What is Concussion?

Original Editor - Megyn Robertson.

Top Contributors - Shaimaa Eldib  

Introduction[edit | edit source]

Concussion is a complex injury that can have far-reaching consequences for an individual, families, and society and it has the potential to be a significant public health burden[1].

The words concussion, sports-related concussion, mild head injury and mTBI ( Traumatic Brain Injury)are used interchangeably in the literature with varying definitions. Here 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 has been described as a metabolic[2], physiological[3], and microstructural[4] injury to the brain. In up to 90% of cases, there is no loss of consciousness (LOC)[1] 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[5]. However, it is associated with alteration of mental status, which usually resolves within 7–10 days for most adults[6].  Approximately twenty percent of concussed patients continue to report post-concussive symptoms for months and even years post-injury[7].

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, phonophobia, trouble focusing, and fatigue. A person with concussion may have slowed mental processing, concentration deficits, memory impairment, irritability, anxiety and depression[8][9].

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[edit | edit source]

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 direct trauma but this is not the case in concussion. For example, a whiplash or contrecoup injury may result in a brain bruise or contusion.

PP TBI.png

Concussion can be the result of acceleration, deceleration or rotational injury[10]. 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. Meaney & Smith[10] compared the force generated in a helmeted head compared with an un-helmeted head. A helmeted head sustained the same degree of angular acceleration as the un-helmeted 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[edit | edit source]

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.

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 causing the left side of the brain to impact 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, and we call this diffuse axonal injury or DAI. 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.[11][12]

Chronic Traumatic Encephalopathy (CTE)[edit | edit source]

CTE is believed to be a neurodegenerative disease caused by repeated head injuries[13][14]. Symptoms may include behavioural, mood and cognitive problems and typically do not begin until years after the injuries. As a neurodegenerative condition, it may worsen 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. CTE can only be officially diagnosed on autopsy through brain tissue analysis[15].

The Neurometabolic Cascade of Concussion[edit | edit source]

Concussion is a metabolic injury[16]. 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[2][17]. 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[18].

So what actually happens?

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, which leads to a neuronal depolarisation 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[16] and becomes neurotoxic. The brain now tries to restore homeostasis but to do this it requires a huge amount of ATP which results in hyperglycolysis or in simpler terms, an energy crisis, This energy crisis results in hyperglycolysis, reduced CBF and inflammation of the brain. A hypometabolic state follows with impaired glucose metabolism and this can last for up to 7-10 days.[19].

Second Impact Syndrome (SIS)[edit | edit source]

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[20].

Summary[edit | edit source]

Concussion is a complex condition. 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[edit | edit source]

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

References[edit | edit source]

  1. 1.0 1.1 Schneider K, Isaac C, Ross C, Miller C. Concussion Management: A Toolkit for Physiotherapists. Physiotherapy Alberta - College and Association, 2017
  2. 2.0 2.1 Giza CC, Hovda DA. The neurometabolic cascade of concussion. Journal of athletic training. 2001 Jul;36(3):228.
  3. McKeag DB, Kutcher JS. Concussion consensus: Raising the bar and filling in the gaps. Clin J Sport Med 2009;19:343-346.
  4. Bazarian JJ. Diagnosing mild traumatic brain injury after a concussion. The Journal of head trauma rehabilitation. 2010;25(4):225.
  5. McCrea MA, Nelson LD, Guskiewicz K. Diagnosis and management of acute concussion. Physical Medicine and Rehabilitation Clinics. 2017 May 1;28(2):271-86.
  6. 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.
  7. 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.
  8. Alexander MP. Mild traumatic brain injury: pathophysiology, natural history, and clinical management. Neurology. 1995 Jul.
  9. Kushner D. Mild traumatic brain injury: toward understanding manifestations and treatment. Archives of internal medicine. 1998 Aug 10;158(15):1617-24.
  10. 10.0 10.1 Meaney DF, Smith DH. Biomechanics of concussion. Clinics in sports medicine. 2011 Jan 1;30(1):19-31.
  11. 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)
  12. McKee AC, Daneshvar DH. The neuropathology of traumatic brain injury. InHandbook of clinical neurology 2015 Jan 1 (Vol. 127, pp. 45-66). Elsevier.
  13. Barr WB, Karantzoulis S. Chronic Traumatic Encephalopathy. InHandbook on the Neuropsychology of Aging and Dementia 2019 (pp. 727-745). Springer, Cham.
  14. Karelina K, Weil ZM. Neuroenergetics of traumatic brain injury. Concussion. 2016 Mar;1(2).
  15. McKee AC, Cairns NJ, Dickson DW, Folkerth RD, Keene CD, Litvan I, Perl DP, Stein TD, Vonsattel JP, Stewart W, Tripodis Y. The first NINDS/NIBIB consensus meeting to define neuropathological criteria for the diagnosis of chronic traumatic encephalopathy. Acta neuropathologica. 2016 Jan 1;131(1):75-86.
  16. 16.0 16.1 Salerno M, Franceschi A, Clifton M, Naser-Tavakolian K, Wengler K, Ouellette D, Wei S, Cruickshank B, Komatsu D, Franceschi D, Bangiyev L. Neurometabolic Disruption Following Sports Concussion Assessed with PET/MRI. Journal of Nuclear Medicine. 2019 May 1;60(supplement 1):391-.
  17. 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
  18. Leddy J, Hinds A, Sirica D, Willer B. The role of controlled exercise in concussion management. PM&R. 2016 Mar;8:S91-100.
  19. Giza CC, Hovda DA. The new neurometabolic cascade of concussion. Neurosurgery. 2014 Oct 1;75(suppl_4):S24-33.
  20. 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.