Essay, 8 pages (2000 words)

Chronic moved to chronic progressive traumatic encephalopathy of

Chronic Traumatic EncephalopathyKaryna LipaiTouro College AbstractThe purpose of this paperis discussing (CTE) cause, diagnosis, treatment, advancements and ways ofprevention. Existing and current methods of treating of CTE have beeninvestigated with the purpose of bringing some more light in diagnose andtreatment of CTE. Deficits of the existing methods have been identified as wellas the probable future ways of mitigating the situation of CTE treatment andprevention. There still identification that researchers of CTE should have aclear understanding of the pathology of CTE. The conclusion is that no currentmethod is available to diagnose CTE in premortem approach; only postmortem isavailable.

Chronic Traumatic EncephalopathyThe disorder is believedto be linked with contact to recurrence of skull trauma. It was realized in the1900’s and it was reported in clinical cases that were defined in boxers. Theterm Chronic Traumatic Encephalopathy is the replacement of the term ‘punch drunk’that was in use by then and was introduced by a Dr. Harrison Martland, about 86years ago (Martland, 1928).

Later, the disorder became popularly known aspugilistic dementia and then the name moved to chronic progressive traumaticencephalopathy of boxers, before changing to the current term, ChronicTraumatic Encephalopathy (Critchley, 1957; Millspaugh, 1937). Furthermore, thedisorder consists of a number of an array of clinical manifestations, whichrange from behavior and motor dysfunction, complete dementia, to mildcognitive.On the other hand, it hasbeen identified that CTE takes place in patients who have a history ofclosed-head trauma. The condition is highly found in individuals that are proneto repetitive symptomatic concussions. The individuals include militaryold-timers, athletes, and domestic violence sufferers. What trauma does is thatit precipitates the neurodegeneration of the flesh found in the brain and thislead to forming of tau protein (Blumbergs et al, 2010). Basically, the point isthat CTE the accumulation of p-tau.More specifically, thetau proteins are neuro-specific initiators of the formation of the microtubule.

The result of this is the issue that the cerebral transportation of wastes andnutrients is affected (Castillo-Carranz, 2014). In addition to this, it isworth noting that cells communicate to enable metabolic processes, and inreference to the buildup of the defective tau, the communication in between thecells is interfered with. On the other hand, McKee et al (2009) identifiedthat lack of healthy tau causes what is death termed as neuronal death. Diagnose of CTEFor the purposes ofdeveloping treatment and diagnostic methodologies, researchers required a clearunderstanding of the CTE pathology.

They are needed to identify differencesthat exist in between neurodegenerative diseases and Chronic TraumaticEncephalopathy. A study conducted in 2009 identified a pervasive cerebral fluidbuildup of mutated tau protein in all the athletes that were used in the study.On the side of the 24 control subjects, there was no accumulation of tau. Theconclusion of the research was that head the athletes; the head injury was aresult of motor neuron degeneration, and in turn, led to a disease and notadvanced life support. The findings of this research helped in defining thevariations that exist in between Chronic Traumatic Encephalopathy and otherneurological degenerative disorders whose basis are tau. The research experienceda development later, and at this time, McKee and Gavett (2011), explained thebuildup of tau protein and the role it has in the degenerative process ofChronic Traumatic Encephalopathy. The report includes that information that thebrain temporary deformation is due to the motion of the initial trauma as wellas the aggravation by traumatic injuries following each other, which wereidentified to cause stretching of the axons (Critchley, 1957). This then wouldlead to damage that in turn changes the degree of the axon membranepermeability, which causes a larger amount of calcium inflow.

Also, thepermeability enhances the release of apoptotic aggregation of tau proteins. Inthis regard, this means that the neurodegeneration was identified to originatefrom the cortical sulci, and before then from the blood vessels surrounding ona small area, which then extends to bigger slices of the brain. On the otherhand, McKee et al (2011) argued that neuropsychological and physical sequelaeof Chronic Traumatic Encephalopathy are caused by the tau-toxic factor that isassociated with systematic degeneration in parts of the brain that have thetask of regulating emotions, memory, and other cognitive functions.McKee et al (2011)research suggested genetic susceptibility to the post-trauma buildup of the tauproteins for the individual who have inherited cholesterol transport gene knownas Apolipoprotein E4 ( McKee et al, 2011). The Apolipoprotein E4 gene has beennoted as the risk factor for a number of Alzheimer’s and Sclerosisdisorders.  The gene can also increase the risk of developing ChronicTraumatic Encephalopathy for about ten times. The gene comprises of one type ofamino acid, where the string of this amino acid has 299 amino acids units thatlead to misfolding.

The brain responds to the abnormality recognizing it, andthen releases enzymes that cut the tail of the protein. The clumping togetherof the brain tau is caused by free-floating pieces of neurotoxic throughmutations (Mahley & Huang, 2012). With this back in mind, can help inexplaining the reason behind the development of Chronic TraumaticEncephalopathy due to repetitive closed-head trauma in some victims whileothers fail to.

Chronic TraumaticEncephalopathy disorder has been on the high profile in the media for itsrelationship with professional athletes. Chronic Traumatic Encephalopathy ismarked depression, aggression, and behavior that appears of more of suicidal(Omalu, 2010).  Currently, there is no consistent way to identify ChronicTraumatic Encephalopathy.

Diagnosis of a disorder needs degeneration evidenceof the tissue of the brain, tau deposits as well as other proteins in thebrain. The drawback associated with evidence is only possible upon inspectionafter death (autopsy) (Fainaru & Fainaru-Wada, 2013). To mitigate the currentsituation, research is continuing with the purpose of finding a test forChronic Traumatic Encephalopathy that can be applied while individuals arestill living (Wetjen, Pichelmann, & Atkinson, 2010).  Anothercontinuing research is on the study brain of people that may be having thedisorder, for example, the footballers.

In attempts to diagnoseCTE, a number of neuropsychological tests are carried out and includebiomarkers and brain imaging (Scrimgeour, 2014).TreatmentDue to the fact thatthere has been a deficit of premortem diagnostic methodology for CTE, theapproach that has been in use is its treatment. However, due to premortemadvances in the process of identifying the tau biomarkers, there has been aclinical progress aimed at treating and preventing CTE has been completed(Small et al, 2013).On the other hand,despite the phenomenon of no clinically proven treatment of CTE, a number ofexperiments have elevated the state of the situation. A recent study hasindicated that an intervention of the treatment by use of a fish that is richin omega-3 oil might need neuroprotective features that can reduce the braininjury of the trauma.  What really happens is that the metabolized fattyacids of the omega-3 resolve and metabolize and fights the inflammation bysuppressing the proinflammatory cytokines (Mills et al, 2011).

The use of thefish oil immediately after traumatic brain injury has taken place can berewarding in the sense that this act would bring down the inflammation,repairing of the damaged cells; and at the same time reduces the incidence ofthe second impact syndrome (Scrimgeour & Condlin, 2014).Towards the success oftreating of CTE, early trials have been made and they are promising, Dr.Trojanowski, from the University of Pennsylvania, has shown that use of anexperimental drug stops tau degeneration progression as well as reversing thetau tangle pathology, hence improving the functionality ofcognitive.(Bachstetter et al, 2012) An additional probableaction that is being researched on by Dr.

William and Margret. The method beingused in this research comprise of LED light being passed through the skull ofthe children’s and veterans with post-concussive symptoms for the purposes ofstimulating the healing after injuries have taken place in the brain. Themotivating thing on this study is on the belief that light is important whenstimulating ATP production, an energy molecule that identified to facilitatethe restoration of the chemical balance of cells of the brain after the injuryhas occurred (Sportingjim, 2013). There is a complicationof the context of the strategic treatment by the intricacies of aiming at thedefective protein by avoiding injuring the protein functionality. Despite advancement inthe area of treatment and prevention of CTE, the available ways of inhibitionsignify dodging of the overall damage of brain by the disturbance (Stoller,2011). The improvements in the area of care apparatus for interactionsporting..

Alteration of the lifestyles, for example, regular practices, havinga diet that is healthy, and at the same time avoiding alcohol and drugs arepreferred. This should be done together with a therapist in order to cope withthe emotional difficulties.  ConclusionCTE is a late impact ofclosed-head trauma that lacks a treatment that is clinically proven. Althoughthis is the case, it is worth noting that CTE diagnosis is done throughpost-mortem examination of the tissues of the cerebral tissues. The researchthat is going on is providing promising advances with the aim of premortemidentification of biomarkers by cutting the edge of the image method (Goldsteinet al, 2012). There exists a belief by clinical investigators that the findingof the researchers that are being carried on, could lead to possible treatmentsand detection in stopping of neurodegeneration. We are having the currentstrategies being focused on the clinical management of symptoms and signsonly.  All in all, prevention of the head trauma is the only optionavailable for preventing Chronic Traumatic Encephalopathy.

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