Long‐term Consequences of Repetitive Brain Trauma: Chronic Traumatic Encephalopathy

Abstract

Chronic traumatic encephalopathy (CTE) has been linked to participation in contact sports such as boxing and American football. CTE results in a progressive decline of memory and cognition, as well as depression, suicidal behavior, poor impulse control, aggressiveness, parkinsonism, and, eventually, dementia. In some individuals, it is associated with motor neuron disease, referred to as chronic traumatic encephalomyelopathy, which appears clinically similar to amyotrophic lateral sclerosis. Results of neuropathologic research has shown that CTE may be more common in former contact sports athletes than previously believed. It is believed that repetitive brain trauma, with or possibly without symptomatic concussion, is responsible for neurodegenerative changes highlighted by accumulations of hyperphosphorylated tau and TDP-43 proteins. Given the millions of youth, high school, collegiate, and professional athletes participating in contact sports that involve repetitive brain trauma, as well as military personnel exposed to repeated brain trauma from blast and other injuries in the military, CTE represents an important public health issue. Focused and intensive study of the risk factors and in vivo diagnosis of CTE will potentially allow for methods to prevent and treat these diseases. Research also will provide policy makers with the scientific knowledge to make appropriate guidelines regarding the prevention and treatment of brain trauma in all levels of athletic involvement as well as the military theater.

Mind the gaps—advancing research into short-term and long-term neuropsychological outcomes of youth sports-related concussions

“…80 These clinical symptoms define disease severity. 81 The neurodegenerative pathophysiology of CTE is complex, and the neurological sequelae are poorly understood. In severe cases, the cerebral cortex and medial temporal lobes seem most profoundly affected, 81,82 with pathology characterized by neurofibrillary tangles composed of phosphorylated tau 79 and, in some cases, TAR DNA-binding protein 43 pathology.…”

“…81 The neurodegenerative pathophysiology of CTE is complex, and the neurological sequelae are poorly understood. In severe cases, the cerebral cortex and medial temporal lobes seem most profoundly affected, 81,82 with pathology characterized by neurofibrillary tangles composed of phosphorylated tau 79 and, in some cases, TAR DNA-binding protein 43 pathology. 83 CTE is also associated with marked atrophy, notably in the frontal cortex and medial temporal lobe, as well as in the mammillary bodies, thalamus and hypothalamus.…”

Cavum Septi Pellucidi in Symptomatic Former Professional Football Players

“…3,7 Moreover, CTE has been found in nonathletes who have experienced repetitive head impacts, including military service members, 2,8,9 persons with medical conditions such as epilepsy and autism, and victims of physical abuse. 2,10 All patients with neuropathologically confirmed CTE reported to date have had a history of brain trauma, typically from repetitive mild or subconcussive head impacts. This suggests that this head impact exposure is a necessary, but not sufficient, condition for the initiation of the pathogenetic cascade that eventually leads to neurodegeneration.…”

Neurodegenerative causes of death among retired National Football League players

“…It is not possible to directly examine mortality from CTE because the pathologic refinement of the CTE diagnosis has only occurred within the last few years, and CTE is not listed as a cause of death in any revision of the International Classification of Diseases (ICD). As an alternative, because it is now known that neurologic conditions previously attributed to AD, PD, and ALS may actually have been related to CTE, 4,9 an analysis that combined all neurodegenerative causes of death was conducted; this analysis included deaths that may be related to CTE even if not reported as such on death certificates.…”