Research Reports - Neurochemical aftermath of repetitive mild traumatic brain injury

JAMA Neurol. 2016 Sep 19. doi: 10.1001/jamaneurol.2016.2038. [Epub ahead of
print]

Shahim P(1), Tegner Y(2), Gustafsson B(3), Gren M(1), Ärlig J(1), Olsson M(1),
Lehto N(2), Engström Å(2), Höglund K(1), Portelius E(1), Zetterberg H(4), Blennow
K(1).

Importance: Evidence is accumulating that repeated mild traumatic brain injury
(mTBI) incidents can lead to persistent, long-term debilitating symptoms and in
some cases a progressive neurodegenerative condition referred to as chronic
traumatic encephalopathy. However, to our knowledge, there are no objective tools
to examine to which degree persistent symptoms after mTBI are caused by neuronal
injury.
Objective: To determine whether persistent symptoms after mTBI are associated
with brain injury as evaluated by cerebrospinal fluid biochemical markers for
axonal damage and other aspects of central nervous system injury.
Design, Settings, and Participants: A multicenter cross-sectional study involving
professional Swedish ice hockey players who have had repeated mTBI, had
postconcussion symptoms for more than 3 months, and fulfilled the criteria for
postconcussion syndrome (PCS) according to the Diagnostic and Statistical Manual
of Mental Disorders (Fourth Edition) matched with neurologically healthy control
individuals. The participants were enrolled between January 2014 and February
2016. The players were also assessed with Rivermead Post Concussion Symptoms
Questionnaire and magnetic resonance imaging.
Main Outcomes and Measures: Neurofilament light protein, total tau, glial
fibrillary acidic protein, amyloid β, phosphorylated tau, and neurogranin
concentrations in cerebrospinal fluid.
Results: A total of 31 participants (16 men with PCS; median age, 31 years;
range, 22-53 years; and 15 control individuals [11 men and 4 women]; median age,
25 years; range, 21-35 years) were assessed. Of 16 players with PCS, 9 had PCS
symptoms for more than 1 year, while the remaining 7 returned to play within a
year. Neurofilament light proteins were significantly increased in players with
PCS for more than 1 year (median, 410 pg/mL; range, 230-1440 pg/mL) compared with
players whose PCS resolved within 1 year (median, 210 pg/mL; range, 140-460
pg/mL) as well as control individuals (median 238 pg/mL, range 128-526 pg/mL;
P = .04 and P = .02, respectively). Furthermore, neurofilament light protein
concentrations correlated with Rivermead Post Concussion Symptoms Questionnaire
scores and lifetime concussion events (ρ = 0.58, P = .02 and ρ = 0.52, P = .04,
respectively). Overall, players with PCS had significantly lower cerebrospinal
fluid amyloid-β levels compared with control individuals (median, 1094 pg/mL;
range, 845-1305 pg/mL; P = .05).
Conclusions and Relevance: Increased cerebrospinal fluid neurofilament light
proteins and reduced amyloid β were observed in patients with PCS, suggestive of
axonal white matter injury and amyloid deposition. Measurement of these
biomarkers may be an objective tool to assess the degree of central nervous
system injury in individuals with PCS and to distinguish individuals who are at
risk of developing chronic traumatic encephalopathy. 

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