What we know about Chronic Traumatic Encephalopathy (CTE)

Share with friends
athletic performance

Twenty years ago, chronic traumatic encephalopathy (CTE) was described as a neurological disorder resulting from repetitive neurotrauma. More recently, it has been definitively shown to be a neurodegenerative condition that has a delayed onset, which means symptoms can show up years, even decades, after the initiation of the process.

Between 2005 and 2012, former athletes were being autopsied and the neuropathology that was described was summarized to be characteristic of CTE. In 2015, the preliminary consensus criteria to define CTE was established and finally published in 2016.

Four Stages

Some neuroscientists like Bennet Omalu insist that cases of CTE fall on a spectrum, while others like Ann McKee and her colleagues at Boston University divide the condition into stages. They suggest that stage I CTE may be asymptomatic or preclinical in some patients. However, not all neuroscientists are in agreement about the criteria of the four stages. Some say it is too difficult to determine progression because the error rate of misdiagnosing stages has yet to be explored. Some say the later stages make it  difficult to differentiate between true CTE criteria, possible sporadic neurodenerative disease, and natural aging. In addition, many late stage cases of CTE have comorbid neurodegenerative conditions, like Alzheimer’s and dementia, which can further complicate an accurate stage diagnosis.

Traumatic Encephalopathy Syndrome

It is important to note, there is a clinical syndrome associated with repetitive head trauma called Traumatic Encephalopathy Syndrome (TES). This syndrome that is observed in the living (as opposed to CTE which currently can only be confirmed after death) has criteria that are as follows:

  • History of multiple impacts to the head
  • No other neurological disorder (including chronic residual symptoms from a single TBI or persistent post-concussion syndrome) that likely accounts for all clinical features, although concomitant diagnoses of substance abuse, PTSD, mood/anxiety disorders, or other neurodegenerative diseases (for example, Alzheimer’s disease and fronto-temporal dementia) or a combination of these can be present.
  • Clinical features must be present for a minimum of 12 months.
  • At least one of the three core clinical features must be present :
    • Cognitive: Cognitive problems reported by the person and/or an informant and low cognitive test scores on one or more tests of episodic memory, executive function, and/or attention
    • Behavioral: Being described as emotionally explosive, physically violent, and/or verbally violent, as reported by self or informant, by history of treatment, or by clinician’s report.
    • Mood: Feeling overly sad, depressed, and/or hopeless, as reported by self or informant, by history of treatment, or by clinician’s report.
  • At least two supportive features must be present. The seven supportive criteria include:
    • Impulsivity (e.g. new behaviors such as excessive gambling, increased or unusual sexual activity, substance abuse, or excessive shopping or unusual purchases)
    • Anxiety (e.g. anxious mood, agitation, excessive fears, obsessive or compulsive behavior, or both)
    • Apathy (e.g. loss of interest in usual activities, loss of motivation and emotions, and/or reduction of voluntary, goal-directed behaviors)
    • Paranoia (e.g. delusional beliefs of suspicion, persecution, and/or unwanted jealousy)
    • Suicidality (i.e. history of suicidal thoughts or attempts)
    • Headache (significant and chronic headache with a least one episode per month for a minimum of 6 months)
    • Motor signs (e.g. dysarthria, dysgraphia, bradykinesia, tremor, rigidity, gait disturbance, falls, and/or other features of parkinsonism)
    • Documented decline (i.e. progressive decline in function and/or a progression in symptoms and/or signs that occurs for a minimum of 1 year)
    • Delayed onset (i.e. delayed onset of clinical features after significant head impact exposure, usually at least 2 years and in many cases several years after the period of maximal exposure)

CTE and the NFL


In 2017, Dr. Ann McKee, a neuropathologist, examined the brains of over 200 deceased football players and published her findings in the Journal of the American Medical Association. Of the 202 brains she dissected, 111 of the brains belonged to former players in the N.F.L. while the others belonged to the Canadian Football League, semi-professional players, college players and high school players. Of those 111 brains belonging to former NFL players, all but one of them was found to have CTE. This is very significant but we have to remember, there is a HUGE selection bias. Some of these players’ families have asked Dr. McKee and her team to dissect their loved one’s brain because they were suspicious of CTE and the former player showed clinical symptoms of  TES/CTE. The brains that were dissected were from players who died as young as 23 and as old as 89.

However, the 110 positive cases are still significant. Since the time when Dr. McKee’s group began examining brains, about 1300 former NFL players have died. If every single one of the remaining ~1200 brains were found NOT to have CTE (which I’m sure you’ll agree is highly unlikely), the minimum prevalence of an NFL player with CTE would be just less than 9% which is much higher than the general population.

“It is no longer debatable whether or not there is a problem in football — there is a problem,” Dr. McKee

Currently CTE can only be diagnosed with an autopsy by using preliminary neuropathological consensus criteria. Since the condition can only be evaluated post-mortem at one static point in time for each case, we cannot say for certain whether the condition is progressive.

Although it is said that some cases of CTE occurs in individuals with no known history of repetitive head trauma, it is impossible to measure the neuro-traumatic events that have occurred in an individual’s lifetime. There are endless possible exposures to environmental, pharmaceutical, nutritional, and other sources that might contribute to pathological changes that develop in the brain over a lifetime.

Although the amount of research about CTE, concussion, and TES has been increasing significantly in the last 10 years, there is still so much that we don’t know. There is so much that we still don’t agree upon. Why do some people develop CTE even without head trauma? Can we do something to stop the condition once it’s already began? It is clear that more published research is crucial to our understanding of this disease. Most importantly, a biomarker is needed so we can identify this condition in the living and ideally, reverse the damage that has the potential to destroy lives.


Picture of Dr. Stephanie Barbakoff DC, DACNB

Dr. Stephanie Barbakoff DC, DACNB

Originally from New York, specializes in women’s health as it relates to post-concussion syndrome, hormones, fatigue, dizziness, and chronic migraines.

Subscribe to our Newsletter

We promise not to spam your inbox.


Our subscribers gain access to brain-based content, backed by research.