Extending the range of differential diagnosis of chronic traumatic encephalopathy of the boxer: Insights from a case report

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ABSTRACT

Sports activities associated with repetitive cranial trauma have become a fad and are popular in gyms and even among children. It is important to consistently characterize the consequences of such sports activities in order to better advise society on the real risks to the central nervous system. We present the case of a former boxer reporting cognitive and behavioral symptoms that began six years after his retirement as a boxer, evolving progressively with parkinsonian and cerebellar features suggestive of probable chronic traumatic encephalopathy (CTE). Using our case as a paradigm, we extended the range of differential diagnosis of CTE, including corticobasal degeneration, multiple system atrophy, vitamin B12 deficiency, neurosyphilis, frontotemporal dementia and Alzheimer’s disease.

RESUMO

As atividades esportivas associadas ao trauma craniano repetitivo tornaram-se uma moda e são populares nas academias e entre as crianças. É importante fazer uma caracterização consistente das consequências de tais atividades esportivas, a fim de aconselhar melhor uma sociedade sobre os riscos reais para o sistema nervoso central. Apresentamos um antigo boxeador relatando sintomas cognitivos e comportamentais que começaram seis anos após sua aposentadoria como boxeador e evoluiu progressivamente com características parkinsonianas e cerebelares sugestivas de provável encefalopatia traumática crônica (ETC). Usando nosso caso como paradigma, ampliamos a gama de diagnóstico diferencial de ETC, incluindo degeneração corticobasal, atrofia de múltiplos sistemas, deficiência de vitamina B12, neurossífilis, demência frontotemporal e doença de Alzheimer.

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Most cited references 19

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Chronic traumatic brain injury associated with boxing.

Barry Jordan (2000)

Chronic traumatic brain injury (CTBI) associated with boxing occurs in approximately 20% of professional boxers. Risk factors associated with CTBI include increased exposure (i.e., duration of career, age of retirement, total number of bouts), poor performance, increased sparring, and apolipoprotein (APOE) genotype. Clinically, boxers exhibiting CTBI will present with varying degrees of motor, cognitive, and/or behavioral impairments. The severe form of CTBI is referred to as dementia pugilistica. The diagnosis of CTBI is dependent upon documenting a progressive neurological condition that is consistent with the clinical symptomatology of CTBI attributable to brain trauma and unexplainable by an alternative pathophysiological process. Pathologically, CTBI shares many characteristics with Alzheimer's disease (i.e., neurofibrillary triangles, diffuse amyloid plaques, acetylcholine deficiency, and/or tau immunoreactivity). The mainstay of treatment of CTBI is prevention, however medications used in the treatment of Alzheimer's disease and/or parkinsonism may be utilized.

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What is the Relationship of Traumatic Brain Injury to Dementia?

Mario Mendez (2017)

There is a long history linking traumatic brain injury (TBI) with the development of dementia. Despite significant reservations, such as recall bias or concluding causality for TBI, a summary of recent research points to several conclusions on the TBI-dementia relationship. 1) Increasing severity of a single moderate-to-severe TBI increases the risk of subsequent Alzheimer's disease (AD), the most common type of dementia. 2) Repetitive, often subconcussive, mild TBIs increases the risk for chronic traumatic encephalopathy (CTE), a degenerative neuropathology. 3) TBI may be a risk factor for other neurodegenerative disorders that can be associated with dementia. 4) TBI appears to lower the age of onset of TBI-related neurocognitive syndromes, potentially adding "TBI cognitive-behavioral features". The literature further indicates several specific risk factors for TBI-associated dementia: 5) any blast or blunt physical force to the head as long as there is violent head displacement; 6) decreased cognitive and/or neuronal reserve and the related variable of older age at TBI; and 7) the presence of apolipoprotein E ɛ4 alleles, a genetic risk factor for AD. Finally, there are neuropathological features relating TBI with neurocognitive syndromes: 8) acute TBI results in amyloid pathology and other neurodegenerative proteinopathies; 9) CTE shares features with neurodegenerative dementias; and 10) TBI results in white matter tract and neural network disruptions. Although further research is needed, these ten findings suggest that dose-dependent effects of violent head displacement in vulnerable brains predispose to dementia; among several potential mechanisms is the propagation of abnormal proteins along damaged white matter networks.

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A critical review of chronic traumatic encephalopathy.

Grant L Iverson, Andrew Gardner, Paul McCrory … (2015)

Chronic traumatic encephalopathy (CTE) has been described in the literature as a neurodegenerative disease with: (i) localized neuronal and glial accumulations of phosphorylated tau (p-tau) involving perivascular areas of the cerebral cortex, sulcal depths, and with a preference for neurons within superficial cortical laminae; (ii) multifocal axonal varicosities and axonal loss involving deep cortex and subcortical white matter; (iii) relative absence of beta-amyloid deposits; (iv) TDP-43 immunoreactive inclusions and neurites; and (v) broad and diverse clinical features. Some of the pathological findings reported in the literature may be encountered with age and other neurodegenerative diseases. However, the focality of the p-tau cortical findings in particular, and the regional distribution, are believed to be unique to CTE. The described clinical features in recent cases are very similar to how depression manifests in middle-aged men and with frontotemporal dementia as the disease progresses. It has not been established that the described tau pathology, especially in small amounts, can cause complex changes in behavior such as depression, substance abuse, suicidality, personality changes, or cognitive impairment. Future studies will help determine the extent to which the neuropathology is causally related to the diverse clinical features.

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Author and article information

Journal

Journal ID (nlm-ta): Dement Neuropsychol

Journal ID (iso-abbrev): Dement Neuropsychol

Journal ID (publisher-id): dn

Title: Dementia & Neuropsychologia

Publisher: Associação de Neurologia Cognitiva e do Comportamento

ISSN (Print): 1980-5764

Publication date (Print and electronic): Jan-Mar 2018

Publication date (Print): Jan-Mar 2018

Volume: 12

Issue: 1

Pages: 92-96

Affiliations

[1 ]Associate Professor of Neurology, Federal University of Goiás, Goiânia, GO, Brazil. Coordinator, Cognitive and Behavioral Neurology Unit, Department of Neurology, Hospital das Clínicas

[2 ]Behavioral and Cognitive Neurology Unit, Department of Neurology, Hospital das Clínicas, Federal University of Goiás, Goiânia, GO, Brazil

Author notes

Leonardo Caixeta, Instituto da Memória Avenida Cristo Rei, 626 / Setor Jaó 74674-290 Goiânia GO - Brazil. E-mail: leonardocaixeta1@ 123456gmail.com

Author contributions. All authors drafted and critically revised the manuscript.

Disclosure: The authors report no conflicts of interest.

Article

DOI: 10.1590/1980-57642018dn12-010014

PMC ID: 5901256

SO-VID: e31b5644-c8fd-4fb6-bd98-910e63a16d07

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.