layer of protein (myelin), which aids transmission of brain signals. Axon’s maintenance cells create and repair the myelin sheath. This is the basic structure of the brain (Steen, et al., 2013).

Multiple Sclerosis damages cells, brain, axon and body through drawing of white blood cells to areas of white matter. This results to an inflammatory response same as of the skin to pathogens that cause pimples. This causes the stripping of myelin from axon. This cause parallels to the myelin coating and soon transmission of nerve impulses stops or slows. Inflammation also kills brain maintenance cells. Once inflammation destroys myelin sheath and axon, it is no longer possible for nervous systems, which coordinate the body activities to take place. This is in turn causes disability of the body (Serafin, et al., 2013).

Nervous system, spinal cord, brain coating and myelin produce substances that attract B cells, which are a sub group of lymphocytes. B cells later produce antibodies when they are mature. Once B cells are in the brain, axon and spinal cord they produce toxic substances, which destroy oligodendrocytes (cells producing myelin). It is through the spread of B cells across the brain and spinal cord that Multiple Sclerosis spreads throughout the brain, axon and spinal cord. B cells regulate other lymphocytes, and it is for this reason they produce toxic substances to counter attack T cells found in the brain (Alastair and Alasdair, 2008).

Multiple sclerosis manifests itself in patients in either one of the four available courses. These are relapsing-remitting, Primary-progressive, secondary-progressive and Progressive relapsing Multiple sclerosis (Talbot, 2010). The four are either placid or severe depending on a patient. Relapsing–remitting is a condition that exhibits clearly defined attacks of worsening neurologic functions. These attacks are relapses, flare-ups, or exacerbation. These attacks occur in the form of the disease worsening after a period of latency. During the remission stages, no progression of the disease occurs. Doctors diagnose about eighty-five percent of Multiple sclerosis patients with relapsing-remitting Multiple sclerosis in the first diagnoses.

The second course of Multiple sclerosis is the primary-progressive sclerosis. Slowly worsening neurologic functions characterize the disease course from the onset without any relapses or remissions. Rate of disease progression varies with minor improvements and latencies. Health care specialists diagnose about ten percent of multiple sclerosis patients with this level of multiple sclerosis.

The third level of the disease is the secondary-progressive multiple sclerosis. After the relapse-remitting stage, many patients develop secondary-progressive multiple sclerosis. The disease in this level worsens steadily without flare-ups and remissions. In the past, about half the number of people diagnosed with remitting-relapsing multiple sclerosis developed this disease in a period of about ten years. No data is available to prove that these medications delay the progress of the disease.

The fourth stage of multiple sclerosis is the progressive-relapsing course. This is a very rare condition affecting about five percent of all multiple sclerosis patients. In progressive-relapsing course, one experiences steadily worsening disease from the onset, but with no clear attacks of worsening nervous system function. Some people experience a bit of recovery in this stage while others do not. The disease continues to progress without any remissions.

Doctors are yet to find exactly what causes multiple sclerosis, but there is interesting information suggesting that a person’s environment, genetics and viruses play a role in the spread of the ailment. Some doctors disagree with these findings while others support them as possible causes of the disease (Richman and Scrub, 2012).

Epidemiological data indicates interesting trends of multiple sclerosis. Different people and population groups have different prevalence of the condition. The disease is common in Scotland, Scandinavia and across the northern part of Europe. In USA, prevalence is higher in whites than among other racial groups. Studies show that some areas have higher multiple sclerosis prevalence than others. These studies also suggest that if one moves from an area with high prevalence to an area with low prevalence of the disease, the risk of acquiring the disease lowers with the risk associated with the new environment. This is the case if the movement occurs before puberty. This data implies that exposure to environmental agents before adolescence poses a threat of multiple sclerosis infection to a person. Both hemispheres of the earth experience high multiple sclerosis levels. This has led to the notion that multiple sclerosis is a disease of temperate climates. As a result, its prevalence increases with distance from the equator (Korteweg, 2011).

Some researchers believe multiple sclerosis is an inherited condition that runs through ancestry lines. These researchers believe there is more than one gene that increases the risk of acquiring this condition. Some argue that multiple sclerosis develops because one has an inborn genetic predisposition to react to environmental agents, which trigger auto immune responses. Auto immune responses refer to the error of genes, which manage to lack of differentiation between body genes and external pathogens (Steen, et al., 2013).

Other studies suggest the cause of the condition is viruses. Studies have suggested that several viruses such as Epstein-Barr, vermicelli zoster and hepatitis vaccine cause of multiple sclerosis. Doctors are yet to prove this study (Serafin, et al., 2013).

At times, multiple sclerosis may not show any symptoms; this makes it hard to detect whether one suffers from it or not. The specialist in such a case uses several strategies to diagnose the condition. These strategies include analysing medical history, brain examination and other test such as magnetic resonance imaging, evoked response techniques and spinal-fluid analysis. To diagnose multiple sclerosis a physician must first find evidence of damage in the central nervous system; then try to find evidence that this damage occurred at least a month apart then later rule out any other possibility for the damage. There is an international guideline, which specialists follow in carrying out the diagnosis. Doctors also use these techniques to assess second area damage in an individual (relapse) of Multiple Sclerosis, also referred to as clinically isolated syndrome (Miller, et al., 2009). An individual with this condition may or may not progress to the multiple sclerosis stage.

A medical history analysis is one of the techniques health specialists use to diagnose multiple sclerosis. In this test, the specialist takes a careful history and any past and present symptoms of multiple sclerosis. The doctor also gathers information such as age, birthplace, ancestry history and places an individual has travelled to find clues of the condition. The physician then performs several tests to assess the mental, speech functions, emotional, coordination, body balance and normal functions of other body senses (Franciotta, et al., 2008).

Magnetic resonance imaging is another method doctors use to diagnose multiple sclerosis. This is so far the best imaging technique that doctors can use to discover lesion (scarring) in the central nervous system. The technique can also differentiate new and earlier scars. However, despite the efficiency of this technique, health practitioners cannot rely solely on this method to diagnose sclerosis since there are other conditions such as cysts, which cause scarring in the central nervous systems. It is essential to realize that about five percent of people diagnosed with multiple sclerosis do not initially have lesions (Korteweg, 2011). Visual evoked techniques record the nervous system’s electrical response through stimulation of certain sensory transmission paths, such as auditory, visual and general sensory. Destroying myelin results to slowing of response, the evoked techniques give evidence for slowed sensory responses. Spinal fluid test is another technique doctors use to detect sclerosis. This method detects the level of certain immune system proteins and presence of oligoclonal bands (Serafin, et al., 2013). The bands that show an immune response within central nervous system are present in spinal fluids of about ninety percent of people with multiple sclerosis (Coles, et al., 2009). Health practitioners cannot rely on this method solely since there are other conditions such as migraine, cysts and malformations, which show similar results.

Health practitioners are yet to find a cure for multiple sclerosis. However, there are therapies, which slow down the disease. The aim of multiple sclerosis’ treatment is to control symptoms and help an individual keep up a normal life style (Hafler, 2013). Therapies available to patients include speech therapy, occupational therapy and support from other groups of people. Speech therapy helps people learn alternative ways of speech if they lose this vital sensory function. Occupational therapy is to help people make a living despite losing their sensory functions. Support group therapy helps a patient over come side effects of the disease such as depression (Darcy, 2012).

Recent studies show that early treatment helps patients delay disability, perhaps through decrease of injury to the nervous system. Treatment of Multiple sclerosis falls into two categories. The first group is the treatments that address symptoms management of the disease such as therapeutic treatments. The second group is of treatments, which change the course of the disease (Alonso and Hernia, 2008). The treatments that alter the course of disease do this via modifying a number of attacks and their severity. FDA has already approved six different multiple sclerosis products. The six are three interferon-beta products (Avonex, Betaseron and Rebif) and three unrelated products (Novantrone, Tysabir and Copaxone).

Betaseron was that first drug that FDA approved and marketed in USA. As with all beta interferon, this product shuts down inflammation of multiple sclerosis lesions through different mechanisms including repairing blood brain-barrier and reducing inflammatory process of lesions. Anovex slows down the rate of disability in relapsing-remitting multiple sclerosis and amount of accumulated multiple sclerosis damage. Rebif is same in structure to anovex. However, Rebif is effective in reducing the number and severity of disability and the number of new lesions (Franciotta, et al, 2008).

Copaxone treatment product differs from beta interferon in chemical composition. These products consist of a group of amino acids, which look like myelin. The drug acts through suppressing the immune system’s attack on myelin. It decreases the frequency and severity of attacks to a similar extent as Betaseron, but with a less effect on lesions. Doctors administer this drug daily to patient through subcutaneous injections. The product is effective for treating relapsing-remitting course of multiple sclerosis. Tysabir is another non-beta inferno product that doctors use to treat multiple sclerosis. This product blocks receptors on white blood cells from entering spinal cord and brain. Tysabir slows down the progress of disability. Novantrone is a non-toxic chemotherapy agent that slows multiple sclerosis progression and reduces relapses through suppressing activities of T Cells and B cells. This product is effective in treating almost all the courses of multiple sclerosis (Franciotta, et al., 2008)

Research shows that more than fifty percent of the world’s population are genetically incapable of developing multiple sclerosis regardless of their environments (International Multiple Sclerosis Genetics Consortium, 2009). The most susceptible areas are northern America and Europe. The two places determine regional variations in disease characteristics. Many of multiple sclerosis patients are women, with about seventy-five percent of all patients been women. Despite the many female patients research records that men have a sixty percent chance of being genetically susceptible. In the recent years, women have shown high response to environmental changes.

Research has also brought developments in diagnoses of the disease. Doctors used assumption methods to diagnose multiple sclerosis in the past. This often led to misdiagnosis and probably wrong medications. In the recent years, research has seen doctors adopt new strategies in diagnoses of the disease. One of the new strategies doctors use in modern diagnosis is the Multiple sclerosis diagnosis international guideline (Alonso and Hernia, 2008). This guideline guides doctors on the techniques and methods they are to use when testing patients for multiple sclerosis. This has contributed to the success of medical practices ion treatment of multiple sclerosis. Modern technologies such as evoked technology systems and Magnetic resonance imaging are able to detect symptoms even when the patient shows no visible symptoms (Serpell, Notcutt and Collin, 2013). Researchers have also provided us knowledge of ailments, which show similar symptoms and signs to multiple sclerosis.

A recent research study has given hope to multiple sclerosis patients. This is the year 2008 Myelin repair research. In the year, 2008 Myelin Repair Foundation got the first patent and in 2010, the second patent of the research. This research has similar suggestions as to the cause of multiple sclerosis with the Professor Jeffrey’s 2001 research on multiple sclerosis. Both studies show that multiple sclerosis might be an autoimmune infection. This supports the idea that multiple sclerosis occurs because of the immune system errors. The Myelin Repair research differs with Jeffrey’s research in treatment for the condition. The research Jeffery did aimed at discovering medications for symptoms while Myelin repair research aims at discovering treatments to control development of the condition. This new development is necessary in helping people at risk of the disease to delay the progression of the condition (Murray, 2008).

In conclusion, Multiple sclerosis is a disease, which destroys an individual’s central nervous system. Once the disease has destroyed the central nervous system, impulses from the brain and spinal cord can longer pass through nervous fibre in a normal way. This altering of transportation of nervous impulses affects normal body and sensory coordination and functions. This is the cause if disability and loss of sensory functions in patients of multiple sclerosis. Researchers have developed new methods and techniques, which make it easy to diagnose and slow the progress of this disease. There are other medicines and treatment options still under study, which has created hope for people with multiple sclerosis.

References

Alastair C and Alasdair A. (2008). Report From request, The Lancet, vol. 372, no 9648, pp1502-1517.

Alonso A and Hernia A. (2008). Temporal trends in the incidence of multiple sclerosis. Neurology, 71(2), 129-135.

Coles J, Compston D, Selma K, et al. (2009). Experimental medicines in multiple sclerosis and compassionate use. J R Coll Physicians Ed in, 39, 35–7.

Darcy C. (2012). Multiple Sclerosis: An overview Clinical review MS part 1. Nursing and Residential Care, 14(8), 335-337.

Franciotta D, Salver M, Lolli F, Aloisi F and Serafini B. (2008). B cells multiple sclerosis. Lancet Neurology Journal, 7( 9), 852 – 858.

Hafler DA.( 2013). Multiple Sclerosis. The journal of Clinical Investigation, 788-792.

International Multiple Sclerosis Genetics Consortium. (2009). SHORT COMMUNICATION The expanding genetic overlap between multiple sclerosis and type diabetes. Genes and Immunity. 10, 11–14.

Korteweg T. (2011). MRI in Multiple Sclerosis:From diagnosis to prognosis. Lancet neurology, 5, 221-227.

Murray T, (2008). Multiple Sclerosis: The History of the Disease, Dalhousie MS Research Unit.

Richman S & Scrub T. (2012). Quick Lessons about Multiple Sclerosis. California, and Clinical information system.

Sandra A, and Hans, V N. (2012). Multiple Sclerosis. Oxford.

Serafin B, Muzio L Rosicarelli B and Aloisi F. (2013). Radioactive in Situ: hybridization for Epstein–Barr virus–encoded small RNA support the presence of Epstein–Barr virus in the multiple sclerosis brain. Brain Journal of Neurology, 1-6.

Serpell G, Notcutt W and Collin C. (2013). Sativex long-term use: an open-label trial in patients with spasticity due to multiple sclerosis. Journal of Neurology, 260(1), 285-295

Steen C, D’haeseleer M, Hoogduin J, Ferns Y, Cambron M, Mostert J, Heersema D, Koch M and De Keyser J. (2013). Cerebral white-matter tissue, blood flow and energy metabolism in multiple sclerosis. Multiple Sclerosis Journal.

Talbot, P. 2010). Understanding the Types of Multiple Sclerosis and Prognostic Indicators. British Journal of Neuroscience Nursing, 6( 4),161-166.

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