Chronic Traumatic Encephalopathy: A Potential Late Effect of Sport-Related Concussive and Subconcussive Head Trauma

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Clinical signs and symptoms of CTE

Whereas concussion and postconcussion syndrome represent temporary states of neuronal and axonal derangement, CTE is a neurodegenerative disease that occurs years or decades after recovery from the acute or postacute effects of head trauma. The exact relationship between concussion and CTE is not entirely clear, although repetitive axonal perturbation may initiate a series of metabolic, ionic, membrane, and cytoskeletal disturbances, which trigger the pathologic cascade that leads to CTE in

Gross Pathology

Neuropathologic studies of athletes with a history of repeated mild head injuries have produced several consistent findings that, together, make CTE a distinctive disorder. On gross examination, there is often anterior cavum septi pellucidi and, usually, posterior fenestrations. These changes may be caused by the force of the head impact being transmitted through the ventricular system, thereby affecting the integrity of the intervening tissue. Enlargement of the lateral and third ventricles is

CTE is a Potential Late Effect of Repeated Head Injuries

CTE is not thought to be a long-term sequela after a specific head trauma. Rather, its clinical symptoms emerge later in life, usually after athletes retire from their sport. Like most other neurodegenerative diseases that cause dementia, CTE has an insidious onset and gradual course. Based on a recent review of neuropathologically confirmed CTE in athletes11, the mean age at onset is 42.8 years (SD = 12.7; range = 25–76 years). On average, onset occurs approximately 8 years after retirement

Summary

CTE is a neurodegenerative disease that occurs later in the lives of some individuals with a history of repeated head trauma. The exact relationship between repetitive mild TBI, with or without symptomatic concussion, and CTE is not entirely clear, although it is possible that repetitive axonal injury sets up a series of metabolic, ionic, and cytoskeletal disturbances that trigger a pathologic cascade, leading to CTE in susceptible individuals. CTE has been reported in association with American

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References (62)

  • H.S. Martland

    Punch drunk

    JAMA

    (1928)
  • M. Critchley

    Medical aspects of boxing, particularly from a neurological standpoint

    Br Med J

    (1957)
  • H. Parker

    Traumatic encephalopathy (‘punch drunk’) of professional pugilists

    J Neurol Psychopathol

    (1934)
  • J.A. Millspaugh

    Dementia pugilistica

    U S Nav Med Bull

    (1937)
  • J.A. Corsellis et al.

    The aftermath of boxing

    Psychol Med

    (1973)
  • H. Miller

    Mental after-effects of head injury

    Proc R Soc Med

    (1966)
  • J.F. Geddes et al.

    Neuronal cytoskeletal changes are an early consequence of repetitive head injury

    Acta Neuropathol

    (1999)
  • B.I. Omalu et al.

    Chronic traumatic encephalopathy in a national football league player: part II

    Neurosurgery

    (2006)
  • B.I. Omalu et al.

    Chronic traumatic encephalopathy in a national football league player

    Neurosurgery

    (2005)
  • S. Cajigal

    Brain damage may have contributed to former wrestler’s violent demise

    Neurology Today

    (2007)
  • A. McKee et al.

    Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injury

    J Neuropathol Exp Neurol

    (2009)
  • B.I. Omalu et al.

    Chronic traumatic encephalopathy, suicides and parasuicides in professional American athletes: the role of the forensic pathologist

    Am J Forensic Med Pathol

    (2010)
  • A.C. McKee et al.

    TDP-43 proteinopathy and motor neuron disease in chronic traumatic encephalopathy

    J Neurol Exp Neuropathol

    (2010)
  • Oldest living pro football players. 2009–2000 Necrology

  • C. Giza et al.

    The neurometabolic cascade of concussion

    J Athl Train

    (2001)
  • T.J. Yuen et al.

    Sodium channelopathy induced by mild axonal trauma worsens outcome after a repeat injury

    J Neurosci Res

    (2009)
  • B.I. Omalu et al.

    Chronic traumatic encephalopathy (CTE) in a national football league player: case report and emerging medicolegal practice questions

    J Forensic Nurs

    (2010)
  • G. Serbest et al.

    Temporal profiles of cytoskeletal protein loss following traumatic axonal injury in mice

    Neurochem Res

    (2007)
  • M.G. Spillantini et al.

    Frontotemporal dementia and Parkinsonism linked to chromosome 17: a new group of tauopathies

    Brain Pathol

    (1998)
  • G.F. Hall et al.

    Human tau filaments induce microtubule and synapse loss in an in vivo model of neurofibrillary degenerative disease

    J Cell Sci

    (2000)
  • G.F. Hall et al.

    Human tau becomes phosphorylated and forms filamentous deposits when overexpressed in lamprey central neurons in situ

    Proc Natl Acad Sci U S A

    (1997)
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      High profile research on professional football players has helped explain neurological system change. Long forming physical processes produce reduced cognitive function, increased confusion, and self-destructive behaviors like substance abuse and self-harm [32,33]. However, CTE alone cannot explain sudden deaths from small concussions or how exposed individuals vary widely in their ability to maintain normalcy in their lives.

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    This work was supported by NIA P30AG13846, Supplement 0572063345-5, National Operating Committee on Standards for Athletic Equipment, and by the Department of Veterans Affairs. This work was also supported by an unrestricted gift from the National Football League. The funding sources were not involved in the preparation, review, or approval of this article.

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