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Identifying Concussion

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Introduction

Concussion is defined as a “clinical syndrome of biomechanically induced alteration of brain function typically affecting memory and orientation, which may involve loss of consciousness.”[1] Diagnosis of concussion relies on a set of clinical criteria rather than imaging findings. This page discusses the American Congress of Rehabilitation Medicine's six criteria for diagnosing mild traumatic brain injury (mTBI), assessment tools, and prognostic indicators.

Note that the terms concussion and mTBI can be used interchangeably, provided neuroimaging is normal or not clinically indicated.[2]

Six Criteria for Diagnosing Concussion

The American Congress of Rehabilitation Medicine identifies six diagnostic criteria for mTBI.

Criterion #1: Mechanically Plausible Mechanism of Injury

There must be a recognised "transfer of mechanical energy to the brain from external forces".[2] Biomechanical causes include a direct head impact or indirect forces transmitted to the brain through the body. The type and direction of force are relevant and will be discussed in the prognosis section.[3]

Criterion #2: Transient Change in Mental Status

There is a transient disruption in brain function.[2] This may include:[3]

  • loss of consciousness (LOC): present in fewer than 10% of concussions
  • amnesia: can be retrograde or post-traumatic
  • other neurological signs: e.g. seizure, tonic posturing (the fencing response), motor incoordination on standing[2]
Criterion #3: At Least Two Acute Symptoms

There are at least two new or worsening symptoms as a result of the disruption in brain function. These symptoms can be cognitive, physical, emotional, and sleep-related.[3][4]

Cognitive symptoms include brain fog, slowed thinking, and difficulty concentrating. Physical symptoms include headache, dizziness, nausea, visual disturbance, balance problems, and fatigue. Emotional symptoms include irritability, sadness, anxiety, and emotional lability. Drowsiness, trouble falling asleep, and hypersomnia are examples of sleep-related symptoms.[4]

Criterion #4: At Least One Clinical or Laboratory Finding

Clinical findings include cognitive impairment, balance impairment, and vestibular or oculomotor dysfunction. These can be identified using standardised assessment tools, selected according to the time since injury and the patient's age. In the acute phase — ideally within 72 hours of injury, and up to seven days — the SCAT6 (Sports Concussion Assessment Tool, 6th edition) can be used for patients aged 13 and older. The Child SCAT6 is used for those aged 5–12. The SCOAT6 (Sports Concussion Office Assessment Tool) can be used in the subacute phase.[3]

Blood biomarkers, such as Glial Fibrillary Acidic Protein (GFAP), Ubiquitin Carboxy-terminal Hydrolase L1 (UCH-L1), S100 calcium-binding protein B (S100B), and tau proteins, are increasingly recognised as promising indicators of neuronal, axonal, and astroglial damage following concussion.[5] However, blood biomarker testing is not yet standard practice in most countries.[3]

Criterion #5: Neuroimaging

Concussion is a functional brain injury and will not appear on standard computed tomography (CT) or magnetic resonance imaging (MRI), and neuroimaging is not required for diagnosis.[6] However, it is indicated when a structural injury, such as a brain bleed or skull fracture, is suspected.[3]

Criterion #6: No Confounding Factors

Signs and symptoms of concussion cannot be better explained by other confounding factors, such as intoxication from drugs or alcohol, metabolic disturbance, or a pre-existing neurological condition.[2][3]

A mild traumatic brain injury can be diagnosed when Criterion 1 and one or more of Criteria 2-5 are met, and there are no confounding factors (Criterion 6).[2]

For more information on the ACRM diagnostic criteria, see: The American Congress of Rehabilitation Medicine Diagnostic Criteria for Mild Traumatic Brain Injury.

Recognising Concussion at the Sideline

For a sideline physiotherapist, rapid and accurate recognition of concussion is the first responsibility. Key observable signs include the spontaneous head shake, Concussion Big Five, concussive convulsion, and fencing response.[3] These signs do not all occur in every concussion, and many concussions present with none of them. However, when any one is observed, it is a strong indicator for immediate removal from play and formal assessment.

Spontaneous Head Shake After a Kinematic Event

The spontaneous head shake after a kinematic event (SHAAKE) is an involuntary, side-to-side rotation of the head occurring within seconds to minutes of impact at a rate of 2–8 movements per second. It has been identified as a reliable indicator of a concussion.[7]

[8]


Concussion Big Five

The Concussion Big Five (Australian CTE Biobank) offers a quick sideline framework and includes the following signs:[3]

  1. Slump: motionless, unconscious, or unresponsive
  2. Sway: unsteady, wobbly, or falling
  3. Slow: delayed movement, slow or wandering gait
  4. Stun: confused, blank, or behaving unusually
  5. Slow speech: slurred or delayed verbal responses

[9]

Concussive Convulsion/Impact Seizure

A concussive convulsion is a brief, tonic-clonic event that begins within seconds of impact. The patient typically displays an initial tonic phase followed by a clonic phase. These are not epileptic seizures and do not correlate with concussion severity.[10][11]

To ensure safety during the seizure, the sideline clinician must position the patient safely on their side to protect the airway. The patient's neck must be stabilised. It is important not to restrain the patient or place objects in their mouth. The clinician must let the seizure run its course.[3]

Fencing Response

The fencing response is a form of tonic posturing in which one arm extends while the other flexes. This position is held involuntarily for several seconds following impact. It resembles the asymmetric tonic neck reflex (ATNR), a primitive reflex seen in infants, and is attributed to acute dysfunction of the lateral vestibular nucleus in the brainstem.[12][3] The fencing response is included in the National Football League's (NFL) No-Go criteria, resulting in immediate removal from play.[13]

The SCAT6

The SCAT6 is a standardised multimodal assessment tool with two phases: an immediate (on-field) assessment and an off-field assessment.[14]

The immediate assessment is ideally completed on-field once first aid priorities are addressed. Throughout, the clinician remains alert for red flags. The patient must be transferred for immediate medical assessment/emergency care if any of the following are observed:[14]

  • neck pain or tenderness
  • seizure or convulsion
  • double vision
  • loss of consciousness
  • weakness or tingling/burning in more than one arm or in the legs
  • deteriorating conscious state
  • vomiting
  • severe or increasing headache
  • increasingly restless, agitated or combative
  • Glasgow Coma Scale (GCS) of less than 15
  • any visible deformity of the skull

The immediate (on-field) assessment itself includes five steps: observable signs, GCS, cervical spine assessment, coordination and oculomotor screen, and a memory assessment using Maddocks questions.[14]

The off-field assessment is conducted in a distraction-free environment once the athlete is in a resting state. The assessment includes athlete background, symptom evaluation (a symptom count out of 22 and a symptom severity score out of 132), cognitive screening (orientation, immediate memory, concentration, delayed recall), and a coordination and balance examination using the Modified Balance Error Scoring System (mBESS) and timed tandem gait.[14]

The full assessment is available here.

The SCAT6 can't be performed correctly in less than 10–15 minutes; a rushed assessment risks missing clinically significant findings.[14]

Note that a patient can score within normal limits on the SCAT6 and still have a concussion. The SCAT6 supports, but does not replace, clinical judgement.[3]

Prognostic Factors in Concussion

Evidence shows that 70–80% of concussions resolve spontaneously within one month.[3] However, the remaining 20–30% of patients experience persistent symptoms. Early identification for these patients is key.[3]

Ten Risk Factors for Prolonged Recovery

Mechanism of injury: Rotational forces cause greater neuronal shearing than linear acceleration forces. Patients with high-rotational mechanisms may face a longer recovery trajectory.[15]

Loss of consciousness (LOC): Brief LOC does not indicate a poor prognosis, but LOC lasting more than one minute may predict a more prolonged recovery.[3]

Amnesia: Greater duration of post-traumatic amnesia correlates with longer expected recovery time.[16][17]

History of previous concussions: A higher number of prior concussions increases the risk of prolonged recovery.[18]

High symptom burden: A greater number and severity of acute symptoms are associated with worse outcomes, particularly cognitive deficits, post-traumatic headache or migraine, dizziness, and oculomotor dysfunction.[19] Tracking symptom severity with a validated outcome measure such as the Post-Concussion Symptom Scale is recommended.

History of mood disorders: A history of depression, anxiety, or other psychological conditions may predispose patients to a longer clinical recovery.[20]

Learning difficulties and ADHD: A specific learning difficulty may be a significant factor moderating long-term concussion outcomes.[21] The relationship between ADHD and concussion is less clear. Some evidence suggests that individuals with ADHD experience worse symptomatology after concussion,[22] while other research indicates a possible neuroprotective effect for those already taking neurostimulant medication, such as methylphenidate (Ritalin/Concerta).[23]

Headache and history of migraine: A personal or family history of migraines, or a new onset of post-traumatic headache or migraine, predicts a more prolonged recovery.[24]

Age: Adolescents are at heightened risk of prolonged recovery due to the recent rapid development of the limbic regions and prefrontal cortex. The frontal lobe, responsible for working memory and other cognitive functions, is more fragile and susceptible to concussion-related damage during this period. Persistent symptoms in adolescents can adversely affect academic performance, social functioning, and emotional regulation, with a heightened vulnerability to psychiatric morbidity.[25] [26][27]

Sex: Growing evidence indicates that females may experience more severe symptoms and longer recovery times following concussion. Hormonal fluctuations across the menstrual cycle may also influence concussion risk in female athletes,[28] and females may be more likely to report symptoms than males.[3]

Immediate Concussion Management

Effective early concussion management centres on conserving brain energy to promote healing.[3]

During the initial 24 to 48 hours following an injury, patients should prioritise rest and sleep in calm, quiet environments, avoiding loud or visually stimulating settings, such as the classroom or office.[29] During this period, all screen time, including television, phones, and computers, should be avoided. Blue light suppresses melatonin production, potentially disrupting sleep and circadian rhythms, and screen use during this window has been linked to longer recovery times.[3][30]

Once the initial 48-hour recovery window passes, patients should implement consistent sleep hygiene practices. This involves establishing a regular sleep-wake schedule, creating a relaxing bedtime routine that includes meditation or breathing exercises, and avoiding screens for one to two hours before bed. Additionally, it is beneficial to avoid caffeine before sleep and napping after 3pm to protect the quality of nocturnal rest.[3]

Current evidence indicates that avoiding physical activity can prolong recovery, and patients do not need to be symptom-free before beginning exercise. After the initial 24 to 48 hours of rest, patients should begin light cardiovascular activity, such as a 10- to 20-minute walk, at a "sub-symptom threshold."[31][29] Symptoms should be monitored during activity: the aim is to exercise without the symptom score rising by more than two points. For example, a headache rated 3 out of 10 on a numerical pain rating scale should not rise beyond 5. If symptoms increase beyond this, the intensity or duration should be reduced.[3]

As recovery progresses, evidence supports physiotherapy intervention, including vestibular and neuromusculoskeletal therapy, to guide a safe return to function.[3]

Clinical vs. Physiological Recovery from Concussion

This distinction between clinical and physiological post-concussion recovery has direct implications for when the medical team can clear a patient to return to activity.

Clinical recovery refers to symptom resolution (i.e. when the patient reports feeling better). Most concussion symptoms (headache, dizziness, brain fog) resolve within a few weeks to a month.[3]

Physiological recovery refers to the normalisation of underlying brain function. Following concussion, cerebral blood flow (CBF) drops significantly and only begins to improve around six weeks post-injury.[32] This hypoperfusion continues to impair brain function even after a patient feels subjectively well. This is also why low-intensity exercise is encouraged after the initial rest period, as it helps restore cerebral blood flow and supports physiological healing.

Recognising this gap matters when interpreting persistent symptoms. A symptom-free patient is not necessarily a physiologically recovered patient, and premature return to high-demand cognitive or physical activity during this window increases the risk of exacerbation and prolonged recovery. Persistent symptoms (i.e. lasting months or even years) may indicate a prolonged physiological recovery process.[3]

Summary

The following table summarises concussion symptoms, assessment and prognosis.

Concussion symptoms, assessment and prognostic factors
Domain Key Points
Diagnosis Six diagnostic criteria have been identified: mechanism of injury, transient mental status change, ≥2 symptoms, ≥1 clinical finding, neuroimaging only if structural injury is suspected, and no confounding factors
Sideline signs SHAAKE, Big Five, concussive convulsion, fencing response. Any of these signs warrant removal from play
Assessment tools SCAT6 (age ≥13) or Child SCAT6 (ages 5–12) ideally within 72 hours, but up to 7 days; SCOAT6 beyond 7 days
SCAT6 limitation Normal score does not exclude concussion; clinical judgement prevails
Recovery 70–80% of concussions resolve within a month; 20–30% have persistent symptoms
Risk factors for prolonged recovery Rotational forces, LOC >1 min, amnesia, prior concussions, high symptom burden, mood disorders, learning difficulties/ADHD, headache/migraine, age, female sex
Recovery gap Clinical recovery precedes physiological recovery; cerebral blood flow only begins to improve around 6 weeks post-injury

Resources

References

  1. ↑ Mullally WJ. Concussion. The American Journal of Medicine. 2017 Aug 1;130(8):885-92.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Silverberg ND, Iverson GL; ACRM Brain Injury Special Interest Group Mild TBI Task Force members:; Cogan A, Dams-O-Connor K, Delmonico R, 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.
  3. ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 3.13 3.14 3.15 3.16 3.17 3.18 3.19 3.20 3.21 3.22 Robertson M. Identifying Concussion Course. Physiopedia Plus, 2026.
  4. ↑ 4.0 4.1 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.
  5. ↑ Kamil R, Atef AbdelAlim Y, Patel S, Sweeney P, Feng H, Hundal J, Goldstein I. Objective Markers for Diagnosing Concussions: Beyond Blood Biomarkers and the Role of Real-Time Diagnostic Tools. J Clin Med. 2025 Oct 30;14(21):7727.
  6. ↑ Khan TF. Defining Concussion: Current Concepts and Diagnostic Criteria. In: Seminars in Pediatric Neurology 2026 Jan 24 (p. 101260). WB Saunders.
  7. ↑ Nowinski CJ, Bureau SC, Rhim HC, Zafonte RD, Cantu RC, Daneshvar DH. Spontaneous Headshake after a Kinematic Event (SHAAKE): Evaluating the Utility of a Potential New Sign in the Diagnosis of Concussion. Diagnostics (Basel). 2024 Oct 17;14(20):2314.
  8. ↑ @StraightArrowNews. Seemingly harmless gesture. Available from: https://www.youtube.com/shorts/ajBcX2ZP3hI [last accessed 1/7/2026]
  9. ↑ The Macquarie University Community. The Australian CTE BioBank - High 5 for the Concussion Big 5! Available from: https://www.youtube.com/watch?v=_SpvSqrC7kE [last accessed 1/7/2026]
  10. ↑ Nass RD, Elger CE, Fink GR, Burghaus L. Kommotionelle Konvulsionen: Epileptischer Anfall oder nicht? [Concussive convulsions: seizure or no seizure?]. Fortschr Neurol Psychiatr. 2011 Nov;79(11):655-9. German.
  11. ↑ Perron AD, Brady WJ, Huff JS. Concussive convulsions: emergency department assessment and management of a frequently misunderstood entity. Acad Emerg Med. 2001 Mar;8(3):296-8.
  12. ↑ Okonkwo DO, Mares A, Wasserman EB, Shrestha R, Terry DP, Solomon G, Sills A, Eagle SR. No Association Between Fencing Response After Concussion and Recovery Time, Concussion Severity, or Clinical Outcomes in Professional American Football Players. Neurosurgery. 2025 Nov 1;97(5):1083-1090.
  13. ↑ NFL Player Health and Safety. Concussion protocol & return-to-participation protocol: overview. Available from: https://www.nfl.com/playerhealthandsafety/health-and-wellness/player-care/concussion-protocol-return-to-participation-protocol (accessed 6 July 2026).
  14. ↑ 14.0 14.1 14.2 14.3 14.4 Echemendia RJ, Brett BL, Broglio S, Davis GA, Giza CC, et al. Introducing the Sport Concussion Assessment Tool 6 (SCAT6). Br J Sports Med. 2023 Jun;57(11):619-621.
  15. ↑ Tierney G. Concussion biomechanics, head acceleration exposure and brain injury criteria in sport: a review. Sports biomechanics. 2024 Nov 1;23(11):1888-916.
  16. ↑ Hart T, Novack TA, Temkin N, Barber J, Dikmen SS, Diaz-Arrastia R, Ricker J, Hesdorffer DC, Jallo J, Hsu NH, Zafonte R. Duration of Posttraumatic Amnesia Predicts Neuropsychological and Global Outcome in Complicated Mild Traumatic Brain Injury. J Head Trauma Rehabil. 2016 Nov/Dec;31(6):E1-E9.
  17. ↑ Ratha Krishnan R, Yang Y, Yee E, Chua KS. Factors Affecting Recovery from Post-Traumatic Amnesia During Inpatient Brain Injury Rehabilitation: A Retrospective Cohort Study. Life. 2026 Jan 26;16(2):203.
  18. ↑ Pertab JL, Merkley TL, Winiarski H, Cramond KMJ, Cramond AJ. Concussion and the Autonomic, Immune, and Endocrine Systems: An Introduction to the Field and a Treatment Framework for Persisting Symptoms. J Pers Med. 2025 Jan 17;15(1):33.
  19. ↑ Iverson GL, Gardner AJ, Terry DP, Ponsford JL, Sills AK, Broshek DK, Solomon GS. Predictors of clinical recovery from concussion: a systematic review. British journal of sports medicine. 2017 Jun 1;51(12):941-8.
  20. ↑ McIntosh SJ, Vergeer MH, Galarneau JM, Eliason PH, Debert CT. Factors Associated With Persisting Symptoms After Concussion in Adults With Mild TBI: A Systematic Review and Meta-Analysis. JAMA Netw Open. 2025 Jun 2;8(6):e2516619.
  21. ↑ Sicard V, Moore RD. The relation of learning disabilities to the long-term outcomes of concussion. Psychology of Sport and Exercise. 2022 Jan 1;58:102101.
  22. ↑ Biederman J, Feinberg L, Chan J, Adeyemo BO, Woodworth KY, Panis W, McGrath N, Bhatnagar S, Spencer TJ, Uchida M, Kenworthy T. Mild traumatic brain injury and attention-deficit hyperactivity disorder in young student athletes. The Journal of nervous and mental disease. 2015 Nov 1;203(11):813-9.
  23. ↑ Rooks LT, Bertò G, Pasquina PF, Broglio SP, McAllister TW, McCrea MA, Pestilli F, Port NL, CARE Consortium Investigators. Factors Associated with Persisting Post-Concussion Symptoms Among Collegiate Athletes and Military Cadets: Findings from the NCAA-DoD CARE Consortium: LT Rooks et al. Sports Medicine. 2025 Jul;55(7):1743-55.
  24. ↑ Sufrinko A, McAllister-Deitrick J, Elbin RJ, Collins MW, Kontos AP. Family History of Migraine Associated With Posttraumatic Migraine Symptoms Following Sport-Related Concussion. J Head Trauma Rehabil. 2018 Jan/Feb;33(1):7-14.
  25. ↑ Leddy JJ, Burma JS, Toomey CM, Hayden A, Davis GA, Babl FE, Gagnon I, Giza CC, Kurowski BG, Silverberg ND, Willer B. Rest and exercise early after sport-related concussion: a systematic review and meta-analysis. British journal of sports medicine. 2023 Jun 1;57(12):762-70.
  26. ↑ Sheldrake E, Al-Hakeem H, Lam B, Goldstein BI, Wheeler AL, Burke M, Dunkley BT, Reed N, Scratch SE. Mental health outcomes across the lifespan in individuals with persistent post-concussion symptoms: a scoping review. Frontiers in neurology. 2022 Apr 11;13:850590.
  27. ↑ Lambert M, Sheldrake E, Deneault AA, Wheeler A, Burke M, Scratch S. Depressive symptoms in individuals with persistent postconcussion symptoms: a systematic review and meta-analysis. JAMA network open. 2022 Dec 27;5(12):e2248453.
  28. ↑ Carr G, Fleddermann MT. The Influence of Menstrual Cycle Phases on Postconcussion Outcomes and Symptom Reporting: A Scoping Review. Scand J Med Sci Sports. 2025 Jul;35(7):e70093.
  29. ↑ 29.0 29.1 Schneider KJ, Leddy JJ, Guskiewicz KM, Seifert T, McCrea M, Silverberg ND, Feddermann-Demont N, Iverson GL, Hayden A, Makdissi M. Rest and treatment/rehabilitation following sport-related concussion: a systematic review. Br J Sports Med. 2017 Jun;51(12):930-934.
  30. ↑ Macnow T, Curran T, Tolliday C, Martin K, McCarthy M, Ayturk D, Babu KM, Mannix R. Effect of Screen Time on Recovery From Concussion: A Randomized Clinical Trial. JAMA Pediatr. 2021 Nov 1;175(11):1124-1131.
  31. ↑ Rahimi A, Ayaz A, Edgar C, Jeyarajan G, Putzer D, Robinson M, Heath M. Sub-symptom threshold aerobic exercise improves executive function during the early stage of sport-related concussion recovery. Journal of Sports Sciences. 2025 Feb 1;43(3):266-79.
  32. ↑ Giza CC, Hovda DA. The Neurometabolic Cascade of Concussion. J Athl Train. 2001 Sep;36(3):228-235.
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