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Brian Springer, MD, Associate Professor, Department of Emergency Medicine, Wright State University, Dayton, OH
Aaron Brooks, MD, Resident Physician, Department of Emergency Medicine, Wright State University, Dayton, OH
Steven M. Winograd, MD, Attending Physician, Mt. Sinai Queens Hospital Center, Assistant Clinical Professor of Emergency Medicine, Mt. Sinai Medical School, Jamaica Queens, New York
• Less than 10% of patients with a concussion have a loss of consciousness.
• Concussion is a clinical diagnosis. It presents with variable neurological symptoms, such as headache, dizziness, and altered judgment following a head injury.
• Many symptoms occur after the initial evaluation. The patient and family should be warned of these and given clear instructions about return to the ED and return to play.
• In the past, patients with a concussion were placed on prolonged rest. Current recommendations include a brief 24 to 48 hours of physical and cognitive rest, followed by progressive return to normal activities, provided the patient remains asymptomatic.
Media coverage of professional athletes experiencing irreversible damage after repeated brain trauma and of the underreported rates and risks of pediatric concussion have heightened awareness surrounding head injury in sports and recreation. Most of the studies prior to the last two decades focused on boxers and assumed concussion was an accepted risk of the sport. Concussion is now known to be a significant public health issue, with high rates of emergency department (ED) visits and hospitalizations. Much of the current concern surrounding concussions revolves around recognition, early diagnosis, treatment modalities, return-to-play, and prevention of recurrent concussions. Recurrent concussions are associated with short- and long-term complications.
The definition of a sports-related concussion (SRC) changed as the understanding of traumatic brain injury (TBI) evolved. As a clinical diagnosis, SRC has no single confirmatory diagnostic test or biomarker; symptoms are variable and highly nonspecific. SRC can be defined simply as the immediate and transient symptoms of TBI.1 SRC often is defined as mild traumatic brain injury (mTBI), a term that is vague and lacks a basis in validated criteria. Concussion may be part of the spectrum of traumatic brain injury with less pronounced structural changes or may be a distinct entity resulting from reversible physiologic change.2 Using terms such as concussion, mTBI, and minor head injury interchangeably creates challenges in communicating well with patients, their families, and other practitioners. The Centers for Disease Control and Prevention (CDC) recommends using the term mTBI, although they acknowledge that such terminology may be frightening to the lay person.3 Traditionally mTBI is based on the Glasgow Coma Scale (GCS) score, whereas concussion is a clinical syndrome defined by multiple signs and symptoms that may overlap with mild, moderate, or severe TBI.4
The 2017 Concussion in Sport Group, an expert panel in the field of concussion, most recently defined SRC with the following criteria:
Previously, concussion was diagnosed only when loss of consciousness occurred, and many athletes still believe this is true.5 The Concussion in Sport Group emphasizes that most individuals with concussion do NOT have a loss of consciousness (as few as 9% experience loss of consciousness).
Biomechanically, SRC occurs not from direct trauma to brain tissue causing structural damage, but from shear forces causing diffuse mechanical injury and functional damage. In recently published biomechanical studies, researchers looked at the head impact exposure patterns in various sports. Sensors placed on helmets and players’ heads provided information on the frequency, kinematics, and location of head impact. While they are useful, these studies do not provide data for noncollision sports, nor do they indicate what is happening to the brain itself on impact.2 Impact may cause rotational, compressive, or tensile forces, and may result in a coup or contrecoup injury. The resulting neuronal damage triggers a cascade of excitatory neurotransmitter release, ion influx, membrane depolarization, and cell dysfunction.5,6 No known threshold for injury exists. SRC occurs across various magnitudes of impact. There is no relationship between the magnitude and location of impact and the development of SRC.5
Following impact, disrupted cell membranes release potassium and depolarize, triggering an abnormal feedback loop of depolarization of undamaged cells and increased neurotransmitter release. These excitatory neurotransmitters also result in the accumulation of intracellular calcium, which causes further cell damage through mitochondrial impairment. The massive depolarization also results in a metabolic mismatch, in which mitochondria struggle to meet enhanced metabolic demand. When energy demand outstrips supply, lactic acid production can enhance injury by breaking down the blood-brain barrier. These changes ultimately result in local neuroinflammatory response and alteration in cerebral blood flow and vasoreactivity. The persistence of these cerebral blood flow alterations is thought to be an underlying cause for development of second impact syndrome, which is discussed later in this article.7
Although gross structural changes are not seen in SRC, shear forces resulting from direct blows to the head or from acceleration-deceleration injuries to the neck can cause diffuse axonal injury and microscopic neuronal pathway disruption. Metabolic impairment further potentiates this microstructural damage, worsening cytoskeletal injury. Advanced imaging techniques have linked the volume of these lesions to the presence of long-term neurocognitive and psychiatric symptoms.6,7
Although most patients will make a complete recovery after concussion, a significant minority develop chronic post-concussive symptoms. Estimates vary widely, with anywhere from 10% to 40% reporting physical, cognitive, emotional, and behavioral changes weeks to months after injury.4 Long-term sequelae of repeated impacts and concussions include increased risk of amyotrophic lateral sclerosis, Alzheimer’s disease, Parkinson’s disease, dementia, and chronic traumatic encephalopathy. Neuroinflammation is present in the pathophysiology of these diseases. Persistent, sustained inflammatory response, especially in the setting of repetitive injury, may play a role in the development of permanent neurologic pathology.4,7
The incidence of TBI and SRC is increasing because of greater awareness and the increased power and strength of athletes.4 Estimates are variable because of a lack of a gold standard definition and diagnostic test, and underreporting by athletes and coaches. CDC estimates of TBI come from administrative claims databases, using patient samples from ED visits and inpatient stays. This fails to capture those seen in primary care offices or other care settings. Other surveillance systems attempt to capture data from school and non-school-based sports and recreational activities, but cannot capture all concussions.5,8
The estimated incidence of TBI-related ED visits, hospitalizations, and deaths in the United States alone ranges from 1.5 million to almost 3 million annually.5,8 Sports-related brain injuries affect between 1.6 million and 3.8 million people annually, accounting for approximately 10% to 15% of all sports-related injuries and about 7% of all sports- and recreation-related ED visits.5,8 Age-adjusted rates of SRC have demonstrated a more than 100% increase during the past two decades.8
Children and adolescents younger than 19 years of age comprise more than 70% of ED visits for SRC, with the highest incidence between 12 and 17 years of age. Males make up the majority of patients, accounting for 77% of all sports- and recreation-related ED visits and between 55% and 60% of SRC visits.6,8,9 Diagnosing concussion in the ED in pediatric patients is challenging and likely underrepresents the true incidence. In younger children, especially those younger than 10 years of age, accidents during activities of daily living and recreational play are common mechanisms of injury.10 The incidence of pediatric SRC likely will continue to rise, as all 50 states have legislation mandating evaluation and clearance by a healthcare professional before return to sport.6
The highest incidence of concussion occurs in contact sports, with football, ice hockey, and wrestling topping the list. Among ED visits for sports- and recreation-related TBI, more than 20% of visits are related to football.8 Linebackers sustain the most concussions among defensive players, while running backs sustain the most on offense. Concussion rates are significantly higher during games than during practice, although practices are a major source of concussion. High school and college football players are at the greatest risk for concussion during practice, although this likely relates to more practice days compared to youth football.8,11 Among gender-matched sports, such as soccer, basketball, softball, and lacrosse, females have similar or higher rates of concussion compared to males, especially at the high school level. Possible explanations include anthropometric differences, such as neck muscle strength, and level of preparation, as well as increased reporting by female athletes.5,8
Surprisingly, there are limited data on the incidence of concussion in professional athletes. The National Hockey League (NHL) and National Football League (NFL) report concussion rates of 1.8 and 6.43 per 1,000 athlete exposures, respectively.5 In a 2018 systematic review of concussion in team sports, researchers found the highest “concussion incident density” (defined by concussion incidence per 1,000 hours and 1,000 athlete exposures) in rugby, and the lowest in soccer. They found a wide variance across context (with matches imposing greater risk than training) and sex (with females at higher risk than males in ice hockey and soccer.)
Clinicians should maintain a high degree of suspicion for SRC when evaluating any patient who presents with a complaint of head trauma. Since concussion results from a disruption in the neural network, the range of potential symptoms is broad, and the corresponding duration and severity are highly variable. In addition, symptoms may alter over time, making surveillance of symptom resolution challenging. SRC symptoms can be nonspecific, and patients’ preexisting conditions can cloud the overall picture. For example, factors such as patient age, previous head trauma, time from injury, history of psychiatric disorders, cognitive behavioral disorders, as well as generalized learning disabilities may affect the clinical presentation of SRC and make diagnosis challenging.13 It is important for the clinician to try to connect symptom onset with an episode of known or suspected physical trauma, as well as an appropriate mechanism of injury.14
It is helpful to break down the signs and symptoms of concussion into broad categories listed in four global frameworks. These are the physical, cognitive, emotional, and sleep-associated signs and symptoms summarized in Table 1.
Loss of consciousness, prolonged altered mental status, focal weakness or numbness, cranial nerve deficits, slurred speech, intractable vomiting, and evidence of increased intracranial pressure (abnormal pupil size or reactivity, papilledema, seizure-like activity) linked to an episode of head trauma should raise concern for more significant TBI. In very young children, it is also important to look for more subtle findings, such as poor oral intake or inconsolability, as indicators of more significant trauma.15,16,17
Many symptoms associated with concussions start within minutes to hours after the initial incident, although delayed presentations of symptoms can occur.13 Symptoms such as headache, nausea, vomiting, memory problems, and confusion can appear in the immediate aftermath of the initial event, while other symptoms, such as sleep disturbance, difficulty concentrating, and emotional instability, may not present until the individuals attempt to return to their regular daily activity days or even weeks later.17
Headache and dizziness are two of the most common presenting symptoms of SRC. The symptoms fit the “physical” context noted in Table 1, and often are the initial presenting symptoms after an SRC.13 Other physical signs and symptoms include visual problems, sensitivity to light and sound, nausea and vomiting, and numbness and tingling.
The most commonly reported symptom following an SRC is headache.18,19 Interestingly, the presence and severity of headache do not correlate with the severity of injury; there is a higher incidence of headache following concussion when compared with more severe TBI.20 Headache associated with a loss of consciousness or an altered level of consciousness, focal neurologic deficits, pain that is progressive in severity, intractable vomiting, and headaches that worsen with changes in the patient’s position may indicate a more severe or structural injury. Other important aspects associated with headache are the timing of the headache in relation to the injury, severity, associated light or sound sensitivity, diffuse or point pain, palpable tenderness, neck pain, or exacerbating factors such as movement. Headaches that begin days after the inciting event may be related to posttraumatic headache or medication-overuse headache, which can arise from poor initial management or follow-up from SRC.20,21
The next most common symptom with SRC is dizziness.19 Differentiating the exact patient complaint being described as “dizziness” is important. Commonly, the separation has been distinguishing between the sensation of the room spinning, or vertigo, and lightheadedness, which is best defined as pre-syncope. The clinician should attempt to differentiate between true vertigo (the sensation of movement while remaining stationary) from disequilibrium, in which balance is impaired. Vertigo most often is secondary to peripheral causes (inner ear dysfunction), whereas even subtle disequilibrium may indicate central neurologic dysfunction due to SRC.22 Children who present with SRC may use the term “dizzy” to describe feelings of anxiety or fear.
Cognitive deficits are a common presenting symptom on initial evaluation after an SRC, and may persist for weeks to months after the initial insult. However, in some patients, cognitive symptoms may not begin to manifest until days to weeks after SRC has been diagnosed.13,20 Common symptoms in this context include difficulty concentrating, memory deficits, decreased mental acuity, and difficulty expressing speech. Anterograde amnesia is the most commonly seen memory deficit.20 Cognitive findings may be subtle and can be clouded by a patient’s pre-existing conditions, such as attention deficit hyperactivity disorder (ADHD), autism, and developmental delays in younger patients, or by dementia in older populations.17 The CDC recommends a detailed patient evaluation for athletes prior to their athletic season to help establish a baseline and increase the sensitivity for detection of subtle cognitive symptoms that may indicate SRC.15,16
Emotional and sleep symptoms tend to develop later, or at least are noticed later, in the course of the SRC process.17 As with cognitive changes, this often requires detailed information gathering both from the patient and from those who witness the patient’s behavior on a daily basis (friends, family). Patients who present for evaluation in the ED may not have developed these symptoms yet, or the symptoms may be subtle. Inform patients and their caregivers that these symptoms may develop, and that it is important for them to communicate those changes to the providers who are tracking their recovery. A clear follow-up plan with a clinician who has an understanding of SRC management and, when appropriate, with concussion or sports medicine specialists, is important. Patients should be informed of the signs and symptoms of SRC. They should be encouraged to document and share these changing findings with their long-term care team.
The most immediate risk to an athlete is sustaining a repeat concussion. Collegiate football players with an initial concussion had a significant risk of sustaining repeat concussions within the same season. Most of these occurred within 10 days of the initial injury.23 Whether subsequent SRCs are associated with increased symptom severity or increased time to resolution is controversial.5,23 Concussed athletes appear to be at increased risk for experiencing lower extremity musculoskeletal injury after return to play.24,25 This finding has been noted in both male and female athletes up to three months after the initial SRC, although the true duration of this increased risk is unknown. Possible explanations include neurocognitive and motor control issues that extend beyond apparent clinical resolution and may not be detectable by current clinical tests. Alternately, the finding simply may reflect a more aggressive style of play. In a study in the British Medical Journal, researchers found that regardless of the sport or athlete’s sex, athletes who sustained a concussion had an equally higher risk of injury both before and after concussion. They concluded that certain athletes display risk behaviors that increase the risk of concussion, and that athletes who sustain concussion have a generally increased risk of sports injury.26
Repeat concussions are associated with a host of long-term complications, although strong studies are lacking. These complications include problems with memory and concentration, chronic headaches, and increased risk for developing depression, anxiety disorders, and dementia. Chronic subconcussive impacts that do not result in immediate symptoms may trigger the same pathologic neurometabolic cascade seen with greater impacts. Cumulatively, these impacts can result in neurodegeneration and are associated with the development of chronic traumatic encephalopathy (CTE).5 First identified in boxers, this syndrome of chronic and progressive neuropsychiatric symptoms had multiple labels over the years, including punch-drunk syndrome, traumatic encephalopathy of professional pugilists, and dementia pugilistica. CTE now is the preferred term.27
The typical age of onset for CTE is 30 to 65 years of age, with a somewhat slower onset than Alzheimer’s disease. Behavioral changes are seen first, with poor impulse control, aggressive and explosive behaviors, apathy and depression, and an elevated suicide risk. Cognitive changes follow, with memory impairment, decreased attention span, and poor executive decision-making. Motor symptoms, such as dysarthria, ataxia, and parkinsonism, come with late-stage disease. The clinical diagnosis remains challenging because of a latent period prior to symptom development, and definitive diagnosis requires pathologic confirmation.27 The literature on the long-term risks of repetitive head trauma remains inconsistent, and the incidence of CTE in athletic populations is unknown.2
Persistent symptoms following SRC occur in a significant minority of patients. The Concussion in Sport Group recommends that “persistent symptoms” be used to describe a failure of normal clinical recovery, with symptoms that persist for more than 10-14 days in adults and more than four weeks in children.2 The expert panel recognizes that this definition does not describe a single pathologic entity, but rather symptoms linked to coexisting or confounding factors that do not necessarily reflect ongoing injury to the brain.
The term postconcussion syndrome (PCS) is defined by ICD-10 as organic and psychogenic disturbances following closed head injuries, with at least three symptom categories occurring within one month of injury. These categories include somatic symptoms such as headache or dizziness, emotional symptoms such as irritability or depression, cognitive symptoms such as concentration and memory impairment, insomnia, and decreased alcohol tolerance. Estimates of the true frequency of PCS vary widely, from 10% to as much as 62.5% of patients following a mild traumatic brain injury or SRC.4,27 No single factor, such as age, gender, prior concussion history, loss of consciousness or amnesia at time of injury, or history of chronic headaches, has been identified clearly as an independent predictor of prolonged symptoms. Clinical scores applied to patients in the ED show only modest discrimination in stratifying risk of PCS. However, greater symptom burden early (within the first one to two weeks) does appear to predict increased risk of prolonged recovery.28,29 Posttraumatic headaches are the most common refractory symptom. Other possible diagnoses include cervical injury, vestibular dysfunction, depression, somatization, and malingering. Management of PCS is multidisciplinary, including neuropsychiatric evaluation and therapy, structured and closely monitored exercise programs, and, when prolonged symptoms negatively affect quality of life, pharmacologic interventions.4,27,30
Second impact syndrome (SIS) is a rare but catastrophic condition that occurs when an athlete who has experienced a mild SRC sustains a second head injury prior to full recovery. Following the second injury, which often is minor, the athlete’s condition rapidly deteriorates, with subsequent collapse, coma, rapidly dilating pupils, loss of eye movement, and respiratory failure. SIS most commonly affects young male athletes between the ages of 10 and 24 years, with those younger than 18 years at greatest risk. The condition often is fatal, and those who survive have severe neurologic disability. American football has the greatest association with the development of SIS. The sport’s popularity among young males with their increased risk-taking behaviors and tendency to underreport concussion may account for the demographics of this entity.27,31,32 The pathologic mechanism of SIS is believed to be a loss of cerebral vascular autoregulation, with resultant brain edema, increased intracranial pressure, and herniation. Decompensation and clinical deterioration occur rapidly, with brainstem failure occurring in less than five minutes from the time of impact.31
There is controversy surrounding SIS and whether it truly exists as a unique clinical syndrome. Researchers question whether the edema is from a second hit or simply is a progression of the primary injury; the maximum time range between the first and second hits; how the presence of intracranial hemorrhage relates to SIS risk and development; and why the incidence of SIS is highest in the United States as opposed to other countries.32 Reviews of the literature have found varying definitions and reported mortality rates for SIS, and they conclude that there is not sufficient high-quality evidence to support a diagnosis of SIS that would be consistent with the World Health Organization and ICD-10 clinical case definitions.33,34 Until more is known, physicians, trainers, coaches, and athletes should continue to be conservative and avoid return to play while still symptomatic. Athletes who collapse on the field require immediate evaluation, airway and breathing support, and rapid transport to the ED. When SIS is suspected, computed tomography (CT) is the initial imaging modality of choice to look for evidence of cerebral edema, herniation, or the presence of acute hemorrhage that may require neurosurgical intervention.27,31
Despite continued interest and research, the diagnosis of SRC remains a clinical one, with no clear imaging or laboratory confirmation. The key components of the clinical diagnosis are a properly performed history and physical exam with emphasis on the signs and symptoms consistent with SRC.2,20 Although clinicians should maintain a high degree of suspicion for SRC when evaluating head trauma, conditions with an immediate threat to life and limb should be ruled out first. These include cervical spine fracture, skull fracture, and intracranial hemorrhage.35,36
The initial evaluation for SRC likely will occur on the field or sideline of an athletic event. The top priority is determining who needs to be transferred to the ED for further care and who can be managed in the outpatient setting.37 The first step is evaluating level of consciousness. If the athlete is unconscious, he or she should be managed with the assumption of a significant intracranial or cervical spine injury.3 The GCS has prognostic value in moderate to severe brain injury and provides a baseline neurologic examination that facilitates reassessment.35,36 The athlete should be evaluated for confusion, lethargy, somnolence, significant changes in behavior such as irritability, or the inability to recognize previously known faces or locations. Other signs and symptoms that should prompt emergency medical services (EMS) transport include a new focal neurologic deficit, posttraumatic seizure, cervical spine tenderness, evidence of skull fracture (mastoid ecchymosis, eyelid hematoma, or bloody otorrhea), slurred speech, difficulty ambulating, severe or worsening headache, or recurrent vomiting.2,35,36,37
On arrival to the ED, an important decision point is if the patient requires neuroimaging.19 CT of the head without contrast is the primary imaging study for evaluating head trauma in the ED. Although CT can effectively evaluate for skull fractures and intracranial bleeding, it is unable to detect either the axonal injury or microscopic neuronal pathway disruption that occurs in SRC.35,38 Magnetic resonance imaging (MRI) with associated advanced techniques such as diffusion tensor, functional, spectroscopy, and perfusion imaging has more sensitivity for subtle white matter lesions that may be present in SRC. Obtaining advanced imaging is a cost- and time-intensive process and may not be readily available in many medical centers. The information gleaned from such testing does not assist in the immediate evaluation and prognostication of SRC. Therefore, the actual clinical usefulness of specialized MRI remains controversial, and its routine use in the evaluation of SRC is not currently recommended.38,39,40 The American Academy of Neurology guidelines for concussion management currently recommend CT imaging for evaluation only in the presence of loss of consciousness, posttraumatic amnesia, persistent GCS score less than 15, focal neurologic deficit, evidence of skull fracture on examination, or signs of clinical deterioration. (See Table 2.) The American Medical Society for Sports Medicine currently recommends imaging when there is concern for intracranial hemorrhage.39 Several clinical decision instruments have been developed to help guide when to forgo imaging. In adult patients, the American College of Radiology currently recommends the use of either the New Orleans Criteria, Canadian CT Head Rule, or the National Emergency X-ray Utilization Study (NEXUS II) to help guide the decision. There are also multiple decision instruments created specifically for use in children. These include the Children’s Head Injury Algorithm for the Prediction of Important Clinical Events (CHALICE), Canadian Assessment of Tomography for Childhood Head injury (CATCH), and Pediatric Emergency Care Applied Research Network (PECARN).40
Once immediate threats to life and limb have been ruled out, the evaluation to determine the presence and severity of SRC can proceed. While the setting may be different, many of the aspects between the evaluation performed on the sideline and in the ED are similar. If they have been completed already in the field, it may be beneficial to repeat them. This provides information on improvement or deterioration of the patient, as minutes to hours may pass from the time of injury to initial ED evaluation.19
The historical aspect of SRC should emphasize the mechanism of injury. Specifics should include the setting in which the injury occurred, the areas of impact, the safety equipment that was in use, and details of any initial evaluation by athletic training staff. Details of the initial evaluation, such as abnormal behavior, neurologic deficits, or loss of consciousness, should be elicited. The clinician should ask about history of prior head injury, history of other medical or behavioral diagnosis, and any current medication or drug use.19,35,37,38 The patient history should be corroborated by family members or training staff, since the patient may not fully remember the event or may not fully comply with the examination because of concern about being held out of future athletic events.41
Head and cervical spine trauma can cause autonomic dysregulation, which can lead to orthostatic hypotension. Orthostatic vital signs with a decreased blood pressure (BP) and increased heart rate (HR) are more consistent with hypovolemia, while a decreased BP without an increased HR is more consistent with a neurogenic cause.42 An accurate core temperature should be obtained, especially in the setting of an athlete coming from the field. Exertional heat stroke (elevated core temperature plus altered mental status) is a time-sensitive and life-threatening emergency that needs to be recognized and treated immediately.19 SRC can affect a patient’s cognitive and behavioral function, so a mental status examination addressing orientation, attentiveness, concentration, short-term and long-term memory, mood, and affect should be performed. The neurological examination should include cranial nerve assessment, sensation and strength testing, cerebellar testing such as rapid alternating movement and finger to nose, and gait and balance evaluation.2,25,42 A tool that can assist with balance evaluation is the Modified Balance Error Scoring System (mBESS). The mBESS compares single and double leg stance and notes the amount of balance errors, giving a standardized method to evaluate balance abnormalities.43 Up to 40% of patients with SRC have some form of visual complaint, and a visual exam emphasizing extraocular movements and oculomotor tracking, pupillary response, accommodation, and convergence can help elucidate some subtle findings in SRC.42 Additionally, patients should be evaluated for the presence of nystagmus. While horizontal unidirectional nystagmus can be a normal finding, the presence of vertical or asymmetric nystagmus in the context of head trauma may be an indication for diagnostic imaging.42
Multimodal evaluation tools have been developed to assist providers in the evaluation of SRC. The Sports Concussion Assessment Tool (SCAT) series, with SCAT5 the most recent iteration, is an example of one such tool, and is currently one of the most thoroughly tested tools of its kind.2,44 The SCAT tools are designed for use by physicians or licensed medical professionals such as athletic trainers. It includes sections for immediate/on-field evaluation, as well as for an office/off-field examination, which can be used in the ED, clinic, or training room setting. SCAT5 alerts initial providers to red flag signs and symptoms, such as focal neurologic deficit, neck pain, loss of consciousness, and vomiting. On-field evaluation includes a GCS score calculator, memory assessment test, and cervical spine screening. Off-field evaluation includes prompts for asking athletes about medical history and previous head trauma. SCAT5 includes a Standardized Assessment of Concussion (SAC) tool that evaluates neurologic status, orientation, memory and concentration, and balance. SCAT5 gives clear instructions on how to perform each aspect and provides guidance on rest, follow-up, and return-to-activity. Although it is not recommended as a stand-alone diagnostic tool, SCAT5 is a convenient and readily accessible means of assisting in the diagnosis and management of SRC.2,36
The King-Devick (KD) test can be performed on the sideline and evaluates saccadic eye movements by showing cards with numbers at varying intervals. Current research on KD has shown that visual scanning ability decreases in the setting of SRC, but more research is needed.45 Video analysis, computer- and tablet-based diagnostic tools, as well as long-distance neurologist evaluation or “teleconcussion” show promise in the early and accurate diagnosis of SRC.46,47,48 Perhaps one of the most anticipated aspects of current research is the use of biomarkers to detect SRC and determine the severity of injury. Biomarkers associated with axonal and astroglial injury, including tau, ubiquitin C-terminal hydrolase 1, glial fibrillary acidic protein, and S100 calcium binding protein B, currently are being studied. While these are important research tools, further study is needed to determine their clinical utility.2,38
The focus of management for SRC is improving symptoms and preventing reinjury.2 The historical cornerstones of management in SRC have been physical and cognitive rest until symptoms resolve.19 Recent literature has suggested that strict rest until complete symptom resolution may not be beneficial, and that levels of activity based on symptomatic tolerance may be better for patients.49 Physical and cognitive rest should start as soon as concern for SRC exists, including removal from the current activity such as a sporting event. The initial rest period should last 24-48 hours until a stepwise protocol is enacted for return to cognitive and sports activities.13
Physical rest is easy for patients and their families to understand, since there is discussion regarding SRC management in popular culture. The initial step is removal from all symptomatic activity. A full description of the complications that can occur from reinjury and the possible progressive nature of symptoms may be necessary to convince patients, families, and coaches about the severity of the situation and the importance of compliance.2,41 After the initial rest period of 24-48 hours, an active rehabilitation period begins that is personalized to the patient’s specific symptoms and prior activity level.35 This period includes a progressive increase in exercise limited by the patient’s symptomatic threshold, as well as possible physical, vestibular, or visual therapies until the patient returns to asymptomatic baseline.2 Although the initial rest period is important, initiating activity within seven days, and in some instances sooner than that, has been shown to be beneficial and to reduce the risk of persistent symptoms, as long as the risk of reinjury is minimized.35,50,51 A specific return-to-play protocol is discussed in the next section.
Cognitive rest may be more difficult for patients and their supporters to grasp and implement. Many activities that patients may think of as restful may be quite stimulating when considering SRC. For example, in the initial rest period of 24-48 hours, screen time (including televisions, gaming systems, and personal mobile devices) should be limited.15,52 Cognitive rest requires communication with the patient’s teachers to reduce cognitive demands during educational activities. Few guidelines exist for return to academics. Just as in physical activity, research suggests that moderate amounts of early cognitive stimulation after the initial rest period are beneficial. This often requires educators to be creative in meeting but not exceeding symptomatic thresholds, such as giving patients multiple cognitive and visual breaks throughout the day, reducing or eliminating classwork or homework, and extending time to completion for projects. Just as with physical rest, much of the direction for returning patients to baseline educational activities should be based on symptomatic thresholds, and the same priority of communicating an initial SRC with athletic staff should occur with educators.25,51,52
The cornerstones of SRC management are rest and progressive activity, but many patients who present to the ED after an SRC may require immediate symptomatic treatment.20 Expert consensus states that early treatment of post-SRC headache may help prevent persistent headache. Common initial treatments include acetaminophen, naproxen, or ibuprofen, with nonsteroidal anti-inflammatory drugs (NSAIDs) given once intracranial pathology has been ruled out.14 Research suggests that post-SRC nausea and vomiting can be treated with ondansetron without significant risk of masking other worrisome conditions. Amantadine, a dopamine agonist, is a potential treatment for persistent SRC-related symptoms, but research is ongoing, and its use in the ED setting is limited.53,54
A key component to ED management of SRC is coordinating appropriate follow-up with outpatient providers; providing educational material to parents and caregivers about return precautions, symptom monitoring, and strategies for care at home; and synchronizing active recovery plans with athletic and educational staff.52 Some facilities may have protocols in place to initiate a plan when a patient is evaluated in the ED, but many facilities require the patient’s direct caregivers and primary care physician to be the main facilitators of a recovery plan. Clear communication with these parties should be made a priority.50,52
Neuropsychological (NP) assessment can be a useful adjunct means of monitoring recovery, especially in cases in which cognitive recovery either precedes or lags behind symptom resolution. Ideally, NP assessment is performed by a neuropsychologist, who is uniquely trained and qualified to interpret the tests and detect subtle abnormalities. Early access to such specialists often is limited. Many high schools, colleges, and professional sports teams use computer-based NP assessment, such as ImPACT, to help guide return-to-play decisions. ImPACT shows good convergent validity when compared to more formal NP assessment.55 However, studies suggest that this test does not correlate with time missed from sport following concussion, and it should not be considered a substitute for a complete NP assessment.2,56,57 NP assessment should never be used in isolation to make management decisions, but rather should be part of an overall assessment.
Once the patient is clinically asymptomatic, NP testing can track recovery of more subtle cognitive deficits. The findings can be used to help educate the athlete, parents, and coaches on the severity of the injury. As noted, the ultimate return-to-play decision is made based on a multidisciplinary approach. If NP and other testing is not available, clinicians should consider a more conservative approach for return to play.2
The range of physiological measures studied following SRC is broad and variable in method of measurement, time to recovery, and clinical significance, with no single measure able to determine an actual time window for recovery. The data suggest that physiologic recovery often extends beyond the recovery of clinical signs and symptoms. As a result, it is suggested that a gradual increase in cognitive and physical activity serves as a buffer zone between symptom recovery and return to full-contact sport.58 Return-to-play (RTP) decisions should be made by providers who are trained in SRC management and must take into consideration the injury severity, clinical progress, and recommended RTP protocols. RTP protocols may come from league and state regulations and may limit who can make RTP decisions. Most states now have recommended RTP protocols, all of which prohibit same-day RTP after a suspected concussion.35 In general, postinjury management and RTP require a careful balance of rest and active treatments. Both too much activity and strict rest may impede recovery from SRC. While a brief period (24-48 hours) of physical and cognitive rest is appropriate following SRC, moderate amounts of closely supervised, gradually increased cognitive and physical activity appear to be beneficial in the recovery process, especially in the athletic population.59,60
The CDC and the Concussion in Sport Group recommend a six-step RTP protocol. (See Table 3.) The athlete follows the initial rest period with daily physical and cognitive activities that stay below the threshold of symptom exacerbation. Once concussion symptoms have resolved, the athlete advances to the next step of increased activity. At each stage, if activity is tolerated without symptom exacerbation, the athlete may proceed to the next stage in 24 hours. This means that RTP requires a minimum of one week to proceed through the entire protocol. If at any stage the athlete has a recurrence of concussion-related symptoms, he or she moves back to the previous stage and can attempt to progress after a 24-hour symptom-free period. Resistance training should be deferred until stages 3 or 4 at the earliest.2,61 Athletes who have prolonged symptoms that impede their ability to progress should be referred to a specialist (neurologist or neurosurgeon) with expertise in concussion management. For adults, 10-14 days of symptoms should prompt referral. Children have longer recovery times, and a more gradual RTP strategy is appropriate, with persistent symptoms greater than one month prompting referral.2,3
Graded RTP protocols have become generally accepted by the medical community as the standard of care for management of SRC. However, the literature lacks comparative, prospective, randomized controlled trials evaluating outcomes and repeat injury risk, and existing protocols lack validation studies.59 In addition, RTP protocols for athletes with multiple concussions or prolonged symptoms are less established, and season-ending or even career-ending decisions are highly individualized. Prolonged symptoms, multiple concussions in a season, decreased athletic or cognitive performance, and abnormal imaging studies are potential indications for ending a season. Lowered concussion threshold (experiencing a concussion from a progressively less forceful injury), prolonged postconcussive symptoms, intracranial hemorrhage, and persistent imaging abnormalities are potential indications for ending a sports career.35
Financial Disclosure: To reveal any potential bias in this publication, and in accordance with Accreditation Council for Continuing Medical Education guidelines, we disclose that Dr. Farel (CME question reviewer), Dr. Schneider (editor), Dr. Stapczynski (editor), Ms. Light (nurse planner), Dr. Springer (author), Dr. Brooks (author), Dr. Winograd (peer reviewer), Ms. Mark (executive editor), Ms. Roberts (associate editor), and Ms. Coplin (editorial group manager) report no financial relationships with companies related to the field of study covered by this CME activity.