In one study, half of a collegiate football team was instructed in helmetless practice, while the other half practiced with helmets. The helmetless group experienced 28% fewer head impacts after just 1 season, suggesting that practicing without helmets in tackle football may be more safe, however the study was limited by small size.22

Players should be advised to follow a brain-healthy lifestyle. Recommendations include cessation of smoking and drug abuse, exercise, proper nutrition, weight loss, stress reduction/mindfulness training, sufficient sleep, and management of cerebrovascular risk factors such as hypertension, hyperlipidemia and diabetes.

In one recent study,  fish oil (containing EPA and DHA), high-potency multivitamins, and supplements containing ginkgo, vinpocetine, acetyl-1-carnitine, phosphatidylserine, n-acetyl-cysteine, and huperizine A seemed to increase cerebral perfusion and improve performance on neuropsychiatric testing after approximately 6 months in players with multiple mTBIs or CTE.23 More research is needed to identify supplements that may be beneficial during rehabilitation from mTBI and CTE.


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Future Research

There is abundant evidence suggesting that repeated mTBIs are related to CTE, but to date, there is insufficient data to confirm a causal link. There is demand for epidemiological, longitudinal, cross-sectional, retrospective and prospective studies to determine the incidence and prevalence of mTBI and CTE — not only in the NFL, but also across the general public and in other contact sports such as soccer, where children as young as 4-5 years of age are already doing “headers”. Every header represents a potential mTBI to the vulnerable young brain.

Continued research should also analyze the relationship between clinical symptoms and pathological features, which would further our understanding of the brain as a whole. Serum and CSF biomarkers, as well as PET neuroimaging using p-Tau radioligands, could be used to achieve an earlier diagnosis of CTE in live patients. Genetic data may identify at-risk individuals, guiding return-to-play counseling.

The relationship between suicidality and multiple mTBIs in former athletes should also be explored, as well as the idea of a “threshold” number of mTBIs for CTE development. Such data would add to the list of known risk factors for suicide, potentially saving hundreds to thousands of lives.

Finally, more research should be geared toward prevention. The early results of helmetless practice are promising, but larger studies need to be conducted to confirm validity.

Conclusion

Chronic traumatic encephalopathy is becoming a ‘hot-button’ issue. American football is a multi-billion dollar industry — the Super Bowl alone has become such a giant event that advertisement revenue is likely to hit record highs this Sunday.

Football scholarships allow many young men to pursue an education they may otherwise not be able to afford, and in states where there are no professional teams, collegiate football is king.

Studies have consistently shown that retired NFL players are at a higher risk of developing CTE.  It is highly unlikely that the current innovations in helmet safety, or instructions on how to properly tackle, are going to reduce that risk enough to make the game safer overall — on the field is where prevention must start.

Until more effort is put into preventing injury in the first place, psychiatrists will likely continue to be key players in the game.

Emily C. Olson, DO, is a psychiatry resident at the Saint Louis University School of Medicine who received her medical degree from Des Moines University College of Osteopathic Medicine. George T. Grossberg, MD, is Director of Geriatric Psychiatry at the SLU School of Medicine and a member of the Psychiatry Advisor editorial board. He is also a past president of both the American Association of Geriatric Psychiatry and the International Geriatric Association

TABLE 1

CTE Stage
(McKee et al.)10
Pathological Features Neuropsychiatric Features
I

Macroscopic:
Grossly Normal

Microscopic:
Perivascular p-Tau NFTs in focal epicenters restricted to the sulcal depths of the superior, superior lateral, or inferior frontal cortex

Cognitive:

  • Memory loss (mild)
  • Executive dysfunction (mild)
  • Inattention (mild-moderate)
  • Difficulty concentrating (mild-moderate)

Behavioral:

  • Aggression
  • Explosivity

Mood:

  • Depression
  • Suicidality
  • Neurologic:

  • Headache
II

Macroscopic:
Mild enlargement of frontal horn and lateral and third ventricles.

Microscopic:
Spread of p-Tau NFTs to the superficial cortical layers next to the focal epicenters as well as the nucleus basalis of Meynert and locus coeruleus

Cognitive:

  • Memory loss (mild-moderate)
  • Executive dysfunction (mild-moderate)
  • Inattention (moderate)
  • Difficulty concentrating (moderate)
  • Language dysfunction

Behavioral:

  • Aggression
  • Explosivity
  • Impulsivity

Mood:

  • Depression
  • Suicidality
  • Mood lability
  • Apathy

Neurologic:

  • Headache
  • Motor Neuron Disease symptoms
III

Macroscopic:
Mild cerebral atrophy, dilation of the ventricles, a sharp concavity of the third ventricle, and loss of pigmentation in the substantia nigra and locus coeruleus

Microscopic:
Dense p-Tau pathology in the medial temporal lobe structures and widespread regions of the septal , frontal, temporal, insular, and parietal cortices, diencephalon, brainstem, and spinal cord

Cognitive:

  • Memory loss (moderate)
  • Executive dysfunction (moderate)
  • Inattention (severe)
  • Difficulty concentrating
  • Language dysfunction

Behavioral:

  • Aggression
  • Explosivity
  • Impulsivity
  • Paranoia

Mood:

  • Depression
  • Suicidality
  • Mood lability
  • Apathy

Neurologic:

  • Headache
  • Motor Neuron Disease symptoms
IV

Macroscopic:
Cerebral, medial temporal lobe, thalamic, hypothalamic, and mammillary body atrophy

Microscopic:
Widespread p-Tau pathology involving regions of the neuraxis (including white matter), extensive neuronal loss and gliosis in the cerebral cortex and sclerosis of the hippocampus

Cognitive:

  • Memory loss (severe)
  • Executive dysfunction (severe)
  • Inattention (profound)
  • Difficulty concentrating (profound)
  • Language dysfunction

Behavioral:

  • Aggression
  • Explosivity
  • Impulsivity
  • Paranoia

Mood:

  • Apathy
  • Suicidality
  • Depression
  • Mood lability

Neurologic:

  • Headache
  • Motor Neuron Disease symptoms
  • Dysarthria
  • Parkinsonian symptoms
  • Gait ataxia
Image 1: According to McKee et al: “The four stages of CTE. In stage I CTE, p-tau pathology is restricted to discrete foci in the cerebral cortex, most commonly in the superior, dorsolateral or lateral frontal cortices, and typically around small vessels at the depths of sulci (black circles). In stage II CTE, there are multiple epicentres at the depths of the cerebral sulci and localized spread of neurofibrillary pathology from these epicentres to the superficial layers of adjacent cortex. The medial temporal lobe is spared neurofibrillary p-tau pathology in stage II CTE. In stage III, p-tau pathology is widespread; the frontal, insular, temporal and parietal cortices show neurofibrillary degeneration with greatest severity in the frontal and temporal lobe, concentrated at the depths of the sulci. Also in stage III CTE, the amygdala, hippocampus and entorhinal cortex show neurofibrillary pathology. In stage IV CTE, there is severe p-tau pathology affecting most regions of the cerebral cortex and the medial temporal lobe, sparing calcarine cortex in all but the most severe cases. All images, CP-13 immunostained 50-µm tissue sections.” 10

References

1.           Martland H. Punch Drunk. J Am Med Assoc. 1924;91(15):1103-1107.

2.           Millspaugh JA. Dementia Pugilistica. U S Nav Med Bull. 1937;35:297-361.

3.           Miller H. Mental after-effects of head injury. Proc R Soc Med. 1966;59(3):257-261.

4.           Corsellis JA, Bruton CJ, Freeman-Browne D. The aftermath of boxing. Psychol Med. 1973;3(3):270-303.

5.           Omalu B, Bailes J, Hamilton RL, et al. Emerging histomorphologic phenotypes of chronic traumatic encephalopathy in american athletes. Neurosurgery. 2011;69(1):173-183.

6.           Gavett BE, Stern RA, McKee AC, et al. Chronic traumatic encephalopathy: a potential late effect of sport-related concussive and subconcussive head trauma. Clin Sport Med Med. 2011;30(1):179-188.

7.           Mez J, Todd S, Deneshvar D, Stein T, McKee A. Pathologically Confirmed Chronic Traumatic Encephalopathy in a 25-Year-Old Former College Football Player. JAMA Neurology.

8.           Broglio SP, Sosnoff JJ, Shin S, et al. Head Impacts During High School Football: A Biomechanical Assessment. J Athl Train (National Athl Trainers’ Assoc. 2009;44(4):342-349.

9.           Azad TD, Li A, Pendharkar A V, Veeravagu A, Grant GA. Junior Seau – An Illustrative Case of Chronic Traumatic Encephalopathy and Update on Chronic Sports-Related Head Injury. World Neurosurg. 2015.

10.         McKee AC, Stein TD, Nowinski CJ, et al. The spectrum of disease in chronic traumatic encephalopathy.

11.         McNamee M, Partridge B, Anderson L. Concussion Ethics and Sports Medicine. Clin Sports Med. 2015.

12.         Giza CC, Kutcher JS, Ashwal S, et al. Summary of evidence-based guideline update: evaluation and management of concussion in sports: report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology. 2013;80(24):2250-2257.

13.         Guskiewicz KM, Marshall SW, Bailes J, et al. Association between recurrent concussion and late-life cognitive impairment in retired professional football players. Neurosurgery. 2005;57(4):719-726.

14.         Guskiewicz KM, Marshall SW, Bailes J, et al. Recurrent Concussion and Risk of Depression in Retired Professional Football Players. Med Sci Sport Exerc. 2007;39(6):903-909.

15.         Giza CC, Hovda DA. The New Neurometabolic Cascade of Concussion. Neurosurgery. 2014;75:S24-S33.

16.         Arun P, Oguntayo S, VanAlbert S, et al. Acute decrease in alkaline phosphatase after brain injury: a potential mechanism for tauopathy. Neurosci Lett. 2015;609:152-158.

17.         McKee AC, Cairns NJ, Dickson DW, et al. The first NINDS/NIBIB consensus meeting to define neuropathological criteria for the diagnosis of chronic traumatic encephalopathy. Acta Neuropathol. 2016;131(1):75-86.

18.         Stein TD, Montenigro PH, Alvarez VE, et al. Beta-amyloid deposition in chronic traumatic encephalopathy. Acta Neuropathol. 2015;130(1):21-34.

19.         Eisenmenger LB, Huo EJ, Hoffman JM, et al. Advances in PET Imaging of Degenerative, Cerebrovascular, and Traumatic Causes of Dementia. Semin Nucl Med. 2016;46(1):57-87.

20.         Wortzel HS, Granacher RP. Mild Traumatic Brain Injury Update : Forensic Neuropsychiatric Implications. J Am Acad Psychiatry Law. 2015;43(4).

21.         Stern R a, Daneshvar DH, Baugh CM, et al. Clinical presentation of chronic traumatic encephalopathy Clinical presentation of chronic traumatic encephalopathy. Neurology. 2013;81:1122-1129.

22.         Swartz EE, Broglio SP, Cook SB, et al. Early Results of a Helmetless-Tackling Intervention to Decrease Head Impacts in Football Players. J Athl Train. 2015;51(1):6-8.

23.         Amen DG, Wu JC, Taylor D, Willeumier K. Reversing brain damage in former NFL players: implications for traumatic brain injury and substance abuse rehabilitation. J Psychoactive Drugs. 2011;43(1):1-5.