mild traumatic brain injury, MTBI, concussion, post-concussive syndrome
About 1.4 million incidents of traumatic brain injury (TBI) are reported in the United States each year,1 of which 75% are classified as "mild."2 Mild TBI (MTBI) results from a number of causes, including falls, interpersonal violence, and motor vehicle collisions.3 Many cases are sports-related; football and wrestling in men and soccer and basketball in women are primary sources.4Patients who have MTBI may present with varying neurologic findings. Intoxication, preexisting conditions, polypharmacy, and dementia are confounders that are frequently encountered during the evaluation. Management decisions may be challenging in the patient who appears well during the evaluation but who was lethargic, confused, or amnestic at the time of the injury. Patients may also present days or weeks after the event with postconcussive symptoms, such as headache, sleep disturbances, memory and concentration problems, and emotional lability.This article presents a pragmatic approach to the patient with MTBI, using evidence-based guidelines when available.CLASSIFICATION OF MTBIMTBI describes a condition in which there is little or no change from the patient's neurologic baseline after the traumatic event. Although the term "head injury" is often used interchangeably with TBI, this usage is inappropriate. Head injury is defined as clinically evident trauma above the clavicles, including scalp lacerations, periorbital ecchymoses, and forehead abrasions. TBI refers to injury to the brain itself; it may occur without visible head injury. TBI manifests as confusion, focal neurologic abnormalities, altered level of consciousness, and/or subtle changes on neuropsychological testing. It may also appear as an abnormality on cranial CT or MRI scans or during intra-cranial surgeries."Concussion" is another term that is used interchangeably with MTBI and defined in various ways in the literature, often in the context of sports injuries.5 Historically, MTBI refers to patients with head injury who have resolving neurologic symptoms and a Glasgow Coma Scale (GCS) score between 13 and 15; concussion refers to patients with head injury who have loss of consciousness (LOC) or amnesia of varying durations. For consistency, we will use the terms "TBI" and "MTBI" unless we refer to a scale or a table using the term "concussion."There is no evidence-based definition of MTBI; inclusion and exclusion criteria vary by classification scheme. The Head Injury Interdisciplinary Special Interest Group of the American Congress of Rehabilitation Medicine defines MTBI according to the following criteria6:- Grade 1: Any alteration in mental state at the time of injury (eg, feeling dazed, disoriented, or confused).- Grade 2: Any loss of memory of the events immediately before or after the injury, with post-traumatic amnesia of less than 24 hours.- Grade 3: Any period of LOC of less than 30 minutes followed by a GCS score of 13 to 15.7.MTBI may not be clinically evident during the initial medical and neurologic evaluations, whether because of symptom resolution or the use of insensitive assessments in very mild cases. The GCS is the most widely used system of global neurologic evaluation and one of the few systems that assigns an evaluation label that is associated with outcome (Table 1).7Initially developed to describe patients who were in a coma after head injury, the GCS score facilitates communication of neurologic status among medical personnel. A score of 13 to 15 typically suggests mild injury; 9 to 12, moderate injury; and less than 9, severe injury. Some experts believe that patients with a GCS score of 13, who have a significantly higher rate of neurosurgical findings on CT, belong in the moderate category. Others only include patients with a GCS score of 15 at the time of evaluation in this category.Although the GCS score is frequently used to grade TBI, the timing of when to determine the score varies considerably in the literature. A single GCS score determination is not sufficient for assessing the severity of a head injury. To optimize its utility, serial GCS measurements are required; the prognosis is worse if the score fails to normalize over time. On the other hand, the initial GCS score is a critical reference point when comparing patient groups and making an initial prognostic judgment.8The GCS score should be obtained through direct interaction with the patient, after the initial assessment and cardiopulmonary resuscitation (if necessary) but before the administration of sedatives or analgesics that may alter the score. To identify the progression or resolution of TBI, a neurologic assessment, including a GCS score, should be performed at regular intervals and when the patient's clinical status changes.PATHOPHYSIOLOGYMTBI can result from a direct blow to the head or from sudden deceleration or rotational forces that do not involve impact. Alteration in the patient's sensorium and cognitive dysfunction stems from direct injury to neurons and surrounding vasculature, with subsequent damage attributable to ischemia and metabolic perturbations.Early studies comparing CT with MRI demonstrated that patients without pathologic findings on head CT scan may exhibit structural abnormalities on MRI, specifically in the cortex of the frontal and temporal lobes.9 These findings correlated with behavioral and neuropsychological abnormalities. Diffuse axonal injury at the gray-white matter interface also has been demonstrated on MRI.10 Subsequent research using dynamic neuroimaging, including positron emission tomography (PET) and single photon emission CT (SPECT), shows impaired cerebral glucose utilization after injury.11 Decreased cerebral blood flow after injury also has been reported.12The current model of brain injury proposes a state of excitatory neurotransmitter toxicity, whereby injury sets off a cascade of neurochemical and metabolic factors resulting in cellular glycolysis with lactate production. These perturbations cause an initial excitatory response followed by a regional metabolic diaschisis and manifest as functional abnormalities.13Metabolic derangement in the injured brain probably contributes significantly to the prolonged period of morbidity experienced by many patients who do not have detectable structural lesions on CT or MRI scans. Some functional abnormalities that persist long after the initial injury are not identified with these anatomic imaging modalities (see "Postconcussive Syndrome" on next page). Future investigations that use more sensitive imaging tests and functional MRI for diffuse axonal injury may clarify the mechanisms and physiology in patients with persistent symptoms.INITIAL EVALUATIONThe condition of patients with TBI may deteriorate rapidly after an ostensibly innocuous presentation. Therefore, an immediate and methodic evaluation in accordance with advanced trauma life support protocols is recommended.14 This includes an assessment of the patient's airways; respiratory, circulatory, and neurologic status; and immobilization of the cervical spine.After this assessment, a more detailed survey and history taking may proceed. If the patient is unable to provide a reliable history, try to secure information from witnesses or family members. Early transfer to an appropriately staffed and monitored emergency department (ED) is critical and should be considered in those with an altered level of consciousness or focal neurologic deficits. Patients with intoxication or bleeding diathesis and those older than 60 years merit special attention because neurologic deficits may not be readily apparent.Important historical aspects of the injury include the mechanism, duration of LOC, post-traumatic amnesia, and other injuries. One potential pitfall in the management of the patient with TBI is to assume that this injury is entirely responsible for the overall clinical picture. A comprehensive approach requires initial consideration of the reversible causes of altered mental status, including hypoperfusion, hypotension, hypoxemia, hypoglycemia, and drug toxicity. Strong consideration of possible antecedent events, such as syncope, transient ischemic attack, orthostasis, or dysrhythmia, is prudent, particularly if the patient is elderly.Evaluation of the patient with dementia may be particularly challenging, especially when an attempt is made to determine whether an acute cognitive deficit is compounding the chronic disease. Cerebrovascular disease and Alzheimer disease may prevent a patient from full participation in the neurologic evaluation. Do not assume that abnormal findings reflect the patient's baseline status or that they are the result of an inability to communicate or participate. A consultation with the caregiver or long-term-care facility may help clarify the patient's preinjury functional status.IMAGING STUDIESCervical spine evaluation. The potential for cervical spine injury is sometimes overlooked in a well-appearing patient with MTBI. Any patient with acute TBI is considered to have an associated spinal injury until proved otherwise.The American Association of Neurological Surgeons' guidelines state that radiographic assessment of a cervical spine injury is not required in trauma patients who are awake, alert, and not intoxicated; who have no neck pain or tenderness; and who do not have significant associated injuries that detract from their general evaluation.15 If these criteria are not met, the patient should have a cervical collar placed immediately. For further evaluation, obtain 3 views of the cervical spine with plain film radiography or cervical spine CT. The modality chosen depends on the patient's concomitant injuries; ability to participate; and preexisting conditions, such as degenerative disease or arthritis.Skull radiography. This modality is neither sensitive nor specific for MTBI and therefore has no role in the evaluation of a child or adult with this condition. Although there is an increased likelihood of intracranial hemorrhage in patients with skull fracture, the prevalence of acute pathology in patients with a positive plain skull film (positive predictive value, 0.41) is low. Normal skull radiographs may be falsely reassuring. Although in one meta-analysis the negative predictive value of skull radiography was 0.94, low sensitivity precludes its use for intracranial pathology screening.16-18Pediatric cerebral neuroimaging. Children with head injury whose mental status is normal at presentation require a thorough history and physical and neurologic examination. If the results are normal, observation for 24 hours by a competent adult in any combination of locations (clinic, office, ED, or home) is recommended for children with minor closed head injury and no LOC.18 In the absence of LOC, head CT or MRI is not required. After the visit, parents should be alert to any new headache, vomiting, drowsiness, balance problems, confusion, emotional lability, seizures, and drainage from the ears or nose of the child.Infants have a higher proportion of intracranial injury with head trauma than do older children.19 Keep in mind that historical signs and symptoms of intracranial pathology are often absent in infants with such injuries. A conservative approach and low head CT threshold are recommended in this age group, particularly if significant scalp hematoma is present.20Cranial CT and careful observation may be used in the initial evaluation of children with MTBI and brief LOC (less than 1 minute). If the child's condition deteriorates during observation, perform a thorough neurologic examination and request a cranial CT scan immediately after the patient is stabilized.Adult cerebral neuroimaging. The indications for CT in adults with MTBI have been reviewed.21,22 According to evidence-based guidelines of the American College of Emergency Physicians, based largely on the New Orleans criteria (NOC),22 urgent head CT is indicated in patients with headache, vomiting, drug or alcohol intoxication, short-term memory deficits, post-traumatic seizure, coagulopathy, or physical evidence of trauma above the clavicle, and in those older than 60 years.17Stiell and colleagues23 formulated a clinical decision rule to standardize the emergency management of patients with minor head injury. The Canadian CT Head Rule (CCHR) consists of 5 high-risk factors (failure to reach a GCS score of 15 within 2 hours, suspected open skull fracture, any sign of basal skull fracture, more than 2 vomiting episodes, or age older than 65 years) and 2 additional medium-risk factors (amnesia before impact of more than 30 minutes and dangerous mechanism of injury).21In a validation study, the CCHR was evaluated and compared with the NOC in adults who presented to the ED with mild TBI and a GCS score of 15. The NOC and the CCHR both had 100% sensitivity for need for neurosurgical intervention and clinically important brain injury, but the CCHR was more specific and would result in lower CT rates.23POSTCONCUSSIVE SYNDROMESymptoms such as headache, dizziness, anxiety, and impaired cognition and memory may persist after MTBI (Table 2). This constellation of symptoms, known as postconcussive syndrome (PCS), affects more than 60% of patients 1 month after the injury24 and 15% at 1 year.25 Besides being distressing to the patient, family, and the primary caregiver, PCS represents a significant economic burden. Patients miss an average of 4.7 workdays after MTBI as a result of PCS symptoms; about 20% of patients are unemployed at 1 year.26 These deficits do not typically have correlating radiographic features on CT or MRI scans. The cognitive impairments may have a profound impact on younger, high-achieving persons; deficits in memory and planning have been detected in amateur athletes as young as high school-age after MTBI.27It is difficult to predict which patients will progress to PCS. Improvement at follow-up has been inversely related to the number of symptoms exhibited at hospital discharge.28 Most symptoms of uncomplicated MTBI display a linear decline during the year after trauma. In one study of 69 patients with MTBI who presented to an ED, predictors of PCS were female sex, non-sports-related mechanism (such as motor vehicle accident or fall), and poor performance on certain neurobehavioral tests (specifically, a score of less than 9 on the Digit Span Forward test for women and a score of less than 11.5 on the Hopkins Verbal Learning Test).29Whether the cause of these long-term impairments is structural or functional is unclear; there is a correlation with PCS symptoms and lesions in the hippocampus and temporal lobe detectable on functional dynamic neuroimaging (PET or SPECT).30 Regardless of the cause, the patient's complaints must be recognized as a clinical entity for which treatment options exist. Identify community resources for patients at risk for PCS. If necessary, arrange for follow-up with a rehabilitation specialist. A multidisciplinary team approach to follow-up is recommended.FOLLOW-UPThe patient with MTBI who has normal results on the neurologic examination and no indications for cerebral or cervical spine neuro-imaging may be discharged. Ideally, a patient should be discharged with written instructions provided to a responsible adult who will be able to check the patient during the subsequent 24 hours. Encourage patients to avoid alcohol for the next several days. Indi-cations for immediate medical attention include new severe headache, vomiting, confusion, emotional lability, drowsiness, seizures, difficulty with coordination or balance, and drainage from the nose or ears. Advise patients with MTBI that symptoms of PCS that last weeks to months may develop.Editor's note: A version of this article was published in the October 2005 issue of Consultant. It has been updated and revised for Applied Neurology.REFERENCES1. Division of Injury and Disability Outcomes and Programs, National Center for Injury Prevention and Control, Centers for Disease Control and Prevention, Department of Health and Human Services. Traumatic brain injury in the United States: emergency department visits, hospitalizations, and deaths. October 2004. Available at: http://www.cdc.gov/ ncipc/pub-res/TBI_in_US_04/TBI_ED.htm. Accessed April 24, 2006.2. National Center for Injury Prevention and Control, Centers for Disease Control and Prevention, Department of Health and Human Services. TBI report to Congress on mild traumatic brain injury in the United States: steps to prevent a serious public health problem. September 2003. Available at: www.cdc.gov/ncipc/pub-res/mtbi/report.htm. Accessed May 5, 2006.3. Guerrero JL, Thurman DJ, Sniezek JE. Emergency department visits associated with traumatic brain injury: United States, 1995-1996. Brain Inj. 2000;14:181-186.4. Powell JW, Barber-Foss KD. Traumatic brain injury in high school athletes. JAMA. 1999;282:958-963.5. Cantu RC. Guidelines for return to contact sports after a cerebral concussion. Physician Sportsmed. 1986;14:75-83.6. Kay T, Harrington DE, Adams R, et al. Definition of mild traumatic brain injury. J Head Trauma Rehabil. 1993;8:86-87.7. Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet. 1974;2:81-84.8. Stuss D. A sensible approach to mild traumatic brain injury. Neurology. 1995;45:1251-1252.9. Levin HS, Amparo E, Eisenberg HM, et al. Magnetic resonance imaging and computerized tomography in relation to the neurobehavioral sequelae of mild and moderate head injuries. J Neurosurg. 1987;665:706-713.10. Mittl RL, Grossman RI, Hiehle JF, et al. Prevalence of MR evidence of diffuse axonal injury in patients with mild head injury and normal head CT findings. AJNR. 1994;15:1583-1589.11. Bergsneider M, Hovda DA, Shalmon E, et al. Cerebral hyperglycolysis following severe traumatic brain injury in humans: a positron emission tomography study. J Neurosurg. 1997;86:241-251.12. Sakurada O, Kennedy C, Jehle J, et al. Measurement of local cerebral blood flow with iodo [14C] antipyrine. Am J Physiol. 1978;234:H59-H66.13. Hovda DA, Lee SM, Smith ML, et al. The neurochemical and metabolic cascade following brain injury: moving from animal models to man. J Neurotrauma. 1995;12:903-906.14. American College of Surgeons. Advanced Trauma Life Support (ATLS) Instructor Manual. 7th ed. Chicago: American College of Surgeons; 2004.15. Radiographic assessment of the cervical spine in asymptomatic trauma patients. Neurosurgery. 2002;50(3 suppl):S30-S35.16. Hofman PA, Nelemans P, Kemerink GJ, Wilmink JT. Value of radiological diagnosis of skull fracture in the management of mild head injury: meta-analysis. J Neurol Neurosurg Psychiatry. 2000;68:416-422.17. Jagoda AS, Cantrill SV, Wears RL, et al. American College of Emergency Physicians, clinical policy: neuroimaging and decision making in adult mild traumatic brain injury in the acute setting. Ann Emerg Med. 2002;40:231-249.18. The management of minor closed head injury in children. Committee on Quality Improvement, American Academy of Pediatrics. Commission on Clinical Policies and Research, American Academy of Family Physicians. Pediatrics. 1999;104:1407-1415.19. Greenes DS, Schutzmann SA. Infants with isolated skull fracture: what are their clinical characteristics, and do they require hospitalization? Ann Emerg Med. 1997;30:253-258.20. Schunk JE, Rodgerson JD, Woodward GA. The utility of head computed tomographic scanning in pediatric patients with normal neurologic examination in the emergency department. Pediatr Emerg Care. 1996;12:160-165.21. Stiell IG, Wells GA, Vandemheen K. The Canadian CT Head Rule for patients with minor head injury. Lancet. 2001;357:1391-1396.22. Haydel MJ, Preston CA, Mills TJ, et al. Indications for computed tomography in patients with minor head injury. N Engl J Med. 2000;343:100-105.23. Stiell IG, Clement CM, Rowe BH, et al. Comparison of the Canadian CT Head Rule and the New Orleans criteria in patients with mild head injury. JAMA. 2005;294:1511-1518.24. Bazarian JJ, Wong T, Harris M, et al. Epidemiology and predictors of post-concussive syndrome after minor head injury in an emergency population. Brain Inj. 1999;13:173-189.25. Rutherford WH, Merrett JD, McDonald JR. Symptoms at one year following concussion from minor head injuries. Injury. 1979;10:225-230.26. Dikmen SS, Temkin NR, Machamer JE, et al. Employment following traumatic head injuries. Arch Neurol. 1994;51:177-186.27. Matser EJ, Kessels AG, Lezak MD, et al. Neuropsychological impairment in amateur soccer players. JAMA. 1999;282:971-973.28. Alves WM, Macciocchi SN, Barth JT. Postconcussive symptoms after uncomplicated mild head injury. J Head Trauma Rehabil. 1993;8:48-59.29. Bazarian JJ, Atabaki S. Predicting postconcussion syndrome after minor traumatic brain injury. Acad Emerg Med. 2001;8:788-795.30. Umile EM, Sandel ME, Alavi A, et al. Dynamic imaging in mild traumatic brain injury: support for the theory of medial temporal vulnerability. Arch Phys Med Rehabil. 2002;83:1506-1513.31. Sports-related recurrent brain injuries-United States. MMWR. 1997;48:224-227.32. Cantu RC. Head injuries in sport. Br J Sports Med. 1996;30:289-296.33. McCrea M, Kelly JP, Randolph C. Standardized Assessment of Concussion (SAC): Manual for Administration, Scoring, and Interpretation. Waukesha, Wis: CNS, Inc; 1996.34. McCrea M. Standardized mental status testing on the sideline after sports-related concussion. J Athl Train. 2001;36:274-279.35. Aubry M, Cantu R, Dvorak J, et al. Summary and agreement statement of the First International Symposium on Concussion in Sport, Vienna 2001. Clin J Sport Med. 2002;12:6-11.36. Lovell MR, Collins MW. Neuropsychological assessment of the college football player. J Head Trauma Rehabil. 1998;13:9-26.37. Wojtys ED, Hovda D, Landry G, et al. Con-cussion in sports. Am J Sports Med. 1999;27:676-686.38. Raimondi AJ, Hirschauer J. Head injury in the infant and toddler. Coma scoring and outcome scale. Childs Brain. 1984;11:12-35.EVIDENCE-BASED MEDICINEExamples of evidence-based medicine related to this article include:- Jagoda AS, Cantrill SV, Wears RL, et al. American College of Emergency Physicians, clinical policy: neuroimaging and decision making in adult traumatic brain injury in the acute setting. Ann Emerg Med. 2002;40:231-249.- Stiell IG, Wells GA, Vandemheen K. The Canadian CT Head Rule for patients with minor head injury. Lancet. 2001;357:1391-1396.MARC ANDREWS, MD, is chief resident and JOHN BRUNS, Jr, MD, is clinical assistant professor of emergency medicine in the Department of Emergency Medicine at Mount Sinai School of Medicine in New York City.---TABLE 2 Symptoms of postconcussive syndromeSOMATICHeadacheSleepDizziness/vertigoNauseaFatiguePhotophobia/phonophobiaCOGNITIVEImpaired attention, concentration, and memoryAFFECTIVEAnxietyDepressionEmotional lability---Sports-Related Mild Traumatic Brain InjuryAbout 300,000 traumatic brain injuries (TBIs) are reported in the United States during sporting and recreational activities each year.31 Most of these occur in younger, healthier patients. In one survey of sports trainers, the mild TBI (MTBI) rate per 100 player-seasons was as high as 3.66 for high school football.4Concussion can be obvious in more severe cases, but in most patients with sports-related MTBI, mild disorientation is the only identifiable abnormality.32 To help identify the subtle memory and concentration deficits that affect persons after a concussion, the Standardized Assessment of Concussion (SAC) was developed to standardize the immediate sideline evaluation of a sports-related head injury.33 The SAC covers the cognitive functions of orientation, immediate memory, delayed recall, and concentration. A decline in the SAC score after injury was sensitive and specific in identifying athletes with concussion on the sideline.34There are numerous guidelines for evaluation and management of MTBI in athletes, including recommendations for when an athlete may safely return to play. However, more recent recommendations for players who exhibit any signs or symptoms of a concussion include the following35:- Removal of the player for the remainder of the competition.- Monitoring by a responsible adult for deterioration.- Medical evaluation.- Medically supervised, stepwise return to play.Optimally, formal neuropsychological testing should be performed within 24 hours of injury.36The American Orthopaedic Society for Sports Medicine recommends that any sideline evaluation after MTBI be performed by a physician and that the patient undergo neuropsychological testing as soon as possible.37 Returning to sports too early may result in cerebral edema, intracranial hypertension, or death from "second-impact syndrome."