There are many definitions of concussion, but it is generally agreed upon that a concussion is a type of mild traumatic brain injury (mTBI) – a traumatically induced, transient disturbance of brain function.1,2 While older data suggests that over 6 per 1000 people worldwide experience a concussion annually, it is estimated that only 1 out of 9 concussions are captured using current data sources.3,4 The Centers for Disease Control and Prevention (CDC) estimates that, when accounting for outpatient visits for TBIs and patients not seeking care for injuries, the incidence may range from 1.4 to 3.8 million concussions per year.1 According to the 2020 National Health Interview Survey, 6.8% of children in the United States, under the age of 18, were reported to have had symptoms of a concussion in their lifetime.5 Populations at high risk of concussions include athletes playing contact sports.

Despite the high incidence of concussion and the associated morbidity, there is no universal consensus on the definition of a concussion6 Furthermore, mTBI and concussion are often used interchangeably because of their overlapping definitions6

The Amsterdam International Consensus Conference on Concussion in Sport defines sport-related concussion as a “traumatic brain injury caused by a direct blow to the head, neck or body”, with the caveat that no abnormalities are noted on traditional modalities of neuroimaging.7 The American Academy of Neurology (AAN) defines a concussion as a “clinical syndrome of biomechanically induced alteration of brain function, typically affecting memory and orientation, which may involve loss of consciousness”.8

The National Institute of Neurological Disorders and Stroke (NINDS) details that a person with mTBI “may remain conscious or may experience a loss of consciousness for a few seconds or minutes”.8 The World Health Organization (WHO) criteria for diagnosing an mTBI includes transient neurologic symptoms (including loss of consciousness for 30 minutes or less) and a Glasgow Coma Scale (GCS) score of 13-15, at least 30 minutes post-injury.8

On the other hand, based on the Mayo Classification System, a concussion could be a Possible TBI, instead of a Probable mTBI, which is described as a “loss of consciousness is momentary to 30 minutes and PTA does not extend beyond 24 hours.” If the individual sustains a depressed, basilar, or linear skull fracture (dura intact), then the TBI is still a Probable mTBI. By this definition, a “diagnosis of Possible TBI is made if one or more of the following symptoms are present: blurred vision, confusion, dazed, dizziness, focal neurological symptoms, headache, or nausea”.8

As with its definitions, the symptoms of a concussion can also be varied, including cognitive, physical, behavioral, and emotional manifestations.9 In this article, we will explore how the understanding of concussion has evolved over the centuries and identify gaps for future research.

To understand the current concepts in concussion, it is essential to first review it through a historical lens. The earliest descriptions can be traced back to the Father of Medicine, Hippocrates, in the 4th century, who identified associations of head injury with loss of consciousness, as well as vision, speech, and hearing impairments.10 While modern translations use the word “concussion” in his writings, this is a word that emerged centuries later.10 In the 10th century, Persian physician Rhazes distinguished a concussion as a transient physiologic alteration or “commotio cerebri”, rather than a structural brain injury.10 Lanfrancus, in the 13th century, further described the latter as “contusio cerebri”.10 In the Renaissance era, Pare called “commotio cerebri” the “moving or concussion of the brain”, thus one of the earliest recorded uses of the phrase.10

Until the 17th and 18th centuries, there was little discussion of the possible mechanisms of a concussion.10 With the advances in science, many hypotheses came into play, including the ideas of a microscopic structural injury as well as functional injury to axons.10

It wasn’t until the turn of the century that we fully developed our modern understanding of the pathophysiology of concussion. Mechanical trauma to the brain sets forth a neurometabolic cascade, which is the sudden release of neurotransmitters, such as glutamate, that bind to NMDA receptors, as well as ionic shifts, leading to neuronal depolarization.11 To return to resting membrane potential, a hypermetabolic phase occurs, resulting in glucose depletion. This energy deficit predisposes the brain to long-term vulnerability.11

After this hypermetabolic state, the brain enters a hypometabolic state.11 Further ionic shifts, including calcium accumulation, impair neuronal structures such as microtubules and neurofilaments, affecting neural connectivity and oxidative metabolism. This leads to glycolysis with lactic acidosis that furthers neuronal vulnerability.11

Diffuse axonal injury from the mechanical stretching of axons can further disrupt membrane integrity and ionic imbalances.12 The effects of these processes on neurotransmission may explain some of the persistent symptoms following a concussion. Clinical studies have also demonstrated an increased permeability of the blood-brain barrier in concussions and mTBI, hypothesised to be secondary to astrocyte dysfunction.13

The approach and evaluation of a suspected concussion often depend on the site of the initial evaluation. While the diagnosis is clinical, there is no single test or criterion to make this diagnosis.2 Clinicians and first responders typically use various standardized diagnostic tools, particularly in a pre-hospital setting.2

It is important to consider pre-morbid conditions, including underlying headache disorders, mental health diagnoses, cognitive concerns, and sleep dysfunction.2 Healthcare providers must distinguish between new and pre-existing symptoms to recognize the risk of worsening of pre-morbid conditions.

Another important consideration is the mechanism of injury. In an injury, two forces are in effect, including contact and inertial forces from head motions.14 Recognizing the movement of the head and the direction of movements is pertinent, as certain planes of movement, e.g., in the coronal plane, may be more likely to lead to a loss of consciousness.14

Symptoms of a concussion can vary and include physical, cognitive, and emotional manifestations.15 Given the heterogeneous presentations of concussions, there have been attempts to categorize them based on symptoms and recovery patterns. Subtypes include 1) headache, 2) cognitive, 3) oculomotor, 4) vestibular, and 5) mood. Associated conditions of concussion include sleep disturbances and cervical strain.16

Headaches are the most common manifestation of a concussion.16 Pre-morbid headaches may increase the risk of post-concussive headaches. Cognitive subtypes of concussion may present as impaired attention, memory, and processing speed.16 Oculomotor deficits may include visual impairments or visual processing concerns, as well as photophobia, blurred vision, and vision-associated nausea.16 The vestibular subtype of concussion includes symptoms such as dizziness, nausea, and dysequilibrium. Mood symptoms can include anxiety, depression, fatigue, or irritability.16

Sleep disturbances can fall anywhere in the spectrum, ranging from insomnia to hypersomnolence.16 Non-restorative sleep can exacerbate other symptoms as well, and in turn, can prolong the recovery from a concussion.16 Cervical strain can also be seen following a head injury. It is essential to note that these subtypes, associations, and symptoms can overlap, despite this attempt at categorization.16

There is increasing recognition of atypical symptoms, including those that traditionally fall under the category of functional neurological disorders.17 These may include transient speech disturbances, functional gait disorders, or unusual hearing changes. These may be responsive to cognitive behavioral therapy and other forms of psychotherapy.17

In some situations, head impacts may not be associated with any recognizable symptoms and may not be classified as a concussion. These can be considered subconcussive injuries.18 However, MR spectroscopy has shown subtle changes, such as an increase in choline, demonstrating potential effects of head injuries even when they are not recognized as a concussion.18

It is also important to recognize that concussions can manifest differently in younger children, making reporting and evaluation of symptoms challenging.15Fig. 1

A thorough history should be gathered to include prior history of learning disability, headaches, or mood symptoms, which can worsen post-concussive symptoms.2 Evaluation should also include the mechanism of injury and current symptoms. A comprehensive physical exam should be conducted to include an examination of the head and neck area for injuries; a complete neurologic exam with a focus on cognitive function, balance, and the vestibular system.2 A detailed neuropsychological test may also be warranted to assess for cognitive changes.2

Various concussion assessment tools have been developed to standardize the evaluation of a suspected concussion.19 The Standardized Assessment of Concussion (SAC) is a quick sideline mental status evaluation that has good sensitivity and specificity. The Sport Concussion Assessment Tool (SCAT), now in its 6th version, is a tool that is more comprehensive, but requires administration by a trained healthcare professional.20 This has most utility in the first 72 hours, but limited utility after a week. It covers various domains, encompassing the numerous symptom subtypes that can be seen following a concussion. There are two versions, Child SCAT for children between ages 6 and 12, and an adult version of the SCAT for those aged 13 and older. There is also an in-office version of the SCAT, called the Sport Concussion Office Assessment Tool 6 (SCOAT 6).21 While the Adult SCAT has been more robustly researched, the Child SCAT has limited data comparing concussed and non-concussed children, particularly in the younger age group. The SCAT also relies heavily on symptom report, which is reliable in older populations but can be challenging to elicit in younger populations.20 Furthermore, the SCAT, in both versions, has limited efficacy beyond the post-injury acute period.20

The Military Acute Concussion Evaluation (MACE), is typically used in the military as a screening tool for concussions.19 The Acute Concussion Evaluation is another clinician-administered tool that can be used to track symptoms.19 The Post-Concussion Symptom Scale (PCSS) can be used to discriminate between concussed and non-concussed athletes, but has not been validated in children under the age of 11.19,20

Neuropsychological evaluation measures, such as the Immediate Post-Concussion Assessment and Cognitive Testing (ImPACT), CogSport, Concussion Resolution Index (CRI), and Automated Neuropsychological Assessment Metrics, can identify signs of cognitive deficits and mood changes when compared to baseline, and have been used in athletes.19

While a concussion is a clinical diagnosis, imaging is reserved for when alternative diagnoses need to be excluded, such as more severe forms of TBI. In the pediatric population, criteria such as the Pediatric Emergency Care Applied Research Network (PECARN) may be applied to assess whether neuroimaging is warranted. In such cases, a computed tomography (CT) scan of the head may be necessary to exclude neurosurgical emergencies.2

In some cases, if the symptoms have not resolved, there may be a role for a magnetic resonance imaging (MRI) of the brain to exclude an underlying etiology. It is important to note that negative neuroimaging does not rule out a concussion. Cortical atrophy can be seen in some pediatric patients up to 4 months post-concussion.22

There may be a future clinical role for such techniques as functional magnetic resonance imaging, magnetic resonance spectroscopy, positron emission tomography, single-photon emission computed tomography, and diffusion tensor imaging, to assess for metabolic shifts, cerebral perfusion, and axonal alterations. However, these techniques are currently used primarily in a research setting to study pathophysiologic changes.19

Biomarkers, including S100 calcium-binding protein, serum Tau-C, T-Tau, and interleukin-6, have been found to be elevated 6 hours post-injury.23 Sex differences have also been noted in biomarkers with higher tau in females.24 Currently, there is limited evidence about the diagnostic utility of these in a clinical setting, but more research is needed.

There may also be a role for electroencephalogram (EEG) and event-related potentials (ERP), to determine recovery. These have been shown to distinguish between concussed and non-concussed individuals.22

A large proportion of emergency department visits for concussion in children are related to sports or recreation, and most of the concussion research is done in athletes.24 However, this does not negate other populations that may be at risk of concussive symptoms. Children with neurodevelopmental disorders may be at a higher risk of concussion and, subsequently, persistent symptoms.25

Despite the consensus about the protective nature of neuroplasticity of the developing brain, studies have demonstrated that injuries sustained in early childhood can disrupt brain development and lead to long-term impairment.15

Younger children may also present differently with irritability, refusing to eat, appearing confused or clumsy, or not wanting to play. It is important to recognize these as likely symptoms of a concussion.26

After a diagnosis of a concussion has been made, the patient will warrant close outpatient observation. Treatment is primarily supportive, with education surrounding a gradual return to learn and play2 Contrary to prior recommendations, absolute rest is no longer recommended; instead, relative rest is encouraged. A stepwise return-to-activity protocol is instituted, where each increase in activity occurs every few days.2 For children, it is essential that caregivers and schools are educated on their role in the recovery process, particularly in the areas of return-to-learn and return-to-play, to allow a safe return to activities.15

There is a role for over-the-counter analgesics.2 In addition, based on the patient’s symptoms, there may be utility for medications to aid cognition, sleep, or mood.2

Concussions generally carry a good prognosis, with most symptoms of a concussion resolving in two weeks. However, it is estimated that up to 30% of people who sustain an mTBI may develop persistent symptoms.27 The transitory phase from concussion to post-concussion is ill-defined. Post-concussion syndrome is characterized by persistent symptoms lasting weeks to months after the initial injury, persisting beyond 3 months, according to some definitions. Still, there is no clear scientific basis for this timeline.28,29

Second impact syndrome is a rare but important complication wherein a second head injury or TBI is sustained before full recovery from the first concussion.30 This may present as a rapid alteration in mentation followed by loss of consciousness. The pathophysiology of second impact syndrome is not fully understood, but it is likely the result of dysfunctional cerebral blood flow, leading to increased intracranial pressure.30 This can quickly lead to cerebral herniation and eventual death.30 Metabolic derangements in the initial concussion are thought to leave the brain prone to further injury.12

Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disorder that is associated with repetitive concussions and mTBIs, and sometimes even repeated sub-concussive injuries.19 Contact sports have a strong association with CTE. This is a pathological diagnosis that is confirmed posthumously. Findings include atrophy of the cerebral cortex (particularly in the frontal and temporal lobes), loss of white matter volume, and thinning of the corpus callosum. Microscopically, there may be an accumulation of hyperphosphorylated tau within neurons and glia.19 This is distinguished from other tauopathies, such as Alzheimer's disease, by abnormal perivascular accumulation of tau in an irregular pattern.19

In cases of an autopsy 6 months after a concussion, there is evidence of multifocal axonal injury and neuroinflammation, almost similar to that seen in military veterans exposed to blast injury.19