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. 2016 Oct;9(2):34-48.

Chronic Traumatic Encephalopathy in Athletes Involved with High-impact Sports

Affiliations

Chronic Traumatic Encephalopathy in Athletes Involved with High-impact Sports

Cyrus Safinia et al. J Vasc Interv Neurol. 2016 Oct.

Abstract

Background and purpose: Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease occurring most commonly in athletes and is caused by repeated concussive or subconcussive blows to the head. The main purpose of this review is to evaluate the published literature on chronic traumatic encephalopathy (CTE) in athletes participating in high-impact sports. In particular, we highlight the significance of concussive and subconcussive impacts in multiple sports, elucidate the differences between clinical/pathological features of CTE and related neurodegenerative diseases, and provide an explanation for the variation in clinical presentation between athletes of different sports.

Methods: A review targeting relevant publications to CTE was performed. The PubMed/MEDLINE index was searched for keywords such as "chronic traumatic encephalopathy," "repetitive traumatic brain injury," "mild traumatic brain injury," and "concussion" from year 1924 through March 1, 2016.

Results: A consensus panel's recent identification of a pathognomonic pathology in CTE, characterized by an irregular distribution of phosphorylated tau deposits, is an important step in developing consensus diagnostic criteria and clinicopathological studies. After review of major clinical studies, evidence suggests that there are clear differences in neuropathological features, clinical progression, and manifestation of symptoms between CTE and other neurodegenerative diseases. The literature suggests boxers tend to have more severe symptoms than other athletes due to more frequent rotational and shearing impacts. Data regarding genetic predispositions of CTE have been inconsistent in part due to low subject populations. Positron emission tomography imaging involving tau-binding ligands has recently proven effective in differentiating CTE from control groups and other neurodegenerative diseases.

Conclusions: Further longitudinal studies should be conducted to correlate the number of suffered concussive/subconcussive forces to the likelihood of developing chronic traumatic brain injury symptoms. Research striving for a reliable antemortem CTE diagnosis would be immensely beneficial, leading to more accurate estimates of prevalence, allowing clinicians to assess future risk of athletes' continued participation in sports, and enabling clinicians to make appropriate preventive recommendations.

Keywords: Chronic traumatic encephalopathy; brain injury; concussion; neurological injury; pathology; traumatic brain injury.

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Figures

Figure 1
Figure 1. Samples head CT images of possible CTE cases. (A) Axial noncontrast head CT scan of a 76-year-old male, retired football player (in college and briefly in NFL), with a medical history of severe cardiac disease presented to the hospital with shortness of breath. The CT scan is remarkable. However, during hospitalization the patient had his pacemaker replaced, and then developed severe postprocedural agitation. The patient’s family stated that approximately 1 month prior to admission, he had an episode of getting lost and was unaware of his surroundings. Since then, his cognition status had continued declining. He was previously diagnosed with frontotemporal lobe dementia. Patient’s family stated that for the last 20 years, he has been extremely agitated. Patient also noted some type of jerking movement of the extremities, and hallucinating (seeing animals) and having delusions. (B) Postmortem CT imaging of a professional boxer who died in his 40s with symptoms of CTE.  This coronal slice shows a cavum septum pellucidum (the authors would like to acknowledge Dr. Gary Hatch for his input in generating this neuroradiographic image).
Figure 2
Figure 2. Differences in 18F-FDDNP signal in patients with suspected CTE versus patients with AD. Note the higher density regions in the CTE case (Adapted, with permission, from Barrio et al. [53]).

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