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October 27, 2015; 85 (17) Views & Reviews

Chronic traumatic encephalopathy and athletes

William Meehan, Rebekah Mannix, Ross Zafonte, Alvaro Pascual-Leone
First published August 7, 2015, DOI: https://doi.org/10.1212/WNL.0000000000001893
William Meehan III
From the Micheli Center for Sports Injury Prevention (W.M.), Waltham; the Brain Injury Center (W.M., R.M.), Sports Concussion Clinic, Division of Sports Medicine (W.M.), and Division of Emergency Medicine (W.M., R.M.), Boston Children's Hospital; the Department of Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital (R.Z.), Massachusetts General Hospital, Brigham and Women's Hospital; and the Berenson-Allen Center and Division of Interventional Cognitive Neurosciences, Department of Neurology (A.P.-L.), Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA.
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Rebekah Mannix
From the Micheli Center for Sports Injury Prevention (W.M.), Waltham; the Brain Injury Center (W.M., R.M.), Sports Concussion Clinic, Division of Sports Medicine (W.M.), and Division of Emergency Medicine (W.M., R.M.), Boston Children's Hospital; the Department of Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital (R.Z.), Massachusetts General Hospital, Brigham and Women's Hospital; and the Berenson-Allen Center and Division of Interventional Cognitive Neurosciences, Department of Neurology (A.P.-L.), Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA.
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Ross Zafonte
From the Micheli Center for Sports Injury Prevention (W.M.), Waltham; the Brain Injury Center (W.M., R.M.), Sports Concussion Clinic, Division of Sports Medicine (W.M.), and Division of Emergency Medicine (W.M., R.M.), Boston Children's Hospital; the Department of Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital (R.Z.), Massachusetts General Hospital, Brigham and Women's Hospital; and the Berenson-Allen Center and Division of Interventional Cognitive Neurosciences, Department of Neurology (A.P.-L.), Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA.
MD
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Alvaro Pascual-Leone
From the Micheli Center for Sports Injury Prevention (W.M.), Waltham; the Brain Injury Center (W.M., R.M.), Sports Concussion Clinic, Division of Sports Medicine (W.M.), and Division of Emergency Medicine (W.M., R.M.), Boston Children's Hospital; the Department of Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital (R.Z.), Massachusetts General Hospital, Brigham and Women's Hospital; and the Berenson-Allen Center and Division of Interventional Cognitive Neurosciences, Department of Neurology (A.P.-L.), Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA.
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Citation
Chronic traumatic encephalopathy and athletes
William Meehan, Rebekah Mannix, Ross Zafonte, Alvaro Pascual-Leone
Neurology Oct 2015, 85 (17) 1504-1511; DOI: 10.1212/WNL.0000000000001893

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Abstract

Recent case reports have described athletes previously exposed to repetitive head trauma while participating in contact sports who later in life developed mood disorders, headaches, cognitive difficulties, suicidal ideation, difficulties with speech, and aggressive behavior. Postmortem discoveries show that some of these athletes have pathologic findings that are collectively termed chronic traumatic encephalopathy (CTE). Current hypotheses suggest that concussions or perhaps blows to the head that do not cause the signs and symptoms necessary for making the diagnosis of concussion, so-called subconcussive blows, cause both the clinical and pathologic findings. There are, however, some athletes who participate in contact sports who do not develop the findings ascribed to CTE. Furthermore, there are people who have headaches, mood disorders, cognitive difficulties, suicidal ideation, and other clinical problems who have neither been exposed to repeated head trauma nor possessed the pathologic postmortem findings of those currently diagnosed with CTE. The current lack of prospective data and properly designed case-control studies limits the current understanding of CTE, leading to debate about the causes of the neuropathologic findings and the clinical observations. Given the potential for referral and recall bias in available studies, it remains unclear whether or not the pathologic findings made postmortem cause the presumed neurobehavioral sequela and whether the presumed risk factors, such as sports activity, cerebral concussions, and subconcussive blows, are solely causative of the clinical signs and symptoms. This article discusses the current evidence and the associated limitations.

GLOSSARY

AD=
Alzheimer disease;
ALS=
amyotrophic lateral sclerosis;
CTE=
chronic traumatic encephalopathy;
FTD=
frontotemporal dementia;
TDP-43=
TAR DNA-binding protein 43

Footnotes

  • Go to Neurology.org for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the article.

  • Editorial, page 1442

  • Received February 19, 2015.
  • Accepted in final form May 20, 2015.
  • © 2015 American Academy of Neurology
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