Home » Head Trauma Strongly Linked To Chronic Traumatic Encephalopathy But Precise Relationship Not Yet Known

Head Trauma Strongly Linked To Chronic Traumatic Encephalopathy But Precise Relationship Not Yet Known

Other risk factors for CTE, incidence rate not yet known; connection has been "greatly overstated" says Cantu



While concussion, as with any form of traumatic brain injury (TBI), needs to be taken seriously, the impact on an athlete's day-to-day life is usually shortlived.  Three-quarters of concussed high school athletes in one recent study [1] were found to be symptom-free within a week; only 15% had symptoms lasting more than a week but less than a month, and only a very small number (1.5%) were still experiencing symptoms more than a month after injury.

Head with question mark post-its inside

Recent evidence, however, suggests that "mild" TBI, including repetitive concussive and subconcussive brain trauma[2] can lead to long-term or progressive symptoms (postconcussion syndrome), disability, and pathologic changes, especially in cases of repetitive concussion:

  • Repeated concussion has been associated with neuropsycyhological deficits, electrophysiologic changes, and metabolic abnormalities measured using brain magnetic resonance spectroscopy (MRS).
  • Closed head injury, even in a mild form, is a leading cause of both short-term and long-term cognitive impairment of athletes, particularly those in contact sports such as football, boxing, soccer, rugby, lacrosse and hockey.
  • While the majority of athletes who experience a concussion can be expected to recover, the risks are increased by a second concussion, or returning to play from a concussion before the brain has fully healed, which recent studies suggest takes much longer than previously thought, particularly in adolescents, who may be peculiarly vulnerable to the lingering effects of concussion on short-term memory than adults or even younger athletes [24], which some experts speculate "could be related to the fact that the frontal part of the brain, responsible for working memory and other executive functions, undergoes its final stages of maturation during adolescence." Indeed, a recent study found that teens are, in fact, slower to regain higher (i.e. 'executive) function after concussion.[25]
More concerning, is that athletes in contact and collision sports have been found, after death, to have been suffering from a neurodegenerative condition called chronic traumatic encephalopathy (CTE), a progressive disease in which symptoms do not appear until many years after an individual finishes their playing career, and have been linked with repeated concussive or subconcussive blows to the head. While most documented cases of CTE have been reported in a highly unrepresentative group of former professional athletes, [3] CTE has more recently been documented in younger, amateur athletes, inclduing an 18-year-old football player.[4]

CTE symptoms  

The reported clinical symptoms of CTE are "tremendously broad" [19], but can include:

  • Memory loss
  • Irritability
  • Outbursts of aggressive or violent behavior
  • Confusion
  • Speech abnormalities (slurred or slowed speech),
  • Cognitive decline (concentration)
  • Gait abnormalities
  • Unsteadiness
  • Headaches
  • Parkinsonism
  • Mood disorders (depression)
  • Paranoia
  • Poor insight/judgment
  • Apathy
  • Hyperreligiousity
  • Visual abnormalities [13,19] 

A 2013 meta-analysis of CTE[19] ("Gardner study") cautions, however, that "It may be that the description of the modern CTE symptomatology is confounded by the retrospective nature of the data collection and the heavily biased case selection. Consequently, the reported clinical observations (ie, suicidality, emotional liability, aggression and disinhibition) are likely to be skewed by selection bias.

Moreover, the Gardner study notes that, because the "clinical features [of CTE] overlap with a number of known psychiatric conditions and neurodegenerative diseases," the recent characterization of CTE "does not adequately consider plausible differential diagnoses, mediating variables, moderating variables, or multifactorial neuropathological processes."  In other words, it is, in the view of many leading concussion experts, overly inclusive and simplistic.  

CTE: not a distinct disorder? 

A controversial 2013 study [26] by Christopher Randolph, PhD, of Loyola University in Chicago, and co-authored by no less a concussion authority than Kevin Guskiewicz,  Kenan Distinguished Professor, Director of the Matthew Gfeller Sport-Related Traumatic Brain Injury Research Center at The University of North Carolina at Chapel Hill, and Director of the Center for the Study of Retired Athletes at UNC, even goes so far as to suggest that CTE may not a distinct neurodegenerative disorder at all.

In a study of retired NFL players - who largely comprise the universe from which the case studies of brains showing the presence of CTE have been drawn, and who the media have widely reported are at high risk of CTE - Randolph found that they did not actually suffer from CTE; when compared with healthy controls and with non-athlete patients with a clinical diagnosis of mild cognitive impairment (MCI), commonly presumed to reflect the earliest stage of Alzheimer's disease, and that the patterns of their impairments were virtually identical to those exhibited by the non-athletes with MCI. 

The study supported, Randolph said, the hypothesis he had proffered in a 2009 paper[30] that a long history of repetitive head trauma in contact sports might eventually result in a diminished cerebral reserve, leading to an earlier expression of common, age-related neurodegenerative diseases such as AD and Parkinson's (PD), but that the ways in which such diminished cerebral reserve would be expressed (e.g. MCI, AD, PD) would not be expected to differ from individuals with those diseases who lacked such a history of head trauma.   

The Randolph study was heavily criticized as flawed by those who viewed CTE as a distinct condition.  Chris Nowinski, co-director of the Center for the Study of Traumatic Encephalopathy at the Boston University School of Medicine (CSTE), told PopSci.com [34] that it was  "preposterous" for Randolph to conclude that CTE might not be its own disease because retired football players had impairments similar to those of other patients with mild cognitive impairment.

While the study was reported by some in the scientific and medical media[34,35,36] at the time it was published, it did not gain a foothold in the mass media and soon faded from view. 

It has since been proved to be an outlier.

In February 2015, a conference of pathologists sponsored by the National Institute of Neurological Disorders and Stroke of the National Institutes of Health convened in Boston to begin the process of generating consensus guidelines for the pathological diagnosis of CET. The group reported "general agreement" that CTE was a distinct neuropathological disease, different from other tauopathies (e.g. neurodegenerative diseases associated with the pathological aggregation of tau protein in the human brain).[69]  The feature considered most specific to CTE, the group reported, and the one that distinguished the disorder from other neurodegenerative diseases such as Alzheimer's, was the where the tau was distributed in different regions of the brain.