Cited by 894Traumatic Brain Injury ResearchTraumatic Brain Injury and Neurovascular DisturbancesAutomotive and Human Injury Biomechanics

Chronic Traumatic Encephalopathy in a National Football League Player

Omalu, Bennet I., DeKosky, Steven T., Minster, Ryan L., Kamboh, M Ilyas, Hamilton, Ronald L., Wecht, Cyril H.·2005·Neurosurgery

Abstract

OBJECTIVE: We present the results of the autopsy of a retired professional football player that revealed neuropathological changes consistent with long-term repetitive concussive brain injury. This case draws attention to the need for further studies in the cohort of retired National Football League players to elucidate the neuropathological sequelae of repeated mild traumatic brain injury in professional football. METHODS: The patient's premortem medical history included symptoms of cognitive impairment, a mood disorder, and parkinsonian symptoms. There was no family history of Alzheimer's disease or any other head trauma outside football. A complete autopsy with a comprehensive neuropathological examination was performed on the retired National Football League player approximately 12 years after retirement. He died suddenly as a result of coronary atherosclerotic disease. Studies included determination of apolipoprotein E genotype. RESULTS: Autopsy confirmed the presence of coronary atherosclerotic disease with dilated cardiomyopathy. The brain demonstrated no cortical atrophy, cortical contusion, hemorrhage, or infarcts. The substantia nigra revealed mild pallor with mild dropout of pigmented neurons. There was mild neuronal dropout in the frontal, parietal, and temporal neocortex. Chronic traumatic encephalopathy was evident with many diffuse amyloid plaques as well as sparse neurofibrillary tangles and tau-positive neuritic threads in neocortical areas. There were no neurofibrillary tangles or neuropil threads in the hippocampus or entorhinal cortex. Lewy bodies were absent. The apolipoprotein E genotype was E3/E3. CONCLUSION: This case highlights potential long-term neurodegenerative outcomes in retired professional National Football League players subjected to repeated mild traumatic brain injury. The prevalence and pathoetiological mechanisms of these possible adverse long-term outcomes and their relation to duration of years of playing football have not been sufficiently studied. We recommend comprehensive clinical and forensic approaches to understand and further elucidate this emergent professional sport hazard.

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Registry

Crossref · 10.1227/01.neu.0000163407.92769.ed

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  • Post mortem chronic traumatic encephalopathy studies reveal cerebral edema, perivascular hemosiderin-burdened macrophages, mural cell mineralization, enlarged perivascular spaces, and leukocyte infiltration.

    “Post mortem CTE studies reveal cerebral edema, perivascular hemosiderinburdened macrophages, mural cell mineralization, enlarged perivascular spaces, and leukocyte infiltration (149, 325, 454, 455)”

    From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [454]

  • Chronic traumatic encephalopathy is characterized by accumulation of TAR DNA-binding protein-43 and neurofibrillary tangles of hyperphosphorylated tau beginning perivascularly, and is reported in football, wrestling, boxing, and soccer players, as well as in veterans.

    “Chronic traumatic encephalopathy (CTE) is characterized by accumulation of TAR DNA-binding protein-43 (TDP43) and neurofibrillary tangles of hyperphosphorylated tau beginning perivascularly (54), and is reported in football (454, 455), wrestling (455), boxing (325), and soccer (366) players, as well as in veterans (237).”

    From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [454]

  • CTE has been diagnosed neuropathologically in American football players, professional and amateur boxers, ice hockey players, professional wrestlers, soccer players, rugby players, and a professional baseball player.

    “Although CTE was first identified in association with boxing, CTE has been diagnosed neuropathologically in American football players, professional and amateur boxers, ice hockey players, professional wrestlers, soccer players, rugby players, and a professional baseball player (Figs. 3, 4, 5, 6) [38, 65, 66, 88, 91, 127, 128, 146–148].”

    From The neuropathology of sport (2014) · cites this paper as [148]

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Authors
Omalu, B. I., DeKosky, S. T., Minster, R. L., Kamboh, M. I., Hamilton, R. L., & Wecht, C. H.
Affiliations
University of Pittsburgh (US)
Venue
Neurosurgery
Published
2005-07
Volume
57
Issue
1
Pages
128-134
ISSN
0148-396X (ISSN-L)
OpenAlex
W4253308936
Cited by
894
References
37
Citations by year
2026: 36 · 2025: 24 · 2024: 42 · 2023: 40 · 2022: 69 · 2021: 58 · 2020: 78 · 2019: 74 · 2018: 78 · 2017: 65 · 2016: 63 · 2015: 61 · 2014: 46 · 2013: 36 · 2012: 28
FWCI
8.89
Type
journal article
Language
en
Open access
closed
Locations
  • Neurosurgery (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
  • Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Automotive and Human Injury Biomechanics
Keywords
chronic traumatic encephalopathy, professional football players, National Football League, repetitive mild traumatic brain injury, neuropathology, tau pathology, neurofibrillary tangles, amyloid plaques, substantia nigra, APOE genotype, cognitive impairment, parkinsonian symptoms, former athletes
MeSH terms
Apolipoproteins E, Athletic Injuries, Central Nervous System, Football, Humans, Immunohistochemistry, Male, Middle Aged, Amyloid beta-Peptides, Brain Injury, Chronic

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