OVERVIEW: What every practitioner needs to knowAre you sure your patient has closed head trauma/concussion? What are the typical findings for this disease?
Closed Head Injury
Closed head injury is the most common type of traumatic brain injury, also called blunt or nonpenetrating head trauma. This brain injury is caused by an external impact from sudden, violent motion that does not include a break in the skull. Closed head injury results in swelling or bleeding within the skull, which can lead to brain damage or death. There are three major consequences of closed head injuries: epidural hematoma, subdural hematoma and concussion. A fourth type, intracerebral hemorrhage, is the same as a hemorrhagic stroke.
Historically the definition of concussion has not been well defined until recently. The word concussion is derived from the Latin word “concutere” (concussus, past participle of concuteere, to strike together). The previous definition narrowly defined concussion as an injury that was associated with a brief loss of consciousness.
Concussion is a kind of mild traumatic brain injury (MTBI) that has been frequently used interchangeably with mild TBI in the medical literature. Here the word “mild” refers to the initial impact of the injury. Concussion refers to the impact of that a relatively low force. These are commonly seen with contact sports, but can also be associated with falls and motor vehicle and bicycle accidents. At the 3rd International Conference on Concussion in Sports in 2008 in Zurich, concussion was defined as “a complex pathophysiologic process affecting the brain, induced by traumatic biomechanical forces.” Several common features to define concussion include the following:
Concussion can be caused by a direct blow to the head, face, neck, or elsewhere on the body, with an impulse force transmitted to the head.
Concussion typically results in the rapid onset of short-lived impairment of neurologic function that resolves spontaneously.
Concussion may result in neuropathologic changes, but the acute clinical symptoms largely reflect a functional disturbance rather than a structural injury.
Concussion results in a graded set of clinical symptoms that may or may not involve loss of consciousness. Resolution of the clinical and cognitive symptoms typically follows a sequential course; however, it is important to note that in a small percentage of cases, postconcussion symptoms may be prolonged.
No abnormality on standard structural neuroimaging studies is seen in concussion.
Concussion is a common sports injury in middle school and high school athletes. The diagnosis is mainly based on history and physical examination. There are no diagnostic studies that help in confirmation of diagnosis. The traditional management of concussion in this age group has changed. Cognitive and physical rest during the recovery phase is a crucial part of management for appropriate healing. New concepts of complete brain rest along with physical rest in school-aged athletes have changed school management decisions.
The lack of prospective studies in the early adolescent age group has been a limitation for definitive recommendations for concussion management. The key component for prevention of closed head injuries like concussion is by education and awareness of safety measures during activities with high risk. It is important to recognize nonspecific signs and symptoms of concussion so that appropriate management can be initiated immediately, which improves the prognosis and prevents long-term sequelae.
The specific signs and symptoms of a concussion, as well as the timing of the appearacne of symptoms and the duration of symptoms can be quite variable. The signs and symptoms can be both acute and chronic. Acute signs and symptoms after concussion are vomiting, headache, inability to console, crying, restlessness or irritability, seizures, dizziness or confusion, visual problems, fatigue, or change in personality.
Chronic symptoms may present as poor cognitive function, persistent headaches, sleep disturbance, and mood disorders like depression and /or anxiety. Loss of consciousness occurs in only 10% of concussion victims and is not a reliable indicator of this condition. Similarly, loss of consciousness is not useful in predicting the severity of concussion.
What other disease/condition shares some of these symptoms?
Signs and symptoms of concussion are also seen with other pathologic conditions. Headache caused by concussion can also be exertional, migraine, or dehydration-induced headache. Poor cognitive function can also be caused by attention deficit disorder, learning disabilities, absence seizures, and mood disorder.
A concussion victim can present with fatigue, which can also be due to anemia, overtraining, or inadequate sleep. The patient can present with classic signs and symptoms of concussion, which can be due to unintentional injury or nonaccidental trauma (child abuse). The diagnosis of concussion should be considered if any individual presents with these signs and symptoms acutely after a traumatic injury to head or body.
What caused this disease to develop at this time?
The leading causes of concussion/MTBI in pediatrics are sports injuries, falls, bicycle or motor vehicle accidents, assaults, or nonaccidental trauma. Any individual without a previous history who presents with any of the signs or symptoms of concussion/MTBI mentioned above after a closed head injury or hit to the body from any cause, should be investigated for concussion. The diagnosis of concussion/MTBI can be challenging because the signs and symptoms can present hours, days, or weeks after the injury.
What laboratory studies should you request to help confirm the diagnosis? How should you interpret the results?
There are no laboratory studies that help in the diagnosis of concussion. The diagnosis is a clinical one, based on thorough history and physical examination, with emphasis on the neurologic examination. Balance deficits are common and should be included in the assessment. There are multiple tests to assess balance, but heel-to-toe walking backward, with eyes closed if possible, is a simple test that can be done by the clinician in any setting. Neuropsychological testing has given clinicians an additional tool to help evaluate and diagnose concussion along with its use in follow-up and recovery after the concussion.
Would imaging studies be helpful? If so, which ones?
The definition of concussion emphasizes that imaging studies are normal and therefore are helpful only to rule out other injuries. There is controversy about the need for urgent computed tomography (CT) after closed head injury. CT of the head is indicated if there are concerns about intracranial hemorrhage or increased intracranial pressure from a pathologic condition. Motor vehicle accidents with a high-risk mechanism for injury, progressive neurologic deterioration, or focal neurologic findings would support the imaging for appropriate diagnosis.
Indiscriminate use of CT is inappropriate from the public health care perspective because of the increased risk of cancer especially in the pediatric age group. A single head computed tomographic scan can lead to about 1/2000 children younger than the age of 2 years having a lifetime risk of cancer.
A large prospective study reported that a history and physical examination with low risk factors supported no CT of the head, with a negative predicted value of 99.95% (with nonsurgical intervention carried out on the missed cases). In this study, the individuals were considered low risk if they had normal mental status, absence of mechanism for severe injury, loss of consciousness, vomiting, severe headache, and no signs of basilar skull fracture.
Radiographs of the skull may be helpful in a suspected skull fracture. A skeletal survey may be indicated when suspected nonaccidental trauma could be the cause of a concussion.
If you are able to confirm that the patient has closed head trauma/concussion, what treatment should be initiated?
Initial treatment in the field at the site of injury should follow the Pediatric Advanced Life Support guidelines, with basic ABCDE evaluation and interventions. One of the key components of the initial management of the injured individual is stabilizing the cervical spine and evaluating for cervical spine injury. If the individual is not conscious or is unable to be adequately assessed, cervical spine precautions should be instituted until the absence of a cervical spine injury is confirmed.In the presence of any suspected cervical spine injury, any neurologic abnormalities or visual changes, further evaluation and management in the hospital setting is needed.
If athletes show any signs or symptoms of concussion during a sports event, the athlete should be immediately removed from the competition and should not return to the game on the same day of injury regardless of the short duration and/or rapid resolution of the signs and symptoms.
Initial treatment of the patient is supportive care. It is important to also rule out other complications or injuries that would require specific intervention. It is critical for the clinician to guide the patient in their recovery with an active management plan based on the current symptoms. Careful care management can facilitate recovery and prevent further injury.
The most effective immediate intervention includes strict physical and cognitive rest. Any activities that cause cognitive exertion such as school work or video games or mild physical exertion like normal play, simple exercises, or participation in any sports should be avoided until the patient is completely asymptomatic and cognitive testing shows no persistent deficits. Patients may then gradually and carefully return to their daily activities under careful supervision and postexertion assessment for return of any symptoms. Children and adolescents will need help and close supervision by their parents/guardians, teachers, coaches, and trainers to monitor and assist their recovery.
The goal of concussion treatment is to minimize environmentally induced symptom exacerbation. Adequate sleep helps in recovery.
Currently there is no strong evidence for any specific treatments. Some common medications have been used to treat symptoms of concussion. Amitriptyline is a tricyclic antidepressant used occasionally to treat migraine headaches. Studies show a variable effect of amitriptyline when used to treat posttraumatic headaches. Despite no prospective studies, there is some anecdotal evidence suggesting the use of melatonin to treat insomnia secondary to concussion.
Management of prolonged symptoms (symptoms continue more than 1 month) with concussion needs a different treatment plan. An animal model study suggests that after concussion, neuroplasticity can be promoted by brain rest during the acute recovery phase (3-4 weeks) followed by increased brain activity during the subacute phase maybe beneficial.
Other studies have recently also suggested the allowance of low-intensity exercise while the patient is still symptomatic during the subacute phase of concussion. The overall consensus recommendations for management include immediate brain rest during the acute phase also known as “metabolic mismatch phase” for 3-4 weeks. During the subacute phase after the acute phase, it is appropriate to gradually introduce cognintive and physical activities, in a slowly increasing fashion under careful supervision, to make sure there is no exacerbation of signs or symptoms.
The following link from the Centers for Disease Control and Prevention (CDC) provides a tool kit for clinicians that includes a patient assessment tool, fact sheets for patients, and a pocket card for on-field sports concussion management.
What are the adverse effects associated with each treatment option?
There can be exacerbation of the signs and symptoms if cognitive and physical rest is not maintained for a sufficient duration or if reintroduction of cognitive and physical acitivities is not done gradually.
What are the possible outcomes of closed head trauma/concussion?
The short-term and long-term outcomes of concussion in children are poorly understood.
One pediatric prospective study showed that in children with loss of consciousness of less than 15 minutes, none had poor outcome (which included severe disabilities, vegetative state, or death). Seizures developed in about 6% of the patients, who had twice the risk of relatively poor outcomes. It is well known that high school players take longer to recover than older adult athletes.
Animal model data suggest the reason for delay in recovery is due to comparative increased sensitivity of the developing brain of young athletes, to the pathologicrelease of glutamine and aspartate.
Adult athletes recover faster, with cognitive test recovery back to baseline in 3-5 days after concussion. College athletes recover in an average of 5-7 days and high school athlete recovery time is seen to be an average of 10-14 days with computerized neuropsychiatric testing. In high school athletes after concussion, more than half took longer than 1 week to recover and 10%-20% took longer than 1 month to become asymptomatic. Other studies showed more than 6 months’ recovery time in 6% of adolescent athletes.
In a study done at a large urban children’s hospital, the pediatric patients presenting to the emergency department with mild TBI (average age 14 years), with a Glasgow Coma Score (GCS) of 14-15 at presentation, were admitted for observation and then followed up in 2-3 weeks. This study suggested that a higher percentage of younger patients will have more prolonged symptoms.
A history of three previous concussions in a high school or college athlete has been well accepted as a risk factor for severe presentation, prolonged recovery time and threefold risk of future injury. There is also an association with decline in cognitive function and long-term neurodeficits. Compared with athletes with no previous history of concussion, athletes with a history of three concussions had a greater neurodeficit decline after a single episode of concussion. Recent study documented that in comparing college athletes with no previous concussion history to athletes with a history of two or more concussions, the athletes with previous concussions had longer recovery times for verbal memory and reaction time on computerized neuropsychiatric testing.
There are gender differences after concussion. Women have a greater decline from their baseline neuropsychological testing and in reaction time. Female athletes have significant worsening of their visual memory compared with male athletes after concussion.
There is no good pediatric age group evidence that comorbidities (like migraine headaches, mood disorder, and attention deficit disorder or sleep disturbance) increase the risk of concussion as seen in adult data. It is also not known if concussion is an environmental stressor that triggers or worsens these underlying comorbidities in susceptible individuals. Currently these comorbities should be considered possible risk factors for a prolonged or complicated recovery phase.
The CDC has a handout for families and caregivers so that they can use the discharge instruction sheet and wallet card to learn about postconcussive symptoms, when to return to the emergency department, and to keep track of follow-up appointments http://www.cdc.gov/concussion/HeadsUp/clinicians_guide.html#downloads.
What causes this condition and how frequent is it?
According to the national emergency department surveillance data, in the United States the estimated incidence of concussion is 1.6-3.8 million/year. The estimated incidence recognizes that only 5.5%-13% of sports-related TBIs are evaluated in the emergency department. From the emergency department surveillance data from 2001-2005, 60% of the sports injuries and 65% of the sports-related TBIs occurred in children between the ages of 5 and 18 years. Breaking the pediatric population into different age subgroups, the highest TBI rates occurs in 10- to 14-year-olds, followed by 15- to 19-year-olds.
Football, basketball, playground activities, soccer, and bicycling are the activities associated with the highest number of TBI-related emergency department visits. According to US high school data reporting, concussions are common injuries in high school sports, which accounts for about 10% of all injuries in contact/collision sports. Male athletes accounted for 70% of the reported emergency department visits, as they commonly play more contact sports.
In certain sports such as soccer, basketball, and college ice hockey, the reported concussion rates were higher in female athletes than in male athletes. The reason for this difference is not entirely clear. Some studies suggest that male athletes have more muscle mass than do female athletes, and stronger neck muscles are better able to absorb force and dampen the forces transmitted to the brain. Some studies have suggested that women are more honest in reporting their concussion symptoms, leading to higher reported rates.
Data show variation from different reporting systems and in different high school sports, suggesting that the actual incidence of concussion may be higher resulting from widespread underreporting of symptoms during sports season. Reasons for underreporting are several. Coaches and sideline personnel may not be able to recognize the concussion symptoms. Up to one third of injured athletes may not recognize their concussion symptoms. Some athletes purposefully do not report the symptoms for fear of being removed from the game or letting their teammates down.
How do these pathogens/genes/exposures cause the disease?
Based on the developed concussion/MTBI study model studies, the concussion injury can be thought of as a two-part process: a primary insult and a secondary inflammatory response.
The primary insult results in excessive release of excitatory neurotransmitters (glutamine and aspartate) that lead to disintegration of cell wall. Increased permeability of the cell wall leads to changes in intracellular sodium and potassium concentration, which in turn cause cell pH changes that cause calcium influx. These changes results in cell injury or cell death, which triggers a cytokine-mediated inflammatory response. During concussion, brain dysfunction also is possibly caused by the axonal stretch injury, which is well recognized in “shaken baby syndrome.” This also leads to a cytokine-mediated inflammatory response.
A recent study demonstrated that mild traumatic forces can cause axonal injury (at an earlier time, without any symptoms), and this trauma before the concussion blow may lower the threshold of the force that leads to symptomatic concussion. This study showed that there was an increase in expression of axonal surface membrane sodium channels within 24 hours, which suggests subclinical injury.
The secondary insult occurs as a result of an increased inflammatory response from the primary insult. This can explain why the concussion symptoms may present or worsen after 6-24 hours after the initial concussion/MTBI.
TBI leads to increased glucose and metabolic needs. Injured neuronal cells can upregulate sodium/potassium-adenosine riphosphatase (Na/K-ATPase)–dependent ion membrane transport proteins and restore the intracellular pH. These ATPase proteins are fueled by glucose. Glucose delivery after brain injury is thus crucial to restoration of intracellular pH and healing of cell membranes.
After concussion, there should be increased blood flow to increase delivery of nutrients, which includes increased glucose delivery to injured neuronal cells. However in both juvenile and adult animal models and in adult trauma victims, it has been shown that the cellular response to injury restricts cerebral blood flow, and the flow metabolism coupling is disrupted. This means that if the demand for glucose is high, the body is unable to upregulate cerebral blood flow, and thus the glucose needs of the injured cells are not met. However, if the glucose needs of the injured brain remain low (with decreased brain activity during pharmacologically induced coma), cerebral perfusion, including glucose delivery is sufficient for the injured cell needs.
The “metabolic mismatch” of increased cerebral glucose needs and inability of the cerebral blood circulation to meet the demands is a fundamental concept in management of concussion during the acute phase. “Concussion penumbra” refers to the development of a tenuous equilibrium between glucose use and delivery, which happens during the early phase of brain healing. In animal models cerebral glucose metabolism is abnormal for about 2 weeks, but the duration associated with MTBI in humans is unknown.
The brain is more vulnerable to additional stress during the early recovery phase. Minimizing glucose demands and avoiding additional strain to the cerebral blood flow by maximum rest would protect the vulnerable neuronal cells. This is the concept, based on the recommendations made for complete cognitive and physical rest during the early phase of recovery until the patient is asymptomatic.
What complications might you expect from the disease or treatment of the disease?
Based on recent evidence, the earlier view that concussion is a brief and uniformly self-resolving injury has changed. Although there are no data on the pediatric population, the chronic repetitive head injury sustained by boxers (chronic traumatic encephalopathy) has been known to cause dementia and more recently other neuropsychiatric disorders. Recent literature also has documented premature dementia and mood disorders in retired professional football player.
The tau proteins seen in other neurodegenerative diseases, have also been seen on autopsies of the brains of past professional contact sports players. The autopsies also showed brain parenchyma with fewer neurons, suggestive of premature neuronal cell death. There is a speculation that the protein deposits on the brain surface are caused by repetitive microtrauma.
How can closed head trauma/concussion be prevented?
For preventive care, clinicians can provide information to patients, families, and caregivers about the behaviors and activities that increase the risk of concussion/MTBI. These tips are also available on the CDC patient information sheet, “Heads Up: Preventing Concussion,” contained in the tool kit. To reduce the risk of concussion, following preventive measures should be advised:
Wear a seat belt in a motor vehicle and having an appropriate car seat according to different pediatric age groups, based on their height and weight.
Never drive under the influence of drugs or alcohol.
Ensure that during high-risk sports, safety rules are followed and appropriately fitted protective equipment is used.
After injury, ensure that appropriate assessment is done to determine if the individual needs further evaluation and treatment and to prevent injuries by avoiding early return to sports activity.
Make living areas and playground surfaces safe according to the safety rules and regulation recommendations.
Wear a helmet that is well fitted and maintained properly when participating in the following activities:
Riding a bicycle, horse, motorcycle, scooter, snowmobile or all-terrain vehicle
Riding a skateboard or other skates, skiing, snowboarding, or sledding
Playing contact sports like football, lacrosse, boxing, ice hockey, or batting or running bases in baseball or softball
What is the evidence?
“Nonfatal traumatic brain injuries from sports and recreation activities–United States, 2001-2005”. MMWR Morb Mortal Wkly Rep. vol. 56. pp. 733-7. (This study provides epidemiologic data on concussion and other TBIs. To characterize sports- and recreation-related (SR-related) TBIs among patients treated in US hospital emergency departments, the CDC analyzed data from the National Electronic Injury Surveillance System–All Injury Program (NEISS-AIP) for the period 2001-2005. This report summarizes the results, indicating that an estimated 207,830 patients with nonfatal SR-related TBIs were treated in emergency departments each year during this period. The highest rates of SR-related TBI emergency department visits for both male patients and female patients occurred among those aged 10-14 years.)
Blinman, TA, Houseknecht, E, Snyder, C. “Postconcussive symptoms in hospitalized pediatric patients after mild traumatic brain injury”. J Pediatr Surg. vol. 44. 2009. pp. 1223-8. (This study sought to clarify the frequency and severity of concussive symptoms reported by children who required hospitalization for MTBI. Symptoms after MTBI are quite common at the time of hospitalization. Symptom scores improve to near normal for most by outpatient follow-up. The most common symptom was headache, but the most severe was fatigue.)
Brenner, D J. “Estimating cancer risks from pediatric CT: going from the qualitative to the quantitative”. Pediatr Radiol. vol. 32. 2002. pp. 228-33.
Cavanaugh, JT, Guskiewicz, KM, Guiliani, C. “Detecting altered postural control after cerebral concussion in athletes with normal postural stability”. Br J Sports Med. vol. 39. 2005. pp. 805-811. (Athletes who demonstrated normal postural stability after concussion nonetheless displayed subtle changes in postural control. Concussion assessment protocols for athletes should include an in-depth assessment of postural control.)
Comper, P, Bisschop, SM. “A systematic review of treatments for mild traumatic brain injury”. Brain Inj. vol. 19. 2005. pp. 863-80. (This systematic review of the literature between the years 1980 and 2003 on treatment of concussion revealed four general categories of interventions: pharmacotherapy, cognitive rehabilitation, patient education, and other. The majority of studies were weak; however there is evidence to support the effectiveness of patient education interventions.)
Davis, GA, Iverson, GL, Guskiewicz, KM. “Contributions of neuroimaging, balance testing, electrophysiology and blood markers to the assessment of sport-related concussion”. Br J Sports Med. vol. 43(suppl 1). 2009. pp. i36-45. (This article reviews the diagnostic tests and imaging used in the management of sports concussion in both adults and pediatric populations to monitor the severity of symptoms and deficits, track recovery, and advance knowledge relating to the natural history and neurobiologic features of the injury. The current status of the diagnostic tests and investigations is analyzed, and potential directions for future research are provided. Currently, all tests and investigations, with the exception of clinical balance testing, remain experimental. There is accumulating research, however, that shows promise for the future clinical application of functional magnetic resonance imaging in sport concussion assessment and management.)
Grady, MF. “Concussion in the adolescent athlete”. Curr Probl Pediatr Adolesc Health Care. vol. 40. 2010. pp. 154-69. (This article reviews the current understanding of the epidemiology, pathophysiology, and clinical presentation of concussion and discusses the unique factors involved in clinical management of concussion in the adolescent student athlete.)
Guskiewicz, KM, Marshall, SW, Bailes, J. “Association between recurrent concussion and late-life cognitive impairment in retired professional football players”. Neurosurgery. vol. 57. 2005. pp. 719-26; discussion 719-26. (The purpose of this study was to investigate the association between previous head injury and the likelihood of the development of mild cognitive impairment and Alzheimer's disease in a unique group of retired professional football players with previous head injury. This is one of several studies that suggest that the onset of dementia-related syndromes may be initiated by repetitive cerebral concussions in professional football players.)
Hahn, YS, McLone, DG. “Risk factors in the outcome of children with minor head injury”. Pediatr Neurosurg. vol. 19. 1993. pp. 135-42. (A subset of children with minor head injury is known to experience serious neurologic consequences, but identifying this subset has been difficult. This study examined various risk factors such as length of unconsciousness, presence of skull fractures, CT findings, posttraumatic seizure, and Glasgow or Children's Coma scores for their impact on clinical outcomes.)
Kuppermann, N, Holmes, JF, Dayan, PS. “Identification of children at very low risk of clinically-important brain injuries after head trauma: a prospective cohort study”. Lancet. vol. 374. 2009. pp. 1160-70. (CT of head-injured children has risks of radiation-induced malignancy. The aim of this study was to identify children at very low risk of clinically important traumatic brain injuries (ciTBI) for whom CT might be unnecessary. The authors provide validated prediction rules that identify children at very low risk of ciTBIs for whom CT can routinely be obviated.)
Leddy, JJ, Kozlowski, K, Donnelly, JP. “A preliminary study of subsymptom threshold exercise training for refractory post-concussion syndrome”. Clin J Sport Med. vol. 20. 2010. pp. 21-7. (This article describes a postconcussion treatment regimen with controlled reintroduction of exercise as a safe program that appears to improve postconcussive symptoms when compared with a no-treatment baseline.)
McAllister, TW, Sparling, MB, Flashman, LA. “Neuroimaging findings in mild traumatic brain injury”. J Clin Exp Neuropsychol. vol. 23. 2001. pp. 775-91. (This article reviews the literature on usefulness of structural and functional imaging in MTBI.)
McCrory, P, Meeuwisse, W. “Consensus statement on Concussion in Sport 3rd International Conference on Concussion in Sport held in Zurich, November 2008”. Clin J Sport Med. vol. 19. 2009. pp. 185-200.
McKeag, DB, Kutcher, JS. “Concussion consensus: raising the bar and filling in the gaps”. Clin J Sport Med. vol. 19. 2009. pp. 343-46.
Mendez, CV, Hurley, RA, Lassonde, M. “Mild traumatic brain injury: neuroimaging of sports-related concussion”. J Neuropsychiatry Clin Neurosci. vol. 17. 2005. pp. 297-303.
Pellman, EJ, Viano, DC. “Concussion in professional football: summary of the research conducted by the National Football League's Committee on Mild Traumatic Brain Injury”. Neurosurg Focus. vol. 21. 2006.
Reddy, CC, Collins, MW. “Sports concussion: management and predictors of outcome”. Curr Sports Med Rep. vol. 8. 2009. pp. 10-5. (This article highlights research on predictors of outcome and treatment protocols that has resulted in the paradigm shift from traditional concussion grading scales to individualized care. Concussion management requires a patient-centered approach with individualized assessment, including risk factor analysis, neurocognitive testing, and a thorough symptom evaluation.)
Saran, A. “Antidepressants not effective in headache associated with minor closed head injury”. Int J Psychiatry Med. vol. 18. 1988. pp. 75-83. (This study questions earlier reports regarding the usefulness of amitriptyline in chronic muscle contraction headache and depression associated with minor closed head injury.)
Sarmiento, KJ, Mitchko, J, Klein, C. “Evaluation of the Centers for Disease Control and Prevention's concussion initiative for high school coaches: "Heads Up: Concussion in High School Sports."”. J Sch Health. vol. 80. 2010. pp. 112-8. (To reduce the number of sports-related concussions, the CDC, with the support of partners and experts in the field, developed a tool kit for high school coaches with practical, easy-to-use concussion-related information. This study explores the success of the tool kit in changing knowledge, attitudes, and practices related to the prevention and management of concussions.)
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- OVERVIEW: What every practitioner needs to knowAre you sure your patient has closed head trauma/concussion? What are the typical findings for this disease?
- What other disease/condition shares some of these symptoms?
- What caused this disease to develop at this time?
- What laboratory studies should you request to help confirm the diagnosis? How should you interpret the results?
- Would imaging studies be helpful? If so, which ones?
- If you are able to confirm that the patient has closed head trauma/concussion, what treatment should be initiated?
- What are the adverse effects associated with each treatment option?
- What are the possible outcomes of closed head trauma/concussion?
- What causes this condition and how frequent is it?
- How do these pathogens/genes/exposures cause the disease?
- What complications might you expect from the disease or treatment of the disease?
- How can closed head trauma/concussion be prevented?
- What is the evidence?