Academic journal article Current Psychiatry

'We Need to Protect the Brain': Addressing the Growing Problem of Chronic Traumatic Encephalopathy

Academic journal article Current Psychiatry

'We Need to Protect the Brain': Addressing the Growing Problem of Chronic Traumatic Encephalopathy

Article excerpt

Football is a multi-billion dollar industry in the United States. Scholarships to play football allow many young men to pursue an education they otherwise might not be able to afford. In states where no professional teams are based, collegiate football is king.

The National Football League (NFL) had its highest concussion tally last year: 182 such injuries reported (1) in the 2014-2015 regular season. The true rate of concussion in the NFL is likely higher, as a result of multiple factors (fear of "letting the team [or the coach] down," fear of retaliation from team owners, (2) etc.).

To simply call a head injury a "concussion" is a disservice to players and their family: Any blow to the head, severe or otherwise, has the potential to cause microvascular disruption in the brain; repeated blows to the head undoubtedly cause further damage.

In reality, a "concussion" is a mild traumatic brain injury (mTBI). With repeated blows, an mTBI can lead to chronic traumatic encephalopathy (CTE). In 2015, eighty-seven of 91 brains from autopsied former NFL players displayed some stage of CTE. (3)

Pathophysiology and presentation

CTE comprises 4 histological stages; Stage 4 is the most advanced. Alzheimer's disease (AD) and CTE display similarities, which suggests a separate classification of CTE-AD; the presence of amyloid [beta] plaques correlates with (1) more severe hyperphosphorylated tau (pTau) pathology and (2) advanced stages of the disease and clinical presentations. Death tends to occur 10 years earlier in CTE-AD than in AD, suggesting that repetitive mTBI might change the deposition and accumulation of amyloid [beta] plaques, and even accelerate the aging process in the brain. (4)

Symptoms. The case series by Omalu et al (4) (which inspired the 2015 motion picture Concussion) and the case series presented by McKee et al (5) described severe psychiatric symptoms associated with CTE:

* decreased speed of information processing

* increase in religiosity

* lack of insight

* poor judgment

* involvement in illegal activities

* substance abuse

* indiscretion

* verbal and physical abuse

* problems with interpersonal relationships

* isolation

* restlessness and hyperactivity

* somatic complaints.

The 2 groups of researchers also noted hopelessness, social, phobia, anxiety, agitation, mania, labile mood, insomnia, explosivity, and suicidal ideation, attempt, and completion. (4,5)

By Stage 4, all affected patients are symptomatic. Cognitive impairment is severe; many are described as having "severe memory loss with dementia," (5) "profound" inattention and loss of concentration, (5) and dysarthria. Paranoia may develop. Mood symptoms can be severe: Approximately 31% of subjects studied have contemplated suicide; of those, 26% had "suicidal tendencies" and 14% completed suicide. (5)

Two distinct types of CTE progression are apparent:

* patients who display cognitive deficits first; they progress to dementia but live longer

* patients who display mood and behavioral symptoms first; they tend to be younger, more violent, depressed, and explosive. (6)

CTE cannot be diagnosed with imaging. There are, however, a few positron emission tomography (PET) ligands for pTau that show promise:

* [F-18]FDDNP, which consistently identifies pTau deposits in brains in which CTE is clinically suspected, in the same distribution of pTau neurofibrillary tangles on autopsy.

* [11C]DPA-713, which detected TBI-related inflammation of neurons in 9 former NFL players in whom CTE was suspected based on the clinical presentation.

* PiB amyloid ligand, under investigation for use in PET neuroimaging. (7)


In January 2016 alone, at least 3 former NFL players were found to have CTE posthumously. …

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