Concussion

Concussion has many different meanings to patients, families, and physicians.[1, 14, 15, 16] One definition of concussion is a condition in which there is a traumatically induced alteration in mental status, with or without an associated loss of consciousness (LOC).[1] A broader definition for concussion is a traumatically induced physiologic disruption in brain function that is manifested by LOC, memory loss, alteration of mental state or personality, or focal neurologic deficits.[1] Concussions usually result in relatively temporary impairment of neurologic function.[8, 16, 17]

Concussion or mild traumatic brain injury (MTBI) is common among most contact and collision sports participants.[1, 2, 3, 4, 5, 6, 7] For many physicians, even those who specialize in MTBI, this area is confusing due to the paucity of scientific evidence to support much of the clinical decision making that is faced in the office.[4, 9, 14, 15, 18] The inconsiderable amount of good scientific research in the area of MTBI is due to problems with ambiguous definitions of concussion, inconsistent criteria when selecting patients to study, variability of injury mechanisms and locations, and differing means of measuring cognitive function.[19, 20] The purpose of this article is to review the epidemiology and diagnosis (but not necessarily the classification) of MTBI, as well as the role of imaging studies, issues regarding return to play, and complications surrounding MTBI.

United States statistics

The incidence of head injury varies with the sport and the age of the participants; many head injuries are likely unreported due to their supposed mild nature; mild concussions may go unnoticed by teammates, coaches, and even the athletes themselves.[1] An athlete's fear of medical disqualification may also lead to underreporting. Studies of high school athletes show the rate of concussions per 1000 exposures as follows: 0.59 for football (boys), 0.25 for wrestling (boys), 0.18 for soccer (boys; 0.23 for girls), 0.09 for field hockey (girls), and 0.11 for basketball (boys; 0.16 for girls). The data from one study noted that concussions account for nearly 15% of all sport-related injuries in high school athletes.[21]

Among National Collegiate Athletic Association (NCAA) soccer players, the rate of injury has been reported as 0.4-0.6 per 1000 athlete exposures[6] ; 72% of these injuries were described as mild and were almost always secondary to direct contact with an opponent. None of the injuries in this group of Atlantic Coast Conference (ACC) soccer players was noted to be a direct result of heading the ball. In contrast, boxing is the sport with the highest rate of head injuries and has more deaths than any other organized athletic activity. At the professional level, many of the boxing bouts end with a technical knockout (ie, brain injury).

Sports activities that place the athlete at high risk for a head injury include boxing, football, ice hockey, wrestling, rugby, and soccer. Physicians and other allied health providers who are responsible for the medical care of such contact or collision sports participants should be adept at evaluating, treating, and making playability decisions related to the short- and long-term consequences of an injury to the brain.

The mechanisms of brain injury may differ among sports activities. Possible mechanisms of injury include compressive forces, which may directly injure the brain at the point of contact (coup); tensile forces produce injury at the point opposite the injury (contrecoup) because the axons and nerves are stretched; finally, rotational forces may result in a shearing of axons. Therefore, the direct force at the point of contact may not be solely responsible for the severity of an injury if a high rotational component with a significant shear effect occurs.

All of the different mechanisms may result in biochemical changes related to perfusion, energy demand, and utilization at the site of injury that are not well understood. At this time, it is unclear whether any experimental animal model or human studies on more severe brain-injured patients accurately reflect the pathophysiology of the typical mild traumatic alteration in brain function.

A previous concussion is a significant risk factor for sustaining a concussion.[2, 3, 7, 22, 23, 24, 25]

One study reported that the risk of sustaining a concussion was 4-5 times higher in patients who had at least 1 concussion in the past. Another study reported that athletes with a history of 3 or more previous concussions were 3-fold more likely to have a concussion than players who had no history of concussion.[24]

Other risk factors for sustaining a concussion that have been suggested but not proven include not wearing mouth guards, poor fitting helmets, and genetic predisposition.[26, 27]  Research in all of these areas continues.

Most patients with an MTBI are able to return to full competition without complication. Because many patients may not report minor head injuries to the athletic trainer, emergency department (ED), or a primary care physician, the overall prognosis of many head injuries is unclear.

A study including male high school football players noted that dizziness at the time of injury is associated with an increased risk of protracted (≥21 d) recovery. Another study involving athletes aged 9-23 years with a diagnosed protracted concussion found that those who have vestibular symptoms after concussion may have slower reaction times than those who do not and thus may be at greater risk for new injury.[28]

A study by Ling and colleagues indicated that at least 4 months after an MTBI, the brain continues to display signs of damage, even if the clinical symptoms of injury have subsided. Evaluation of patients with mild brain injury, however, revealed no evidence of cortical or subcortical atrophy. The study involved 50 patients with MTBI and 50 matched controls. In the first 2 weeks following injury (the semiacute injury phase), patients with concussion complained of more cognitive, somatic, and emotional symptoms than did the controls. These symptoms, however, were significantly reduced at 4-month follow-up (at which time, 26 of the patients were evaluated).[29, 30]

In a prospective cohort study of 280 patients aged 11 to 22 years who presented to an emergency department with acute concussion, repeat concussions increased the risk for prolonged recovery.[31]  Patients with a history of previous concussions had symptoms that lasted twice as long (24 days) as those who did not have such a history (12 days).

An analysis of children presenting to the ED with concussion showed that the patients were still struggling with a significant burden of symptoms 1 week after injury.[32, 33]  Headache was the most common initial symptom; by day 7, 69.2% were still experiencing headaches. Fatigue persisted in 59.8% of children at day 7, and poor concentration persisted in 56.8% 1 week later. Emotional symptoms (eg, depression, frustration, irritability, and restlessness) also developed and increased by day 7 but were largely resolved by day 90.

A retrospective study by Kontos et al showed that adolescent athletes with concussion who received clinical care within 7 days of the injury recovered in a mean of 20 days more quickly than athletes who received care 8-20 days after the injury. The researchers suggest that the earlier initiation of active rehabilitation strategies may explain the more rapid recovery.[34]

Chronic postconcussive syndrome can be quite severe, with the most dramatic presentation including dementia pugilistica, which is associated with boxing. This Alzheimer-like condition has a reported incidence of 15% among professional boxers. Fortunately, this condition is rare in most other sports. Hopefully, more frequent, detailed neuropsychologic testing will decrease the frequency of postconcussive syndrome among elite and professional athletes by detecting more subtle injuries earlier. For further information on this topic, see Repetitive Head Injury Syndrome.

Complications

Chronic traumatic encephalopathy (CTE) 

Persons with a history of repetitive brain trauma, including boxers and football players, are at risk for developing chronic traumatic encephalopathy (CTE), a progressive degenerative disease. Degenerative changes, which can begin months to decades after the patient’s last brain trauma, include atrophy of the cerebral hemispheres, medial temporal lobe, thalamus, mammillary bodies, and brainstem. The condition is also characterized by ventricular dilatation and by fenestration of the cavum septum pellucidum, as well as the accumulation of phosphorylated tau in the brain, with deposits of the protein being found in the sulci and in perivascular areas of the cerebral cortex. Symptoms of CTE include memory loss, confusion, impaired judgment, reduced impulse control, aggression, explosive anger, depression, and progressive dementia.[35, 36, 37, 38]

According to a report from the US Department of Veterans Affairs and Boston University, 87 of 91 deceased former players for the National Football League (NFL) (96%) who donated their brains for study were found to have changes consistent with CTE. These finding need to be tempered by the fact the donors had, prior to death, expressed concern that they might have CTE and so may have had a higher proportion of the disease than does the overall population of former NFL players. In addition these individuals had not necessarily had clinical symptoms of CTE, but felt they might be at risk.[39, 40]

A study by Mez et al diagnosed CTE in 177 (78%) of 202 samples from deceased American football players. The samples included 111 former NFL players of which, 110 (99%) were diagnosed with CTE. The study also found that among the 26 participants diagnosed with mild CTE, 96% had behavioral or mood symptoms or both, 85% had cognitive symptoms, and 33% had signs of dementia. In the 84 participants diagnosed with severe CTE, 89% had behavioral or mood symptoms, 95% had cognitive symptoms, and 85% had signs of dementia.[41]

A study by Alosco et al showed that a distinct pattern of frontal-temporal atrophy on MRI may suggest CTE. Compared with persons with normal cognition, those with CTE had significantly greater atrophy in several brain regions, including the orbital-frontal cortex, dorsolateral frontal cortex, superior frontal cortex, anterior temporal lobes, and medial temporal lobe.[42]

Athletes with an MTBI often appear acutely with a confused or blank expression or blunted affect. Delayed response to simple questioning may be demonstrated, along with emotional lability. The emotional lability may become more evident as the athlete attempts to cope with their confusion. Many athletes report an associated headache and dizziness. Visual complaints may include seeing stars, blurry vision, or double vision.[43]

In a study of 48 athletes aged 9-23 years with a diagnosed protracted concussion, Kontos et al found that those who have vestibular symptoms after concussion may have slower reaction times than those who do not and thus may be at greater risk for new injury.[28]

Patients with vestibular dizziness and those with vestibulo-ocular symptoms had significantly slower reaction times than those without these impairments (P = .05 and P = .04, respectively).[28] Athletes with vestibular dizziness and vestibulospinal and vestibulo-ocular impairments also had more total symptoms than those without these impairments. Furthermore, vestibular impairments were associated with greater cognitive impairment and somatic symptoms. Abnormal (>6 cm) convergence distance was associated with a significantly slower reaction time (P = .05).[28]

Both pretraumatic (retrograde) amnesia and posttraumatic (antegrade) amnesia may be present. Usually, the duration of retrograde amnesia is quite brief, with a more variable duration of posttraumatic amnesia (seconds to minutes), depending upon the injury.

A history of persistent vomiting may suggest a significant brain injury with associated elevated intracranial pressure. Other signs of increased intracranial pressure include worsening headache, increasing disorientation, and changing level of consciousness. Possible causes of increasing intracranial pressure include subdural hematomas, epidural hematomas, or some other type of intracranial hemorrhage.

It is important to document a previous history of concussions. Multiple concussions with prolonged neurologic symptoms (eg, headache, hyperacusis, dizziness) suggest postconcussive syndrome and should influence return-to-play decisions.[2, 3, 7, 22, 23, 24, 25]

Assessment tools

The Glasgow Coma Scale (GCS) is routinely used to assess head injuries in an emergency department. This 15-point scale is used to assess eye (spontaneous opening = 4 to no response = 1), motor (obeys commands = 6 to no response = 1), and verbal responses (oriented = 5 to no response = 1) in an attempt to quantify the patient's level of consciousness. This tool is not sensitive enough to evaluate more mild injuries and should not be used on the playing field to judge playability. See the Glasgow Coma Scale calculator.

McCrea et al developed a sideline evaluation to help the practitioner evaluate the more subtly injured brain.[20, 44] A 30-point scale is used to assess an athlete's orientation, concentration, immediate memory, and delayed recall. Preseason testing must be done if a practitioner is hoping to use this tool as a supplement to the neurologic and mental status exam; if the baseline status of an individual is not known, assessment for change after a head injury is useless. McCrea's sideline evaluation uses recitation of the months of the year in reverse order after a study by Young et al showed the lack of reliability of the "serial 7s" test (serial subtraction by 7 from 100) in the baseline evaluation of mental status even in non–head-injured athletes.[45]

Interestingly, the results from one study noted that administering preseason baseline neurocognitive tests in a group versus individual setting resulted in significantly lower verbal memory, visual memory, motor processing speed, and reaction time scores and a greater rate of invalid baselines.[46]

Sport Concussion Assessment Tool, 3rd edition, (SCAT3) is another standardized tool. SCAT3 combines multiple assessments into a single instrument. This combined tool was first produced as a part of the Summary and Agreement Statement of the Second International Symposium on Concussion in Sport,[47] and it has been updated twice since then (SCAT2, 2009; SCAT3, 2013).

A study investigated acute lower extremity musculoskeletal injury rates pre- and post-concussion in concussed (n=44) and matched control athletes (n=58). The study reported that within 1-year post-concussion, the concussed group was 1.97 times more likely to have suffered an acute lower extremity musculoskeletal injury like an ankle sprain, post-concussion than prior to concussion, and 1.64 times more likely to have suffered an acute lower extremity musculoskeletal injury post-concussion than their matched non-concussed cohort over the same time period.[48]

Classification

Many different classification schemes have been proposed over the last 2 decades. No one classification system is necessarily better than another classification system. No scientific basis for any of the classification systems exists.

Cantu's guidelines,[7, 49] Ommaya and Gennarelli's guidelines,[50] the Colorado guidelines,[51] and the 1997 American Academy of Neurology (AAN) guidelines[52] were proposed to aid in the evaluation of a concussion. The free CDC Tool Kit on Concussion for High School Coaches is available online in English and Spanish and uses the 1997 AAN guidelines to support a classification scheme.[53] The authors prefer to characterize concussions as follows[53] :

• A simple concussion injury progressively resolves after 7-10 days without complication. The key to return to play is to hold the athlete from practice or competition until all symptoms have resolved.

• A complex concussion consists of persistent symptoms that may include those that recur with exertion, specific sequelae such as seizure associated with the injury, prolonged LOC (>1 min), or prolonged impairment of cognitive function.

Some studies have suggested that LOC may not be a great predictor of short-term or long-term neurologic functioning, which makes the guidelines more controversial.[54, 55]

Regardless of the classification scheme that is used, all concur with the ultimate recommendation: Do not allow the concussed athlete to return to play until the patient is completely asymptomatic. The athlete must be free of headache, dizziness, amnesia, blunted affect, and delayed verbal or ocular responses, and all cognitive functioning must have returned to normal.

Perform a thorough, organized assessment to better define the degree of injury when a player is brought to the sidelines or emergency department for evaluation.

The initial evaluation should focus on airway, breathing, and circulation for any unconscious patient. Assume all unconscious or mentally impaired patients have sustained an injury to their cervical spine until proven otherwise.

For conscious patients, the remainder of the examination should be performed in a quiet place, on the sidelines or in the locker room away from teammates and coaches, or in a private room in an emergency department in order to get an accurate assessment of the cognitive status of the injured athlete.

The initial clinical examination should include a careful inspection of the athlete's general appearance.

Palpating the head and neck is important when looking for an associated skull or cervical injury.

Palpate the facial bones and the periorbital, mandibular, and maxillary areas after any head trauma. (See also the Medscape Drugs & Diseases articles Sports-Related Facial Trauma, Maxillary and Le Fort Fractures, and Management of Panfacial Fractures [in the Plastic Surgery section].)

Open and close the mouth to help in the evaluation of possible temporomandibular joint (TMJ) pain, malocclusion, or mandible fracture. (See also the Medscape Drugs & Diseases articles Initial Evaluation and Management of Maxillofacial Injuries [in the Trauma section], Mandibular Fracture Imaging [in the Radiology section], and Mandibular Body Fractures [in the Otolaryngology and Facial Plastic Surgery section].)

Inspect the nose for deformity and tenderness, which may indicate a possible nasal fracture. (See also the Medscape Drugs & Diseases articles Nasal and Septal Fractures [in the Otolaryngology and Facial Plastic Surgery section], Nasal Fracture [in the Sports Medicine section], and Nasal Fracture Surgery [in the Plastic Surgery section].)

Persistent rhinorrhea or otorrhea (clear) indicates a possible associated skull fracture. (See also the Medscape Drugs & Diseases articles Imaging in Skull Fractures [in the Radiology section] and Skull Fracture [in the Neurosurgery section].)

Perform a careful detailed neurologic examination to include examinations of the visual fields, extraocular movements, pupillary reflexes, and level of the eyes.

Assess upper-extremity and lower-extremity strength and sensation.

Assess coordination and balance. Concussed patients often have difficulty with the finger-nose-finger test and will use slow, purposeful movements to complete the task.[56]

Catena et al compared the immediate versus long-term effects of concussion on balance control.[57]  Individuals with concussion (n = 30) and matched controls (n = 30) performed a single task of level walking, attention divided walking, and an obstacle-crossing task at 2 heights, with testing occurring 4 times postinjury.

The investigators demonstrated no significant difference between the 2 groups in the single-task level walking task. However, although concussed individuals walked slower within 48 hours of the injury and had less motion of their center of mass in the sagittal plane with divided attention during walking, there were no group differences by day 6 for the same task.[57]

In addition, there were no significant group differences in balance control during obstacle crossing during the first 2 testing sessions, but by day 14, concussed individuals had less mediolateral motion of their center of mass. Catena et al concluded that attention divided gait is better at distinguishing gait adaptations immediately postconcussion, but obstacle crossing can be used further along in the recovery process to detect new gait adaptations.[57]

Significant sway in Romberg testing may indicate persistent injury.

Adding a simple vision test performed on the sidelines to standard tests based on balance symptoms and cognition tasks can improve the detection of concussion in sports players who have experienced a head injury, according to a study of 217 young athletes. The King-Devick test involves reading a series of numbers and takes about 1 minute to complete. A baseline test is given at the start of the season, and tests are repeated after injuries occur. Concussion is diagnosed if the injured athlete takes longer to complete the test.[58]

Among the 30 study subjects with a first concussion, 79% showed worsening of time scores on the King-Devick vision test, while the Standardized Assessment of Concussion (SAC) test detected 52% of concussions and the Balance Error Scoring System (BESS) test detected 70%. Combining the King-Devick vision test with the SAC detected 89% of concussions, and combining all 3 tests identified 100% of concussions.[58]

When examining an athlete on the sideline, perform repeat examinations every 15 minutes until the symptoms have cleared. Repeat the examinations even if the athlete is allowed to return to play.

The patient should not be allowed to return to competition if his/her symptoms or physical examination findings do not return to normal after 15 minutes. For a few hours after the initial injury, close observation and monitoring of the athlete for worsening mental status or neurologic status is warranted on the sideline or in the emergency department.

It is important to be cognizant of the fact that although the following studies may be useful in the evaluation of head trauma, they will be negative for a concussion with no other injury.

CT scanning

In an emergency department-based study, the percentage of abnormal CT scans in adult patients increased from 13% for patients with a perfect GCS score to 37% for those with a GCS score of 13.

In a different study that assessed 712 patients with LOC or amnesia and a perfect GCS, the rate of abnormal CT scans was 9%, with less than 1% requiring surgical intervention.[59]

Indications for ordering a CT scan include focal neurologic examination findings, signs or symptoms of increased intracranial pressure, GCS score less than 15, and seizures related to trauma. Some authors suggest that any athlete with loss LOC (grade 3 concussion) should have a CT scan obtained.[60] This area is controversial. Athletes with a brief LOC are at no higher risk for long-term neurologic sequelae, and indications for imaging should not differ from those listed above.

CT scanning continues to be the imaging study of choice in evaluating an acute head injury. Better imaging of an acute hemorrhage, speed of the study, and improved ability to monitor the patient are the reasons for using CT scanning rather than magnetic resonance imaging (MRI).

MRI

MRI is the imaging study of choice for patients who have prolonged symptoms (> 7 d) or for a late change in an individual's neurologic signs or symptoms.

MRI offers a more detailed examination and possibly detects more subtle findings.

Delayed or slowly developing bleeds may be easier to detect on MRI.

A study by Strauss et al identified early diffusion tensor imaging (DTI) biomarkers of mild traumatic brain injury that significantly relate to outcomes at 1 year following injury. The study found that abnormally high fractional anisotropy is significantly associated with better outcomes and might represent an imaging correlate of postinjury compensatory processes.[61, 62]

Neuropsychologic testing

Detailed neuropsychologic testing is employed more often at the professional level and in research in athletes with MTBI.

When evaluating an athlete's performance on the neuropsychologic tests, it is best to compare results with the athlete's previous tests.

The National Hockey League (NHL), National Football League (NFL), Major League Baseball (MLB) as well as many college teams are utilizing limited neuropsychologic testing to document the possible prolonged effects of presumed minor head injuries and to assist the clinician in determining possible retirement issues.

Neuropsychologic testing is indicated in cases of complex concussions.[47]

Although positron emission tomography (PET) scanning and functional MRIs (fMRIs) may be used, their clinical application in most cases of MTBI is uncertain.[8, 9, 10]

A study by Papa et al evaluated the serum levels of two biomarkers, glial fibrillary acidic protein (GFAP) and ubiquitin C-terminal hydrolase (UCH-L1) that show promise for clinical usefulness in suspected traumatic brain injury (TBI) and concussion. The study found that GFAP performed consistently in detecting MMTBI, CT lesions, and neurosurgical intervention across 7 days and that UCH-L1 performed best in the early postinjury period.[63, 64]

In March 2013, the American Academy of Neurology (AAN) updated its 1997 guidelines on the evaluation and management of sports concussion. A major change is the removal of return-to-play recommendations. The current recommendation for athletes who have sustained a concussion is immediate removal from play. Return to play should not be allowed until after assessment by a healthcare professional. Young athletes should be managed even more conservatively; their symptoms and neurocognitive performance take longer to improve after a concussion.

Highlights from the revised recommendations include the following[13, 65] :

• There is no evidence that medication improves recovery after concussion

• The risk for concussion is greatest in football and rugby, followed by hockey and soccer; for young women and girls, the risk is greatest in soccer and basketball

• An athlete who has a history of 1 or more concussions is at greater risk for being diagnosed with another concussion

• The first 10 days after a concussion appears to be the period of greatest risk for being diagnosed with another concussion

• Evidence suggests that use of helmets may prevent concussion versus no helmet, but there is no clear evidence that one type of football helmet can better protect against concussion over another kind of helmet

• Licensed health professionals trained in treating concussion should look for ongoing symptoms, history of concussions, and younger age in the athlete

• Risk factors linked to chronic neurobehavioral impairment in professional athletes include prior concussion, longer exposure to the sport, and having the ApoE4 gene

• Symptom checklists, the Standardized Assessment of Concussion (SAC), neuropsychological testing (paper-and-pencil and computerized), and the Balance Error Scoring System may be helpful tools in diagnosing and managing concussions but should not be used alone for making a diagnosis

• Although an athlete should immediately be removed from play after a concussion, there is insufficient evidence to support absolute rest after concussion

A clinical report by the American Academy of Pediatrics (AAP) provided information regarding the diagnosis and management of sports-related concussions in adolescents and children.[11] The recommendations explained that appropriate management is essential in order to reduce the risk of long-term symptoms and complications. The team physician and athletic trainer must maintain a high index of suspicion to detect more mild concussions. The report also noted that cognitive and physical rest is the mainstay of management after diagnosis in these patients, and ongoing neuropsychological testing is a helpful tool during management.

Updated guidance from the AAP continues to recommend immediate removal from play; however, athletes do not need to avoid all activity while they have symptoms but should instead limit their physical exertion to brisk walking. Similarly, although a reduction in academic workload is recommended, prolonged absence from school should be discouraged.[66]

The AAP report notes that a return to sports and physical activity should not occur the same day as a concussion. Return to sports and physical activity requires a progressive exercise program, a complete absence of symptoms, successful completion of a standardized neuropsychological test, and continuing evaluation for any recurring signs or symptoms. The recovery for pediatric and adolescent athletes is generally longer than for older athletes.

Use of standardized tools in ED management of concussion

In a study of 164 patients 5 to 21 years old, use of the CDC’s Acute Concussion Evaluation (ACE) tools modified for use in a pediatric emergency department (ED) increased patient follow-up and improved recall of, and adherence to, ED discharge recommendations.[67, 68] With implementation of the tools, the percentage of patients following up with their primary care provider increased from 23% to 39% in the first week following discharge; from 31% to 55% in the second week; and from 32% to 61% in the fourth week.[67, 68]

Failure on validity tests has been shown to help detect exaggerated or feigned problems in adults with mild traumatic brain injury (TBI), and a study by Kirkwood and colleagues suggests that validity testing may also help identify noninjury effects in children and adolescents.[69] In their study of 191 patients aged 8 to 17 years with mild TBI, the 23 patients (12%) who failed the Medical Symptom Validity Test endorsed significantly more postconcussive symptoms than those who passed the test, with a large effect size (P< .001).[69]

Medical issues/complications

Most of the complications listed below probably already existed when the athlete sustained the initial head injury; in other words, they are not caused by an MTBI. These conditions may be associated with what was thought of as an MTBI. Therefore, the reader should not think of these conditions as a complication of an MTBI but must consider these other conditions when evaluating an athlete with a head injury.

A subdural hematoma is a rare injury in the athlete who presents with a presumed concussion. The classic presentation of a subdural hematoma is an acute and persistent LOC associated with the initial injury.

No association between epidural hematoma and brain injury exists. This condition classically presents with a brief period of unconsciousness, followed by a lucid period, and then a subsequent deterioration over 15-30 minutes. Tearing of the middle meningeal artery secondary to an associated temporal skull fracture is the usual cause of an epidural hematoma.

Subarachnoid bleeding may also occur with a head injury of any type. Worsening headache and other signs of increasing intracranial pressure will gradually grow after the initial event.

Second impact syndrome has been described in many review articles. In this condition, fatal brain swelling occurs after minor head trauma in individuals who still have symptoms from a previous minor head trauma. Thus far, all cases of second impact syndrome have been described in relatively young patients (age < 20 y). Significant controversy exists over the etiology of this condition, although it is thought to be secondary to loss of autoregulation of cerebral blood flow in an already injured brain.

Authors have questioned the validity of second impact syndrome due to problems with the documentation of the (1) initial event, (2) persistent symptoms, and (3) severity of the second impact. Despite these problems, practitioners should be aware of this possible complication, especially when treating the relatively immature brain of a young athlete. Treatment of second impact syndrome requires immediate recognition and immediate treatment with hyperventilation and osmotic agents. Surgical treatment for this condition is ineffective. The overall prognosis is usually grim.

Postconcussive syndrome consists of prolonged symptoms that are related to the initial head injury. Unfortunately, the severity of the concussion does not necessarily predict who will experience prolonged symptoms. Similarly, the number of concussions is not necessarily predictive of future problems. Symptoms usually consist of persistent recurrent headaches, dizziness, memory impairment, loss of libido, ataxia, sensitivity to light and noise, concentration and attention problems, depression, and anxiety.

A retrospective case-control study indicated that children with a personal or family history of mood disorders who sustain a sports-related concussion have a significantly increased risk for developing postconcussive syndrome.[70]

A study that included 2413 participants by Grool et al reported a lower risk of persistent postconcussive symptoms in those who participated in early physical activity compared to those with no physical activity (24.6% vs 43.5%; Absolute risk difference, 18.9% [95% CI,14.7%-23.0%]). However, further clinical studies are needed to examine this association.[71]  

Most patients with MTBI recover in 48-72 hours, even with detailed neuropsychologic testing, and are headache free within 2-4 weeks of the injury. Obtain a more detailed history of emotional, concentration, and associated symptoms for patients who have persistent symptoms that last longer than 1 week.

A double-blind study by Miller and colleagues indicated that hyperbaric oxygen (HBO) is no better than sham therapy in the treatment of postconcussive syndrome. The study involved 72 persons, 94% of whom were enlisted in military service, with participants experiencing ongoing postconcussion symptoms for a period of at least 4 months after sustaining an MTBI. Patients received HBO treatment, sham air-compression therapy, or routine care alone.[72, 73]

A study of retired professional football players (average age 53.8 +/– 13.4 y) by Guskiewicz et al reported significant memory changes in those players with a history of recurrent concussions.[3] Another report by the same authors of these retired football players suggested a link between recurrent sports-related concussions and an increased risk of clinical depression.[23]

Concussion information from the NFL Players' Association, the American Academy of Neurology, and the American College of Emergency Physicians can be found here.

Consultations

Consultation with a neurologist or primary care sports medicine physician is indicated for patients who have prolonged symptoms. Neuropsychologic consultation may also be considered to document any deficits that may interfere with the athlete's return to sport, school, or work.

Recommendations on the diagnosis and management of mild traumatic brain injury in children were released on September 4, 2018, by the CDC.[74, 75]  Key recommendations include:

• Refrain from routinely imaging children to diagnose mild traumatic brain injury (mTBI). Weigh multiple risk factors for further injury against the risks associated with radiation exposure and possible sedation when evaluating a child with possible mTBI.
• Validated, age-appropriate symptom scales in diagnosis should be used.
• Assess risks for sustained recovery. Risks include history of mTBI or other brain injury, severe symptoms immediately after the injury, and personal characteristics and family history, such as learning difficulties and family and social stressors.
• Provide instructions about returning to activity appropriate for patients' symptoms.
• Counsel patients and their parents/caregivers to return gradually to non-sports activities after no more than a 2-3 days of rest.

Overall, no medical therapy is usually prescribed for patients after an acute brain injury. Pain control is usually achieved with over-the-counter medications, such as acetaminophen. Avoid narcotics so that clouding of the patient's mental status or neurologic examination does not occur.

In a retrospective study of adolescent patients with concussion, researchers found that overuse of analgesics following injury may exacerbate concussion-related headaches or make them chronic.[76]

Of 104 patients in the study, 77 had chronic posttraumatic headache lasting between 3 and 12 months, and 54 of these patients (70.1%) met criteria for probable medication overuse for headache. Patients with medication overuse were significantly more likely to have daily headaches, to have nausea, to have throbbing associated with their headaches, and to be female. Headaches subsided or improved to preconcussive patterns in 37 patients (68.5%) within 2 months of discontinuing analgesics.

Class Summary

Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who have sustained trauma or those who have sustained injuries.

Acetaminophen (Tylenol, Aspirin-Free Anacin, Feverall, Q-Pap, Mapap)

Acetaminophen may work peripherally to block pain impulse generation; it may also inhibit prostaglandin synthesis in the CNS.

Return-to-play criteria are controversial. Similar to classification guidelines, several different guidelines regarding return to play have been established. No scientific evidence exists to justify one criterion versus another criterion. The main criteria for an athlete's return to play include complete clearing of all symptoms, complete return of all memory and concentration, and no symptoms after provocative testing. Provocative testing includes jogging, sprinting, sit-ups, or push-ups—in other words, some type of exercise that raises the athlete's blood pressure and heart rate.

The rules are the same for athletes who have a concussion that prohibits return to play during competition. Only after all symptoms have cleared both at rest and with exertion should an athlete even consider returning to practice or competition. In addition, the athlete has to show complete resolution of any emotional lability, mood disturbance, attention, or concentration difficulty. Relatively minor concussions may have more prolonged neurologic deficits. Therefore, the most important aspect of all published guidelines is the concept of an athlete not being allowed to return to play until he/she is completely asymptomatic.

A study of high school concussion patients reports that most assessments are performed by athletic trainers and the timing of return to play was similar whether the decision was made by a physician or an athletic trainer.[21]

In 2010, the AAN issued a brief position statement on sports concussion, recommending caution and protection first. If an athlete is suspected of having a concussion or closed head injury, then first remove the athlete from practice or competition, and do not allow return to play until he or she is evaluated by a physician with experience in treating concussions and cleared for return. Further recommendations are available in the 2013 AAN guidelines on evaluation and management of sports concussion.[13]

Injury prevention methods are currently being studied. In the past, rule changes that barred spearing in football and teaching football players not to lead with their head have significantly reduced the frequency of severe head injuries in American football.

Equipment and environmental changes can also prevent injury. Soccer goals must be anchored to the ground because many deaths secondary to head injury in soccer have been the direct result of a goal tipping over onto a player.

There is controversy regarding possible helmet wearing in soccer. Although helmets have been shown to clearly reduce the risk of head injury in recreational bicycle riding, no clear evidence exists that the type of headgear proposed for youth soccer will prevent acute or chronic head injury among soccer players.[26] Long-term studies that examine soccer players over time and that compare the players to themselves in a longitudinal fashion have not been completed. Thus far, studies that suggest long-term damage from heading have been methodologically flawed by comparing soccer players to other athletes, and these studies have not been able to distinguish heading from previous concussions. Most concussions in soccer are the result of direct contact rather than heading of the ball.

Even if helmets are used, no guarantee exists that they will necessarily fit. Studies of football helmet use in high school have demonstrated that only 15% of the helmets fit properly.[27] Further documentation of the possible increase in the risk of head injury associated with poor helmet fit has not been completed.

Although mouth guards have been advocated for injury prevention purposes, no controlled study has proven their usefulness in concussion prevention.

It is important to educate allied health professionals, coaches, families, and athletes about the recognition and acute management of a concussion, the difficulties involved with a concussion, the difficulty in managing and treating concussions, and the subtle problems with long-term complications. Understanding and recognition of these issues by all of the above may help to prevent recurrent concussion problems. Inexperienced healthcare providers may want to use some type of published guideline when initially managing these injuries.