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What is Concussion?

Original Editor - Megyn Robertson.

Top Contributors - Ewa Jaraczewska, Jess Bell, Stacy Schiurring, Kim Jackson, Shaimaa Eldib, Naomi O'Reilly, Wanda van Niekerk, Tarina van der Stockt, Olajumoke Ogunleye and Robin Tacchetti  

Concussion Overview

The American Academy of Neurology (2013) describes concussion as a “clinical syndrome of biomechanically induced alteration of brain function typically affecting memory and orientation, which may involve loss of consciousness.”[1]

The Amsterdam consensus defines sport-related concussion as a "traumatic brain injury caused by a direct blow to the head, neck or body resulting in an impulsive force being transmitted to the brain that occurs in sports and exercise-related activities. This initiates a neurotransmitter and metabolic cascade, with possible axonal injury, blood flow change and inflammation affecting the brain. Symptoms and signs may present immediately, or evolve over minutes or hours, and commonly resolve within days, but may be prolonged."[2]

The traumatically induced, transient disturbance of brain function in concussion is predominantly functional and microstructural, with no macroscopic structural damage visible on routine CT or MRI. This distinction fundamentally shapes both diagnosis and management in clinical rehabilitation settings.

Concussion and Traumatic Brain Injury

The Glasgow Coma Scale is a bedside assessment used to evaluate a person's level of consciousness following a brain injury.

In a medical and rehabilitation context, concussion is considered a subtype of mild traumatic brain injury (mTBI). Both terms describe brain dysfunction resulting from biomechanical forces, such as a blow or jolt to the head. The American Congress of Rehabilitation Medicine report that mTBI can be used interchangeably with concussion, but only when neuroimaging is normal or not clinically indicated.[3]

In approximately 90% of concussion cases, loss of consciousness does not occur and amnesia is not required for a diagnosis.[4] However, longer durations of loss of consciousness and longer periods of amnesia (anterograde or retrograde) indicate a more severe injury.[5] Concussion typically presents with a Glasgow Coma Scale score of 13 to 15.[6]

Common Causes of Concussion

The most common cause of concussions is falls, particularly in older adults and young children. Motor vehicle accidents are another leading cause, as are physical assaults[7] and sports-related injuries, particularly in contact sports, such as American football, rugby, and hockey.[5] Research also suggests that subconcussive impacts, such as heading a soccer ball, may cause neurophysiological changes in the brain. These impacts have been associated with long-term risks like chronic traumatic encephalopathy.[8] [9][10][11] This is an emerging area of research and safe impact thresholds in sports have not yet been established.[12]

Biomechanics of Injury

Concussion results from forces that cause rapid acceleration-deceleration or rotational movement of the brain within the skull. It occurs through two primary mechanisms: direct impact and indirect forces.[13] Direct injuries happen when an object strikes the head or the head hits a hard surface. Indirect injuries result from rapid acceleration or deceleration movements, such as whiplash or blast-related pressure waves, which affect the brain without physical contact to the head.[3]

Whatever the mechanism, two components of acceleration occur in nearly every concussion: linear and rotational. Linear acceleration moves the head in a straight line, while rotational acceleration causes the brain to twist or spin. Brain tissue deforms more readily in response to shear forces, so rotational acceleration causes more extensive damage than linear forces alone. This is compounded by the density differences between grey and white matter, which cause them to respond differently to shear forces.[6][14]

These shear forces can stretch and damage thousands or even millions of scattered axons, leading to diffuse axonal injury. Because standard neuroimaging is designed to detect larger bleeds rather than individual axonal injuries, the microstructural axonal injury of concussion cannot be seen on routine CT or MRI scans. This is one reason why so many concussions go undiagnosed.[6]

How Rotational Forces Affect the Corpus Callosum

The brain consists of two hemispheres connected by a bundle of axons called the corpus callosum, which allows communication between the left and right sides. The hemispheres are separated by the falx cerebri, a sickle-shaped fold of dura mater.[15]

During an impact with deceleration and rotational forces, the brain experiences three types of strain.

  • Compression strain: tissue on the side of impact is pressed against the rigid falx cerebri
  • Tensile strain: tissue on the opposite side is stretched as it pulls away from the falx cerebri
  • Shearing: because the falx cerebri is rigid, the axons of the corpus callosum are stretched and strained (in concussion, there is microstructural axonal injury)
Neurometabolic cascade of concussion. Permission for re-use granted by Complete Concussions.

Neurometabolic Cascade and the Energy Crisis of Concussion

The neurometabolic cascade begins the moment a biomechanical force is transmitted to the brain.[16] At impact, stretching and shearing forces temporarily damage the neurons, in a process called mechanoporation.[17] This triggers a massive, uncontrolled release of neurotransmitters (e.g. glutamate) and disrupts the electrochemical gradients that neurons depend on, causing a sudden shift in ion levels: potassium rushes out of cells while calcium and sodium rush in.[18][19]

The calcium influx is particularly damaging. Intracellular calcium activates destructive enzymes, impairs mitochondrial function, and drives the further release of glutamate, the brain's main excitatory neurotransmitter.[20] Glutamate activates further depolarisation in a self-reinforcing cycle, producing a spreading depression-like state (a state where normal brain waves are temporarily suppressed across the cerebral cortex). This widespread disruption contributes to the immediate changes in mental status, confusion, and cognitive symptoms seen clinically.[6][19]

To restore ionic homeostasis, ATP-dependent membrane pumps are activated, which sharply increases glucose demand. This triggers a period of hyperglycolysis (intense glucose consumption) that begins almost immediately. At the same time, cerebral blood flow is significantly reduced. This creates a situation where the brain needs more energy to restore normal function after injury, but blood flow is reduced. Thus, there is a mismatch between supply and demand,[20] and a resulting cellular energy crisis.[18]

Following this, the brain enters a prolonged period of glucose hypometabolism that can last two to four weeks.[21][22]

Symptomatic recovery typically takes around 2-4 weeks in adults, but this does not mean the brain has fully healed. Cerebral blood flow can take several weeks to fully stabilise post-injury and persistent neuroinflammation, including microglial activation, can outlast symptom resolution.[6][5][21][16] During this period, the brain is highly vulnerable, and a second injury can lead to serious cell damage or even cell death.

The following video explains biochemical and structural changes in the brain that are associated with the symptoms of a concussion.

[23]

Clinical Presentation

Concussion causes a diverse range of symptoms that typically fall into four categories.[24]

  • Cognitive: confusion, memory or concentration difficulties
  • Physical (somatic): headache, dizziness, balance problems
  • Emotional: irritability, mood changes
  • Sleep-related: insomnia, fatigue

There is also a notable clinical overlap between concussion and whiplash, and these two conditions can often co-occur. Both share an acceleration-deceleration mechanism and cause similar symptoms, including headache, dizziness, fatigue, and cognitive impairment. They both also lack a definitive diagnostic test, which can make differentiation challenging.[6]

Diagnosis remains clinically driven, relying on a careful history of the mechanism of injury and evolving symptoms, supported by functional assessment rather than imaging.[6]

Concussion Red Flags

While most concussions resolve without complication, certain signs and symptoms suggest more serious underlying injury and require urgent medical assessment. Clinical red flags include prolonged loss of consciousness, worsening headache, repeated vomiting, seizures, slurred speech, unequal pupil size, weakness or numbness in the limbs, and increasing confusion or agitation. In children, signs such as persistent crying, refusal to eat, or difficulty waking should also raise concern. These signs warrant urgent referral to emergency medical services, as they may suggest complications such as intracranial bleeding, skull fracture, or more severe traumatic brain injury. Prompt recognition and response are critical for patient safety and optimal outcomes.[25][26]

Symptoms such as dizziness and headache can also indicate other serious conditions, including cervical artery dysfunction (CAD). When assessing head injury, clinicians should evaluate cranial nerve function and consider the "5 Ds" (dizziness, diplopia, dysphagia, dysarthria, drop attacks) and "3 Ns" (nystagmus, numbness of the lips, face, and tongue, nausea). Tinnitus may also be relevant.[6]

Conclusion

Most concussions resolve within days to weeks, but approximately 20–30% of patients may experience prolonged symptoms.[27] Early recognition of this group, combined with education, reassurance, and graded return to activity, is central to physiotherapy management.

Additional Resources

References

  1. ↑ Mullally WJ. Concussion. The American Journal of Medicine. 2017 Aug 1;130(8):885-92.
  2. ↑ Patricios JS, Schneider KJ, Dvorak J, Ahmed OH, Blauwet C, Cantu RC, et al. Consensus statement on concussion in sport: the 6th International Conference on Concussion in Sport-Amsterdam, October 2022. Br J Sports Med. 2023 Jun;57(11):695-711.
  3. ↑ 3.0 3.1 Silverberg ND, Iverson GL; ACRM Brain Injury Special Interest Group Mild TBI Task Force members, et al. The American Congress of Rehabilitation Medicine Diagnostic Criteria for Mild Traumatic Brain Injury. Arch Phys Med Rehabil. 2023 Aug;104(8):1343-1355.
  4. ↑ Kamins J, Giza CC. Concussion—mild traumatic brain injury: recoverable injury with potential for serious sequelae. Neurosurgery Clinics of North America. 2016 Oct 1;27(4):441-52.
  5. ↑ 5.0 5.1 5.2 Giza CC, Kutcher JS. An introduction to sports concussions. Continuum (Minneap Minn). 2014 Dec;20(6 Sports Neurology):1545-51.
  6. ↑ 6.0 6.1 6.2 6.3 6.4 6.5 6.6 6.7 Robertson M. What is Concussion Course. Physiopedia Plus, 2026.
  7. ↑ Hon KL, Leung AK, Torres AR. Concussion: a global perspective. In Seminars in Pediatric Neurology 2019 Jul 1 (Vol. 30, pp. 117-127). WB Saunders.
  8. ↑ D’Arcy RC, McCarthy D, Harrison D, Levenberg Z, Wan J, Hepburn A, Kirby ED, Yardley T, Yamada-Bagg N, Fickling SD, Munce TA. An objective neurophysiological study of subconcussion in female and male high school student athletes. Scientific reports. 2024 Nov 22;14(1):28929.
  9. ↑ Johnson B, Neuberger T, Gay M, Hallett M, Slobounov S. Effects of subconcussive head trauma on the default mode network of the brain. J Neurotrauma. 2014 Dec 1;31(23):1907-13.
  10. ↑ Nowinski CJ, Rhim HC, McKee AC, Zafonte RD, Dodick DW, Cantu RC, Daneshvar DH. 'Subconcussive' is a dangerous misnomer: hits of greater magnitude than concussive impacts may not cause symptoms. Br J Sports Med. 2024 Jul 1;58(14):754-756.
  11. ↑ Hack L, Singh B, Binkofski F, Helmich I. Repetitive subconcussive head impacts in sports and their impact on brain anatomy and function: a systematic review. Int J Sports Med. 2024 Oct;45(12):871-883.
  12. ↑ Ntikas M, Binkofski F, Shah NJ, Ietswaart M. Repeated Sub-Concussive Impacts and the Negative Effects of Contact Sports on Cognition and Brain Integrity. Int J Environ Res Public Health. 2022 Jun 9;19(12):7098.
  13. ↑ Meaney DF, Smith DH. Biomechanics of concussion. Clin Sports Med. 2011 Jan;30(1):19-31, vii.
  14. ↑ Mesfin FB, Gupta N, Hays Shapshak A, et al. Diffuse Axonal Injury. [Updated 2025 Jul 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2026 Jan-. Available from https://www.ncbi.nlm.nih.gov/books/NBK448102/ [last accessed 3.6.2026]
  15. ↑ Meybodi AT, Tabani H, Benet A. Chapter 2 - arachnoid and dural reflections. In: McDermott MW, editor. Handbook of clinical neurology. Vol 169. Elsevier. 2020. p17-54.
  16. ↑ 16.0 16.1 Giza CC, Hovda DA. The new neurometabolic cascade of concussion. Neurosurgery. 2014 Oct 1;75:S24-33.
  17. ↑ LaPlaca MC, Lessing MC, Prado GR, Zhou R, Tate CC, Geddes-Klein D, Meaney DF, Zhang L. Mechanoporation is a potential indicator of tissue strain and subsequent degeneration following experimental traumatic brain injury. Clin Biomech (Bristol). 2019 Apr;64:2-13.
  18. ↑ 18.0 18.1 Romeu-Mejia R, Giza CC, Goldman JT. Concussion pathophysiology and injury biomechanics. Curr Rev Musculoskelet Med. 2019 Jun;12(2):105-116.
  19. ↑ 19.0 19.1 Toman E, Hodgson S, Riley M, Welbury R, Di Pietro V, Belli A. Concussion in the UK: a contemporary narrative review. Trauma Surg Acute Care Open. 2022 Oct 19;7(1):e000929.
  20. ↑ 20.0 20.1 Fineman I, Hovda DA, Smith M, Yoshino A, Becker DP. Concussive brain injury is associated with a prolonged accumulation of calcium: a45Ca autoradiographic study. Brain research. 1993 Oct 8;624(1-2):94-102.
  21. ↑ 21.0 21.1 Neumann KD, Broshek DK, Newman BT, Druzgal TJ, Kundu BK, Resch JE. Concussion: beyond the cascade. Cells. 2023 Aug 22;12(17):2128.
  22. ↑ Giza CC, Hovda DA. The neurometabolic cascade of concussion. J Athl Train. 2001 Sep;36(3):228-235.
  23. ↑ Neuroscientifically Challenged. 2-Minute Neuroscience: Concussions. Available from: https://www.youtube.com/watch?v=gLwtJcKh4gQ [last accessed 28/08/2026]
  24. ↑ Bishay AE, Hughes NC, Albert AN, Dugan JE, De Oliveira N, Williams KL, et al. Atypical symptoms following concussion: a comprehensive review of functional deficits. Archives of Clinical Neuropsychology. 2025;40(7):1415-26.
  25. ↑ Quick BL, Glowacki EM, Kriss LA, Hartman DE. Raising concussion awareness among amateur athletes: an examination of the Centers for Disease Control and Prevention’s (CDC) Heads Up campaign. Health communication. 2023 Jan 28;38(2):298-309.
  26. ↑ McCrory P, Meeuwisse W, Dvorak J, Aubry M, Bailes J, Broglio S, Cantu RC, Cassidy D, Echemendia RJ, Castellani RJ, Davis GA. Consensus statement on concussion in sport—the 5th international conference on concussion in sport held in Berlin, October 2016. British journal of sports medicine. 2017 Jun 1;51(11):838-47.
  27. ↑ Leddy JJ, Sandhu H, Sodhi V, Baker JG, Willer B. Rehabilitation of concussion and post-concussion syndrome. Sports health. 2012 Mar;4(2):147-54.
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