The aftermath of boxing revisited: identifying chronic traumatic encephalopathy pathology in the original Corsellis boxer series

Goldfinger, Marc; Ling, Helen; Tilley, Bension S.; Liu, Alan King Lun; Davey, Karen; Holton, Janice L.; Révész, Tamás; Gentleman, Steve

doi:10.1007/s00401-018-1926-8

Cited by 33 publications

(26 citation statements)

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“…All cases were reported to have been boxers with the exception of a circus clown who was an achondroplastic dwarf, aged 33 at the time of death, who had 15 years of exposure as a circus clown and participation in dwarf throwing competitions reported by Williams and Tannenberg ( 89 ). * 1967 = Constantinidis and Tissot ( 90 ), 1968 = Payne ( 64 ), 1973 = Corsellis et al ( 4 ), 1992 = Hof et al ( 91 ), 1996 = Williams and Tannenberg ( 89 ), 1999 = No listed authors ( 92 ), 2018 = Goldfinger et al ( 88 ); ** Case 28 said to have boxed professionally in his youth. He was described as being “considered active and mentally alert up to the time of his death” (4); AD, Alzheimer's disease; ARTAG, Aging-related tau astrogliopathy; CTE, chronic traumatic encephalopathy; N/A, not applicable; NR, not reported; § Case 17 “Age at Death” reported as 63 years in Corsellis et al ( 4 ) and 62 years in Goldfinger et al ( 88 ); Case 26 “Age at Death” reported as 57 years in Corsellis et al ( 4 ) and 56 years in Goldfinger et al ( 88 ); *** Obvious neurological abnormality includes two or more of the following: movement abnormalities, decreased facial movement, slowed movements, tremor, rigidity, falls, ocular abnormalities, ptosis, reduced upgaze, gait problems: staggered gait, slowed gait, shuffled gait, ataxia, reduced coordination, speech changes: slowed speech, slurred speech, dysarthria, dysphagia, spasticity .…”

Section: Discussionmentioning

confidence: 99%

“… * 1967 = Constantinidis and Tissot ( 90 ), 1968 = Payne ( 64 ), 1973 = Corsellis et al ( 4 ), 1992 = Hof et al ( 91 ), 1996 = Williams and Tannenberg ( 89 ), 1999 = No listed authors ( 92 ), 2018 = Goldfinger et al ( 88 ); …”

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Risk for Misdiagnosing Chronic Traumatic Encephalopathy in Men With Anger Control Problems

Gardner

2020

Front. Neurol.

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Background: There are no validated or agreed upon criteria for diagnosing chronic traumatic encephalopathy (CTE) in a living person. In recent years, it has been proposed that anger dyscontrol represents a behavioral clinical phenotype of CTE. This is the first study to examine the specificity of the diagnostic research criteria for traumatic encephalopathy syndrome (TES, the clinical condition proposed to be CTE) in men from the US general population who have anger dyscontrol problems. It was hypothesized that a substantial percentage of these men would meet the research criteria for TES. Methods: Data from 4,139 men who participated in the National Comorbidity Survey Replication, an in-person survey that examined the prevalence and correlates of mental disorders in the United States, were included in this study. Men who were diagnosed with intermittent explosive disorder in the past year were the clinical sample of interest (n = 206; 5.0% of all men in the database), and the remaining men were used as a comparison sample. They were classified as meeting the research criteria for TES if they presented with the purported supportive clinical features of CTE (e.g., impulsivity/substance abuse, anxiety, apathy, suicidality, headache). Results: In this sample of men from the general population with intermittent explosive disorder, 27.3% met a conservative definition of the proposed research criteria for CTE (i.e., traumatic encephalopathy syndrome). If one assumes the delayed-onset criterion is present, meaning that the men in the sample are compared to former athletes or military veterans presenting with mental health problems years after retirement, then 65.0% of this sample would meet the research criteria for TES. Conclusions: These results have important implications. Using conservative criteria, at least one in four men from the general population, who have serious anger control problems, will meet the symptom criteria for TES. If one considers former athletes and Iverson and Gardner Anger Control Problems and CTE military veterans with anger control problems who present many years after retirement and who experienced a documented decline in their mental health, nearly two-thirds will meet these research criteria. More research is needed to examine risks for misdiagnosing TES and to determine whether anger dyscontrol is a clinical phenotype of CTE.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Risk for Misdiagnosing Chronic Traumatic Encephalopathy in Men With Anger Control Problems

Gardner

2020

Front. Neurol.

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“…A more prudent explanation for the lack of cerebellar pathology observed in modern boxers is that changes in boxing regulations over the past 50 years, including the elimination of blows to the back of the head (the "rabbit punch"), result in less direct cerebellar injury. Recently, Goldfinger et al used p-tau immunocytochemistry to investigate tissue available from 14 of the original 15 Corsellis cases, 15 tissue that had been in fixative for 50 years and sampled by many investigators. Goldfinger et al systematically examined serial sections from multiple sites within the frontal and temporal lobes.…”

Section: Beta-amyloid Pathology Is Not a Primary Feature Of Ctementioning

confidence: 99%

“…Perivascular ptau immunoreactive astrocytes alone are not considered evidence of CTE, and, if present in isolation, they most likely represent aging-related tau astrogliopathy (ARTAG). [13][14][15] Defining the Neuropathological Criteria for CTE…”

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confidence: 99%

The Neuropathology of Chronic Traumatic Encephalopathy: The Status of the Literature

McKee

2020

Semin Neurol

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Chronic traumatic encephalopathy (CTE) is a tauopathy associated with repetitive mild head trauma, including concussion and asymptomatic subconcussive impacts. CTE was first recognized in boxers almost a century ago and has been identified more recently in contact sports athletes, military veterans exposed to blast, and victims of domestic violence. Like most neurodegenerative diseases, CTE is diagnosed conclusively by a neuropathological examination of brain tissue. CTE is characterized by the buildup of hyperphosphorylated tau (p-tau) in neurofibrillary tangles (NFTs), neurites, and, sometimes, astrocytes, surrounding small blood vessels in a patchy distribution at the sulcal depths of the cerebral cortex. In 2015, using the McKee proposed criteria for the neuropathological diagnosis of CTE, a consensus panel of expert neuropathologists confirmed CTE as a unique neurodegenerative disease with a pathognomonic lesion and published the preliminary NINDS (National Institute of Neurological Disorders and Stroke) criteria for CTE. Since that time, the NINDS criteria for CTE have been implemented and validated in multiple international publications. Using the NINDS criteria, the largest clinicopathological series of CTE to date was reported that included 177 former American football players, including 110 (99%) of 111 former National Football League players, 48 (91%) of 53 former college football players, and 3 (21%) of 14 former high school players. Studies have also shown a significant association between cumulative exposure to repetitive head trauma, as judged by the length of American football playing career, and risk for and severity of CTE. There is also a significant relationship of the length of football playing career with p-tau pathology, inflammation, white matter rarefaction, and age at death in CTE. While p-tau pathology, inflammation, white matter rarefaction, and arteriolosclerosis contribute to dementia in CTE, whether they also influence the behavioral and mood symptoms in CTE has yet to be determined. There have been several instances of aging-related tau astrogliopathy (ARTAG), a common astrocytic pathology in the elderly, misdiagnosed as CTE in the recent literature, provoking claims that CTE pathology is present in people not known to have experienced repetitive head trauma. Although ARTAG is often found in CTE, the pathognomonic lesion of CTE is a neuronal lesion consisting of NFTs and neurites, with or without p-tau immunoreactive astrocytes. Some authors consider β-amyloid (Aβ) to be a primary feature of CTE, yet the data indicate that CTE is a primary tauopathy, with Aβ deposition a function of age and inheritance of the ApoEe4 allele. Some authors also question the progressive nature of CTE pathology, although there is clear evidence in most individuals that p-tau pathology increases in density and affects more brain regions with survival. This review is intended to outline the status of the evidence-based literature regarding CTE neuropathology and to address the misrepresentations and confusions that have arisen in recent reviews and a letter of correspondence.

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Late Presentation of Chronic Traumatic Encephalopathy in a Former Association Football Player

Cullinane,

Wrigley,

Bradshaw

et al. 2023

Movement Disord Clin Pract

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BackgroundChronic traumatic encephalopathy (CTE) is a neurodegenerative disease characterized by widespread accumulation of hyperphosphorylated tau that typically occurs in people who have suffered repetitive head impacts. To date, very few cases have been reported in association football players.ObjectivesTo describe the clinicopathological features of a case of CTE in an 84‐year‐old former football player who was clinically diagnosed as having dementia with Lewy bodies (DLB).MethodsA retrospective review of the patient's primary care and hospital medical records was performed along with a comprehensive neuropathological examination.ResultsThis patient presented at age 84 with symmetrical parkinsonism and cognitive impairment that was exacerbated by prochlorperazine. His condition was rapidly progressive with recurrent falls within 1 year. Other features included headaches, depression, anxiety, suicidal ideation, disturbed sleep and aggression. He received a clinical diagnosis of DLB and died approximately 2 years after the onset of symptoms. A post‐mortem examination revealed stage 4 CTE.ConclusionsWhile the contemporaneous onset of parkinsonism and cognitive symptoms in the context of possible neuroleptic sensitivity is suggestive of DLB, the additional symptoms of aggressive behavior, depression and suicidality in a former football player are consistent with the neuropathological diagnosis of CTE. This case, which is notable for the late presentation, demonstrates that CTE may masquerade as other dementias and highlights the importance of seeking a history of repetitive head impacts.

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The aftermath of boxing revisited: identifying chronic traumatic encephalopathy pathology in the original Corsellis boxer series

Cited by 33 publications

References 12 publications

Risk for Misdiagnosing Chronic Traumatic Encephalopathy in Men With Anger Control Problems

Risk for Misdiagnosing Chronic Traumatic Encephalopathy in Men With Anger Control Problems

The Neuropathology of Chronic Traumatic Encephalopathy: The Status of the Literature

Late Presentation of Chronic Traumatic Encephalopathy in a Former Association Football Player

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