Authors: Mara S. Aloi, MD, RDMS, Assistant Professor of Emergency Medicine, Drexel University School of Medicine, Program Director, Emergency Medicine Residency, Allegheny General Hospital, Pittsburgh, PA; and Brian Rempe, MD, Assistant Professor of Emergency Medicine, Drexel University School of Medicine, Assistant Program Director, Emergency Medicine Residency, Allegheny General Hospital, Pittsburgh, PA.
Peer reviewer: John P. Santamaria, MD, Affiliate Professor of Pediatrics, USF School of Medicine, Tampa, FL.
Traumatic brain injury (TBI) is an important public health problem. It has the potential for long-term complications with persistent morbidity, and also can result in missed school and workdays. The medical literature is replete with studies defining the management of moderate to severe TBI, but much controversy still exists concerning the management of mild TBI. Most of the literature deals with adult patients; therefore, less is known about mild TBI in children.
Some of the problems that may result from a concussive injury are subtle and are often missed or attributed to something else, such as psychogenic factors. This can result in further injury when a child is prematurely allowed to return to play.
With nearly 60% of all high school students in the United States participating in organized sports, there is a huge population at risk for concussive injury.1 The rate of hospital admission for children with mild TBI has been decreasing despite increases in estimated rates of emergency department visits for TBI.2 This suggests that the burden of managing these cases is being shifted toward emergency physicians and other healthcare providers in outpatient settings. It is crucial that acute care providers accurately identify pediatric patients with mild TBI who may be at risk of developing the symptoms of postconcussive syndrome (PCS).
Much of the literature on concussion indicates significant underdiagnosis and underreporting.3 It is estimated that 1 million cases occur annually, with 80-90% being classified as mild TBI.4 According to the Centers for Disease Control and Prevention, more than 500,000 pediatric TBI patients are treated and released annually.5 It is estimated that an additional 250,000 cases are seen in outpatient, non-hospital settings. It is unknown how many patients never seek medical attention because they deem their injury to be mild, even though they may have suffered a concussion. Patients with mild cases may not seek medical care if they do not experience any limitation of daily functioning;6 thus, their cases may go unreported. In one self-report study, many athletes described concussive injuries without realizing they had sustained a concussion.7 Even if patients do present for care, many healthcare providers rely on the Glasgow Coma Scale for assessment; this tool is insensitive for mild cases of TBI. Therefore, the true incidence of mild TBI and PCS is unknown.
The highest-risk sports for TBI and PCS are boxing, football, hockey, wrestling, and soccer.8 More than 60,000 high school athletes suffer PCS injuries each year.9 The majority of these are football players. In almost every age group, the incidence of concussion is higher in males than in females, but this gap is narrowing as more females join organized sports.
The term "postconcussion syndrome" was first used in 1934 to describe the "subjective post-traumatic syndrome due directly to the blow on the head."10 Since that time, much discussion and controversy has arisen concerning attempts to further delineate and categorize this disease process. The word "concussion" refers to mild TBI that is caused by an impact or jolt to the head. All concussive injuries involve rotation, acceleration, and/or deceleration forces that result in stress to brain tissue and associated vascular and neural tissues.11 Concussion also may result from a direct blow elsewhere on the body from which force is transmitted to the head.12 The exact mechanism of injury will depend on the sport or activity. In animal models of concussion, changes include neuronal depolarization; release of excitatory neurotransmitters; and impairment of glucose metabolism, axonal function, and cerebral blood flow.13,14
Although there are more data on adult patients, several interesting findings have been published on the unique characteristics of the pediatric brain. In the past, it was believed that the pediatric brain was more resilient and could more easily recover from injury than the adult brain. However, it has been discovered that the immature brain is actually more vulnerable to injury.
The developing brain is 60 times more sensitive to glutamine-mediated N-methyl-D aspartate (NDMA) excitotoxic brain injury.15 This NDMA-hypersensitivity may make the young brain more susceptible to injury from excitatory amino acids (EAAs), which are present after brain trauma. The injury induced by these EAAs results in post-traumatic dysautoregulation and a subsequent decrease in cerebral blood flow. These effects may not be seen until 2-3 days after injury and may persist for up to 1 week. It is during this period, when the brain is hypersensitive and autoregulation has not normalized, that the brain may be more vulnerable to another concussive injury. In fact, previous injury has been shown to impart a 3- to 6-times higher risk of sustaining a subsequent concussion.16,17
The pediatric brain may be more prone to diffuse and prolonged cerebral edema after injury than the adult brain.1,18 This may result in a longer recovery time and render the child susceptible to more severe damage or permanent deficit if another injury occurs while edema is still present. More protracted recovery rates have been reported in high school athletes suffering from PCS than in college athletes, suggesting that younger athletes take longer to return to baseline.15
The significance of head injury also may be greater in children because their young brains are still developing skills. Impact to areas of the brain important for skill acquisition is more likely to affect developing skills than well-established ones. Injury in preschool-age children (< 5 years) may be even worse because this age is critical for the development of many important skills. Research has shown that mild TBI in preschool children may affect their ability to learn to read.19 Early diagnosis of injuries in these children may allow for early intervention that focuses on these affected skills, as well as teacher notification. Normal neurobehavioral and neurobiological development may depend on a precise balance of chemical and anatomic factors, so any derangement of these factors may have serious consequences. The hippocampus is especially sensitive to repeated injury, which may account for memory disturbance seen after concussion.20
There may be a chemical and biological basis for the development of PCS. The apolipoprotein E epsilon-4 (apoE) gene has been implicated as a susceptibility gene for Alzheimer's disease. This gene is involved with neuronal repair and antioxidant activity and has been associated with poor outcomes after TBI.12 The apoE gene has been shown to be a risk factor for chronic traumatic encephalopathy in boxers.21 Despite this evidence, there is no role at present for routine genetic screening as part of sports physicals. Pre-morbid behavioral disorders (such as attention-deficit/hyperactivity disorder) may affect vulnerability to concussion as well.4 There is some evidence that greater force is required to bring about symptoms after TBI in children.22,23 Fortunately, younger athletes are smaller in size and in strength than their adult, professional counterparts, which reduces the force of collisions.
Clinical Features of Concussion. Clinical features associated with concussion vary significantly. Detecting the often subtle signs and symptoms is important to the clinician as there are no objective radiographic tests to diagnose a concussion. Recognition is particularly important in sports, where a re-injury could result in postconcussive syndromes or the second impact syndrome, which involves a second head injury while the patient is still symptomatic from the original injury. The second impact syndrome, addressed more thoroughly later in this discussion, is rare but can lead to devastating outcomes that include brain damage and death.
Currently, the American Academy of Neurology (AAN) defines concussion as "a trauma-induced alteration in mental status that may or may not involve a loss of consciousness."24 These alterations cause a spectrum of signs and symptoms that can be divided into three categories:1,25,26
Somatic: headache, fatigue, sleep disturbance, nausea, visual changes, tinnitus, dizziness, balance problems, light/noise sensitivity.
Emotional/Behavioral: lowered frustration tolerance, irritability, increased emotional lability, depression, anxiety, clinginess, personality changes.
Cognitive: slowed thinking or response speed, mental fogginess, poor concentration, distractibility, memory/learning difficulty, disorganization, problem-solving difficulties.
Two commonly used diagnostic guidelines come from the International Classification of Diseases, 10th revision (ICD-10) and the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV). The ICD-10 criteria are: history of TBI plus three of the following eight symptoms: headache; dizziness; fatigue; irritability; insomnia; intolerance of stress, emotion, or alcohol; difficulty concentrating; and memory impairment.
Critics of this method fault the lack of requirement of objective cognitive deficit or exclusion of other disorders.27
The DSM-IV criteria require a history of TBI causing "significant cerebral concussion" and:
1) cognitive deficit in attention or memory;
2) the presence of at least 3 out of 8 symptoms (fatigue, sleep disturbance, headache, dizziness, irritability, affective disturbance, personality changes, apathy) that appear after injury and last > 3 months;
3) symptoms that begin or worsen after injury; and
4) interference with social role functioning.
The DSM-IV also requires the exclusion of dementia or other disorders that might account for symptoms.
Unfortunately, there is limited agreement between the DSM-IV and the ICD-10 criteria. For example, in one study, only 17% of patients who met the criteria for PCS using the ICD-10 set also met the DSM-IV requirements.27 When healthcare workers have multiple diagnostic criteria sets to choose from, with varying inclusion criteria and reliability, the result may be inaccurate classification of patients.
The symptom pattern seen after concussive injury is multifactorial. The mechanism and force of injury, as well as the patient's genetic makeup/susceptibility, gender, previous injury history, preexisting conditions/learning difficulties, psychiatric status, and psychosocial factors, all contribute to the severity and duration of symptoms.28-30 This is where much of the controversy regarding the diagnosis of PCS arises. Some authors believe that symptom-based diagnosis may include those with pre-injury symptoms, malingering, or post-injury psychological factors that may exacerbate symptoms.4 Many of the criteria listed above are subjective and nonspecific. Patients and their parents can report these complaints even in the absence of history of brain trauma, leading some authors to question the validity of diagnosis based purely on reported symptoms.31 The symptom expectation factor cannot be underestimated. Parents of head-injured children are up to 3 times more worried about "brain damage," which may result in unintentional false reporting of PCS symptoms. Even if symptoms exist, are they attributable to the brain trauma or the overall stress from the trauma? At least one study found that symptoms developed with the same frequency in head-injured and non-head-injured trauma patients.31 This calls into question whether objective symptoms specifically related to brain concussion actually exist.
Loss of consciousness was once considered a cardinal feature of concussion, but research has shown it to be somewhat less important clinically.32-35 Particularly in sports-related concussion, post-traumatic amnesia (PTA) is probably more important prognostically.26,36 PTA may be associated with a worse functional outcome. Specific symptoms of depression and cognitive deficits vary significantly based on the duration of PTA. Amnesia of any duration after trauma is associated with a greater incidence of dizziness.37 Asplund and coworkers reported that more than 3 hours of headache, difficulty concentrating, retrograde amnesia, and loss of consciousness may be predictive of a more prolonged recovery.26 Patients experiencing PTA for more than 30 minutes may have a more severe concussion than others. However, determination of the actual duration of PTA is difficult and usually relies on a retrospective account of recent events (obtained by asking the patient how far back he or she can remember). At present, there is no standardized method of determining the duration of PTA.
The Glasgow Coma Scale, a well-known 15-point scale used to assess head injury, is insensitive for detecting milder degrees of impairment. There is a limited role for its use for sideline testing. Computerized testing has some benefit over symptom-report diagnosis because it also can assess reaction time. This has been shown to be very sensitive in detecting mild TBI.38 Several well-validated neuropsychological tests are available as computer models and allow both baseline (pre-injury) and post-trauma testing. This may be a more objective method of evaluating PCS. Many athletic organizations require baseline neuropsychological testing at the start of the season so that after injury, the player can be retested and scores compared with the baseline.
Concussion in Sports, Management on the Sidelines. Concussion is a common occurrence in sports activities. Issues include recognition and sideline testing, management of concussion, and when to allow athletes to return to play. This is still the subject of much debate and controversy. Several sets of guidelines have been presented that are meant to grade concussions and then direct return-to-play decisions accordingly.39 However, there is no universally accepted grading system, and no guideline has been scientifically established. Lovell and co-workers wrote, "At the current time, there is no consensus on the definitive diagnosis of concussion, parameters regarding return to sport participation following injury and the short-term and long-term neurologic consequences associated with concussion."27 This has led to the general rule: "When in doubt, sit them out."1
Three of the most commonly used guidelines are discussed. (See Table 1.) It should be mentioned that these guidelines are generalized to all genders, ages, and levels of skill. A "one-size-fits-all" application of these guidelines does not take into account the differences between the pediatric and adult brain.
Cantu published sport-related concussion guidelines in 1986. The symptoms measured in his guidelines include loss of consciousness and post-traumatic amnesia.40 He, as well as those publishing later guidelines, divides concussion into three grades based on severity. Grade 1 involves no loss of consciousness and post-traumatic amnesia lasting less than 30 minutes. Grade 2 involves a loss of consciousness for less than 5 minutes and amnesia of more than 30 minutes but less than 24 hours in duration. Grade 3 involves post-traumatic amnesia lasting more than 24 hours or loss of consciousness for more than 5 minutes. Later, Cantu created another set of guidelines including assessment based on the duration of concussive systems other than amnesia, including loss of consciousness and confusion.15
In 1991, the Colorado Medical Society published guidelines again utilizing amnesia and loss of consciousness. Grade 1 concussions involved transient confusion without PTA or loss of consciousness. Grade 2 added PTA, and Grade 3 involved any loss of consciousness.41
The AAN guidelines, published in 1997, also split concussion into three grades,24 but they involve confusion rather than amnesia and consider any loss of consciousness very serious. Grade 1 involves no loss of consciousness, only transient confusion, and all symptoms resolving in less than 15 minutes. Grade 2 involves similar symptoms lasting more than 15 minutes. Grade 3 includes concussion with any loss of consciousness.
The guidelines summarized in Table 1 also have associated return-to-play recommendations based on the grade of the concussion. (See Table 2.) These recommendations for return to play are similar for a given grade of concussion, but differ widely in the grade assigned to specific symptoms. All allow individuals with grade 1 concussions to return to play if symptoms resolve and the results of examination on the sidelines are normal. Unfortunately, objective neuropsychological testing of reaction time and cognitive function has shown that, even in athletes with grade 1 concussions whose symptoms resolve within 15 minutes after injury, deficits may persist until day 6.42
Athletes with grade 2 concussion are removed from play and may return in one to two weeks if symptoms resolve. For grade 3 concussions, The Colorado Medical Society and AAN recommend hospital evaluation as well as a delayed return to play. Cantu recommends removal from play for a month with a grade 3 concussion. He also recommends longer play restriction in athletes with recurrent injury. Particularly, he recommends ending the season for an athlete sustaining his/her third concussion even if it is mild.27,40,41 These guidelines rely heavily on the presence or absence of symptoms to guide decision-making. The use of quick sideline testing may result in neurocognitive deficits being missed and may place the athlete at risk if he or she is allowed to return to play prematurely. In addition, practitioners should bear in mind that some patients might minimize or deny symptoms to get clearance to play. There also exists the mentality that athletes are expected to "tough it out" or "play through an injury."
Traditionally, many athletes have not been allowed to return to play for 7 days. There is evidence that this one-week recovery time may not be long enough. McClincy et al studied recovery times in 104 high school and college athletes who sustained concussions.43 They graded concussions using AAN scales, and also used neuropsychological testing before and repeatedly after a concussive event. Neurocognitive defects persisted for up to 14 days. Alarmingly, concussion recovery times had little to do with AAN grade; 80% of concussed athletes would have returned to play with persistent neurocognitive defects. This is potentially dangerous, as research has demonstrated risks associated with repeated injury prior to full recovery.15
The International Conference on Concussion in Sport met and published guidelines in Vienna in 2001 and in Prague in 2004.21 They offered a new definition for sports concussion as "a complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces." Their consensus was that loss of consciousness had likely been overstated as an indicator of injury severity, and that amnesia was possibly a valuable indicator of severity. The group abandoned previous concussion grading based on initial symptoms and instead separated concussion into two groups, simple and complex, based on pattern of recovery. They also indicated that in contrast to statements from previous grading scales, any child with concussion mandated an evaluation by a physician.
A simple concussion is defined as one that "resolves without complication over a 7-10 day period." A graded increase in activity is recommended before these patients return to full sport participation. A complex concussion is one that leads to persistent symptoms or involves seizure or prolonged loss of consciousness (more than 1 minute). This category also includes those with recurrent injury. Formal neuropsychological testing is recommended for this group, as well as more intensive evaluation by physicians who specialize in concussion. (See Table 3.)
To address the concerns that symptom-based guidelines were resulting in athletes being returned to play prematurely, the conference statement from Prague made several additional recommendations:21 A key instruction is that no player goes back into the current game after a concussion. This differs significantly from the previously mentioned guidelines, which may allow return to play after a short rest (15-20 minutes) and sideline testing. Another recommendation is the return to play in a stepwise fashion. This begins with light activity and progresses to sport-specific exercise; followed by drills; full-contact practice; and finally, return to game play. If any symptom occurs during this process, the athlete should return to the level of exercise not associated with symptoms. The athlete may then attempt a higher level of activity after 24 hours. The statement also recommended cognitive rest, which had not been mentioned in previous return-to-play guidelines.
In addition, the Prague statement included the Sport Concussion Assessment Tool (SCAT), which is meant to be used for the sideline assessment of athletes and also for pre-season assessment.21 The SCAT card is available from the Clinical Journal of Sport Medicine (www.cjsportmed.com, search for "Sport Concussion Assessment Tool") and consists of a scorecard for concussion symptoms, as well as an organized outline of a neurocognitive assessment tool. However, unlike professional sports organizations that require the presence of on-site trainers or sports medicine physicians, amateur sporting events may not have these resources present at each game. If an assessment by a trained individual cannot be done on the sidelines, the patient should be removed from play until a proper evaluation has been completed.4
ED Management: When to Order a CT Scan
Perhaps the most important step in evaluating the emergency department patient with concussion is ruling out more significant pathology such as brain hemorrhage. Some common symptoms of concussion also may indicate more severe pathology. Concussed patients often complain of a headache,26 but severe headache may indicate a more serious intracranial injury.44,45 Some vomiting may be present in the setting of concussion, but recurrent or projectile vomiting may be an indication that further testing is warranted.46,47
The question of when to obtain imaging to exclude an intracranial injury has been the topic of numerous studies over several years, yet there is not a clear consensus.44-52 Computed tomography (CT) is expensive, and it also exposes patients to significant doses of radiation, which may increase the future risk of cancer. The risk of cancer death in a 1-year-old who undergoes a CT scan of the brain approaches 1/1000.53 Unfortunately, the youngest members of the pediatric population are the most difficult to assess for more serious injury and also may suffer the greatest risk of radiation exposure.44,53,54
In 1999 the American Academy of Pediatrics, in concert with the American Academy of Family Physicians, published a consensus guideline on the management of minor closed head injury in children older than age 2. For the patient with a normal neurological exam following a mild head injury without a loss of consciousness, they recommend only observation. If there is a brief loss of consciousness, then a CT scan or observation is appropriate. The period of observation should be 24 hours, but that can include at-home observation by a reliable caregiver as well as time in the emergency department, physician's office, or hospital. Notably, this guideline is meant to include those who have symptoms of concussion including episodes of vomiting or lethargy, but it excludes patients with evidence of a skull fracture, as well as those with multiple traumas, intentional trauma, intoxication, or bleeding diathesis.55
Later investigation has attempted to close the 0- to 2-year-old age gap with the development of criteria to determine when these youngest of patients should receive brain CT scans.45,47,48 This group traditionally has been considered at higher risk and more difficult to assess.48,54 In addition to brain injury, other complications such as growing skull fractures and leptomeningeal cysts must be considered in this age group.54 In 2001, Schutzman and colleagues published guidelines for those younger than age 2.48 The recommendations included exceptions to the previously mentioned AAP guidelines. They advocated dividing patients into four groups depending on risk. In their guidelines, risk is determined by age, with lower ages at higher risk. Symptoms such as vomiting, loss of consciousness, and lethargy are considered, as is the mechanism of injury. Lower-risk infants can be discharged. Radiographs are considered for those with potential skull fracture. Those with intermediate risk are scanned or observed, and all high-risk patients receive CT scans.48 Notably, the authors pointed out that loss of consciousness and vomiting had not been demonstrated to be predictive of intracranial injury (ICI). The guidelines do not offer strict cut-offs between their risk groups, which could lead to clinician judgment playing a very significant role.
In 2003, Palchak et al published a decision rule for determining when to scan those age 2 or younger.44 They studied 2043 children who underwent CT scan following a head injury. The decision rule involved the following:
- Abnormal mental status;
- Clinical evidence of skull fracture;
- History of vomiting;
- Scalp hematoma in those younger than age 2; and
The authors demonstrated a sensitivity of 99% for detecting lesions present on CT scans and 100% sensitivity for lesions requiring intervention. There was a specificity of 42.7% for those requiring intervention.
More recently, NEXUS II data have yielded more specific criteria for use in children in general and in the difficult 0- to 2-year-old group.47 Published in 2006, this study involved 1666 children, 309 of whom were younger than age 3. The authors began by analyzing 19 variables potentially associated with significant ICI. They selected eight variables based on the association with ICI in the study cohort, including:
- Evidence of significant skull fracture;
- Altered level of alertness;
- Neurological deficit;
- Persistent vomiting;
- Presence of scalp hematoma;
- Abnormal behavior;
- Coagulopathy; and
- Age older than 65.
Utilizing the NEXUS II cohort, the authors reported 98.3% sensitivity with 100% in the population younger than age 3, but noted that these criteria should be validated in a separate cohort of patients. Specificity was only 13.7% for the group, but these data could still be used to decrease unnecessary CT scan utilization.
In 2007, Sun et al used the NEXUS II cohort data to validate a slight modification of the Palchak et al rule (the UC-Davis Pediatric Head Injury Rule).45 They demonstrated a sensitivity of only 90.4% and specificity of 42.7%. This Modified UC-Davis Pediatric Head Injury Rule involves five elements, including:
- Abnormal mental status;
- Signs of skull fracture;
- Scalp hematoma in children younger than age 2;
- High-risk vomiting; and
- Severe headache.
High-risk vomiting in this scenario refers to recurrent, forceful, or projectile vomiting, according to the authors. This was only a slight modification of the UC-Davis Pediatric Head Injury Rule, which had demonstrated a sensitivity of 100%.
To date, there is no universally accepted guideline to instruct physicians when to order CT scans on children with concussion or head injury. Physicians should use their clinical assessment of the patient along with knowledge of the currently available guidelines in determining which patients to scan.
Adjunctive Tests. Conventional neuro-radiologic studies are usually normal in mild TBI, although CT scan is still used liberally in the acute setting to rule out serious pathology such as intracranial bleed or subarachnoid hemorrhage. Magnetic resonance imaging (MRI) can be used for certain situations including prolonged recovery time, focal neurologic deficits, or worsening symptoms. In rare cases, delayed or slowly developing intracerebral hemorrhage (ICH) has been detected by MRI.
Single photon emission computerized tomography (SPECT) and positron emission tomography (PET) scanning may be useful as diagnostic modalities. They can assess regional blood flow and cerebral blood volume.56 SPECT also can evaluate blood-brain barrier integrity. SPECT and PET are much more sensitive than CT or MRI, which are negative in the majority of patients with PCS. They have been found to have a sensitivity of 90%.57 SPECT is much more readily available and less costly. Using these modalities, researchers have found a high incidence of medial temporal hypo-perfusion (MTH) in children with mild TBI.57,58 This may account for the memory impairment seen with PCS because the hippocampus is located in the medial temporal lobe. Researchers hypothesize that this hypo-perfusion results in ischemic injury. Symptoms of PCS correlated with abnormal SPECT scans. SPECT may prove to be a useful screening tool to determine if any hypo-perfusion has occurred in children who have suffered a concussive injury, but at present, it is not widely used for that purpose.
Electroencephalogram (EEG) may show abnormal slowing after concussion.59 This can be coupled with low-resolution brain electromagnetic tomography (LORETA), which localizes areas of slowing to pathologic areas found on SPECT scan. It is currently unclear if these abnormalities are associated with the symptoms of PCS.
Ideally, serum biochemical markers could be used instead of expensive radiologic studies, some of which incur the risk of radiation exposure. It is presumed that if the blood-brain barrier is damaged by a traumatic injury, brain-related proteins may be identifiable in the peripheral circulation. Astroglial protein (S100B) may indicate brain injury, but diagnostic tests for it are still experimental. S100 protein is released from astrocytes. However, this isoform is not isolated to brain tissue. In addition, its relationship to outcome after TBI is variable. Recent investigations suggest that using a creatine kinase correction factor may aid in accounting for extracranial S100B release.60 Further research needs to be undertaken to determine if this is a useful tool in the evaluation of patients with mild TBI. Neuron-specific enolase (NSE) is an enzyme important for glycolysis in neurons. It is not isolated to the brain. Cleaved tau protein (CTP), found in axons, is presumed to be released after mild TBI when diffuse axonal injury has occurred. This marker may be useful in combination with S100B protein.61 At present, the value of these markers is questionable.
It should be mentioned that objective measures of brain injury, such as radiologic tests and serum markers, cannot be used as the only predictors of mild TBI outcome. Numerous other factors come into play, such as pre-morbid characteristics (e.g., attention-deficit/hyperactivity disorder, socioeconomic setting) and coping mechanisms, which account for the variability in symptom severity and duration in patients with seemingly similar injuries. It has been shown that children with persistent symptoms of concussion have poorer pre-injury behavioral adjustment than children without persistent symptoms.62 The emotional and behavioral symptoms of PCS may be affected by post-injury parent and family adjustment, family stressors, and resources unrelated to the injury.63 Below-average parenting skills and family functioning may worsen the negative effects of PCS, but higher-functioning families may be able to lessen these effects, especially the behavioral symptoms.4 Children who have adjustment difficulties may not have the necessary coping skills to deal with the acute stress of an injury. Families who function poorly may not serve as a resource to help children cope. There is a significant relationship between the number of problems reported and the level of parental stress.64 Failure to reasonably cope with the acute stress of injury may result in persistent symptoms, even when the tangible effects on brain function have resolved as evidenced by neuropsychological testing.
The individual's recovery course is more important than the initial grade of concussion. Grading concussions immediately after injury may not be an accurate assessment because individual recovery varies. Loss of consciousness is one indication of concussion severity, but it is by no means the most important. Many recover quickly despite suffering a loss of consciousness; conversely, others who do not lose consciousness may experience a prolonged recovery period.65
It is crucial to identify patients who are at risk for developing PCS early so that treatment can be started and assistance can be offered with psychosocial and family issues.
Optimal management requires ongoing assessment to make sure secondary problems have not developed (such as depression, family dysfunction, post-traumatic stress disorder, attention-deficit/hyperactivity disorder). Therefore, appropriate follow-up instructions and referrals should be offered.
To reduce some of the negative psychosocial effects of PCS, it is important to educate families and school personnel. They may be able to adjust the child's schedule and their own expectations while healing is occurring. Specialized educational help can be arranged. This and other early psychosocial intervention, such as cognitive-behavioral therapy, may lessen the severity of some of the emotional and behavioral symptoms resulting from PCS.66,67 If a patient is not improving as expected, referrals to specialists in neuropsychology, neurology, rehabilitation, sports medicine, or behavioral health should be considered.
Pharmacologic Therapy. Several medications have been recommended for PCS based on their efficacy in treating similar symptoms in the non-concussed population. Few have been studied. Levels of dopamine and serotonin are reduced in the cerebrospinal fluid of TBI victims,68 which is the basis for use of antidepressants in patients with TBI. Methylphenidate and sertraline have been found to be better than placebo for treating depression. Their efficacy in treating the other neuropsychological symptoms of PCS, including sleep disturbances and cognitive function, has not been proven. Sertraline has been found safe for use in children as young as age 6. Symptomatic relief of headache can be achieved with acetaminophen or non-steroidal anti-inflammatory agents.
Investigative studies have explored the role of functional neurogenesis. Using a rat model, fibroblast growth factor-2 and epidermal growth factor have been found to encourage repopulation of hippocampal neurons in an area of injury.69 To document similar results in humans, researchers may need to use SPECT scanning, as histopathology tests of treated human subjects cannot be done.
Disposition. Hippocrates once said, "No head injury is too trivial to ignore."70
The emergency department physician should not halt treatment and assessment of a child following a negative head CT scan. Parents should be educated about the symptoms and natural history of concussion, and appropriate follow-up should be recommended. Parents often want to know when their child can return to sports or to physical education class, but children should be managed very conservatively. Field and colleagues compared collegiate and high school athletes and determined that the younger athletes took longer to recover, particularly in memory testing.15 As previously mentioned, it also is suspected that the pediatric brain is more susceptible to second insult until injury has fully resolved. The Concussion in Sport Group recommends guidelines for stepwise return to play.21 The athlete/student can advance through each level if symptoms do not develop with the activities described. If PCS symptoms develop at a particular level, the patient should return to the previous level for 24 hours before attempting that level again. The group recommends the following steps for return to play:21
1) No activity. Complete rest while still symptomatic. When symptoms have resolved, proceed to level 2;
2) Light aerobic exercise (walking, stationary bike), no resistance training;
3) Sport-specific exercise (e.g., running for soccer or football);
4) Non-contact training drills;
5) Full-contact training after medical clearance; and then
6) Game play.
Retirement From Play
Retirement from play should be considered for athletes with a persistently abnormal neurologic exam or persistent concussive symptoms, and those with neuropsychological testing scores that are not at the patient's baseline.40 Also included are those with abnormal neuroimaging studies, those with increasing recovery times after successive injuries, and those who require less force to suffer a concussion after subsequent injuries.71 There are no absolute numbers of concussions to guide clinicians at this point. Cantu has recommended retiring players for the season if they've had two to three lower-grade concussions or one to two grade 3 concussions.40 Patients should be referred to their primary care providers for further guidance on when they may return to play. Preseason concussion assessment and baseline neuropsychological testing could potentially identify those at high risk for injury.21 If retirement from play is considered too extreme, recommendations for special protective gear or a change in playing position may be given, but this should be done with the cooperation of the primary care provider, coach, and family.
The risk of recurrent concussions also is subject to debate. It used to be accepted dogma that each concussion rendered the brain more susceptible to subsequent injury, but it has not been scientifically proven. A "three-strike rule" requiring removal of an athlete from play if he or she has sustained three concussions has been used.72 Recent literature suggests that recurrent concussions have some cumulative effects. In one study of high school athletes, children who had suffered more than two concussions but were currently asymptomatic had neuropsychological test scores that were indistinguishable from those of children with recent concussions.68 Academic grade point average was also lower in those with multiple concussions, although it is unclear whether this was a result of injury or if it indicates a predisposition of some children to concussive injury. In another study, memory deficits were found to be more pronounced in children with multiple concussions. The evaluation of a child after head injury should include a history of all prior head injuries, previous symptoms of PCS, and documented concussions. This may be difficult because many patients will not recognize all prior concussive injuries. Recollections of coaches or teammates can be unreliable. All previous injuries to the maxillofacial area and neck should be looked into, as these may have been associated with an undiagnosed PCS. The families of children who have sustained multiple concussions should be advised about the risks of repeated injury. Referral for further evaluation and neuropsychological testing should be considered after the patient is evaluated following an acute injury.
Chronic Postconcussive Syndrome (Dementia Pugilistica). Chronic postconcussive syndrome is an Alzheimer's-like condition seen in professional boxers. It is rarely described in other sports. A less severe form is persistent postconcussion syndrome, which is defined as the presence of PCS symptoms after 3 months post-injury. This may be seen in up to 30% of patients.58 Due to the previous lack of objective, sensitive diagnostic tools, many physicians may have attributed persistent symptoms to a psychological origin rather than an organic one. Secondary gain issues have also been thought to come into play. Children with persistent symptoms have been grouped in with these even though secondary gain may play less of a role. Objective neuropsychological tests will aid in identifying those with true deficits.
Second Impact Syndrome. The second impact syndrome refers to fatal cerebral edema following relatively minor head trauma that occurs while a patient is recovering from a prior injury and is still symptomatic. The second blow to the head can be remarkably minor, with the patient becoming obtunded within a few seconds or minutes.73 The syndrome is thought to relate to a disruption of the autoregulation of cerebral blood flow and is characterized by the abrupt onset of cerebral edema.1,73 On most recent review, only 17 cases have been described and all patients were 13-18 years of age.74 This syndrome is a rare occurrence and the reported incidence is 1 to 2 in 1.5 million players. The prognosis for this condition is dismal. Potential interventions include osmotic agents. Surgery has no role.
There is no proven medical therapy for concussion, so prevention is crucial.
Pre-participation Assessment. Baseline testing is currently recommended by the International Conference on Concussion in Sport.21 They recommend conducting baseline cognitive assessment and symptom score as pre-participation evaluation in all players in high-risk organized sports, regardless of age or level of performance. This has sparked some debate. Some experts feel the immense output of resources needed to put all amateur athletes through baseline testing is not justifiable.1 Comprehensive tests take hours and are costly. Many districts do not have access to the testing tools. It has been suggested that comprehensive testing be used only in certain situations, including: multiple concussions; no improvement within 1-2 weeks; and difficulty at school. Three widely available systems are the Immediate Post-Concussion Assessment and Cognitive Testing (IMPACT), the Concussion Resolution Index, and CogSport.
Proper Head Protection. The majority of concussive injuries are sustained while playing football or hockey, both of which require helmet use. Unfortunately, it has been found that only 15% of high school football players' helmets fit.75 The American Academy of Pediatrics and the American Dental Association recommend the use of mouth guards in high school football players. Mouth guards not only protect the teeth but also realign the mandible. This allows the force of blunt trauma to the jaw and head to be absorbed by the cartilaginous cushion between the top of the jaw and the skull. The New England Patriots team has had no PCS since fitting players with mouth guards. It is presumed that similar protective effects will be seen in athletes playing other sports. The assessment of a head-injured child should include questioning about protective gear worn during injury, and is similar to assessment used for patients involved in motor vehicle or bicycle accidents. This may help guide modification of equipment to prevent future injury.
Education. Athletes, coaches, and families should be educated at the beginning of the season so they can recognize PCS and seek medical attention promptly. They also should be informed of the potential risks and long-term complications so they will take the problem seriously. It's important to note that many individuals in the lay public still believe loss of consciousness is required for concussion to have taken place. Whenever young athletes are seen for any trauma, clinicians should take the opportunity to educate them on the necessity of reporting injuries early and resisting the urge to be stoic and "play through the injury." This can be difficult because adolescents often have some feeling of indestructibility. They also may fear having to sit out of games, thereby losing potential opportunities for higher level of play or scholarships.
Professional athletes are subject to baseline assessment, education, and prevention. These standards also should apply to young amateur athletes, given the risks to brain development and the possibility of long-term complications. Educational programs targeting young athlete groups should be developed. To deliver appropriate care after an acute injury, healthcare providers must be cognizant of the ramifications of concussion.7
Resource Note from the authors: A new resource from the CDC is available free to physicians. It is a kit called "Heads' Up: Brain Injury in Your Practice" and includes fact sheets to prevent concussions and a palm card on the management of on-field sports-related concussions.
It is available at www.cdc.gov/ncipc/pub-res/tbi_toolkit/toolkit.htm
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