This document summarizes the neurometabolic cascade that occurs following a concussion. It describes the initial events such as neurotransmitter release and ion influx that lead to hyperactivity and then depressed metabolism. Functional MRI studies have shown increased brain activation and axonal damage in concussed athletes. There is also evidence that concussions can lead to long term neurological disorders like chronic traumatic encephalopathy and increased risk of conditions like Alzheimer's disease and Parkinson's disease. The document concludes that repeated concussions are definitely linked to early onset neurological disorders and that concussion protocols and education need to be improved.

1. St. Lawrence University
Amanda McClure
The Neurometabolic Cascade of a Concussion
INTRODUCTION
o ¼ of adults, ¼- ½ young athletes could only recall one symptom
of a concussion, ¼ of these athletes did not know if a player
experiencing concussion symptoms should continue competing
(Cusimano, 2009).
o Concussion: a clinical syndrome characterized by immediate and
transient alteration in brain function, including alteration of
mental status and level of consciousness, resulting from
mechanical force or trauma (AANS, 2005).
o Symptoms include (but are not limited to):
o Headache, dizziness, and/or nausea
o Poor memory and/or concentration
o Irritability, depression
o Sleep disturbance
o Loss of consciousness
POST-CONCUSSIVE PATHOPHYSIOLOGY
o Initial Sequence of Events (Frost,2011)
o Abrupt, involuntary release of neurotransmitters
(glutamate), and ion influx (Ca2+)
o Sodium-Potassium Pump (Na+/K+ pump) activated
o Hyperactivity soon turns into a period of depressed
metabolism
o At-risk time period to develop cerebral hemorrhage and/or
elevated intracranial pressure
PHYSIOLOGICAL DAMAGE
o Functional Magnetic Resonance Imaging (fMRI) showed a
significant increase in cortical activation in patients who suffered
from a concussion in-season versus a patient who had not
(Jantzen, 2004).
o Increases in brain activation were in regions associated with
executive function including working memory and motor
planning (Jantzen, 2004).
o Axonal Damage: reduces efficiency of processing in the brain;
more neuronal resources needed to carry out the same function
as a healthy brain (Jantzen, 2004).
o Chronic Traumatic Encephalopathy (CTE) linked with
neuropsychiatric consequences including cognitive decline, mood
and anxiety disorders (Coughlin et al, 2015).
o Increased binding of [11C] DPA-713 to the translocator protein,
suggesting permanent damage to the brain after a concussion
(Coughlin et al, 2015).
SHORT TERM EFFECTS
o Cerebral glucose levels completely diminished by 24 hours
after injury, remain low for 5 to 10 days (Giza et al, 2001).
o Post Concussion Syndrome (PCS) (White, 2012)
o Experiencing symptoms longer than 10 days, lasting
several weeks or months
o Most commonly suffer from severe headaches, dizziness
and irritability
CONCLUSION
REFERENCES
Coughlin, J.M. et al (2015). Neuroinflammation and Brain Atrophy in Former NFL Players: An in vivo Multimodal Imaging Pilot Study. Neurobiology of Disease, 74, 58-65. http://ac.els-cdn.com/S0969996114003325/1-s2.0-
S0969996114003325-main.pdf?_tid=f576a062-75f7-11e5-a34a- 00000aab0f27&acdnat=1445214534_9773418293812cafeb298bf6820edc47
Cusimano, M.D., Chipman M.L. Volpe, R., Donnelly, P (2009). Canadian Minor Hockey Participants’ Knowledge about Concussion. The Canadian Journal of Neurological Sciences, 36 (03), 315-320. http://
journals.cambridge.org/download.php?file=%2FCJN%2FCJN36_03%2FS0317167100007046a.pdf&code=085ea5e64672c161d36eebf438633b36
DeKosky, ST et al (2010). Traumatic brain injury- football, warefare and long-term effects. The New England Journal of Medicine. 363:1293-1296.
Frost, C (2011). Anatomy of the Concussion: More Serious than Meets the Eye? https://honors.usf.edu/documents/Thesis/U78133303.pdf
Giza, C.C., et al (2001). The Neurometabolic Cascade of Concussions. Journal of Athletic Training, 36(3),228-235. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC155411/pdf/attr_36_03_0228.pdf
Guskiewicz, K.M., et al (2007). Recurrent Concussion and Risk of Depression in Retired Professional Football Players. Journal of Medicine & Science in Sports & Exercise. http://indianasportsconcussionnetwork.com/
recurrentriskofdepressionnfl.pdf
Jantzen, K.J., et al (2004). A Prospective Functional MR Imaging Study of Mild Traumatic Brain Injury in College Football Players. American Journal of Neuroradiology, 25, 738-745. http://www.ajnr.org/content/25/5/738.full.pd
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Lehman, E.J., et al (2012). Neurodegenerative Causes of Death Among National Football League Players. The Official Journal of the American Academy of Neurology, 79(19), 1970-1974. http://www.neurology.org/content/
79/19/1970.short
McCroy, P., et al (2015). Sport Psychology and Concussion: New Impacts to Explore. British Journal of Medicine. http://bjsm.bmj.com/content/38/5/519.full.pdf+html
Maroon, JC et al (2012). Post concussion syndrome: a review of pathophysiology and potential nonpharmacological approaches to treatment. Phys. Sportsmed. 40: 73-87
Rudelli,R., et al (1982). Posttraumatic Premature Alzheimer’s Disease. Journal of the American Medical Association, 39(9), 570-575. http://archneur.jamanetwork.com/article.aspx?articleid=5811
White, J. (2012). CONCUSSION: Short and Long-Term Impact. Retrieved November 14, 2015, from http://mnepilepsy.org/patient-information/concussion-short-and-long-term-impact/
LONG TERM EFFECTS: NEUROLOGICAL DISORDERS
o TBI can progress into later-onset, chronic neurodegenerative disorders of the brain (caused by repeated
concussions).
o Can result in Dementia Pugilistica (DP) , CTE, Parkinson’s Disease (PD) and Alzheimer’s Disease (AD)
o 20-30% of patients with AD or PD suffered a single-incident traumatic brain injury.
o Death caused by neurodegenerative disorders is 3 times greater in previously concussed population than
that of the general US population (Lehman et al, 2012).
o Prevalence rate of ALS and AD is 4 times higher in previously concussed individuals than the general US
population (Lehman et al, 2012).
Figure 2 Reproduced from Jantzen, KJ et al (2004). A
prospective functional MR imaging study of mild traumatic
brain injury in college football players. American Journal or
Neuroradiology. 25: 738-745.
Figure 1 Reproduced from Maroon, JC et al (2012). Post concussion syndrome: a
review of pathophysiology and potential nonpharmacological approaches to
treatment. Phys. Sportsmed. 40: 73-87.
o Correlation between TBI and Chronic Depression (Guskiewicz, 2006)
o Prevalence rates from 6% (mild TBI) to 77% (more severe TBI)
o 18.5% lifetime prevalence of depression in individuals who suffered from head injury vs. 13.4% for those
with no history of head injury
o Rudelli’s research in 1982 was the first to suggest that dementia may be attributed to brain contusions
formed following head injury as a result of cerebral edema or swelling
o In 2004, it was proven that children are more resilient to traumatic brain injuries than adults are however:
o Concussions have potential to affect a child’s social, and educational success
o “It takes a 2 to 3 fold greater impact force to produce clinical symptoms in children compared to adults”
Figure 3 Reproduced from Coughlin, JM et al (2015). Neuroinflammation and
brain atrophy in former NFL players: an in vivo multimodal imaging pilot study.
Neurobiology of Disease. 74: 58-65.
Figure 4 Reproduced from DeKosky, ST et al (2010). Traumatic brain injury-
football, warefare and long-term effects. The New England Journal of Medicine.
363:1293-1296.
o Definite trend between multiple concussions and early on-set neurological disorders can be inferred from research
o Must re-evaluate concussion protocol in sports, inform the sports community more on the long-term effects concussions
have on the human brain.