Sports Concussion and Chronic Traumatic Encephalopathy (CTE)

Rosabel Rivares Young, M.D., M.S. Pharm, F.A.A.N., Q.M.E.

In the 1990s, Dr. Rivares Young was the “ringside doctor” for the Juvenile Justice
Correctional programs for the California Athletic Commission.  In that capacity, her job
was to examine Juvenile delinquents as young as 12 years old that were participating in
boxing, Mixed Martial Arts, and football as part of the Corrections Department
rehabilitation activities.

Dr. Young observed that some of these juveniles exhibited more severe behavioral
derangements after these activities, including poor school performance, loss of
socialization, more violent behavior, and epilepsy.  Joined by her colleagues in
Neurology, Psychiatry, Psychology, and Behavioral Medicine, Dr. Young advised the
State of California to discontinue sports activities that might cause head injuries. 
Eventually other activities did replace the violent sports, with more focus on
rehabilitation and skills development training programs.

How do you determine the risk for future cognitive impairment and epilepsy for a high
school football player after a concussion on the field?

The current protocol requires that the full SCAT (Sports Concussion Assessment Tool)
testing be performed as soon as possible after the injury. Testing includes mental
status, speech, vision, coordination, and balance. All parts should be performed even if
the Glasgow Coma Score (GCS) is 15 and the athlete appears to have recovered.
Despite almost a century of recognition that athletes would get “punch drunk” after head
injuries, the first version of the SCAT was not published until 2005. The current SCAT6
version is used to evaluate athletes aged 13 years and older on the field immediately
after a head injury. There is also a Child SCAT6 for children 12 years of age and under.
A pre-season SCAT6 should be performed along with the annual physical to provide a
baseline should a concussion occur. If the student had prior head injuries, ADHD,
learning disability, or has active psychological symptoms, the family should be advised
that their child is at greater risk of permanent brain damage even if only a mild sports
concussion occurs.

What testing do neurologists obtain for a young athlete who suffers a concussion?

A thorough neurological examination is the most important and probably still the most
sensitive test when done well. The face-to-face examination should include cranial
nerves, neuromuscular coordination, and mental status, with detailed testing of all
cognitive functions related to the frontal, temporal, parietal, and occipital lobes, as well
as their interconnections.

An Electroencephalogram should also be performed in all cases of head injury with altered mental status even if symptoms resolve. This is the test with wires on the head attached to the skin with a washable cream. It can identify abnormal brain activity and possibly determine what type of seizures you have but not necessarily what caused them.

Prognosis – What is Chronic Traumatic Encephalopathy (CTE)?

The old opinion was that children and teens will always “grow out of it” and would not
suffer permanent brain damage after a head injury. The truth is that brain injuries can
reduce cognitive reserve at any age. Brain cells diminish in number with age anyway,
but we are all born with a surplus and a lot of redundancy, so most people will not get
dementia during their productive adult years. Surplus and redundancy allow other parts
of the brain to take over functions lost after an injury. This is what we call compensatory
cognitive reserve. However, with repetitive brain injuries, cognitive reserve is reduced
to the point that the brain is no longer able to compensate, and cognitive impairment,
behavioral, and mood symptoms appear even without subsequent injury. This is what
we call Chronic Traumatic Encephalopathy (CTE). That’s why if you had several
concussions and feel OK for many years, you can still get CTE when you get older,
even if you have no other head injuries for the rest of your life.

Symptoms of CTE are more often noticed by family, not by the patients themselves.

My husband used to play pro football, then worked for 20 years with no problems at all. But now at just age 50, he seems to be getting forgetful, has angry outbursts, and wakes up in the middle of the night for no apparent reason.

This patient appears to be developing CTE. Although CTE has been staged
anatomically from brain samples of patients who have died of CTE, the four stages are
based on analysis of chemical markers (like tau) and do not necessarily correspond to
the sequence of symptoms. In the last stage (IV), the whole body slows down, as in
Parkinson’s disease.

Patients are often in denial when they begin to have difficulties – a product of years of
professional athletic conditioning to “play hurt.” Athletes were trained to endure pain, to
get back on the field and continue the game even with severe headaches, ringing in the
ears, and mental fog. With time, over the years after they retired, the physical pain
symptoms may have improved, giving them a “false sense of security” that their injuries
are behind them. But as the brain’s cognitive reserve depletes and reaches the critical
threshold, they are surprised by these “new” symptoms, and resort to the only way they
know how to cope – denial – and they continue to work hard. By the time they lose their
jobs, their family, and their home, it may be too late for treatment.

Some symptoms could be due to complex partial (focal impaired awareness) epilepsy,
such as memory lapses, angry outbursts, and even mood swings. This is why it is
critical to see a neurologist as soon as possible after retiring from contact sports, even if
there are no active symptoms. A neurologist can perform an EEG and other tests that
may reveal epilepsy is part of the problem, and this can be controlled with medications.

What can you do now if you had a concussion in the past and want to reduce your chances of getting CTE?

A neurologist can also detect and treat early deficits, even if not seizures, by
recommending changes in diet, nutritional supplements, improved sleep habits, and
other lifestyle changes to reduce your risk. Certain supplements that have been found
helpful in medical studies include Vitamin D (2000-3000 International Units daily),
Vitamin B12 (1000 micrograms weekly), Vitamin B1 Thiamine (200 mg daily), Vitamin
B2 Riboflavin (200 mg daily), Coenzyme Q10 (100 mg daily), and Magnesium Oxide or
Magnesium Glycinate (200-400 mg daily). However, as these have the potential to
interact with some medications, such as blood thinners, and safety during pregnancy or
with reduced kidney function has not been ascertained, it is important to always check
with your neurologist before starting supplements on your own.

Although the current data is anecdotal, a group of retired NFL players that decided to go
on a vegetarian diet seem to doing better cognitively and emotionally than their age-
matched NFL counterparts on regular diets. Some athletes living in regions of the
country with high fish content diets also seem to do better. Based on what we now
know about CTE, the underlying pathology is inflammation, as in other types of
dementia, and thus a diet low in animal meat (beef, pork, venison) may reduce
progression of CTE.

About the Author

Rosabel Rivares Young, M.D., M.S. Pharm, F.A.A.N., Q.M.E.
Board Certified in Brain Injury Medicine
Certified, American Board of Psychiatry and Neurology with Added Qualifications in Neurophysiology
Certified, American Board of Electrodiagnostic Medicine
Certified, American Board of Clinical Neurophysiology

References

Characterizing Tau Deposition in Chronic Traumatic Encephalopathy (CTE): Utility of the McKee CTE Staging Scheme
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Baucom  5 , Neil W Kowall  1,2,3 , Nicole Saltiel  1 , Lee E Goldstein  1,2,7,8,9,10 , Douglas I Katz  1,11 , Brigid
Dwyer  1,11 , Daniel H Daneshvar  1 , Joseph N Palmisano  1,12 , Brett Martin  1,12 , Robert C Cantu  1,13,14,15 , Robert A
Stern  1,13,16 , Victor E Alvarez  1,3,4 , Jesse Mez  1 , Thor D Stein  1,2,3,4 , Ann C McKee  1,2,3,4
Acta Neuropathol. 2020 Aug 11;140(4):495–512. doi: 10.1007/s00401-020-02197-9


The spectrum of disease in chronic traumatic encephalopathy
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Brain. 2013 Jan; 136(1): 43–64.
Published online 2012 Dec 2. doi: 10.1093/brain/aws307

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