Discussion: Traumatic Brain Injuries In Football Research Paper

Discussion: Traumatic Brain Injuries In Football Research Paper ORDER NOW FOR CUSTOMIZED AND ORIGINAL ESSAY PAPERS ON Discussion: Traumatic Brain Injuries In Football Research Paper This will be a 10-15 review paper- done in APA-style- that follows from the content you developed in Assignment One . You will be evaluated on your degree of success in applying the feedback from your first assignment toward your second assignment. This may take various forms, including- enhanced organization of your work, sharpening your take-home message or position, adhering more to APA-style, more careful editing of your writing, etc. Attached is the outline(Assignment 1). Also attached is a sample paper. Suffolk University PS 215 Traumatic Brain Injuries In Football Research Paper attachment_1 attachment_2 Discussion: Traumatic Brain Injuries In Football Research Paper TRAUMATIC BRAIN INJURIES IN FOOTBALL Christian Restrepo NEUR-101 March 9, 2020 Abstract There have been increasing cases of Traumatic Brain Injury (TBIs) in football in recent years. The situation has been partly because of their likely long-term effects, such as neurodegeneration on players. The emphasis of studies has been on incidences of concussions that have been presented at emergency centers. Few studies propose solutions to post-injury long-term effects of traumatic brain injuries. Most studies suggest withdrawal from football to mediate against neurodegeneration. Although there is no exact pathological mechanism of neurodegenerative disorders, studies have associated post-injury oxidative stress to the high risk of neurodegenerative processes. Oxidative stress, therefore, may play a significant part in the working mechanism of neurodegenerative diseases. Accordingly, reactive oxygen species may serve as fluid markers to define and monitor cellular damage. Hence, this study proposes the need to investigate the pathophysiology of TBIs and neurodegenerative disorders to understand factors that elevate the risk of neurodegenerative diseases among footballers. Keywords: Traumatic Brain Injury, Football, Pathophysiology, Oxidative Stress, Reactive Oxygen Species TRAUMATIC BRAIN INJURIES IN FOOTBALL Statement of the Problem Incidences of traumatic brain injuries (TBIs) in football have received considerable attention in recent years. This condition has been partly because of the growing interest in the literature concerning their potential long-term impact (Manley et al., 2017). TBI is among the leading cause of death as well as disability among youth and adult football players. Some studies have shown the association between the long-term effect of TBIs and neurodegenerative diseases. The main ones include Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS), which have been linked with the brain injuries that happen during football matches (Cruz-Haces et al., 2017). Although there has been a high prevalence of TBIs for neurodegenerative disorders, few preventive treatments have been proposed besides withdrawal from football. Partly, this is because the mechanisms that result in neurodegeneration remain unclear. Oxidative stress has been associated with neurodegeneration (Cruz-Haces et al., 2017). Reactive oxygen species are promising as a therapeutic mediation in AD pathogenesis (Cruz-Haces et al., 2017). As such, there is a likelihood that oxidative stress after a brain injury could be a vital primary mechanism that associates TBIs with increase risks of neurodegeneration. Therefore, there is a need to examine the pathophysiology of TBIs and neurodegeneration to determine factors that trigger neurodegenerative developments. Introduction and Purpose of the Study TBI and Degenerative disorders Incidence of Traumatic Brain Injury There are about 1.6 million reported TBI cases globally each year, out of which, 173,285 are associated with sports activities (Cruz-Haces et al., 2017). As the number of participants continues to increase, the prevalence of TBIs also increases proportionally (Randolph et al., 2013). This study’s purpose is to examine the pathophysiology of TBIs and neurodegeneration to identify factors that trigger neurodegenerative developments Why is it a Health Concern? Acute sports-related TBI can result in concussions and hemorrhage, as well as structural brain damages (Cruz-Haces et al., 2017). Apart from initially causing mechanical damage, TBI can trigger a secondary injury that may result in long-term neurological disorders; hence, it is a severe global public health issue (Montenigro et al., 2017). Pathological Mechanisms of TBIs in Football Acute TBI Brain Injuries In most instances, TBI arises from a physical blow targeting an individual’s head when experiencing a traumatic event in football (Randolph et al., 2013). Clinically, TBI is categorized as mild, moderate, or severe according to history, such as the length of unconsciousness as well as clinical observations (Lehman et al., 2012). Varying clinical descriptions between governing institutions leads to difficulties in comparing incidence rates of mild TBI (Montenigro et al., 2017). These inconsistencies can be severe because of the acute effects of TBI, like second impact syndrome (Ling et al., 2015). Secondary Impact Syndrome Second impact syndrome is a highly feared complication among footballers, which involves a sustained brain injury for the second time even before the symptoms of the first have not completely cleared (Manley et al., 2017). Typically, the second injury involves a minor blow on a footballer’s head, but shortly, the footballer collapses into a coma. Suffolk University PS 215 Traumatic Brain Injuries In Football Research Paper It is proposed that a footballer experiences cerebral edema after the second impact syndrome, which results in herniation. Secondary Impact Syndrome is prevalent in children as well as adolescents, especially males between 10 and 24 years, and 71% happened in American Footballers, mostly at the high school level (Manley et al., 2017). Pathological Mechanisms of Neurodegenerative disorders Although there is an inconsistent clinical representation, AD, PD, and ALS possess many similar characteristics. And although most instances are idiopathic, all three diseases have defined genetic risk factors (Lehman et al., 2012). These illnesses are pathologically defined by the degeneration of particular neuronal individuals connected to the clinical symptoms (Cruz-Haces et al., 2017). Although there are no precise pathogenesis mechanisms, studies suggest that oxidase stress and neuroinflammation significantly contribute to the pathophysiology of neurodegeneration, especially in AD, PD, and ALS (Montenigro et al., 2017). AD has a considerably high incidence in older people, which substantially decreases the quality and expectancy of life (Cruz-Haces et al., 2017). AD’s pathology entails neuritic plaques, including the loss of the brain’s cholinergic neurons, although the mechanisms resulting in this situation remain unclear (Montenigro et al., 2017). Conclusion and Proposed Research Available Studies Oxidative stress has been linked with neurodegeneration as well as secondary brain injury, which suggests that oxidative stress after a brain injury among footballers is a most likely mechanism which relates TBIs to the high prevalence of neurodegenerative disorders (Grimberg-Peters et al., 2016). Studies show that oxidative stress is a critical determinant of AD pathogenesis because of the evidence of high neurotoxic markers of lipid peroxidation (Lehman et al., 2012). As a result, reactive oxygen species, including their byproducts, may help as fluid markers to identify and monitor damages to the cells (Cruz-Haces et al., 2017). Also, the reactive species may be an effective therapy to decrease the incidence of neurodegeneration resulting from brain injuries (Grimberg-Peters et al., 2016). Besides, they can also offer long-term improvement of life for individuals with TBIs. Gaps in Research Although there is an increased incidence of TBIs for neurodegenerative diseases, few studies have proposed prophylactic treatments apart from a recommendation for footballers to withdraw from football. Current research proposal Examine the pathophysiology of TBIs and neurodegeneration to define factors that increase the prevalence of neurodegenerative disorders. Suffolk University PS 215 Traumatic Brain Injuries In Football Research Paper References Cruz-Haces, M., Tang, J., Acosta, G., Fernandez, J., & Shi, R. (2017). Pathological correlations between traumatic brain injury and chronic neurodegenerative diseases. Translational Neurodegeneration, 6(1), 1-10. Grimberg-Peters, D., Büren, C., Windolf, J., Wahlers, T., & Paunel-Görgülü, A. (2016). Hyperbaric Oxygen Reduces Production of Reactive Oxygen Species in Neutrophils from Polytraumatized Patients Yielding in the Inhibition of p38 MAP Kinase and Downstream Pathways. PLOS ONE, 11(8), e0161343. Lehman, E., Hein, M., Baron, S., & Gersic, C. (2012). Neurodegenerative causes of death among retired National Football League players. Neurology, 79(19), 1970-1974. Ling, H., Hardy, J., & Zetterberg, H. (2015). Neurological consequences of traumatic brain injuries in sports. Molecular and Cellular Neuroscience, 66, 114-122. Manley, G., Gardner, A., Schneider, K., Guskiewicz, K., Bailes, J., & Cantu, R. et al. (2017). A systematic review of potential long-term effects of sport-related concussion. British Journal of Sports Medicine, 51(12), 969-977. Montenigro, P., Alosco, M., Martin, B., Daneshvar, D., Mez, J., & Chaisson, C. et al. (2017). Cumulative Head Impact Exposure Predicts Later-Life Depression, Apathy, Executive Dysfunction, and Cognitive Impairment in Former High School and College Football Players. Journal of Neurotrauma, 34(2), 328-340. Randolph, C., Karantzoulis, S., & Guskiewicz, K. (2013). Prevalence and Characterization of Mild Cognitive Impairment in Retired National Football League Players. Journal of The International Neuropsychological Society, 19(8), 873-880. Get a 10 % discount on an order above $ 100 Use the following coupon code : NURSING10

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