Chronic Traumatic Encephalopathy In order to discuss Chronic Traumatic Encephalopathy (CTE) and the potential risks related to the disease one must first understand what CTE is. CTE is a degenerative disease of the brain caused by repetitive head trauma (What is CTE?, 2016). Athletes that participate in contact sports such as football, hockey, rugby, and even soccer are most at risk due the nature of their sports. Former participants of all these sports have been diagnosed with CTE posthumously, and during their declines have suffered from fits of rage, dementia, substance abuse, and suicide. These are all thought to be symptoms caused by CTE (Karantzoulis, 2013). Is the entertainment provided by these events worth the possibility of these
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Dr. Harrison Martland examined retired professional boxers in 1928; he descried them as “cuckoo”, “goofy”, and “slug nutty”. Later, Dr. Martland called the compilation of these symptoms in boxers Punch Drunk (SpringerPlus, 2016). This was later formally named Chronic Traumatic Encephalopathy. Further research showed that symptoms of CTE became apparent between seven and thirty-five years after the start of a boxer’s career, and that seventeen percent of boxers will experience these symptoms after their career (Karantzoulis, 2013). Some argue that because ninety percent of sport related head injuries are mild traumatic brain injuries (mTBI) not to the extent of the injuries sustained by boxers, CTE is not a prominent concern for most athletes in contact sports. However, in a study where lab mice received repeated mTBIs they showed CTE-like changes such as increased expression of glial fibrillary acidic protein …show more content…
The images in the middle and on the right show brain tissue of two individuals with significant tau protein build up and CTE. This discovery was first made by Brain Injury Research Institute doctors Bennet I. Omalu, M.D. and Julian Bailes, M.D. in a professional football player in 2002 (What is CTE?, 2016). While research on CTE has grown tremendously in the past five years, there is still much about the disease that is not understood (Iverson, 2013). Boston University’s Center for the Study of CTE has received more than 260 brain and spinal cord donations from retired athletes. These will provide better models than animals and aid in expanding the understanding of CTE (Karantzoulis, 2013). Further research may provide information about genetic variants which put certain individuals at greater risk for CTE. (SpringerPlus, 2016). This could provide insight on why two individuals with the same amount of head trauma may not both have CTE. Research may also be done on treatment for CTE and managing its symptoms as suicide is a common result of the disease (Iverson, 2013). More information on the exact determinants of mild traumatic brain injuries is needed as it can help stop CTE before it even begins (SpringerPlus, 2016). Prevention and understanding of CTE requires more knowledge on what triggers these chemical changes in the brain, and how to reduce the
Dr. Harrison Martland examined retired professional boxers in 1928; he descried them as “cuckoo”, “goofy”, and “slug nutty”. Later, Dr. Martland called the compilation of these symptoms in boxers Punch Drunk (SpringerPlus, 2016). This was later formally named Chronic Traumatic Encephalopathy. Further research showed that symptoms of CTE became apparent between seven and thirty-five years after the start of a boxer’s career, and that seventeen percent of boxers will experience these symptoms after their career (Karantzoulis, 2013). Some argue that because ninety percent of sport related head injuries are mild traumatic brain injuries (mTBI) not to the extent of the injuries sustained by boxers, CTE is not a prominent concern for most athletes in contact sports. However, in a study where lab mice received repeated mTBIs they showed CTE-like changes such as increased expression of glial fibrillary acidic protein …show more content…
The images in the middle and on the right show brain tissue of two individuals with significant tau protein build up and CTE. This discovery was first made by Brain Injury Research Institute doctors Bennet I. Omalu, M.D. and Julian Bailes, M.D. in a professional football player in 2002 (What is CTE?, 2016). While research on CTE has grown tremendously in the past five years, there is still much about the disease that is not understood (Iverson, 2013). Boston University’s Center for the Study of CTE has received more than 260 brain and spinal cord donations from retired athletes. These will provide better models than animals and aid in expanding the understanding of CTE (Karantzoulis, 2013). Further research may provide information about genetic variants which put certain individuals at greater risk for CTE. (SpringerPlus, 2016). This could provide insight on why two individuals with the same amount of head trauma may not both have CTE. Research may also be done on treatment for CTE and managing its symptoms as suicide is a common result of the disease (Iverson, 2013). More information on the exact determinants of mild traumatic brain injuries is needed as it can help stop CTE before it even begins (SpringerPlus, 2016). Prevention and understanding of CTE requires more knowledge on what triggers these chemical changes in the brain, and how to reduce the