What is Concussion?

Original Editor - Megyn Robertson.

Top Contributors - Samuel Adedigba and Mandy Roscher  


Concussion has been described as a metabolic[1], physiological[2], and microstructural[3] injury to the brain. The words concussion, sports related concussion, mild head injury and mTBI are used interchangeably in the literature with varying definitions. For the purposes of this course, we will use the term ‘Concussion’ with the following definition.

Concussion is a trauma-induced transient alteration in brain function, in the absence of gross structural abnormalities. It is associated with alteration of mental status and level of consciousness, which usually resolves within 7–10 days for most adults[4].  Approximately twenty percent of concussed patients continue to report post concussive symptoms for months and even years post-injury[5].

In up to 90% of cases there is no loss of consciousness (LOC) with the result that almost half of all concussions go unidentified or undiagnosed. Concussion may or may not include retrograde or anterograde amnesia, but again this is not the case in all concussions[6].

Concussion results in a constellation of physical, cognitive, visual, emotional, and sleep-related disturbances. Signs and symptoms are broad and include headache, dizziness, gait and balance disturbance, nausea, vomiting, photophobia, trouble focusing, and fatigue. A person with concussion may have slowed mental processing, concentration deficits, memory impairment, irritability, anxiety and depression[7][8].

For ease of reference we will divide the symptomatology of concussion into four categories:

  • Cognitive (that’s memory and concentration).
  • Sleep or Fatigue (some patients can’t sleep, others want to sleep all the time),
  • Emotional (irritable, short, tearful, anxious).
  • Somatic (headaches, dizziness, neck pain).

Mechanism of Injury

Concussion occurs as a result of a direct blow to the head or forces elsewhere on the body that are transmitted to the head.  In other words, concussion can occur in the absence of your head striking an object, such as whiplash. Mostly moderate to severe TBI’s with skull fractures and brain bleeds are the result of blunt trauma but this is not the case in concussion.

A whiplash or contrecoup injury results in a brain bruise or contusion.

Coup-contrecoup Injury.png

Concussion can be the result of an acceleration, deceleration or rotational injury[9]. With the head/neck motions that occur during a typical impact or whiplash, there are two components of acceleration that occur in nearly every instance of concussion — linear AND rotational acceleration.

Brain tissue deforms more readily in response to shear forces from rotational acceleration than other biologic tissues. Rapid head rotations generate shear forces throughout the brain, and, therefore have a high potential to cause greater tissue damage.

It is interesting to note that rotational acceleration creates greater damage to the brain than linear acceleration, even though both are present in any head impact.  In a study by Meaney & Smith (2011)[9] they compared the force generated in a helmeted head compared with an unhelmeted head. A helmeted head sustained the same degree of angular acceleration as the unhelmeted head for the same impact, but its linear acceleration was decreased significantly.

So, in essence a helmet won’t decrease your risk of concussion caused by rotational acceleration. However, it will reduce linear acceleration forces and reduce the risk of a moderate to severe TBI such as occurs with a skull fracture or brain bleed. The bottom line is that players must still wear protective headgear!

Neuropathology of concussion

View the impact of the brain against the skull in slow motion, can you see the shock waves that travel through the brain on impact?
Coup-contrecoup Injury Demonstration.gif

The brain consists of two hemispheres that are connected by a few central structures, one being the corpus callosum, a fibrobundle consisting of axons which allows for communication between the left and right hemispheres. The two hemispheres of the brain are separated by a tough ligamentous structure, the falx cerebri.

During an impact involving combined sudden deceleration and rotational forces, the corpus callosum can often become injured. The injuries occur because the soft brain reacts in shock waves. The left side of the brain impacts against the falx, and the right side of the brain pulls away from the falx. Because the falx is rigid, the axons that comprise the corpus callosum are torn and broken.

Shearing forces with partial and complete axonal injuries also occur within the hemispheres. Grey matter comprises of cell bodies and the white matter is comprised of axons, resulting in two different densities. These density differences also lead to shearing injuries. Thousands or even millions of scattered axons may be torn or diffuse axonal injury. It is important to note that no bleeding occurs unless some of the larger and more resilient arteries are also torn.

CT and MRI are designed to detect a relatively large bleed, so these neuroimaging techniques are not sensitive enough to detect individual axonal injuries so we cannot see a concussion on a CT scan or MRI. This is why so many concussions go undetected or undiagnosed.[10][11]

What is Chronic Traumatic Encephalopathy (CTE)?

CTE is believed to be a neurodegenerative disease caused by repeated head injuries. Symptoms may include behavioural, mood and cognitive problems. Symptoms typically do not begin until years after the injuries. CTE often gets worse over time and can result in dementia. If we consider that concussion is due to dissociation between the left and right hemispheres, then repeated concussions could lead to a decrease in thickening of the corpus callosum and increased space in all other ventricles, as seen in the image below and right.

It is understood that long term damage of repeated concussions can lead to Chronic Traumatic Encephalopathy (CTE) but only be officially diagnosed on autopsy through brain tissue analysis.

The Neurometabolic cascade of concussion

Concussion is a metabolic injury. The metabolic cascade happens immediately after concussion and involves the autonomic nervous system (ANS) and its control of both cerebral blood flow (CBF) and cardiac rhythm. This physiological dysregulation typically resolves, assuming no recurrent insult, within days to weeks after the injury is sustained[1][12]. Evidence has shown that a vulnerable period of brain metabolic imbalance occurs after concussion, the resolution of which does not necessarily coincide with resolution of clinical symptoms[13].

So what actually happens? Let’s explore this further.

Immediately after a biomechanical injury to the brain, there is a massive release of neurotransmitters. The binding of excitatory transmitters such as glutamate combines with NMDA receptors leads to a neuronal depolarization causing an efflux of potassium and influx of calcium, resulting in a depression like state in the brain. The brain’s metabolism essentially slows down and becomes neurotoxic.

In an effort to restore ionic and cellular homeostasis, we need additional ATP (energy) which leads to hyperglycolysis. Hyperglycolysis is the relative depletion of intracellular energy reserves and increase in ADP 6, that results in an energy crisis, reduced cerebral blood flow (CBF) and inflammation. After an initial period of hyperglycolysis and metabolic uncoupling, glucose metabolic rates go into a state of impaired metabolism that can last up to 7-10 days[14].

What is Second Impact Syndrome?

This has become a very controversial topic of late as SIS is believed to be a cause of sudden death in athletic children and young adults. SIS occurs when a second concussion occurs before symptom resolution from the first concussion, resulting in diffuse and often catastrophic cerebral oedema. Reports of SIS are few, and some argue that SIS is simply diffuse cerebral swelling unrelated to the first concussion[15].


Hopefully you now have a better understanding on how exceptionally complex concussion is! There is a vast multidisciplinary role in the treatment of concussion as so many biological systems can be affected. It is imperative that we as physiotherapists know what to look for and address, so that we can refer to the relevant specialists (if need be) and provide a holistic treatment for our concussion patients.

Glossary of Terms

Abbreviation Meaning
ANS Autonomic Nervous System
ATP Adenosine Triphosphate (an energy molecule)
CBF Cerebral Blood Flow
CN Cranial nerve
CTE Chronic Traumatic Encephalopathy
HRV Heart rate variability
ISF Interstitial fluid
PCS Post Concussion Syndrome
SIS Second Impact Syndrome
TBI Traumatic Brain Injury


  1. 1.0 1.1 Giza CC, Hovda DA. The neurometabolic cascade of concussion. Journal of athletic training. 2001 Jul;36(3):228.
  2. McKeag DB, Kutcher JS. Concussion consensus: Raising the bar and filling in the gaps. Clin J Sport Med 2009;19:343-346.
  3. Bazarian JJ. Diagnosing mild traumatic brain injury after a concussion. The Journal of head trauma rehabilitation. 2010;25(4):225.
  4. McCrory P, Meeuwisse WH, Aubry M, Cantu B, Dvořák J, Echemendia RJ, Engebretsen L, Johnston K, Kutcher JS, Raftery M, Sills A. Consensus statement on concussion in sport. Br J Sports Med. 2013 Apr 1;47(5):250-8.
  5. Ruff R. Two decades of advances in understanding of mild traumatic brain injury. The Journal of head trauma rehabilitation. 2005 Jan 1;20(1):5-18.
  6. McCrea MA, Nelson LD, Guskiewicz K. Diagnosis and Management of Acute Concussion. Phys. Med. Rehabil. Clin. N. Am. 2017;28:271–286. doi: 10.1016/j.pmr.2016.12.005.
  7. Alexander MP. Mild traumatic brain injury: pathophysiology, natural history, and clinical management. Neurology. 1995 Jul.
  8. Kushner D. Mild traumatic brain injury: toward understanding manifestations and treatment. Archives of internal medicine. 1998 Aug 10;158(15):1617-24.
  9. 9.0 9.1 Meaney DF, Smith DH. Biomechanics of concussion. Clinics in sports medicine. 2011 Jan 1;30(1):19-31.
  10. Mesfin FB, Taylor RS. Diffuse Axonal Injury (DAI) [Updated 2019 Jun 4]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK448102/ (accessed 23/8/2019)
  11. McKee AC, Daneshvar DH. The neuropathology of traumatic brain injury. InHandbook of clinical neurology 2015 Jan 1 (Vol. 127, pp. 45-66). Elsevier.
  12. McCrea M, Guskiewicz KM, Marshall SW, Barr W, Randolph C, Cantu RC, Onate JA, Yang J, Kelly JP. Acute effects and recovery time following concussion in collegiate football players: the NCAA Concussion Study. Jama. 2003 Nov 19;290(19):2556-63
  13. Leddy J, Hinds A, Sirica D, Willer B. Controlled Exercise and Concussion Management. Physical Medicine and Rehabilitation. 2016;8:91–100
  14. Giza CC, Hovda DA. The new neurometabolic cascade of concussion. Neurosurgery. 2014 Oct 1;75(suppl_4):S24-33.
  15. McLendon LA, Kralik SF, Grayson PA, Golomb MR. The controversial second impact syndrome: a review of the literature. Pediatric neurology. 2016 Sep 1;62:9-17.