Chronic Traumatic Encephalopathy: A Critical Appraisal

Levin, Benjamin D.; Bhardwaj, Anish

doi:10.1007/s12028-013-9931-1

Cited by 21 publications

(16 citation statements)

References 56 publications

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“…Case 2 ( E–H ): A 61‐year‐old former professional boxer had a similar degree of CTE ‐related tauopathy ( E , AT 8 immunostain). In fact, both the NFL player and the boxer met neuropathological criteria for CTE stage III tauopathy. However, in contrast to the NFL player, there is marked degeneration within the cerebellum with marked P urkinje cell loss ( F , B ielschowsky silver stain; arrowhead, B asket cell processes without P urkinje cells “empty B askets”).…”

Section: Boxing and American Footballmentioning

confidence: 99%

“…However, the ability to diagnose CTE during life is critical to conduct epidemiologic studies on CTE and to eventually plan treatment trials. To address this gap, Montenigro et al proposed new clinical research diagnostic criteria for CTE (61) that overcome the limitations identified (49,58) in the previous criteria (40,43,44,92). The new criteria are based on a systematic review of the previous literature, as well as on the clinical features reported in neuropathologically confirmed cases of CTE without comorbid disease (52,53,86).…”

Section: Clinical Diagnostic Criteriamentioning

confidence: 99%

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Clinical Features of Repetitive Traumatic Brain Injury and Chronic Traumatic Encephalopathy

2015

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Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease characterized by a distinct pattern of hyperphosphorylated tau (p-tau). Thought to be caused by repetitive concussive and subconcussive injuries, CTE is considered largely preventable. The majority of neuropathologically confirmed cases have occurred in professional contact sport athletes (eg, boxing, football). A recent post-mortem case series has magnified concerns for the public's health following its identification in six high school level athletes. CTE is diagnosed with certainty only following a post-mortem autopsy. Efforts to define the etiology and clinical progression during life are ongoing. The goal of this article is to characterize the clinical concepts associated with short- and long-term effects of repetitive traumatic brain injury, with a special emphasis on new clinical diagnostic criteria for CTE. Utilizing these new diagnostic criteria, two cases of neuropathologically confirmed CTE, one in a professional football player and one in a professional boxer, are reported. Differences in cerebellar pathology in CTE confirmed cases in boxing and football are discussed.

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Section: Boxing and American Footballmentioning

confidence: 99%

Section: Clinical Diagnostic Criteriamentioning

confidence: 99%

Clinical Features of Repetitive Traumatic Brain Injury and Chronic Traumatic Encephalopathy

2015

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“…44 The average age of diagnosis for CTE is 54 years old with the youngest case at 18 years old. 45 Young age of disease onset manifests with mood and behavioral disturbances, while older age at time of onset primarily presents with cognitive decline. 46 The latency of onset is variable ranging from a few months to several decades following neurotrauma exposure.…”

Section: Introductionmentioning

confidence: 99%

Alzheimer’s disease and chronic traumatic encephalopathy: Distinct but possibly overlapping disease entities

et al. 2016

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Background Alzheimer’s disease (AD) and chronic traumatic encephalopathy (CTE) have long been recognized as sharing some similar neuropathological features, mainly the presence of neurofibrilary tangles and hyperphosphorylated tau, but have generally been described as distinct entities. Evidence indicates that neurotrauma increases the risk of developing dementia and accelerates the progression of disease. Findings are emerging that CTE and AD may be present in the same patients. Clinical presentation We present a series of previously unpublished cases with one case demonstrating possible neurotrauma-related AD, one pure CTE, and an example of a case exhibiting features of both AD and CTE. The future significance of this work lies not only in the confirmation of AD-CTE coexistence but more importantly, ways of generating a hypothesis about the possibility that CTE may accelerate AD development. Understanding the relationship between neurotrauma and neurodegenerative disease, will help elucidate how distinct disease entities can co-exist in the same patient. It will ultimately require the use of preclinical animal models and repeat injury paradigms to investigate clinically relevant injury mechanisms. These models should produce a CTE-like phenotype that must be both neuropathologically and behaviorally similar to human disease. Conclusion In this case series and review of the literature, we present a discussion of AD and CTE in the context of neurotrauma. We highlight recent work from repetitive neurotrauma models with an emphasis on those exhibiting a CTE-like phenotype. We briefly address potential mechanisms of interest shared amongst AD and CTE and advocate for future experiments to enhance understanding of CTE pathophysiology and the relationship between CTE and AD.

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“…95 Because of the neuropathological similarities with AD and TBI, potential pharmacological and behavioral interventions for these conditions could also be applied to CTE. 74,191 Discussion CTE represents a major public health issue, given the number of athletes and service members who are exposed to concussive and/or subconcussive events. The current state of the science has generated an initial consensus on the neuropathology of CTE.…”

Section: Treatment and Prevention Strategiesmentioning

confidence: 99%

The Biological Basis of Chronic Traumatic Encephalopathy following Blast Injury: A Literature Review

Aldag

Armstrong

Bandak

et al. 2017

Journal of Neurotrauma

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The United States Department of Defense Blast Injury Research Program Coordinating Office organized the 2015 International State-of-the-Science meeting to explore links between blast-related head injury and the development of chronic traumatic encephalopathy (CTE). Before the meeting, the planning committee examined articles published between 2005 and October 2015 and prepared this literature review, which summarized broadly CTE research and addressed questions about the pathophysiological basis of CTE and its relationship to blast- and nonblast-related head injury. It served to inform participants objectively and help focus meeting discussion on identifying knowledge gaps and priority research areas. CTE is described generally as a progressive neurodegenerative disorder affecting persons exposed to head injury. Affected individuals have been participants primarily in contact sports and military personnel, some of whom were exposed to blast. The symptomatology of CTE overlaps with Alzheimer's disease and includes neurological and cognitive deficits, psychiatric and behavioral problems, and dementia. There are no validated diagnostic criteria, and neuropathological evidence of CTE has come exclusively from autopsy examination of subjects with histories of exposure to head injury. The perivascular accumulation of hyperphosphorylated tau (p-tau) at the depths of cortical sulci is thought to be unique to CTE and has been proposed as a diagnostic requirement, although the contribution of p-tau and other reported pathologies to the development of clinical symptoms of CTE are unknown. The literature on CTE is limited and is focused predominantly on head injuries unrelated to blast exposure (e.g., football players and boxers). In addition, comparative analyses of clinical case reports has been challenging because of small case numbers, selection biases, methodological differences, and lack of matched controls, particularly for blast-exposed individuals. Consequently, the existing literature is not sufficient to determine whether the development of CTE is associated with head injury frequency (e.g., single vs. multiple exposures) or head injury type (e.g., impact, nonimpact, blast-related). Moreover, the incidence and prevalence of CTE in at-risk populations is unknown. Future research priorities should include identifying additional risk factors, pursuing population-based longitudinal studies, and developing the ability to detect and diagnose CTE in living persons using validated criteria.

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Chronic Traumatic Encephalopathy: A Critical Appraisal

Cited by 21 publications

References 56 publications

Clinical Features of Repetitive Traumatic Brain Injury and Chronic Traumatic Encephalopathy

Clinical Features of Repetitive Traumatic Brain Injury and Chronic Traumatic Encephalopathy

Alzheimer’s disease and chronic traumatic encephalopathy: Distinct but possibly overlapping disease entities

The Biological Basis of Chronic Traumatic Encephalopathy following Blast Injury: A Literature Review

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