Chronic traumatic encephalopathy

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Chronic traumatic encephalopathy (dementia pugilistica, punch drunk syndrome, DP, CTE ) results from head injury and classically presents as mood and impulse control disorders evolving into Parkinsonism and/or dementia years after one or more cerebral traumatic insults. These do not have to have been associated with severe head injury and indeed there is a distinctly increased risk in any contact sport where repetitive minor head injury is a feature. While first recognised in boxers, it has been recognised now to be associated with many ball games and even domestic violence victims. It is likely to be an occupational hazard in some military and paramilitary occupations. Cases could be induced by psychiatric disorder involving self harm. A relatively distinct neuropathological patterned of change has been described at post mortem and this remains the gold standard for diagnosis. Indeed investigations in life can not at present distinguish between multiple other potential causes of Parkinsonism and dementia. A clinical history of head trauma is the single most predictive factor of the characteristic neuropathology.



The area continues to be a medico-legal minefield with vested interests in the sporting and employment field historically resisting attempts to make their sports and employment safer and challenging causality with the potential for substantial settlements. However useful changes that lower individual risk have occurred in sports such as boxing[1] over the last half century or so, even if at the most extreme some have recommended banning the sport[2][3]. The names of Karel Henner and Bennet Omalu are associated with the difficult progress made to date in prevention.


There is an association between any brain damage and the late development of neurodegenerative conditions. This is likely to be related to autoimmune stimulus being more likely after neuronal damage. Such autoimmune stimulus will have both genetic and environmental components and must be understood in the context that the brain also has mechanisms that allow plasticity and early in life effectively repair. The secondary injury cascade is very complex[4]. As of 2016 addressing chronic endoplasmic reticulum stress and neurology-protein homeostasis appears to be the most promising mechanism of intervention after the CNS injury has occurred[5].


It is one of the neurogenerative conditions associated with abnormal patterns of disposition of tau protein in the brain. The characteristic findings appear to be very common in participants of some sports and predate the onset of severe neurological symptoms, as demonstrated by post-mortems in very young contact sports participants who have died of other causes. As the standard of neuropathological examination required now to make the diagnosis includes specific immuno-staining of CNS histopathological specimens it may not be done routinely. Provisional diagnostic criteria have been defined[6].


Symptoms typically manifest five or more years after exposure and certainly up to 40 or more years. The psychiatric symptoms usually develop first with dementia or movement disorder being late.

  • Behavioural
    • Explosivity
    • Violence
  • Mood disorders
    • Depression
    • Hopelessness
  • Cognitive impairment
    • Impaired memory
    • Impaired executive function
    • Impaired attention
    • Dementia
  • Movement disorders

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