Sport-Related Concussion

Abstract

Purpose of Review

The incidence of sport-related concussion (SRC) has been increasing in different sports and its impact on long-term cognitive function is increasingly recognized. In this study, we review the epidemiology, neuropathophysiology, clinical symptoms, and long-term consequences of SRC with a specific focus on cognition.

Recent Findings

Repeated concussions are associated with an increased risk of several neurologic diseases and long-term cognitive deficits. To improve cognitive outcomes in athletes with SRC, standardized guidelines for the assessment and management of SRC are vital. However, current concussion management guidelines lack procedures for rehabilitating acute and long-term cognitive symptoms.

Summary

Increased awareness for the management and rehabilitation of cognitive symptoms in SRC is needed in all clinical neurologists treating professional and amateur athletes. We propose cognitive training as a prehabilitation tool to alleviate the severity of cognitive symptoms and as a rehabilitative tool to improve cognitive recovery postinjury.

Cognitive impairment is a common sequela of acquired brain injury and a growing area of interest for the management of sport-related concussion (SRC). Challenges in managing cognitive impairment after SRC arise not only from the heterogeneity of neural injuries and resulting effects on cognition but also from the implications these may have within individual circumstances, goals, and prior cognitive abilities. These natural complexities are further compounded by challenges in measurement and monitoring, given the temporal dynamics of impact and measurement remain largely unclear.

In this article, we provide a state-of-the-art overview of current evidence and research directions in SRC, with a particular emphasis on the link between injury, cognition, and functional sequalae. We further introduce cognitive training as a potential mitigation and prevention measure and its potential role to improve field performance by targeting cognitive skills that underpin performance of different sports. We review potential mechanisms, practical considerations, and areas for further mechanistic and clinical research.

Definition and Epidemiology

Concussion, defined as a temporary disturbance of brain function, is a form of traumatic brain injury (TBI). TBI is listed as an intracranial injury in the International Classification of Diseases, 10th Revision (ICD-10) and can be mild, moderate, or severe. In addition to concussion, cerebral edema, diffuse and focal brain injury, and various forms of traumatic hemorrhage fall under TBI. Concussion is the mildest and most common variant of TBI, but given the heterogeneity in the literature regarding definitions, the term concussion is often interchangeably used with the term mild TBI; because the differences in injury are vague, there is debate on whether concussion and mild TBI are unique constructs.¹ This article will therefore use the term concussion to also represent mild TBI. The term TBI will be used when referring to all levels of TBI. Globally, 50 million people experience TBI annually²; however, given that many cases may receive outpatient treatment, are undiagnosed, untreated, or not the primary injury, the true prevalence is likely considerably greater.³ Forward estimates suggest that half of the global population will have at least 1 TBI over their lifespan.² SRCs occur specifically due to biomechanical forces induced on the body or head, which in turn lead to acceleration, deceleration, and rotational forces on the brain. Repetitive head injuries (RHIs), which may follow similar mechanisms as concussion but do not meet the clinical criteria, are also very common in sport and can be less symptomatic or even asymptomatic. Contrary to common belief, more than 90% of concussions do not involve a loss of consciousness, which, combined with the absence of objective biomarkers, can make them challenging to diagnose.

SRCs have become such a serious concern that an international workgroup of leading researchers and clinicians was formed to guide policy, clinical practice, and future research.¹ Consensus statements¹ by this workgroup and the resulting awareness have led many sports to introduce new rules and mandatory requirements around player safety, assessment, management, and monitoring of concussion injuries and protective equipment.

Sports-Related Concussion Epidemiology

Beyond increasing public awareness, the statistics of SRCs tell an alarming story. Estimates suggest that 3.8 million concussions occur in the United States annually because of sport and recreation with up to 50% of concussions going unreported.⁴ The incidence of concussion in sport has been steadily increasing over previous decades, with 2 comprehensive studies of collegiate athletes in North America showing an increase in concussion rates from 1.7 per 10,000 athlete exposures (1 athlete exposure is defined as 1 athlete participating in 1 practice or game) in 1988–1989 to 3.4 in 2003–2004⁵ and to 4.47 in the period between 2009 and 2014.⁶ Similar incidence trends are also found in high school athletes⁷ and school children.⁸ For comparison, the incidence of concussion injuries was almost double that of the seemingly more common anterior cruciate ligament injuries.⁵ Exacerbating this is the fact that 35%–62% of concussion injuries in high school and collegiate athletes are not reported.⁹ In collegiate athletes, the greatest number of concussion injuries were observed in men's American football, while the highest rates of concussion were noted in men and women's ice hockey and women's soccer.^5,6 In 2017, approximately 2.5 million American high school students self-reported having at least 1 physical activity–related or SRC in the preceding 12 months, while 1 million reported 2 or more.¹⁰ At the elite level, concussions are more common, with an analysis of head injuries during the 2012–2013 and 2013–2014 National Football League (NFL) seasons illustrating a concussion rate of 66.1 (per 10,000 athlete exposures).¹¹

Neuropathophysiology, Clinical Symptoms, and Long-term Consequences

Neuropathophysiology

SRCs are heterogeneous because severity and location of impact, age, and sex play key roles in the subsequent neuropathophysiology and clinical symptoms. Concussion generally results in diffuse injuries that can be difficult to detect and generally refer to axonal injury, but also include vascular injury and brain edema.^12,13 In a primary concussion phase, diffuse axonal injury is the most common form of injury and results from acceleration, deceleration, and rotational forces that cause the differently weighted brain tissues to move at different rates resulting in the shearing of axons.¹² In a secondary phase, diffuse axonal injury leads to a series of metabolic disturbances known as the hypermetabolic or neurometabolic cascade of concussion.¹⁴ This is characterized by an influx of calcium and sodium ions and efflux of potassium ions, leading to an increased activation of the sodium-potassium pump and thus hyperglycolysis.¹⁵ In addition, shearing of endothelial cells in small vessels can cause reduced cerebral blood flow,¹² leading to a mismatch between glucose supply and demand¹⁵ and eventually an acute failure in neuronal function.¹² The aforementioned ionic dysregulation also results in the release of excitatory amino acids such as glutamate that binds to NMDA receptors and causes further depolarization. Concurrently, there is a calcium influx into mitochondria, which leads to oxidative stress and exacerbates the disruption in cellular energy supply.¹⁶ Furthermore, excess intracellular calcium can also phosphorylate neurofilament microstructures leading to further axonal damage and disrupted axonal transport, continuing the cycle.¹⁵

Using a combination of rodent and human studies, links have been proposed between pathophysiologic changes and postconcussive symptoms. Cognitive impairment and slower speed of processing could be a consequence of axonal injury and altered neurotransmission; increased sensitivity to repeated injuries could be a result of the glycolysis imbalance.¹⁵ In the long term, dysfunctional neurotransmission in NMDA receptors in the hippocampus could result in memory deficits and cognitive deterioration.¹⁷ Recent hypotheses on cognitive dysfunction after concussion suggest that diffuse axonal injury in the hippocampus leads to persistent deficits in intrahippocampal synchronization and memory consolidation, to reduced input to hippocampal structures and diffuse damage to long-range connections between the hippocampus and other brain regions such as the prefrontal cortex and amygdala,¹⁸ explaining some of the most common postconcussive symptoms, such as impaired memory and attention deficits. However, the outlined neuropathophysiological cascade and its proposed links to postconcussive symptoms should be interpreted with caution. First, most pathophysiologic hypotheses are based on animal models that usually reflect moderate-to-severe TBI. Second, given the heterogeneity of concussion, the level of contribution of specific damage cascades to pathophysiology in individual cases is difficult to determine.

SRC Symptoms

Similar to its neuropathophysiology, symptoms after SRC can also be rather heterogeneous and difficult to separate from depressive mood or general fatigue induced by sport. The prevalence of certain symptoms after concussion in comparison with moderate-to-severe TBI is currently debated. Nonetheless, there is consensus¹ that symptoms of SRC may include 1 or more of the following:

1. Headache

2. Confusion

3. Disorientation

4. Emotional lability or irritability

5. Somnolence or drowsiness

6. Cognitive impairment

7. Gait unsteadiness

8. Amnesia

9. Loss of consciousness

10. Sleep disturbances

11. Vestibular-ocular impairments

When present, cognitive symptoms most commonly manifest as impairments in processing speed, attention, memory, and executive functions.^19,20 The duration of symptom resolution after SRC varies, but many studies illustrate cognitive symptoms resolve largely within a few days^21,22 to 1 month.²³ However, some observations indicate persistence of cognitive impairments beyond this interval, with a recent review suggesting approximately 50% of individuals who experience a single concussion (not specifically SRC) still exhibit cognitive impairment 3 or more months postinjury.²⁰ There is also evidence that RHI may affect cognition; increased heading in soccer players has been associated with lower memory scores,²⁴ and high school American football players, despite not being diagnosed with concussion, have been shown to exhibit cognitive impairment.²⁵ However, 2 well-sized systematic reviews of investigating RHI in soccer have concluded that either more research is needed²⁶ or that heading does not lead to adverse outcomes.²⁷

Long-term Cognitive Effects

Symptom resolution may not mean complete cognitive recovery because neuropsychological testing may show persistent cognitive deficits in 80%–90% of individuals with typical recovery.⁴ Longer recovery duration could be categorized as postconcussion syndrome (PCS), but whether PCS is a different to long-term effects of concussion remains unclear.²⁸ Studies on retired American football players with a history of head injuries have illustrated that recurrent concussion lead to an increased risk of late-life cognitive decline^29,30 and depression.³¹ Furthermore, former athletes who sustained their last SRC more than 3 decades earlier were shown to have lower performance on tests of episodic memory and response inhibition.³²

Concussion is a risk factor for several different diseases that affect cognition. There is clear evidence that previous concussion is the greatest risk factor for future concussion injuries,³³ with some studies illustrating an almost 6-fold increase in one's relative risk.³⁴ This could be caused by each subsequent concussion potentially reducing the level of impact needed to induce neuropathophysiological changes and clinical symptoms. There is increasing evidence suggesting that repetitive concussion can lead to chronic traumatic encephalopathy (CTE), a progressive neurodegenerative disease.³⁵ However, recent studies suggests that CTE may be linked more closely to head injury, irrespective of concussive symptoms (i.e., subconcussive damage).³⁶ CTE can result in perivascular tau pathology (e.g., neurofibrillary tangles and hyperphosphorylation), diffuse axonal injury, and cerebral atrophy. Clinical symptoms can include memory and executive function impairments, parkinsonism, impulsive behavior, emotional instability, apathy, depression, and suicidality.^35,37 A recent study found that from 202 brains of deceased American football players of all ages and levels examined, 87% had CTE neuropathology, including 110 from 111 former NFL players³⁷. Despite the selection bias given the convenience sampling of donated brains, the results show a clear link between American football and CTE, likely resulting from repetitive head trauma. Furthermore, repeated concussions have been linked to an increased risk of multiple sclerosis,³⁸ Alzheimer disease,³⁹ stroke,⁴⁰ Parkinson disease,⁴¹ and epilepsy.⁴² Given the potential long-term consequences, the assessment and management of SRC is paramount, especially given that athletes are generally at a greater risk of repeated injury than nonathletes.

Assessment, Management, and Rehabilitation

Assessment—Neuropsychological and Behavioral

In addition to neurologic examination, patient medical history, and symptom questionaries, ancillary methods such as motor testing, neuropsychological testing, neuroimaging, and vestibular-ocular testing are used to aid TBI diagnosis. Vestibular-ocular symptoms such as dizziness and blurred vision are associated with a greater risk of protracted recovery.⁴³ Vestibular-ocular tests such as the Vestibular/Ocular Motor Screening (VOMS)⁴⁴ assess vestibular-ocular dysfunction by testing domains such as visual motion sensitivity, rapid eye movements, and smooth visual pursuits. While VOMS does not provoke symptoms in healthy individuals,⁴⁵ athletes with concussions will likely experience symptoms such as dizziness or nausea.

A number of sports have improved their safety guidelines and furthermore introduced compulsory baseline testing such as the Sport Concussion Assessment Tool 5 (SCAT-5). The SCAT-5 is currently the most commonly used clinical test for concussion, having been implemented by many professional bodies such as International Association Football Federation (FIFA) NFL, and World Rugby. Although not necessary for effectiveness, many teams administer a preseason baseline of the SCAT-5 for later postinjury comparison. The SCAT-5 combines athlete self-evaluation of symptoms with objective cognitive and neurologic screening administered by a healthcare professional. The self-evaluation can be disadvantageous because it could result in athletes underreporting their symptoms and thus misleading healthcare professionals. Furthermore, there have been reports that the orientation questions used (Maddock questions)⁴⁶ are sometimes memorized by athletes. Perhaps the largest limitation of SCAT-5 is that—similar to many standardized assessments for concussion—it currently cannot be effectively used as an on-field or sideline test for removal from activity. This is because many sports have strict rules about stoppage and substitution, which does not allow for the SCAT-5 to be conducted and scored in its entirety. For instance, in soccer, stoppage time is limited to 3 minutes and players cannot be substituted off for assessment.⁴⁷ Rule changes allowing for temporary concussion substitutions during assessment, and the introduction of technical aids replaying videos of a potential concussive event are being discussed to facilitate the SCAT-5–based diagnostic process.^48,49 Indeed, technical video and communication aids have already been implemented at the Union of European Football Associations (UEFA) European Championship 2020 and in the German professional football league.^48,50 Until changes to stoppage time or substitution guidelines have been fully implemented, SCAT-5 and similar standardized tests are better served to assist in the diagnosis of concussion and return-to-play decisions, but not necessarily in removal from activity decisions. There are a number of quicker commercial tests and products that claim to assist in the latter, but many of them can only focus on 1 aspect of concussion, e.g., vestibulo-ocular function, and thus may have limited sensitivity and specificity.⁵¹

Assessment—Imaging

There is an increasing use of brain imaging in the assessment of concussion. In severe cases, CT can rapidly be administered to rule out intracranial hemorrhage. However, given the lower sensitivity of CT for other concussion-related brain changes, MRI remains the preferred imaging modality, especially in the subacute and chronic phases, where recovery is worse than expected or neurologic deficits remain.^2,52 In research settings, advanced MRI techniques such as susceptibility-weighted imaging (SWI) and diffusion tensor imaging (DTI) are increasingly used, given their greater sensitivity to structural change. SWI has been shown to be specifically sensitive to microhemorrhage, a marker of white matter injury after TBI.¹⁹ DTI shows promise as a potential diagnostic tool across varying TBI severities, with mean diffusivity (MD) being more sensitive to mild injuries such as SRC and fractional anisotropy to more severe injuries.⁵³ MD was significantly increased in acute and postacute phases of mild TBI, even when athletes showed no more symptoms and was associated with worse clinical outcome.⁵⁴ Using different imaging modalities such as functional imaging, magnetic resonance spectroscopy, and PET, recent studies have shown that SRC can lead to altered functional connectivity between brain regions,⁵⁵ neurometabolic changes,⁵⁶ and neuroinflammation.⁵⁷ While these advanced neuroimaging techniques show higher sensitivity than standard MRI and CT in detecting a multitude of acute, subacute, and chronic structural and functional brain changes and could have prognostic value in the future, their translation into clinical practice remains challenging, given the availability of appropriate equipment, temporal constraints of clinical environments, and a lack of standardization.⁵⁴ Given the extensive literature of imaging studies in concussion, an in-depth discussion of the topic is not within the scope of this article. Please see Koerte et al.⁵⁸ for a comprehensive review.

Assessment—Specimen Biomarkers

Blood biomarkers have received considerable interest recently, specifically to guide injury management and return-to-play decisions. Higher plasma tau levels after concussion (less than 6 hours postconcussion) have been linked to longer return-to-play time and correlate with the duration of symptoms.^59,60 Neurofilament light has been shown to be elevated in American football players after a season, both compared with their own baseline and noncontact athletes.^e1 Furthermore, neurofilament light has been used to identify individuals at risk of persistent PCS and similar to plasma tau, has the potential to assist in return-to-play decisions.^e2 A number of other measures, such as neurogranin, oligodendrocyte myelin glycoprotein, synuclein beta,^e3 high-sensitivity C-reactive protein,^e4 and S100 calcium-binding protein B,^e5 have likewise been proposed as potential blood-based biomarkers for concussion. Subacute biomarkers such as neurofilament light, as well as autoantibody biomarkers, and chronic biomarkers such as plasma tau are investigated for their potential in tracking disease progression, long-term consequences of TBI, and guide return-to-play decisions. Protein biomarkers such as glial fibrillary acidic protein and ubiquitin C-terminal hydrolase-L1 are closest to broader clinical implementation, with S100 calcium-binding protein B already being implemented in Scandinavian guidelines for patient selection for CT imaging after TBI.² Nevertheless, using serum biomarkers to detect concussion may be difficult because their low specificity could result in false-positives.⁴⁷ With advances in scientific methodology and technology, new pitch-side diagnostics are being investigated. Recently, specific MicroRNAs (miR-425-5p and miR-502) were discovered to be downregulated postconcussion.^e6 As a result, researchers are collecting urine and saliva samples from rugby players with suspected concussion, both during suspected concussion and throughout their recovery, with the aim of improving on-field diagnostics and return-to-play decisions.^e7

Assessment—Medical Devices

There has also been promising research into the biomechanics and physics of collisions, with rugby union players wearing accelerometers to measure the g-force of impact as a potential measure of severity of concussion.^e8 However, it has been argued that most forms of head impact measurement systems such as accelerometers, telemetry, and sensors are not sensitive or specific enough to detect concussion.^e9 The United States Food and Drug Administration (FDA) has approved a number of medical devices for the assessment of head injury using a range of different approaches, including analysis of blood samples for known protein biomarkers of head injury, computerized neuropsychological tests and devices based on portable imaging modalities (EEG and near infrared spectroscopy) and eye tracking. There are also a number of companies marketing unapproved “medical devices” for the diagnosis, treatment, and management of concussion, and the FDA has recently had to release a statement warning consumers against these and that no medical device can assess head injuries without the presence of a healthcare professional.⁶¹

While combined neurologic, neuropsychological, and vestibular-ocular testing are still the primary methods for assessing potential SRC, the potential of specimen biomarkers and the creation of new highly mobile medical devices illustrate a new era that could enable faster and more precise pitch-side assessments of SRC. Ultimately, these different methods could be combined to produce more sensitive and objective measures for removal from activity decisions, SRC diagnoses, and return-to-play decisions.

Management

Given that concussion may often present with symptoms that do not seem to warrant medical intervention, many individuals who have sustained a concussion do not see a medical professional. However, as outlined earlier, concussion can result in a series of underlying neuropathophysiological changes, which, in some cases, can lead to long-term cognitive, behavioral, and psychosocial impairment. For moderate and severe TBI, management and treatment after acute care generally revolves around occupational, speech, physical, and psychological rehabilitation and improving independent functioning. However, cognitive rehabilitation is sometimes overshadowed by rehabilitation of these other domains. For SRC, most sporting bodies now follow specific management guidelines published by the Concussion in Sport Group¹ (Table). After an initial 24–48 hours of rest, the concussed player can begin the graded return to sport. The guidelines suggest a minimum of 24 hours between each stage, which in theory could result in a concussed athlete returning to play within a week.

Table.

Graded Return-to-Sport Guidelines From the Fifth International Conference on Concussion¹

These guidelines reduce the immediate likelihood of sustaining an additional concussion, which is vital given that further concussion during this acute phase can exacerbate the neuropathophysiological cascade. As described earlier, the immediate neuropathophysiological consequences of a concussion are an uncoupling of cerebral blood flow and glucose metabolism, making cells particularly vulnerable during recovery. Any further dysregulation of energy demand due to additional injury in the immediate aftermath of a concussion might render the recovery of an injured cell impossible and instead lead to cell death. Other sources of potentially increased vulnerability such as intracellular Ca²⁺ accumulation or alterations in NMDA receptor composition can last up to 4 weeks postconcussion,¹⁷ making graded return-to-sports guidelines imperative. The guidelines can also mitigate short-term physical symptoms, but one could argue they fail to holistically rehabilitate the player. For example, rehabilitation of a torn muscle fiber will involve stretching, weight-bearing, deep-tissue massage, or dry needling among other activities. Thus, the injured muscle is actively rehabilitated before return to play. Furthermore, these activities are not restricted to postinjury and are often suggested for injury prevention as prehabilitation. By contrast, this form of rehabilitation is rarely followed for cognition after SRC because a disproportionate emphasis is placed on motor and vestibular-ocular symptoms. This is also noted with moderate and severe TBI in a clinical setting because more focus is placed on rehabilitation of physical abilities over cognitive and psychosocial symptoms. However, this approach is changing with recent clinical guidelines, suggesting cognitive remediation should play a larger role,² especially restorative treatments and compensatory strategies.^e10

Perhaps the cornerstone of current concussion management, the recommendation of cognitive and physical rest is now being questioned. While there is broad evidence supporting rest, some experts are in agreement that there is inadequate empirical evidence for the effectiveness of prescribed physical and cognitive rest and furthermore that active rehabilitation may improve symptom recovery.^e11 Firsthand investigations have shown that cognitive rest is not significantly associated with time to symptom recovery^e12 and in some cases too much rest could prolong recovery.^e13,e14 Individualized subthreshold aerobic exercises following SRC have been shown to speed recovery time compared with stretching,^e15 a result also supported by a systematic review on rest after SRC.^e16 This raises the question as to whether subthreshold cognitive exercise could have a similar effect. Of interest, there is evidence showing that moderate activity (both physical and cognitive) leads to optimal neurocognitive outcomes postconcussion when compared with high activity and no activity.^e17 More research, specifically RCTs, is needed to investigate the effects of immediate postconcussive cognitive activity on neurocognitive outcomes. Other factors beyond activity intensity, such as type of cognitive activity, whether it is combined with physical activity, the duration of the activity, and when it is instigated after concussion, could all hypothetically have an effect on neurocognitive outcomes. Ultimately, while rest may still play an important factor in recovery, perhaps it should not be a blanket recommendation but instead a guideline that could be superseded by cognitive activity to a level of intensity as tolerated by the patient.

Rehabilitation—Cognitive Training

Cognitive training is a general term that covers an array of structured interventions aiming to enhance or maintain cognitive performance using repeated practice of cognitively challenging tasks.^e18 It is one of the 3 overarching types of cognition-focused interventions (interchangeably referred to in the literature as neuropsychological, neurocognitive, or simply cognitive interventions), alongside cognitive rehabilitation and cognitive stimulation (for a comprehensive review, see Wilson^e19). Cognitive rehabilitation focuses on the cognitive underpinning of individual functional deficits and is more individualized in nature. Cognitive stimulation is a more generic approach that aims to create opportunities for cognitively engaging activities, which is much more common in populations with severe impairments (e.g., people with dementia) than those with potentially reversable cognitive impairment. The overarching idea of cognitive training is to induce experience-dependent neuroplasticity through structured and controlled learning events, in contrast to the more sporadic exposure to cognitive challenges experienced with cognitive rehabilitation or stimulation.^e20 Training will often combine explicit teaching of compensatory strategies alongside restorative drill and practice exercises and typically delivered to people with brain injury as part of a comprehensive rehabilitation program.^e19

If properly targeted, such neural changes could build over time and lead to reduced cognitive dysfunction (rehabilitation), lead to a reduced risk of severe cognitive dysfunction after trauma (prerehabilitation), or improve cognitive functioning, which could translate to superior performance in the field (enhancement). Similar to how professional athletes undertake preseason strength and conditioning training to increase sporting performance and lower the risk of injury throughout the season (i.e., prerehabilitation),^e21,e22 cognitive training has the potential to work in a similar capacity, by improving sporting performance,^e23 reducing the risk of injury, and supporting rehabilitation.

Despite robust evidence for its efficacy on cognitive performance in healthy individuals^e24,e25 and those with acquired brain injury^e26,e27 or other cognitive disorders,^e28,e29 the mechanisms underlying cognitive training effects—and therefore their clinical implications—remain largely unclear. Despite some claims that cognitive training effects do not extend beyond trained tasks,^e30 the bulk of the evidence points to robust efficacy on untrained cognitive tasks within the same domain (i.e., near transfer) and limited “far” transfer to domains not targeted by the intervention.^e18,e25,e31 Rehabilitation interventions based on explicit teaching of cognitive strategies would tend to be task specific and therefore not directly relevant or efficacious for other cognitive domains.^e19,e32 There is even less clarity about the mechanisms underlying process-based training (predominantly computerized cognitive training) because these may simply improve problem-solving efficiency without changing cognitive capacity, a notion partially supported by neuroimaging studies, although the link between training content and its associated neural effects are not well understood.^e18,e33

Although solid mechanistic theory is still lacking, several important practical implications can already be drawn. Perhaps most critical is that cognitive training must be targeted at the cognitive skills that are most important for the individual and their specialization. For example, recent studies in soccer players^e34 and lacrosse players^e35 have shown that cognitive training can improve sport-specific performance, with soccer players improving on-field passing and lacrosse players improving shooting accuracy. These studies tailored the intervention to specific cognitive skills believed to underpin performance in the respective sports, such as field of view, processing speed, or visuospatial skills, whereas other unrelated cognitive abilities (e.g., verbal memory) are less likely to be relevant to on-field performance. Similarly, the content and approach in postinjury rehabilitation must take into account individual areas of impairment, individual goals, and critical abilities required to return to activity.^e19

Planning cognitive prehabilitation may be more complex because the impact of injury is less predictable. In populations such as in surgical patients, prehabilitation interventions tend to be comprehensive and multidomain, i.e., training a wide array of processes targeting global cognitive performance and requiring larger doses and exposure than more targeted approaches.^e36 Theoretically, cognitive prehabilitation can leverage on cognitive reserve, commonly defined as the adaptivity of cognitive abilities and therefore their potential susceptibility to injury.^e37 Cognitive reserve has been used to explain why individuals with similar brain pathology may present significant differences in cognitive performance and is often linked to lifestyle exposures such as educational attainment, occupation, physical exercise, and general cognitive abilities before brain injury.^e37 In light of these interindividual differences, studies of rehabilitative methods will need to carefully balance their study populations to provide actionable results.

Because high cognitive reserve in the form of higher educational attainment has been associated with less cognitive impairment after TBI,^e38,e39 undertaking cognitive training as prehabilitation, or as part of general training and conditioning, may have the potential to reduce the severity of cognitive side effects.^e23 Indeed, cognitive training has already been shown to be effective in improving cognition in postacute TBI,^e26 with several feasibility studies also highlighting the potential of cognitive training as a therapeutic tool in patients with moderate-to-severe TBI with varying time since injury.^e40,e41 Whether the effects are similar during the acute phase (i.e., immediately after injury) is still unknown. Given that there is now agreement that active rehabilitation could improve symptom recovery, future research should focus on investigating the potential of CCT to alleviate cognitive symptoms immediately after SRC.

Conclusion

The incidence of SRC has become a major concern for many sporting bodies and athletes. Given its heterogeneity, research in the field is mainly targeted toward making diagnoses methods more sensitive and return-to-play decisions more objective. SRC can often lead to cognitive symptoms, which, in some cases, develop into long-term impairments. Currently, concussion management guidelines lack procedures for rehabilitating these acute or long-term cognitive symptoms. Cognitive training could be an added option because it has the potential to improve sport-specific performance, reduce the risk of cognitive symptoms postconcussion, and rehabilitate cognitive impairment. However, more research, specifically randomized controlled trials, are needed to investigate the effectiveness and feasibility of cognitive training for SRC.

Appendix. Authors

Study Funding

This review was funded by the Bundesinstitut für Sportwissenschaft (Aktenzeichen: ZMVI4-070106/19–20).

Disclosure

H. Hallock was using ImPACT Applications, Inc then as a paying customer for separate ongoing research; C. Reinsberger receives scientific funding by the Federal Institute of Sports Sciences (Germany) and the Heinz Nixdorf Westfalian Foundation. He examines and treats patients with sport-related concussion on a regular basis in an outpatient concussion clinic. He is a member of the medical committee of the German Football association (DFB) and provides counselling to the Union of European Football Associations (UEFA); C. Finke received scientific funding by the Federal Institute of Sports Sciences (Germany). C. Finke was using ImPACT Applications, Inc then as a paying customer for separate ongoing research. The other authors report no relevant disclosures. Full disclosure form information provided by the authors is available with the full text of this article at Neurology.org/cp.