CHRONIC TRAUMATIC ENCEPHALOPATHY IN A NATIONAL FOOTBALL LEAGUE PLAYER: PART II.
Omalu, Bennet I. M.D., M.P.H.; DeKosky, Steven T. M.D.; Hamilton, Ronald L. M.D.; Minster, Ryan L. M.S.I.S.; Kamboh, M. Ilyas Ph.D.; Shakir, Abdulrezak M. M.D.; Wecht, Cyril H. M.D., J.D.
59(5):1086-1093, November 2006.
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OBJECTIVE: We present the second reported case of autopsy-confirmed chronic traumatic encephalopathy in a retired professional football player, with neuropathological features that differ from those of the first reported case. These differing pathological features underscore the need for further empirical elucidation of the pathoetiology and pathological cascades of long-term neurodegenerative sequelae of professional football.
METHODS: A psychological autopsy was performed with the next-of-kin and wife. Medical and hospital records were reviewed. A complete autopsy was accompanied by a comprehensive forensic neuropathological examination. Restriction fragment length polymorphism analysis was performed to determine apolipoprotein-E genotype.
RESULTS: Pertinent premortem history included a 14-year span of play in organized football starting from the age of 18 years. The subject was diagnosed with severe major depressive disorder without psychotic features after retirement, attempted suicide multiple times and finally committed suicide 12 years after retirement by ingestion of ethylene glycol. Autopsy revealed cardiomegaly, mild to moderate coronary artery disease, and evidence of acute ethylene glycol overdose. The brain showed no atrophy, a cavum septi pellucidi was present, and the substantia nigra showed mild pallor. The hippocampus and cerebellum were not atrophic. Amyloid plaques, cerebral amyloid angiopathy, and Lewy bodies were completely absent. Sparse to frequent [tau]-positive neurofibrillary tangles and neuropil threads were present in all regions of the brain. Tufted and thorn astrocytes, as well as astrocytic plaques, were absent. The apolipoprotein-Egenotype was E3/E4.
CONCLUSION: Our first and second cases both had long careers without multiple recorded concussions. Both manifested Major Depressive Disorder after retirement. Amyloid plaques were present in the first case and completely absent in the second case. Both cases exhibited neurofibrillary tangles, neuropil threads, and coronary atherosclerotic disease. Apolipoprotein-E4 genotypes were different. Reasons for the contrasting features in these two cases are not clear. Further studies are needed to identify and define the neuropathological cascades of chronic traumatic encephalopathy in football players, which may form the basis for prophylaxis and therapeutics.
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