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Chronic traumatic encephalopathy (CTE) in a National Football League Player: Case report and emerging medicolegal practice questions

Omalu, Bennet I. MD, MBA, MPH1; Hamilton, Ronald L. MD2; Kamboh, Ilyas M. PhD3; DeKosky, Steven T. MD4; Bailes, Julian MD5

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Journal of Forensic Nursing: March 2010 - Volume 6 - Issue 1 - p 40-46
doi: 10.1111/j.1939-3938.2009.01064.x
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Chronic Traumatic Encephalopathy (CTE) represents the cumulative, long-term neurologic consequences of repetitive concussive and subconcussive blows to the brain, which may be sustained in contact sports such as boxing, ice hockey, martial arts, and American football (Rabadi & Jordan, 2001). Guskiewicz et al., 2005 and Guskiewicz et al., 2007 reported that onset of dementia-related syndromes and clinical depression can be initiated by repetitive cerebral concussions in professional football players. Omalu et al., 2006 and Omalu et al., 2005 reported the first and second cases of autopsy-confirmed CTE in National Football League (NFL) players in 2005 and 2006. This case report establishes a case series and identifies emerging common denominators and characteristics of CTE in NFL players.

Case report

Premortem history

The person featured in this case died at the age of 44 years. He began playing football in high school at the age of 15 years. He played Division 2 college football for 4 years and in the NFL for 9 years. He was known as an aggressive player and a hard hitter. He was not known to have abused steroids or other illicit drugs during his career in the NFL. He admitted to his family members and journalists that he sustained many concussions during his career in the NFL, losing count after his 15th concussion. He did not report many of them to his team mates, coaches, or physicians. He once suffered from a documented seizure after a game, was admitted into a hospital overnight, practiced 2 days after his discharge, and played in another game within 7 days.

After his retirement from the NFL, he taught elementary school for a short time then spent time coaching college football but did not stay at any institution long, living in five different states within several years. He suffered chronic musculoskeletal pain from the many injuries he had sustained while he played football. He suffered constant headaches and at some point he began taking Percocet (oxycodone and acetaminophen) for his pain. He began drinking brandy the year he retired from the NFL and continued for 5 years, when he began drinking less. He stopped drinking completely 9 years after retirement, 2 years before his death.

After his retirement from the NFL, he made some business investments, which did not do well. He invested money in several other businesses with his friends, which came to naught. He made bad judgments and spent money injudiciously. He started becoming forgetful 3–4 years after he retired from the NFL. While holding conversations, he would forget what he was talking about and would circumlocute. He forgot about conversations he had with people including schedules, agreements, and plans. He frequently forgot where he kept his wallet, check books, and keys and would constantly search for them even when he lived in a one-bedroom apartment. He once got lost while driving home and had to call a close friend to help him find his way home.

Our case never married. Over the years he had many girlfriends, but none of his girlfriends lived with him. He always had a cousin, niece, or nephew live with him. He fathered three children, two sons and a daughter with three different women. He was known to be an exuberant, outgoing, and sociable person who liked family and social gatherings. Following his retirement, he progressively began to avoid these events for no clear reason. On weekends, he would remain in bed all day and not engage in any activities. He developed a needy, dependent persona, and became more private, withdrawn, seclusive, and reclusive. Beginning 5 years after retirement, he began to get upset and angry if people did not do what he wanted. He exhibited exaggerated responses to minor life events, would blow things out of proportion, and worried about everything. He overreacted to letdowns and disappointments and would get very angry and upset over trivial issues that would not upset the average person.

Approximately, 8 years after his NFL retirement, he became excessively driven during the college football seasons as a college football coach. He would stay awake all night at his office working on plays, watching films of games, and breaking down plays. Early in the mornings he would return home to sleep, but as time went by he would merely go home to take a shower and then return to the office to continue working. He became constantly restless and tossed, turned, and moved constantly even while sleeping. He developed insomnia and sometimes would go to bed around 2:00 A.M. just to wake up 2 or 3 hours later because he could not sleep.

He progressively exhibited fluctuations in mood. He became progressively isolated and did not want to be around people. He stopped attending parties, visiting places of interest, and socializing with his friends. He frequently told his relatives that he was very depressed and was thinking of committing suicide, and did attempt suicide a number of times by consuming prescription drugs and by deliberate carbon monoxide exposure. In his final years he was constantly depressed, exhibited frequent tearful episodes, and frequently verbalized suicidal ideations. He manifested a major fear of financial ruin. However, he became less and less restrained and discreet with his spending. He would complain about money one day and would come home the next day having gone on a shopping spree buying clothing and accessories for men. He readily gave money to family members, friends, and acquaintances.

He was evidently aware that something was wrong with him; he once told a girlfriend that he needed help and that someone should help him. He read the bible and religious books seeking a deeper faith in God. He exhibited paranoid ideations, once telling his mother that someone was against him and out to destroy him. He believed that people were not helping him to move up and some of his superiors were not treating him well. He felt comfortable only at home and was not comfortable in social gatherings. He always thought that someone was going to steal his car when he visited nightclubs with his cousin, and would rather stay outside sometimes to watch over his car. His friends jokingly told him he was bipolar and should consult a psychiatrist. It was not clear to his friends and family if he consulted a psychiatrist before he died.

Our case committed suicide in his home by shooting himself in the mouth approximately 11 years after his retirement from the NFL. According to his family, there was no history of depression in his immediate family and there was no documented head trauma outside football.

Autopsy findings

A full autopsy was performed on the body of our deceased player and revealed a gunshot wound of entrance in the soft palate with surrounding soot deposits. The bullet perforated the oro- and nasopharynx, perforated and fractured the base of the skull, perforated, lacerated, and contused the pons, basal ganglia, third and lateral ventricles, and the right parietal lobe. Deformed fragments of a jacketed bullet were recovered from the right parietal lobe and right basal ganglia. The brain weighed 1,140 grams and revealed no remote contusions, lacerations, or necrosis.

The coronary arteries revealed mild segmental atherosclerosis of the left anterior descending coronary artery and the right coronary artery with approximately 30% and 20% intraluminal occlusion, respectively. The liver revealed focal macrovesicular hepatocellullar steatosis involving less than 10% of hepatocytes. The forensic pathologist who performed the autopsy had thought that the brain appeared grossly normal except for the evidence of a gunshot wound of the brain. He cut the brain in the fresh state and saved five topographically targeted archival pieces of brain tissue in formalin.

Brain tissue findings

Five pieces of brain tissue submitted for study included irregularly cut samples of neocortex, hippocampus, cerebellum, cerebellum with brainstem, basis pontis, and ventral medulla. Microscopic sections were stained with hematoxylin and eosin, and Bielschowsky silver stain; and were immunostained for beta-A4 amyloid, polyclonal tau, glial fibrillary acidic protein (GFAP), CD-68, ubiquitin, neurofilament, Amyloid Precursor Protein (APP), and alpha-synuclein.

Microscopic examination of the hematoxylin and eosin-stained sections of the neocortex revealed the expected columnar and laminar organization with mild neuronal loss. The hippocampus revealed no dysplasia of the dentate fascia or cornu ammonis. There was mild neuronal loss in the Sommer's sector of the hippocampus. The cornu ammonis and parahippocampal gray cortex revealed acute contusional microhemorrhages extending to the superficial subcortical white matter. Examination of hematoxylin and eosin-stained sections of the cerebellar cortex revealed focal acute subarachnoidal microextravasations. There was mild neuronal loss of the Purkinje neurons accompanied by mild Bergmann astrogliosis.

Irregular sections of the brain stem revealed discernible pigmented nigral neurons, basis pontis, pontine nuclei, transverse and descending pontine fibers, ventral and tegmental medulla, inferior olivary nucleus, and basal arachnoid mater. There were multiple randomly situated contusional parenchymal microhemorrhages of the identifiable fragments of the brain stem with arachnoidal microextravasations. Several penetrating parenchymal vessels revealed focal perivascular and intramural infiltration by lymphocytes.

Examination of beta-A4 amyloid immunostained sections of the submitted hippocampus, neocortex, cerebellum, pons, and medulla revealed no diffuse or neuritic plaques or evidence of cerebral amyloid angiopathy. Examination of polyclonal tau immunostained sections revealed sparse-to-moderate-to-frequent densities of NTs and band-shaped, flame-shaped, and small globose perikaryal NFTs in the neocortex, pyramidal cells of the CA-1, CA-2, and CA-3 regions, the subiculum/presubiculum, entorhinal cortex, pigmented and nonpigmented neurons of the ventral and tegmental pons and medulla, pontine nuclei and small identifiable fragments of the substantia nigra and locus ceruleus. Some ghost tangles were noted in the neocortex and hippocampus (Figures 1A–C). There were no NFTs or NTs in the cerebellum.

Figure 1.
Figure 1.:
(A) Photomicrographs of polyclonal tau-protein immunostained sections of the neocortex (×100 magnification) showing frequent NFTs and NTs. (B) Photomicrographs of polyclonal tau-protein immunostained sections of the neocortex (×200 magnification) showing frequent NFTs and NTs. (C) Photomicrograph of a polyclonal tau-protein immunostained section of the neocortex (×400 magnification) showing NFTs and NTs.

Examination of alpha-synuclein immunostained sections revealed no Lewy bodies, Lewy neurites, or glial inclusions in all the sections of the brain examined. Examination of ubiquitin immunostained sections revealed focal staining of some NFTs and NTs. Some neurons showed nondescript diffuse or granular cytoplasmic immunopositivity for polyclonal tau. Argyrophilic grains were absent. Examination of CD-68 immunostained sections revealed patchy immunopositivity of astrocytic cytoplasms and processes in the gray and white matter, accentuated in the white matter. Examination of GFAP immunostained sections revealed mildly increased staining in the gray and white matter. Examination of Bielschowsky silver-stained sections revealed NFTs and no diffuse or neuritic amyloid plaques in the areas described above for tau immunostains. APP and neurofilament stains did not reveal any axonal spheroids or axonal degeneration.

Apolipoprotein E (ApoE) genotype: Genomic deoxyribonucleic acid (DNA) was extracted from peripheral blood leukocytes using the QIAamp DNA BloodMini Kit (Qiagen, Valencia, CA). Restriction Fragment Length Polymorphism analysis was accomplished using Hha I (New England Biolabs, Beverly, MA) according to protocols previously published (Kamboh, Aston, & Hamman, 1995; Omalu et al., 2006; Omalu et al., 2005). The ApoE genotype was determined to be E3/E3 (Figure 2).

Figure 2.
Figure 2.:
Polyacrylamide gel electrophoresis showing deoxyribonucleic acid (DNA) stained with ethidium bromide visualized with ultraviolet light. Lanes 1 and 2 contain duplicate samples of the extracted DNA amplified and digested as described in the text. The restriction fragment pattern in lanes 1 and 2 with bands at 92 and 48 bp corresponds to the genotype E3/E3. Lane 3 is a sample known to be E2/E4 prepared in parallel with the samples from lanes 1 and 2. Lane 4 is a negative template control. Lane 5 contains a 50 to 2,000 base-pair ladder.


Table 1 shows the football profiles and neuropathologic features of this case compared to the only two previously reported cases in the medical literature (Omalu et al., 2006; Omalu et al., 2005). Table 2 summarizes the emerging syndromic components common to these case series (Omalu, 2008). Neurodegenerative disease diagnosis can only be confirmed by direct tissue examination. Without full autopsies, histochemical, and immunohistochemical analyses of brain tissues in this case and the two previously reported cases, which we have reported, could not have been identified. This emphasizes the need to perform full autopsies and comprehensive neuropathologic examinations of the brain on deceased NFL players to confirm the presence or absence of CTE for forensic epidemiological purposes and for evidentiary medicolegal purposes, especially when such deceased players manifested premortem behavioral profiles that are similar to the syndromic components in Table 2.

Table 1
Table 1:
Common and contrasting features of this case and two previously reported cases of chronic traumatic encephalopathy in the medical literature constituting a case series
Table 2
Table 2:
Common syndromic components and behavioral profiles of our case and two previously reported cases of chronic traumatic encephalopathy in the medical literature constituting a case series

CTE is the term applied to chronic neurodegeneration following a single episode of severe traumatic brain injury or (more commonly) repeated episodes of mild traumatic brain injury. It is a syndrome of chronic progressive cognitive and neuropsychiatric symptoms or dementia manifesting with contemporaneous, multidomain impairment of intellectual functioning including language, visuospatial skills, personality, cognition, emotion, and mood disorders.

Head injury has been convincingly implicated as a risk factor for Alzheimer's Disease—like neurodegenerative diseases in epidemiological studies (Clinton, Ambler, & Roberts, 1991; Gualtieri & Cox, 1991; Mayeux et al., 1993; Mortimer et al., 1991). Following the development of tissue immunohistochemistry methods in the 1980s and 1990s, researchers have confirmed neuronal cytoskeletal changes to be consequences of repetitive head injuries especially in boxers. (Allsop, Haga, Bruton, Ishii, & Roberts, 1990; Geddes, Vowles, Nicoll, & Revesz, 1999; Geddes, Vowles, Robinson, & Sutcliffe, 1996).

The immunohistology of our case does not indicate a diagnosis of Alzheimer's disease (Ellison & Love, 2004). Rather it may resemble, in part, the immunohistology of Tangle-Only Dementia (TOD) (Noda et al., 2006; Yamada, 2003; Yamada et al., 2001). The underlying neuropathologic tissue substrates of TOD are sparse to frequent tau-immunoreactive NFTs and NTs primarily in the limbic cortex and possibly in the neocortex and subcortical ganglia, with or without diffuse amyloid plaques (Itoh et al., 1996; Noda et al., 2006). TOD is a rare type of dementia with a reported prevalence of 0.7% to 7.7% in several autopsy series (Noda et al., 2006). TOD occurs in the oldest old people in their 80s and 90s, and in most reported cases the antemortem diagnosis was Alzheimer's Disease. The topographic spread of NFTs and NTs in our case is broader than the topographic spread of NFTs and NTs that is typically seen in TOD.

While the possession of the ApoE4 allele is thought to be a risk factor for adverse outcomes of brain trauma and for Alzheimer's Disease, our case was homozygous for E3. ApoE is a circulating 34-KDa glycosylated protein, the gene for which is mapped to chromosome 19q (Bales, Dodart, DeMattos, Holtzman, & Paul, 2002; Ellison & Love, 2004). It is primarily synthesized in the liver and is involved in lipid metabolism, with triglyceride, phospholipid, cholesteryl ester, and cholesterol transport in and out of cells. ApoE is a ligand for low density lipoprotein (LDL) receptors and mediates the receptor binding of ApoE containing lipoproteins to the LDL receptor for cellular uptake and intracellular cholesterol metabolism. In the central nervous system ApoE is synthesized and secreted primarily by astrocytes and microglia, and its importance is underscored by the absence of most other plasma apolipoproteins in the brain. It is the primary cholesterol transporter in the brain, where it is proposed to function as a ligand directing the delivery of lipids for neuronal repair and remodeling after injury (Bales et al., 2002; Greenfield, Graham, & Lantos, 2002). In humans there are three ApoE isoforms, E2, E3, and E4, with three corresponding ApoE alleles, E2, E3, and E4. Although the underlying mechanism remains poorly defined, the alleles for ApoE represent important genetic risk factors for late-onset forms of Alzheimer's Disease and adverse outcomes following traumatic brain injury (Mayeux et al., 1995; Millar, Nicoll, Thornhill, Murray, & Teasdale, 2003; Teasdale, Nicoll, Murray, & Fiddes, 1997), with the E4 allele increasing the risk for developing Alzheimer's Disease by 19-fold for E4/E4 homozygotes (Bales et al., 2002; Ellison & Love, 2004). On the contrary, an overrepresentation of the E3 allele has been reported in patients who suffer from TOD with lower prevalence of E4 alleles than in Alzheimer's Disease patients (Bancher, Egensperger, Kosel, Jellinger, & Graeber, 1997; Yamada et al., 2001).

NFTs and NTs are principally composed of abnormally hyperphosphorylated, paired helical filaments of tau protein, which is a microtubule associated protein (MAP). Tau is a phosphoprotein, the gene of which is mapped to Chromosome 17q, and occurs normally in axons of neurons in the central and peripheral nervous system, where it binds to and stabilizes microtubules in their polymerized state (Greenfield et al., 2002). Microtubules are neuroaxonal cytoskeletons composed of alpha and beta tubulins, and are important in the maintenance of cell shape, motility, transport, and mitosis. MAPs such as tau help to regulate the transport of vesicles or organelles among the microtubules, support axonal outgrowth, and anchor enzymes. Gene induction, increased synthesis, and upregulation of tubulins occur during neuroaxonal regeneration following lesioning and axotomy (Greenfield et al., 2002). Experimental models of traumatic brain injuries have also shown that proteolytic cleavages, disintegration, abnormal metabolism, and accumulation of neuronal cytoskeletal and transmembrane proteins, including APP and tau protein, may follow severe or repeated mild traumatic brain injuries both acutely and chronically (Gabbita et al., 2005; Geddes et al., 1999; Uryu et al., 2002). Repeated mild traumatic brain injuries may also initiate progressive widespread neuronal loss in selectively vulnerable brain regions for months to years after the initial insult. The mechanisms underlying these delayed neuronal injuries are believed to result from the activation of endogeneous autodestructive biochemical pathways induced by traumatic brain injuries (Gabbita et al., 2005).

Our case report adds to the reported autopsy evidence and establishes an autopsy case series for CTE in NFL players since a case series comprises 3 to 10 cases of a disease occurrence without predefined denominators. This case emphasizes the indispensable role of forensic pathologists and nurses in the surveillance and identification of CTE in professional contact sport athletes. We recommend that full autopsies and comprehensive neuropathological examinations of the brain be performed on every retired NFL player who dies with a premortem history of the syndromic components listed in Table 2. Autopsies will confirm the incident cases of CTE since CTE cannot be confirmed without direct tissue examination. Autopsy findings can serve as prevailing evidentiary findings for all types of medicolegal questions and proceedings, which may arise. With the performance of autopsies and identification of more cases, and with further longitudinal prospective studies involving all football players from the prehigh school to professional levels, we can begin to elucidate the full epidemiological and pathologic spectrum of CTE in football players.


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Chronic traumatic encephalopathy; football players; forensic nursing; National Football League

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