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Acute mild traumatic brain injury (concussion) in adults

Acute mild traumatic brain injury (concussion) in adults
Literature review current through: Jan 2024.
This topic last updated: Feb 22, 2022.

INTRODUCTION — Mild traumatic brain injury (TBI) is common and, while typically benign, has a risk of serious short- and long-term sequelae.

Important considerations in the management of mild TBI include [1]:

Identification of immediate neurologic emergencies

Recognition and management of neurologic sequelae

Prevention of cumulative and chronic brain injury

An overview of the clinical presentation, evaluation, and management of mild TBI in adults is presented here. The epidemiology and classification of TBI, mild TBI in children, postconcussion syndrome (PCS), and other sequelae of mild TBI are discussed separately.

(See "Traumatic brain injury: Epidemiology, classification, and pathophysiology".)

(See "Minor blunt head trauma in infants and young children (<2 years): Clinical features and evaluation".)

(See "Minor blunt head trauma in children (≥2 years): Clinical features and evaluation".)

(See "Postconcussion syndrome".)

(See "Sequelae of mild traumatic brain injury".)

DEFINITIONS — TBI occurs with head injury, usually due to contact. Acceleration/deceleration forces have also been postulated to cause TBI in the absence of contact injury. (See "Traumatic brain injury: Epidemiology, classification, and pathophysiology".)

Mild TBI is typically defined as mild by a Glasgow Coma Scale (GCS) score of 13 to 15, measured at approximately 30 minutes after the injury (table 1). Some recommend classifying patients with a GCS score of 13 as moderate head injury (defined as GCS score of 9 to 12) because they seem more similar with regard to prognosis and incidence of intracranial abnormalities [2-5]. According to the American Congress of Rehabilitation Medicine, mild TBI is "a traumatically induced physiological disruption of brain function," as manifested by any one of several features, including "any period of loss of consciousness, any loss of memory for events immediately before or after the accident, [or] any alteration in mental state at the time of the accident" as long as the severity of deficits doesn't lead to an initial GCS score of less than 13 (table 1) [6].

The term "concussion" is often used in the medical literature as a synonym for mild TBI, but it is used more specifically to describe the characteristic symptoms and signs that an individual may experience after a mild TBI. The Quality Standards Subcommittee of the American Academy of Neurology defines concussion as a trauma-induced alteration in mental status that may or may not involve loss of consciousness [1].

Definitions of mild TBI/concussion often do not explicitly require a normal head computed tomography (CT). A minority of patients who present with mild TBI are found to have significant intracranial abnormalities, including contusion and hemorrhage (subarachnoid, subdural, epidural, or intracerebral), either at presentation or at follow-up. When these are identified, patients may no longer be considered to have mild TBI as their primary diagnosis but are more appropriately diagnosed and managed according to the identified lesion (eg, acute subdural hemorrhage). However, such patients may still be subject to other sequelae of mild TBI. (See "Postconcussion syndrome" and "Sequelae of mild traumatic brain injury".)

EPIDEMIOLOGY — Approximately 2.5 million people sustain a TBI in the United States every year [7]. Most, 75 to 95 percent, are mild [8,9]. The annual incidence of mild head injury per 100,000 population has been estimated to be 131 for San Diego County, California [10]; 149 for Olmsted County, Minnesota [11]; and 749 for Auckland, New Zealand [12]. However, the incidence of mild head injury may be significantly higher, as many cases go unreported [13,14].

For an industrialized country such as the United States, estimates of the relative causes of TBI are as follows: motor vehicle accidents (20 to 45 percent), falls (30 to 38 percent), occupational accidents (10 percent), recreational accidents (10 percent), and assaults (5 to 17 percent) [12,15]. In older adults, falls are more likely the cause, and motor vehicle accidents are more common in the young.

Mild TBI also occurs in contact sports; American football, ice hockey, soccer, boxing, and rugby have a particularly high incidence [16]. The annual incidence of sports-related concussion in the United States is 1.6 to 3.8 million, and the likelihood of an athlete in a contact sport experiencing a concussion is as high as 20 percent per season [17]. In football alone, an estimated 10 percent of United States college and 20 percent of United States high school players sustain brain injuries each season [18-20].

Mild TBI is also a common injury among soldiers who have participated in combat [14]. In a survey of 2525 Army infantry soldiers performed three to four months after their return from a one-year deployment in Iraq, 5 percent reported injuries with loss of consciousness and 10 percent reported injuries with altered consciousness [21]. The mechanisms of injury (in order of frequency) included blasts or explosions, falls, motor vehicle accidents, and fragment, shrapnel, and bullet wounds.

Males are more commonly head-injured, with a ratio between 2.0:1 and 2.8:1 [9,12]. This likely reflects the greater participation of men in high-risk activities that lead to TBIs. Approximately one-half of all patients with mild TBI are between the ages of 15 and 34 years. Patients at moderate risk include those less than 5 years and those over 60 years. Lower socioeconomic status, lower cognitive function, and a history of hospital admissions for intoxications are also risk factors for head injury [9,22].

PATHOPHYSIOLOGY — Mild TBI results from direct external contact forces or from the brain being slapped against intracranial surfaces with acceleration/deceleration trauma. Concussion may result in neuropathologic changes, but the acute clinical symptoms are believed to reflect a disturbance of function rather than structural injury [23].

Mild TBI may result in cortical contusions due to coup and contrecoup injuries [24]. While axonal rupture from shear and tensile forces can occur at the time of severe head injury, milder degrees of axonal damage are postulated to play a role in mild TBI. Disruption of axonal neurofilament organization impairs axonal transport, leading to axonal swelling, Wallerian degeneration, and transection [25]. Release of excitatory neurotransmitters acetylcholine, glutamate, and aspartate, and the generation of free radicals may contribute to secondary injury [26]. There is also emerging evidence that inflammatory mediators promoting repair and regeneration may also contribute to secondary injury and neurodegeneration [27]. One somewhat controversial theory regarding blast trauma is that the transfer of kinetic energy through the vascular system to the brain can lead to TBI in the absence of a direct head injury [28].

That these processes occur in mild TBI is supported by findings in animal models of brain injury [25,29]. Evidence of microscopic axonal injury, axon retraction bulbs, and microglial clusters has also been described in the pathologic examination of patients with minor head injury who died of other injuries [30,31]. Diffusion tensor magnetic resonance imaging (MRI) studies in patients with mild TBI demonstrate increased fractional anisotropy and decreased diffusivity in the corpus callosum and other white matter tracts that is suggestive of cytotoxic edema [32-35]. Functional MRI studies demonstrate additional abnormalities [36,37]. Imaging studies have shown that patients with mild head injury may have more frequent and more extensive areas of abnormality as measured by Technetium-99m (Tc-99m) hexamethylpropylene amine oxime single-photon emission computed tomography (HMPAO SPECT), fludeoxyglucose positron emission tomography (FDG-PET), computed tomography (CT) perfusion, and MRI than can be seen on a conventional noncontrast CT, supporting a role for diffuse structural and/or physiologic derangement in mild TBI [38-44]. The advanced neuroimaging techniques described above may one day be helpful in identifying sequelae of TBI when conventional noncontrast CT and MRI are normal; however, the data currently available for the use of these techniques are insufficient for clinical use and application to individual patients [45]. There is interest in leveraging artificial intelligence and big data, including conventional and advanced neuroimaging, to develop algorithms for providing integrated evidence-based patient care, which assists and improves triage, diagnosis, treatment, and prognosis [46].

CLINICAL FEATURES

Acute symptoms and signs — The hallmark symptoms of concussion are confusion and amnesia, sometimes with, but often without, preceding loss of consciousness [1,47]. These symptoms may be apparent immediately after the head injury or may appear several minutes later [48]. It is important to emphasize that the alteration in mental status characteristic of concussion can occur without loss of consciousness. In fact, the majority of concussions in sports occur without loss of consciousness and are often unrecognized [49].

The amnesia almost always involves loss of memory for the traumatic event and frequently includes loss of recall for events immediately before (retrograde amnesia) and after (anterograde amnesia) the head trauma. An athlete with amnesia may be unable to recall details about recent plays in the game or details of current events. Amnesia also may be evidenced by the patient repeatedly asking a question that has already been answered.

Other early symptoms of concussion include headache, dizziness (vertigo or imbalance), lack of awareness of surroundings, and nausea and vomiting; these may immediately follow the head trauma or evolve gradually over several minutes to hours [48]. Over the next hours and days, patients may also complain of mood and cognitive disturbances, sensitivity to light and noise, and sleep disturbances [50].

While many concussions occur without observed findings [47], signs observed in someone with a concussion may include [48]:

Grossly observable incoordination (stumbling, inability to walk tandem/straight line)

As well as neuropsychiatric impairments, including:

Vacant stare (befuddled facial expression)

Delayed verbal expression (slower to answer questions or follow instructions)

Inability to focus attention (easily distracted and unable to follow through with normal activities)

Disorientation (walking in the wrong direction, unaware of time, date, place)

Slurred or incoherent speech (making disjointed or incomprehensible statements)

Emotionality out of proportion to circumstances (appearing distraught, crying for no apparent reason)

Memory deficits (exhibited by patient repeatedly asking the same question that has already been answered or inability to recall three of three words after five minutes)

Occasionally, associated transient neurologic deficits, such as global amnesia or cortical blindness, can occur. The pathogenesis underlying these symptoms is not well understood; it is speculated that vascular hyperreactivity and trauma-induced, migraine-equivalent phenomena may play a role [51-53].

Less common are cranial nerve deficits such as extraocular muscle weakness, vertigo, and nystagmus. (See "Sequelae of mild traumatic brain injury", section on 'Other cranial nerve injuries' and "Sequelae of mild traumatic brain injury", section on 'Posttraumatic vertigo and dizziness'.)

Clinical findings not consistent with mild, uncomplicated TBI include focal neurologic findings such as limb weakness or hemiparesis, visual field deficit, pupillary abnormality, or Horner syndrome. These should be evaluated independently. A stroke syndrome, in particular, raises suspicion for traumatic vascular injury, while paraparesis or paraplegia suggests spinal cord injury. These presentations and their evaluation and management are discussed separately in individual topic reviews.

Seizures — Early posttraumatic seizures are those that occur within the first week after head injury. These seizures are considered to be acute symptomatic events and not epilepsy. Posttraumatic seizures occur in less than 5 percent of mild or moderate TBI, and they are more common with more severe TBI, especially if complicated by intracranial hematoma [54,55].

Approximately half occur within the first 24 hours of the injury; one-quarter occur within the first hour [55,56]. The earlier a seizure begins, the more likely it will be generalized in onset; after the first hour more than half are either simple partial (pure motor) seizures or focal with secondary generalization [54,55].

Early posttraumatic seizures increase the risk of posttraumatic epilepsy by fourfold, to more than 25 percent [55]. While antiseizure medications may be used in the treatment of early seizures, they are not helpful in the prevention of posttraumatic epilepsy. (See "Posttraumatic seizures and epilepsy".)

Complicated mild traumatic brain injury — With uncomplicated, mild TBI, limited structural axonal injury may be present but not overtly evident on computed tomography (CT) or routine conventional magnetic resonance imaging (MRI). However, mild TBI can be complicated in 6 to 10 percent of cases by existent cortical contusions and the development of intracranial hemorrhage, which may be intracerebral, subdural, epidural, or subarachnoid [57]. Worse functional outcomes are seen in patients with mild TBI with imaging evidence of intracranial injury when compared with those without [58].

Brain contusions are areas of injury with associated localized ischemia, edema, and mass effect [59]. Signs of cortical contusions vary based on their number, size, and location within the brain but include focal neurologic signs as well as confusion and impaired consciousness. Brain contusions may delay recovery from a concussion.

Neurologic deterioration after mild TBI is highly suggestive of an evolving intracranial hematoma, which may be intracerebral, subdural, or epidural and usually occurs due to a tear in an intracranial artery or vein [60]. Signs include worsening headache, focal neurologic signs, confusion, and lethargy, which may progress to loss of consciousness or even death. In the setting of substantive secondary hemorrhage with deterioration in the Glasgow Coma Scale (GCS), the TBI would be reclassified as moderate or severe.

Subdural hemorrhage occurs when trauma results in the tearing of bridging veins or dura. The presentation may be acute, subacute, or chronic. (See "Subdural hematoma in adults: Etiology, clinical features, and diagnosis" and "Subdural hematoma in adults: Management and prognosis".)

Epidural or intracerebral hemorrhage is usually arterial in origin and has an acute, abrupt presentation, which might be delayed by minutes to hours from the original injury. It is estimated that before neurologic deterioration, up to half of persons with epidural hemorrhage have a "lucid interval" following a brief loss of consciousness or period of confusion. (See "Intracranial epidural hematoma in adults" and "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis" and "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis".)

In addition to concussion, head trauma may result in injuries to other parts of the head or neck, including skull or facial bone fractures, spine or spinal cord injuries, eye injuries, and damage to major blood vessels within the neck. A skull fracture may be accompanied by underlying pathologic findings, including brain contusions, dural tears, and vascular trauma [61]. Skull fractures and traumatic cervical vascular injuries are discussed separately. (See "Skull fractures in adults" and "Blunt cerebrovascular injury: Mechanisms, screening, and diagnostic evaluation" and "Blunt cerebrovascular injury: Treatment and outcomes" and "Acute traumatic spinal cord injury" and "Overview of eye injuries in the emergency department" and "Approach to diagnosis and initial treatment of eye injuries in the emergency department".)

EVALUATION — Patients suspected of concussion or mild TBI should be medically evaluated by a trained licensed health professional, whether in a doctor's office, in an emergency department, or on an athletic field sideline. (Related Pathway(s): Mild head trauma: Evaluation of adults in the emergency department.)

The acute evaluation of an individual includes a neurologic assessment and mental status testing [62]. Prolonged unconsciousness (greater than one minute), persistent mental status alterations, or abnormalities on neurologic examination require urgent imaging and neurologic or neurosurgical consultation [1]. Standardized examinations may aid in the sideline evaluation of concussion but have not been well validated when used without a baseline score.

It is important to note that mild TBI and concussion may be unrecognized by both the injured and nonmedically trained observers, particularly if there is no loss of consciousness [47]. Some surveys have found that more than 80 percent of individuals with a past concussion did not recognize it as such [63,64].

Neurologic assessment — Patients should be asked to describe the incident in as much detail as they can, including the events leading up to the injury, and those that immediately followed it. This history can assess the degree of amnesia associated with the concussion. Symptoms should be specifically elicited; a symptom checklist, such as the one used in the Standardized Assessment of Concussion (SAC), can be helpful (table 2).

An evaluation of mental status is required. Simple questions of orientation have inadequate sensitivity to detect mild TBI after head injury [65]. The mental status examination should include an assessment of short-term memory as well as attention and concentration. While standardized examinations can be used in this regard, most have not been validated for concussion diagnosis in the absence of a baseline score. More detailed descriptions of mental status examinations are described separately. (See "The mental status examination in adults", section on 'Attention and concentration' and "The mental status examination in adults", section on 'Memory' and "The detailed neurologic examination in adults".)

Finally, a neurologic examination should include at minimum an assessment of cranial nerves III through VII (extraocular movements, pupillary reactivity, face sensation, and movement) as well as limb strength and coordination and gait.

Standardized examinations — Standardized examinations may aid in the identification of individuals, particularly athletes, with concussion. While a number of diagnostic tools have been developed to aid in concussion recognition, none of these substitute for a more thorough medical evaluation, nor are they intended to be able to rule out concussion [66]. Some (eg, SAC, Sport Concussion Assessment Tool [SCAT5]) are validated only in the setting of a preinjury assessment.

Standardized Assessment of Concussion – The SAC was developed as a standardized tool for the sideline evaluation of athletes who suffer a head injury [1,65]. The SAC includes measures of orientation, immediate memory, concentration, delayed recall, neurologic screening, and exertional maneuvers (table 3). Although not part of the scored assessment, the SAC also includes a graded symptom checklist and a brief neurologic examination, and records the presence of posttraumatic and retrograde amnesia (table 2) [65,67].

Most studies evaluating the SAC have examined football players and compared scores after head injury with a preinjury baseline score [65,67-72]. In this regard, it has an estimated sensitivity and specificity of 80 to 94 percent and 76 to 91 percent, respectively [66].

The validity of this assessment in the absence of a baseline score is uncertain. Patients with concussion have significantly lower scores than those without, but a cutoff score to diagnose concussion has not been identified [65]. The SAC was also used as an evaluation tool in 165 children (ages 6 to 18 years) who presented to an emergency department with concussion and were compared with a control group with minor extremity injury, rather than with a premorbid baseline score as in the studies above [73]. SAC scores were slightly lower in the concussion group, but this reached statistic significance only in the group age 12 to 14 years. However, when the graded symptoms checklist (table 2) was summed, this score was significantly higher in concussion patients compared with controls, with patients scoring a mean of 8 to 14 points, while controls scored 1 to 2 points.

The SAC should not be used in isolation to determine the readiness of athletes to return to play. (See 'Return to play for athletes' below.)

Post-Concussion Symptom Scale and Graded Symptom Checklist – Use of the Post-Concussion Symptom Scale and Graded Symptom Checklist requires the patient to rate severity of symptoms on a 7-point scale (0 = none; 6 = severe) for 15 to 30 symptoms associated with concussion (eg, headache, dizziness, irritability, difficulty concentrating). A score greater than a baseline preinjury score is considered indicative of a concussion, and has been found to have a sensitivity and specificity of 64 to 89 percent and 91 to 100 percent, respectively [66].

While not validated for diagnosis of concussion in the absence of a baseline score, reviewing such symptoms with a patient who had not been assessed preinjury may still be useful to the clinician in determining the presence and severity of a concussion.

Sport Concussion Assessment Tool – The most recent revision of the SCAT5 was endorsed by a consensus statement on concussion in sport in 2016 [74,75]. Although no version has been well validated, the tool is increasingly used. The SCAT5 is freely accessible.

SCAT5 provides a detailed clinical assessment that includes a review of subjective symptoms, the Glasgow Coma Scale (GCS), the SAC cognitive assessment, and an evaluation of balance and coordination. Although scored on a point scale, normative data and a cutoff scores have not been defined. As with other standardized assessments discussed here, using the tool to guide the examination may provide a reasonable approach to patient evaluation, even in the absence of validated scoring [76].

In one cross-sectional study, a 3.5-point drop in the SCAT2 score had a sensitivity and specificity of 96 and 81 percent, respectively, while a postinjury score of 74.5 or lower was associated with a sensitivity and specificity of 83 and 91 percent, respectively [77].

Westmead posttraumatic amnesia scale – Two studies have demonstrated that a revised version of the Westmead posttraumatic amnesia scale (WPTAS) is simple to perform, taking less than one minute in the emergency department setting, and correlates with the findings in more detailed neuropsychologic testing [78,79]. An incorrect response to any one question on the WPTAS is considered a positive test for cognitive impairment after head injury:

What is your name?

What is the name of this place?

Why are you here?

What month are we in?

What year are we in?

What town/suburb are you in?

How old are you?

What is your date of birth?

What time of day is it? (morning, afternoon, evening)

Three pictures are presented for subsequent recall

Other measures – Other standardized measures used to assess posttraumatic amnesia and other cognitive neurologic deficits associated with mild TBI include the Immediate Post-Concussion Assessment and Cognitive Testing (ImPACT), the Galveston Orientation and Amnesia Test (GOAT), the Military Acute Concussion Evaluation (MACE), and Balance Error Scoring System (BESS), but these have not been well validated [74,78,80-84].

Imaging — Imaging, usually head computed tomography (CT) without contrast, is recommended for a subset of patients with mild TBI in the acute setting. (Related Pathway(s): Mild head trauma: Evaluation of adults in the emergency department.) The primary purpose of imaging in the acute setting is to identify injuries requiring immediate neurosurgical intervention or early neurologic evaluation with medical management. Imaging is also used to assess prognosis for long-term management [57]. (See 'Complicated mild traumatic brain injury' above.)

While imaging is usually normal in patients with a concussion or mild TBI, studies suggest that there is a sufficient incidence of abnormalities to make imaging worthwhile in a subset of at-risk patients. One systematic review of the literature estimated a prevalence of CT abnormalities of 5 percent among patients presenting to a hospital with a GCS = 15 and 30 percent for those presenting with a GCS = 13 [85]. The incidence of abnormalities leading to neurosurgical intervention was approximately 1 percent.

Selection of patients — There is evidence that patients with mild TBI can be selected for CT based on clinical criteria. (Related Pathway(s): Mild head trauma: Evaluation of adults in the emergency department.) Three such criteria, the Canadian CT head rule (CCHR), the New Orleans criteria (NOC), and the National Emergency X-Radiography Utilization Study II (NEXUS II) criteria, have been developed and prospectively validated. A conservative approach to selecting individuals for imaging based on these combined criteria is presented in the algorithm (algorithm 1). These criteria prioritize a high sensitivity for identifying patients with clinically important CT findings over reducing the number of examinations performed.

The CCHR requires a head CT for patients with mild TBI and any one of the following [86]:

GCS <15 two hours after injury

Suspected open or depressed skull fracture

Any sign of basilar skull fracture: hemotympanum, raccoon eyes (intraorbital bruising), Battle sign (retroauricular bruising), or cerebrospinal fluid leak, oto- or rhinorrhea

Two or more episodes of vomiting

Sixty-five years of age or older

Amnesia for events occurring more than 30 minutes prior to impact

Dangerous mechanism (pedestrian struck by motor vehicle, occupant ejected from motor vehicle, fall from ≥3 feet or ≥5 stairs)

Patients with certain high-risk features were excluded in the population in which these criteria were originally developed and tested. Hence, the presence of any of these is also an indication for head CT in this protocol:

Neurologic deficit

Seizure

Presence of bleeding diathesis or oral anticoagulant use

Return visit for reassessment of a head injury

The NOC apply to patients with a GCS of 15 and require CT if there is headache, vomiting, age >60 years, drug or alcohol intoxication, persistent anterograde amnesia, seizure, or visible trauma above the clavicle [87].

In the NEXUS II criteria, CT is indicated for significant skull fracture, scalp hematoma, neurologic deficit, altered level of alertness (GCS ≤14), abnormal behavior, coagulopathy, or persistent vomiting [88].

These criteria were applied prospectively within a multicenter study population of more than 7000 patients. Sensitivities for clinical outcomes were highest for the NOC. For patients requiring neurosurgical intervention, sensitivities for NOC, CCHR, and NEXUS II were 100, 100, and 95 percent, respectively. For patients with clinically important brain injury, sensitivities for NOC, CCHR, and NEXUS II were 92, 79, and 89 percent, respectively. Specificity of these criteria is predictably low (<50 percent) with the NOC typically having the lowest specificity (<25 percent) [89]. Other studies have generally found similar relative performance of these rules [90-94].

A conservative approach to selecting individuals for imaging based on these criteria is presented (algorithm 1). Combining these criteria in this way will increase the sensitivity and further reduce the specificity for clinical outcomes. The American College of Emergency Physicians has endorsed indications for imaging that are concordant with the NOC [95,96]. The National Institute for Health and Care Excellence guidelines for performing a head CT are similar to the CCHR, and apply to patients with GCS score 14, signs of basal skull fracture, vomiting, >30 minutes of retrograde amnesia for events prior to injury, posttraumatic seizures, coagulopathy, dangerous mechanism of injury, focal neurologic deficit, or age >64 years [97].

Another potential indication for CT may be to avoid in-hospital observation, for patients who live alone. Neurologically normal patients with a normal CT examination are at low risk for subsequent neurologic deterioration [2,98,99]. In one study, for example, none of 542 patients admitted to the hospital with a "mild" head injury and a normal initial CT showed subsequent deterioration, and none required surgery [2]. (See 'Indications for admission' below.)

Selection of modality — In patients with mild TBI who meet criteria for imaging, head CT without contrast is the most appropriate examination choice. Head magnetic resonance imaging (MRI) without contrast can be sensitive in detecting intracranial injury that is occult on CT, such as subtle blood products or secondary signs of injury like edema, but is not indicated for initial evaluation as the examination does not seem to impact the disposition of the patient. MRI is considered more appropriate for evaluating TBI in the subacute (eg, 8 to 89 days after injury) or chronic (eg, >90 days after injury) setting, particularly when clinical symptoms persist.

Computed tomography — Head CT without contrast is recommended for imaging of patients with acute TBI, as it is the best modality to detect injuries that may require neurosurgical intervention. Examples include:

Mass effect (basal cistern compression or midline shift), sulcal effacement, or herniation

Substantial epidural or subdural hematoma (>1 cm in width, or causing mass effect)

Substantial cerebral contusion (>1 cm in diameter, or more than one site)

Extensive subarachnoid hemorrhage, posterior fossa, intraventricular or bilateral hemorrhage

Depressed or diastatic skull fracture

Pneumocephalus

Cerebral edema

Clinically important and neurosurgical abnormalities are visible on initial CT [57,100]. In one large multicenter study, the initial CT scan had a 99.7 percent predictive value for excluding an injury requiring neurosurgical intervention [101].

Intravenous contrast is not routinely administered in evaluating patients with mild TBI but may be required to perform CT angiography (CTA) of the head and neck when vascular injury is suspected.

Magnetic resonance imaging — In the acute setting, head MRI without contrast is usually not indicated for mild TBI. MRI is more sensitive than CT in detecting small amounts of parenchymal, subdural, and epidural hemorrhage; contusion; and posterior fossa, brainstem, and diffuse axonal injuries. MRI is generally less sensitive than CT at detecting subarachnoid hemorrhage. While MRI after CT reveals additional findings in up to one-third of patients, this additional information does not alter the initial patient triage [39,102-104]. However, in patients with a negative CT with persistent or progressive unexplained neurologic deficits, MRI can be used to evaluate for occult injury. (See 'Follow-up imaging' below and "Postconcussion syndrome", section on 'Neuroimaging'.)

Intravenous contrast administration for magnetic resonance angiography (MRA) of the head and neck is sometimes required in patients where the noncontrast images suggest a vascular injury to perform MRA. The evaluation of these patients is discussed separately. (See "Blunt cerebrovascular injury: Mechanisms, screening, and diagnostic evaluation".)

In case series of patients with acute mild TBI, MRI abnormalities were reported in 30 percent of cases with normal CT [39,104,105]. Most of these additional abnormalities were lesions "consistent with axonal injury," but small contusions and subarachnoid hemorrhage have also been described. Some nonspecific magnetic resonance (MR) findings may be unrelated to TBI, and others do not clearly correlate with TBI severity or outcome; however, the presence of one or more brain contusions or foci of hemorrhagic axonal injury has been associated with poorer three-month outcomes (odds ratio [OR] 4.5 and 3.2, respectively) [104]. Nonetheless, as there is no specific treatment for these lesions, MRI is typically reserved for patients who do not recover as expected as well as for those with other unexplained focal neurologic deficits. (See 'Follow-up imaging' below and "Postconcussion syndrome", section on 'Neuroimaging'.)

When comparing a cohort with a history of TBI with a control group, MRI with diffusion tensor imaging (DTI) may find lower factional anisotropy and higher mean diffusivity in the TBI population [106]. However, there is insufficient evidence to recommend DTI to diagnose mild TBI in individual patients [107].

Biomarkers — Not currently used in routine clinical practice, biomarkers are being investigated in the diagnosis and assessment of mild TBI. In one study of professional hockey players, plasma levels of tau protein were significantly increased compared with baseline levels when measured one hour after concussion and remained elevated for as long as six days, correlating with the duration of symptoms [108]. Two other potential biomarkers appeared less useful; neuron-specific enolase levels were not significantly elevated after TBI, and S-100 calcium-binding protein B levels, while initially increased, returned rapidly to baseline levels. These findings require replication before this testing can be recommended in clinical practice.

DIAGNOSIS — The diagnosis of concussion or mild TBI is made in an individual with a head injury due to contact; brief loss of consciousness may or may not have occurred. The patient typically has neurologic symptoms, including confusion or memory loss as described above, but does not have neurologic deficits that are associated with a Glasgow Coma Scale (GCS) score of less than 13, measured at approximately 30 minutes after the injury (table 1). (See 'Clinical features' above.)

While there are often no specific exclusions in the definition of concussion or mild TBI for complications of intracranial hemorrhage or skull fracture, when these are identified, it is appropriate to include these as additional diagnoses when determining management or discussing prognosis, rather than making a diagnosis of isolated mild TBI or concussion.

OBSERVATION AND DISPOSITION — Some form of inpatient or at-home observation is recommended for at least 24 hours after a mild TBI because of the risk of intracranial complications [98,109]. A conservative approach to the initial evaluation and disposition of patients with mild TBI is presented (algorithm 1) [8,85]. (Related Pathway(s): Mild head trauma: Evaluation of adults in the emergency department.)

If the patient's condition deteriorates during observation, a thorough neurologic examination should be performed, and an immediate head computed tomography (CT) without contrast should be obtained [98,110].

In-hospital observation

Indications for admission — Hospital admission is recommended for patients at risk for immediate complications from head injury [2,61,111-113]. These include patients with:

Glasgow Coma Scale (GCS) <15

Abnormalities on head CT (eg, intracranial hemorrhage, ischemia, mass effect, midline shift)

Seizures

Abnormal bleeding parameters from underlying bleeding diathesis or oral anticoagulation

Other neurologic deficit

Recurrent vomiting

While it is preferable that the admitting hospital have neurosurgical service, it may not be required, particularly if the CT is normal [114]. Decisions regarding transfer to a hospital with neurosurgical service should be individualized and the choice to intervene with neurosurgery is based on clinical signs and symptoms in combination with imaging.

In-hospital observation should also be considered if no responsible person is available at home to monitor the patient for progression of symptoms. In such patients, a normal head CT may obviate the need for admission and should be considered specifically for this purpose, even if not otherwise indicated according to the criteria discussed above and shown in the algorithm (algorithm 1). In one study, 575 patients with GCS = 15 were randomized to immediate CT versus in-hospital observation [99,115]. Similar clinical outcomes were seen in the two groups; CT was the more cost-effective strategy. No patient with a normal immediate CT later suffered neurologic complications. Another report also found that strategies of observation and monitoring versus more liberal CT imaging yielded similar clinical outcomes, but emphasized that the latter approach was associated with higher average radiation exposures [116].

Management of complications and associated injuries

Seizures – Although seizures in the setting of acute mild TBI are often self-limited and do not recur, patients are often treated with antiseizure medications because of the risk of status epilepticus or aggravation of a systemic injury. The management of early posttraumatic seizures is discussed separately. (See "Posttraumatic seizures and epilepsy".)

There is no role for prophylactic antiseizure medications in patients with mild TBI in the absence of seizures.

Intracranial hemorrhage – Intracranial hemorrhage may be subdural, epidural, subarachnoid, or intracerebral. The management of these is discussed separately.

(See "Subdural hematoma in adults: Management and prognosis".)

(See "Intracranial epidural hematoma in adults".)

(See "Nonaneurysmal subarachnoid hemorrhage".)

(See "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis".)

Skull fracture – The management of skull fractures is presented separately. (See "Skull fractures in adults".)

Hypopituitarism – Posttraumatic hypopituitarism can be a complication of mild TBI and can have clinical features similar to postconcussion syndrome. However, there is controversy over the utility and recommendations for screening [117].

Follow-up imaging — Most patients with mild TBI do not require subsequent imaging. Evidence does not support its routine use, so patient selection is needed. In patients with mild TBI, a repeat head CT has been reported to change management in 2 to 4 percent of cases [118].

If follow-up imaging is necessary, magnetic resonance imaging (MRI) may be preferred over CT in some patients because of its higher sensitivity for nearly all abnormalities and its lack of ionizing radiation. With patients in a head brace where hardware artifact will likely degrade image quality, CT may be the better choice. Timely availability and easy comparison with the prior study may also favor CT. CT angiography (CTA) and magnetic resonance angiography (MRA) of the head and neck are comparable in diagnostic performance for detection of occult vascular abnormalities and the choice is driven by institutional technology and expertise.

Patients in whom follow-up imaging is often indicated include:

Neurologic deterioration – Patients who have a clinically significant neurologic decline should have an urgent follow-up imaging study. CT scan is appropriate as the initial follow-up test in most patients [57].

Unexplained neurologic findings – Patients with neurologic deficits that are not adequately explained by CT, in particular, those whose specific neurologic syndrome is felt to be secondary to a vascular injury, may require MRI and/or vascular imaging. The evaluation of these patients is discussed separately. (See "Blunt cerebrovascular injury: Mechanisms, screening, and diagnostic evaluation".)

Patients with persistent neurologic complaints following mild TBI may also warrant imaging. (See "Postconcussion syndrome", section on 'Neuroimaging'.)

Anticoagulation – Patients who are anticoagulated may be at risk for delayed intracranial hemorrhage, even when the initial CT is normal. We individualize decisions in this setting, reimaging selected patients at higher risk (eg, high international normalized ratio [INR], older age, more severe injury, initial abnormal CT). All patients with neurologic decline should be reimaged.

A repeat head CT was performed in two prospective studies of 137 and 97 anticoagulated patients with mild TBI and initial normal CT examination [113,119]. New hemorrhagic lesions were identified in 1.4 and 6 percent, respectively. Only one patient in the latter series required neurosurgical intervention. An initial INR >3 was identified as a risk factor. According to another study, GCS <15 may be another risk factor for delayed hemorrhage after mild TBI in anticoagulated patients [120].

Patients on antiplatelet therapy are likely at lower risk of delayed complications than those taking anticoagulants. In a series of 424 patients on either anticoagulant or antiplatelet therapy, new hemorrhagic lesions were identified on repeat CT in just 1 percent [121]. In a second series of patients who were taking either anticoagulant or antiplatelet therapy prior to a low-altitude fall (<6 feet), only 0.5 percent of those with an initial normal CT scan had delayed hemorrhage [122].

Initial abnormal CT – Select patients with intracranial hemorrhage, mass effect, midline shift, and/or hydrocephalus on initial CT may require subsequent imaging.

Whether follow-up imaging is required in clinically stable patients with contusion or minor intracerebral hemorrhage (<10 mL) is a matter of clinical judgement [57,123,124]. Some physicians would choose to repeat imaging in stable patients with intracerebral hemorrhage or contusion, particularly to support an early discharge and/or in the setting of anticoagulation therapy. There are limited data to support this approach. A meta-analysis of observational studies of patients with mild TBI found that a repeat head CT (all had an initial abnormal CT, some may have been preceded by clinical change) prompted a change in management in 2.3 percent and neurosurgical intervention in 1.5 percent [118]. Worsening of imaging findings was reported in approximately 30 percent. Advanced age, anticoagulation, and larger volume of blood were predictors of hemorrhage progression in some studies [124,125].

Isolated subarachnoid hemorrhage may be a relatively benign finding in this population [126,127]. In one retrospective registry review, isolated subarachnoid hemorrhage in patients with mild TBI (GCS ≥13) was associated with a benign neurologic outcome in all 478 patients; only one developed bilateral subdural hematomas that subsequently required intervention [126].

The evaluation and management of patients with subdural and epidural hemorrhage and those with skull fractures are discussed separately. (See "Intracranial epidural hematoma in adults" and "Subdural hematoma in adults: Management and prognosis" and "Skull fractures in adults".)

Outpatient observation — Outpatient observation may be permitted for the patient whose neurologic condition is very unlikely to deteriorate. There is substantial evidence that patients with a GCS = 15, normal examination and head CT, and no predisposition to bleeding are unlikely to suffer subsequent neurologic deterioration [95,98,109,128].

The observer should be given explicit and understandable instructions on patient monitoring and how and when to seek medical help [109]. The following warning signs should prompt the caregiver to seek immediate medical help:

Inability to awaken the patient at time of expected wakening

Severe or worsening headaches

Somnolence or confusion

Restlessness, unsteadiness, or seizures

Difficulties with vision

Vomiting, fever, or stiff neck

Urinary or bowel incontinence

Weakness or numbness involving any part of the body

Return to work — For patients with uncomplicated concussion, a period of physical and cognitive rest is often recommended for at least 24 hours and pending resolution of symptoms; this is followed by a gradual return to work, school, and physical activity [23]. However, the benefit of such recommendations has not been carefully evaluated [129]. One randomized study in children found that five days of strict cognitive rest did not improve outcomes and appeared to be associated with slower symptom resolution [130,131]. (See "Concussion in children and adolescents: Management", section on 'Cognitive rest'.)

Patients with prolonged symptoms may benefit from reevaluation and treatment [132]. (See "Postconcussion syndrome".)

Avoidance of activities that may place the patient at risk of subsequent concussion during the acute symptomatic period seems sensible.

Return to play for athletes — It is likely that premature return to play, when an athlete is still symptomatic, places that athlete at great risk for subsequent injury, including recurrent concussion. In one prospective cohort study of 2905 college football players, 1 in 15 players with concussion had additional concussions in the same season, most occurring 7 to 10 days after the first concussion [133]. With each concussion, the risk of future concussions increased. Individuals with three concussions had a three times greater risk of future concussion compared with those without concussion. Another important consideration is the fact that premature return to play by a symptomatic athlete places that athlete at greater risk for subsequent concussion and potentially for cumulative brain injury [48,49,134]. (See "Sequelae of mild traumatic brain injury", section on 'Chronic traumatic encephalopathy'.)

The concern that recurrent concussions may lead to serious sequelae such as second impact syndrome and dementia has led to the development of a series of guidelines that address concussion severity and return to play for athletes [135,136]. These include the 2012 Consensus Statement on Concussion in Sport [23], the 2013 American Academy of Neurology systematic review and evidence-based guideline [66], and the 2013 American Medical Society for Sports Medicine position statement [137]. However, there is a paucity of prospective data on which to base recommendations, and current guidelines are largely consensus- rather than evidence-based.

Based on these concerns, it is recommended that:

Athletes suspected of having a concussion should be removed from play and evaluated by a licensed health professional. An emergency department evaluation is indicated for any athlete who suffers loss of consciousness [1,138]. (See 'Evaluation' above.)

Athletes with diagnosed concussion should be removed from play or practice (contact-risk activity) until symptoms have resolved off medication.

A more conservative approach is probably appropriate for children and adolescents. (See "Minor head trauma in infants and children: Management", section on 'Return to play'.)

Individuals with a history of multiple concussions should undergo a more detailed evaluation regarding neurobehavioral symptoms; if these are present, they should be referred for neurologic and neuropsychologic assessments [139]. Patients with persistent neurobehavioral complaints or objective deficits should be counseled about the risk of chronic traumatic encephalopathy and possible retirement from contact sports.

The 2012 Consensus Statement on Concussion in Sport was written by a multidisciplinary, international group and proposes a six-day graduated return-to-play protocol in which the athlete makes a stepwise increase in functional activity, is evaluated for symptoms, and is allowed to progress to the next stage each successive day if asymptomatic (table 4) [23]. If symptoms occur, then the patient should drop back to the previous asymptomatic level and reattempt progression after 24 hours. While these guidelines further suggest that a more rapid return to play may be possible for asymptomatic adult athletes, same-day return to play is not recommended. They also suggest that a more conservative approach be followed for adolescents and children [140]. (See "Minor head trauma in infants and children: Management", section on 'Return to play' and "Sports participation in children and adolescents: The preparticipation physical evaluation", section on 'Sports participation'.)

PROGNOSIS — The symptoms and disability attributed to postconcussion syndrome (PCS) are greatest within the first 7 to 10 days for the majority of patients. At one month, symptoms are improved and in many cases resolved [141]. A minority of patients have symptoms that persist or are permanent. (See "Postconcussion syndrome", section on 'Prognosis' and "Sequelae of mild traumatic brain injury".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Increased intracranial pressure and moderate-to-severe traumatic brain injury" and "Society guideline links: Minor head trauma and concussion".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Concussion in adults (The Basics)" and "Patient education: Skull fractures (The Basics)" and "Patient education: Head injury in adults (The Basics)")

Beyond the Basics topics (see "Patient education: Head injury in children and adolescents (Beyond the Basics)" and "Patient education: Vertigo (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

A mild traumatic brain injury (TBI) or concussion is an injury to the brain that may result after blunt force or an acceleration/deceleration head injury. Its occurrence is most obvious when the individual has experienced brief loss of consciousness or demonstrates overt confusion or amnesia. Subtler degrees of neurologic impairment are common and may be unrecognized by the individual and observer. (See 'Definitions' above and 'Clinical features' above.)

All patients with mild TBI or concussion should be medically evaluated. An athlete with known or suspected head injury should be evaluated by a trained observer for potential concussion. Simple orientation questions are inadequate to detect concussion. One suggested tool for nonmedically trained personnel is the Standardized Assessment of Concussion (SAC) (table 3). (See 'Standardized examinations' above.)

Patients who have suffered loss of consciousness or have persistent symptoms should be referred to an emergency department. At-risk patients should have a head computed tomography (CT) without contrast in the acute setting (algorithm 1). Intravenous contrast administration for CT angiography (CTA) of the head and neck is sometimes required in patients where the noncontrast images suggest a vascular injury. (See 'Evaluation' above and 'Imaging' above.)

Neurosurgical or neurologic evaluation is indicated if CT shows any of the following findings (see 'Management of complications and associated injuries' above):

Mass effect (basal cistern compression or midline shift), sulcal effacement, or herniation

Substantial epidural or subdural hematomas (>1 cm in width, or causing mass effect)

Substantial cerebral contusion (>1 cm in diameter, or more than one site)

Extensive subarachnoid hemorrhage, posterior fossa, intraventricular or bilateral hemorrhage

Depressed or diastatic skull fracture

Pneumocephalus

Cerebral edema

Some form of observation is recommended for at least 24 hours after a mild TBI because of the risk of intracranial complications; while the incidence is low, sequelae are potentially life threatening. Some patients may be safely monitored at home by a responsible caregiver, while inpatient observation is recommended for others (algorithm 1). (See 'Observation and disposition' above.)

Follow-up imaging (CT or magnetic resonance imaging [MRI]) is indicated for those who experience clinical deterioration, and may also be appropriate for some with an initial abnormal CT and/or high-risk patients who are anticoagulated. MRI should be performed in patients whose neurologic deficits cannot be explained by the CT findings. In patients with suspected vascular injury, CT or magnetic resonance angiography (MRA) of the head and neck with intravenous contrast should also be performed. (See 'Follow-up imaging' above.)

We recommend that athletes not return to play the same day after concussion, and also that athletes NOT return to play until asymptomatic off medication (Grade 1C). A more conservative approach is probably appropriate for children and adolescents. (See 'Return to play for athletes' above.)

  1. Practice parameter: the management of concussion in sports (summary statement). Report of the Quality Standards Subcommittee. Neurology 1997; 48:581.
  2. Stein SC, Ross SE. The value of computed tomographic scans in patients with low-risk head injuries. Neurosurgery 1990; 26:638.
  3. Servadei F, Teasdale G, Merry G, Neurotraumatology Committee of the World Federation of Neurosurgical Societies. Defining acute mild head injury in adults: a proposal based on prognostic factors, diagnosis, and management. J Neurotrauma 2001; 18:657.
  4. Uchino Y, Okimura Y, Tanaka M, et al. Computed tomography and magnetic resonance imaging of mild head injury--is it appropriate to classify patients with Glasgow Coma Scale score of 13 to 15 as "mild injury"? Acta Neurochir (Wien) 2001; 143:1031.
  5. Culotta VP, Sementilli ME, Gerold K, Watts CC. Clinicopathological heterogeneity in the classification of mild head injury. Neurosurgery 1996; 38:245.
  6. Kay T, Harrington DE, Adams R, et al. Definition of mild traumatic brain injury. J Head Trauma Rehabil 1993; 8:86.
  7. Centers for Disease Control and Prevention. Injury Prevention & Control: Traumatic Brain Injury. Traumatic Brain Injury. Available at: http://www.cdc.gov/TraumaticBrainInjury/index.html (Accessed on March 27, 2017).
  8. Vos PE, Alekseenko Y, Battistin L, et al. Mild traumatic brain injury. Eur J Neurol 2012; 19:191.
  9. Kraus JF, McArthur DL. Epidemiologic aspects of brain injury. Neurol Clin 1996; 14:435.
  10. Kraus JF, Nourjah P. The epidemiology of mild, uncomplicated brain injury. J Trauma 1988; 28:1637.
  11. Annegers JF, Grabow JD, Kurland LT, Laws ER Jr. The incidence, causes, and secular trends of head trauma in Olmsted County, Minnesota, 1935-1974. Neurology 1980; 30:912.
  12. Feigin VL, Theadom A, Barker-Collo S, et al. Incidence of traumatic brain injury in New Zealand: a population-based study. Lancet Neurol 2013; 12:53.
  13. Bernstein DM. Recovery from mild head injury. Brain Inj 1999; 13:151.
  14. Xydakis MS, Ling GS, Mulligan LP, et al. Epidemiologic aspects of traumatic brain injury in acute combat casualties at a major military medical center: a cohort study. Ann Neurol 2012; 72:673.
  15. Jennett B, Frankovyski RF. The epidemiology of head injury. In: Handbook of Clinical Neurology, Braakman R (Ed), Elsevier, New York 1990. Vol 13, p.1.
  16. Guerriero RM, Proctor MR, Mannix R, Meehan WP 3rd. Epidemiology, trends, assessment and management of sport-related concussion in United States high schools. Curr Opin Pediatr 2012; 24:696.
  17. McKee AC, Cantu RC, Nowinski CJ, et al. Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injury. J Neuropathol Exp Neurol 2009; 68:709.
  18. Kelly JP, Rosenberg JH. The development of guidelines for the management of concussion in sports. J Head Trauma Rehabil 1998; 13:53.
  19. Powell JW, Barber-Foss KD. Traumatic brain injury in high school athletes. JAMA 1999; 282:958.
  20. Marar M, McIlvain NM, Fields SK, Comstock RD. Epidemiology of concussions among United States high school athletes in 20 sports. Am J Sports Med 2012; 40:747.
  21. Hoge CW, McGurk D, Thomas JL, et al. Mild traumatic brain injury in U.S. Soldiers returning from Iraq. N Engl J Med 2008; 358:453.
  22. Nordström A, Edin BB, Lindström S, Nordström P. Cognitive function and other risk factors for mild traumatic brain injury in young men: nationwide cohort study. BMJ 2013; 346:f723.
  23. McCrory P, Meeuwisse WH, Aubry M, et al. Consensus statement on concussion in sport: the 4th International Conference on Concussion in Sport held in Zurich, November 2012. Br J Sports Med 2013; 47:250.
  24. Goodman JC. Pathologic changes in mild head injury. Semin Neurol 1994; 14:19.
  25. Povlishock JT, Katz DI. Update of neuropathology and neurological recovery after traumatic brain injury. J Head Trauma Rehabil 2005; 20:76.
  26. Hayes RL, Dixon CE. Neurochemical changes in mild head injury. Semin Neurol 1994; 14:25.
  27. Simon DW, McGeachy MJ, Bayır H, et al. The far-reaching scope of neuroinflammation after traumatic brain injury. Nat Rev Neurol 2017; 13:171.
  28. Bhattacharjee Y. Neuroscience. Shell shock revisited: solving the puzzle of blast trauma. Science 2008; 319:406.
  29. Ommaya AK, Gennarelli TA. Cerebral concussion and traumatic unconsciousness. Correlation of experimental and clinical observations of blunt head injuries. Brain 1974; 97:633.
  30. Oppenheimer DR. Microscopic lesions in the brain following head injury. J Neurol Neurosurg Psychiatry 1968; 31:299.
  31. Blumbergs PC, Scott G, Manavis J, et al. Staining of amyloid precursor protein to study axonal damage in mild head injury. Lancet 1994; 344:1055.
  32. Wilde EA, McCauley SR, Hunter JV, et al. Diffusion tensor imaging of acute mild traumatic brain injury in adolescents. Neurology 2008; 70:948.
  33. Mayer AR, Ling J, Mannell MV, et al. A prospective diffusion tensor imaging study in mild traumatic brain injury. Neurology 2010; 74:643.
  34. Aoki Y, Inokuchi R, Gunshin M, et al. Diffusion tensor imaging studies of mild traumatic brain injury: a meta-analysis. J Neurol Neurosurg Psychiatry 2012; 83:870.
  35. Croall ID, Cowie CJ, He J, et al. White matter correlates of cognitive dysfunction after mild traumatic brain injury. Neurology 2014; 83:494.
  36. Mayer AR, Bellgowan PS, Hanlon FM. Functional magnetic resonance imaging of mild traumatic brain injury. Neurosci Biobehav Rev 2015; 49:8.
  37. van der Horn HJ, Liemburg EJ, Scheenen ME, et al. Graph Analysis of Functional Brain Networks in Patients with Mild Traumatic Brain Injury. PLoS One 2017; 12:e0171031.
  38. McAllister TW, Sparling MB, Flashman LA, Saykin AJ. Neuroimaging findings in mild traumatic brain injury. J Clin Exp Neuropsychol 2001; 23:775.
  39. Hughes DG, Jackson A, Mason DL, et al. Abnormalities on magnetic resonance imaging seen acutely following mild traumatic brain injury: correlation with neuropsychological tests and delayed recovery. Neuroradiology 2004; 46:550.
  40. Kant R, Smith-Seemiller L, Isaac G, Duffy J. Tc-HMPAO SPECT in persistent post-concussion syndrome after mild head injury: comparison with MRI/CT. Brain Inj 1997; 11:115.
  41. Korn A, Golan H, Melamed I, et al. Focal cortical dysfunction and blood-brain barrier disruption in patients with Postconcussion syndrome. J Clin Neurophysiol 2005; 22:1.
  42. 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.
  43. Chen SH, Kareken DA, Fastenau PS, et al. A study of persistent post-concussion symptoms in mild head trauma using positron emission tomography. J Neurol Neurosurg Psychiatry 2003; 74:326.
  44. Metting Z, Rödiger LA, Stewart RE, et al. Perfusion computed tomography in the acute phase of mild head injury: regional dysfunction and prognostic value. Ann Neurol 2009; 66:809.
  45. Wintermark M, Sanelli PC, Anzai Y, et al. Imaging evidence and recommendations for traumatic brain injury: advanced neuro- and neurovascular imaging techniques. AJNR Am J Neuroradiol 2015; 36:E1.
  46. Agoston DV, Langford D. Big Data in traumatic brain injury; promise and challenges. Concussion 2017; 2:CNC45.
  47. Duhaime AC, Beckwith JG, Maerlender AC, et al. Spectrum of acute clinical characteristics of diagnosed concussions in college athletes wearing instrumented helmets: clinical article. J Neurosurg 2012; 117:1092.
  48. Kelly JP, Rosenberg JH. Diagnosis and management of concussion in sports. Neurology 1997; 48:575.
  49. Collins MW, Grindel SH, Lovell MR, et al. Relationship between concussion and neuropsychological performance in college football players. JAMA 1999; 282:964.
  50. Cantu RC. Posttraumatic Retrograde and Anterograde Amnesia: Pathophysiology and Implications in Grading and Safe Return to Play. J Athl Train 2001; 36:244.
  51. Yamamoto LG, Bart RD Jr. Transient blindness following mild head trauma. Criteria for a benign outcome. Clin Pediatr (Phila) 1988; 27:479.
  52. Haas DC, Ross GS. Transient global amnesia triggered by mild head trauma. Brain 1986; 109 ( Pt 2):251.
  53. Harrison DW, Walls RM. Blindness following minor head trauma in children: a report of two cases with a review of the literature. J Emerg Med 1990; 8:21.
  54. Lee ST, Lui TN. Early seizures after mild closed head injury. J Neurosurg 1992; 76:435.
  55. Barry E. Posttraumatic epilepsy. In: The treatment of epilepsy: Principles and practice, 3rd ed, Wyllie E (Ed), Lippincott Williams, Philadelphia 2001. p.609.
  56. Pagni CA. Posttraumatic epilepsy. Incidence and prophylaxis. Acta Neurochir Suppl (Wien) 1990; 50:38.
  57. Wintermark M, Sanelli PC, Anzai Y, et al. Imaging evidence and recommendations for traumatic brain injury: conventional neuroimaging techniques. J Am Coll Radiol 2015; 12:e1.
  58. Hsiang JN, Yeung T, Yu AL, Poon WS. High-risk mild head injury. J Neurosurg 1997; 87:234.
  59. Williams DH, Levin HS, Eisenberg HM. Mild head injury classification. Neurosurgery 1990; 27:422.
  60. Liau LM, Bergsneider M, Becker DP. Pathology and pathophysiology of head injury. In: Neurological surgery: A comprehensive reference guide to the diagnosis and management of neurosurgical problems, 4th ed, Youmans JR, Becker DP, et al (Eds), Saunders, Philadelphia 1996. p.1549.
  61. Dacey RG Jr, Alves WM, Rimel RW, et al. Neurosurgical complications after apparently minor head injury. Assessment of risk in a series of 610 patients. J Neurosurg 1986; 65:203.
  62. McCrory P. Do not go gentle into that good night... Br J Sports Med 2005; 39:691.
  63. Delaney JS, Abuzeyad F, Correa JA, Foxford R. Recognition and characteristics of concussions in the emergency department population. J Emerg Med 2005; 29:189.
  64. Delaney SJ, Lacroix VJ, Leclerc S, et al. Concussions during the 1997 Canadian football league season. Clin J Sports Med 2000; 54:1488.
  65. McCrea M, Kelly JP, Kluge J, et al. Standardized assessment of concussion in football players. Neurology 1997; 48:586.
  66. Giza CC, Kutcher JS, Ashwal S, et al. Summary of evidence-based guideline update: evaluation and management of concussion in sports: report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology 2013; 80:2250.
  67. McCrea M, Kelly JP, Randolph C, et al. Standardized assessment of concussion (SAC): on-site mental status evaluation of the athlete. J Head Trauma Rehabil 1998; 13:27.
  68. Barr WB, McCrea M. Sensitivity and specificity of standardized neurocognitive testing immediately following sports concussion. J Int Neuropsychol Soc 2001; 7:693.
  69. McCrea M, Guskiewicz KM, Marshall SW, et al. Acute effects and recovery time following concussion in collegiate football players: the NCAA Concussion Study. JAMA 2003; 290:2556.
  70. McCrea M. Standardized Mental Status Testing on the Sideline After Sport-Related Concussion. J Athl Train 2001; 36:274.
  71. McCrea M, Barr WB, Guskiewicz K, et al. Standard regression-based methods for measuring recovery after sport-related concussion. J Int Neuropsychol Soc 2005; 11:58.
  72. Daniel JC, Nassiri JD, Wilckens J, Land BC. The implementation and use of the standardized assessment of concussion at the U.S. Naval Academy. Mil Med 2002; 167:873.
  73. Grubenhoff JA, Kirkwood M, Gao D, et al. Evaluation of the standardized assessment of concussion in a pediatric emergency department. Pediatrics 2010; 126:688.
  74. McCrory P, Meeuwisse W, Johnston K, et al. Consensus statement on Concussion in Sport 3rd International Conference on Concussion in Sport held in Zurich, November 2008. Clin J Sport Med 2009; 19:185.
  75. Echemendia RJ, Meeuwisse W, McCrory P, et al. The Sport Concussion Assessment Tool 5th Edition (SCAT5): Background and rationale. Br J Sports Med 2017; 51:848.
  76. Guskiewicz KM, Register-Mihalik J, McCrory P, et al. Evidence-based approach to revising the SCAT2: introducing the SCAT3. Br J Sports Med 2013; 47:289.
  77. Putukian M, Echemendia R, Dettwiler-Danspeckgruber A, et al. Prospective clinical assessment using Sideline Concussion Assessment Tool-2 testing in the evaluation of sport-related concussion in college athletes. Clin J Sport Med 2015; 25:36.
  78. Shores EA, Lammél A, Hullick C, et al. The diagnostic accuracy of the Revised Westmead PTA Scale as an adjunct to the Glasgow Coma Scale in the early identification of cognitive impairment in patients with mild traumatic brain injury. J Neurol Neurosurg Psychiatry 2008; 79:1100.
  79. Ponsford J, Willmott C, Rothwell A, et al. Use of the Westmead PTA scale to monitor recovery of memory after mild head injury. Brain Inj 2004; 18:603.
  80. Levin HS, O'Donnell VM, Grossman RG. The Galveston Orientation and Amnesia Test. A practical scale to assess cognition after head injury. J Nerv Ment Dis 1979; 167:675.
  81. Mayers LB, Redick TS. Clinical utility of ImPACT assessment for postconcussion return-to-play counseling: psychometric issues. J Clin Exp Neuropsychol 2012; 34:235.
  82. Elbin RJ, Schatz P, Covassin T. One-year test-retest reliability of the online version of ImPACT in high school athletes. Am J Sports Med 2011; 39:2319.
  83. Valovich McLeod TC, Bay RC, Lam KC, Chhabra A. Representative baseline values on the Sport Concussion Assessment Tool 2 (SCAT2) in adolescent athletes vary by gender, grade, and concussion history. Am J Sports Med 2012; 40:927.
  84. Schatz P, Sandel N. Sensitivity and specificity of the online version of ImPACT in high school and collegiate athletes. Am J Sports Med 2013; 41:321.
  85. Borg J, Holm L, Cassidy JD, et al. Diagnostic procedures in mild traumatic brain injury: results of the WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury. J Rehabil Med 2004; :61.
  86. Stiell IG, Wells GA, Vandemheen K, et al. The Canadian CT Head Rule for patients with minor head injury. Lancet 2001; 357:1391.
  87. 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.
  88. Mower WR, Hoffman JR, Herbert M, et al. Developing a decision instrument to guide computed tomographic imaging of blunt head injury patients. J Trauma 2005; 59:954.
  89. Ro YS, Shin SD, Holmes JF, et al. Comparison of clinical performance of cranial computed tomography rules in patients with minor head injury: a multicenter prospective study. Acad Emerg Med 2011; 18:597.
  90. Stiell IG, Clement CM, Rowe BH, et al. Comparison of the Canadian CT Head Rule and the New Orleans Criteria in patients with minor head injury. JAMA 2005; 294:1511.
  91. Smits M, Dippel DW, de Haan GG, et al. External validation of the Canadian CT Head Rule and the New Orleans Criteria for CT scanning in patients with minor head injury. JAMA 2005; 294:1519.
  92. Bouida W, Marghli S, Souissi S, et al. Prediction value of the Canadian CT head rule and the New Orleans criteria for positive head CT scan and acute neurosurgical procedures in minor head trauma: a multicenter external validation study. Ann Emerg Med 2013; 61:521.
  93. Papa L, Stiell IG, Clement CM, et al. Performance of the Canadian CT Head Rule and the New Orleans Criteria for predicting any traumatic intracranial injury on computed tomography in a United States Level I trauma center. Acad Emerg Med 2012; 19:2.
  94. Kavalci C, Aksel G, Salt O, et al. Comparison of the Canadian CT head rule and the new orleans criteria in patients with minor head injury. World J Emerg Surg 2014; 9:31.
  95. Jagoda AS, Bazarian JJ, Bruns JJ Jr, et al. Clinical policy: neuroimaging and decisionmaking in adult mild traumatic brain injury in the acute setting. Ann Emerg Med 2008; 52:714.
  96. Centers for Disease Control and Prevention. Injury Prevention & Control: Traumatic Brain Injury. Heads Up to Clinicians: Updated Mild Traumatic Brain Injury Guideline for Adults. http://www.cdc.gov/concussion/HeadsUp/clinicians_guide.html (Accessed on October 23, 2010).
  97. https://www.nice.org.uk/guidance/cg176/chapter/1-Recommendations#investigating-clinically-important-brain-injuries (Accessed on April 28, 2017).
  98. 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.
  99. af Geijerstam JL, Oredsson S, Britton M, OCTOPUS Study Investigators. Medical outcome after immediate computed tomography or admission for observation in patients with mild head injury: randomised controlled trial. BMJ 2006; 333:465.
  100. Manolakaki D, Velmahos GC, Spaniolas K, et al. Early magnetic resonance imaging is unnecessary in patients with traumatic brain injury. J Trauma 2009; 66:1008.
  101. Livingston DH, Lavery RF, Passannante MR, et al. Emergency department discharge of patients with a negative cranial computed tomography scan after minimal head injury. Ann Surg 2000; 232:126.
  102. Hesselink JR, Dowd CF, Healy ME, et al. MR imaging of brain contusions: a comparative study with CT. AJR Am J Roentgenol 1988; 150:1133.
  103. Wilberger JE Jr, Rothfus WE, Tabas J, et al. Acute tissue tear hemorrhages of the brain: computed tomography and clinicopathological correlations. Neurosurgery 1990; 27:208.
  104. Yuh EL, Mukherjee P, Lingsma HF, et al. Magnetic resonance imaging improves 3-month outcome prediction in mild traumatic brain injury. Ann Neurol 2013; 73:224.
  105. 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 Am J Neuroradiol 1994; 15:1583.
  106. Douglas DB, Muldermans JL, Wintermark M. Neuroimaging of brain trauma. Curr Opin Neurol 2018; 31:362.
  107. ACR Appropriateness Criteria: Head Trauma. American College of Radiology. Available at: https://acsearch.acr.org/docs/69481/Narrative (Accessed on February 22, 2022).
  108. Shahim P, Tegner Y, Wilson DH, et al. Blood biomarkers for brain injury in concussed professional ice hockey players. JAMA Neurol 2014; 71:684.
  109. Lawler KA, Terregino CA. Guidelines for evaluation and education of adult patients with mild traumatic brain injuries in an acute care hospital setting. J Head Trauma Rehabil 1996; 11:18.
  110. Sifri ZC, Nayak N, Homnick AT, et al. Utility of repeat head computed tomography in patients with an abnormal neurologic examination after minimal head injury. J Trauma 2011; 71:1605.
  111. Atzema C, Mower WR, Hoffman JR, et al. Defining "therapeutically inconsequential" head computed tomographic findings in patients with blunt head trauma. Ann Emerg Med 2004; 44:47.
  112. Nishijima DK, Offerman SR, Ballard DW, et al. Immediate and delayed traumatic intracranial hemorrhage in patients with head trauma and preinjury warfarin or clopidogrel use. Ann Emerg Med 2012; 59:460.
  113. Menditto VG, Lucci M, Polonara S, et al. Management of minor head injury in patients receiving oral anticoagulant therapy: a prospective study of a 24-hour observation protocol. Ann Emerg Med 2012; 59:451.
  114. Joseph B, Aziz H, Pandit V, et al. Prospective validation of the brain injury guidelines: managing traumatic brain injury without neurosurgical consultation. J Trauma Acute Care Surg 2014; 77:984.
  115. Norlund A, Marké LA, af Geijerstam JL, et al. Immediate computed tomography or admission for observation after mild head injury: cost comparison in randomised controlled trial. BMJ 2006; 333:469.
  116. Mahoney E, Agarwal S, Li B, et al. Evidence-based guidelines are equivalent to a liberal computed tomography scan protocol for initial patient evaluation but are associated with decreased computed tomography scan use, cost, and radiation exposure. J Trauma Acute Care Surg 2012; 73:573.
  117. Tan CL, Alavi SA, Baldeweg SE, et al. The screening and management of pituitary dysfunction following traumatic brain injury in adults: British Neurotrauma Group guidance. J Neurol Neurosurg Psychiatry 2017; 88:971.
  118. Reljic T, Mahony H, Djulbegovic B, et al. Value of repeat head computed tomography after traumatic brain injury: systematic review and meta-analysis. J Neurotrauma 2014; 31:78.
  119. Kaen A, Jimenez-Roldan L, Arrese I, et al. The value of sequential computed tomography scanning in anticoagulated patients suffering from minor head injury. J Trauma 2010; 68:895.
  120. Mason S, Kuczawski M, Teare MD, et al. AHEAD Study: an observational study of the management of anticoagulated patients who suffer head injury. BMJ Open 2017; 7:e014324.
  121. Peck KA, Sise CB, Shackford SR, et al. Delayed intracranial hemorrhage after blunt trauma: are patients on preinjury anticoagulants and prescription antiplatelet agents at risk? J Trauma 2011; 71:1600.
  122. Bauman ZM, Ruggero JM, Squindo S, et al. Repeat Head CT? Not Necessary for Patients with a Negative Initial Head CT on Anticoagulation or Antiplatelet Therapy Suffering Low-Altitude Falls. Am Surg 2017; 83:429.
  123. Bee TK, Magnotti LJ, Croce MA, et al. Necessity of repeat head CT and ICU monitoring in patients with minimal brain injury. J Trauma 2009; 66:1015.
  124. Thorson CM, Van Haren RM, Otero CA, et al. Repeat head computed tomography after minimal brain injury identifies the need for craniotomy in the absence of neurologic change. J Trauma Acute Care Surg 2013; 74:967.
  125. Washington CW, Grubb RL Jr. Are routine repeat imaging and intensive care unit admission necessary in mild traumatic brain injury? J Neurosurg 2012; 116:549.
  126. Quigley MR, Chew BG, Swartz CE, Wilberger JE. The clinical significance of isolated traumatic subarachnoid hemorrhage. J Trauma Acute Care Surg 2013; 74:581.
  127. Borczuk P, Penn J, Peak D, Chang Y. Patients with traumatic subarachnoid hemorrhage are at low risk for deterioration or neurosurgical intervention. J Trauma Acute Care Surg 2013; 74:1504.
  128. Jagoda AS, Cantrill SV, Wears RL, et al. Clinical policy: neuroimaging and decisionmaking in adult mild traumatic brain injury in the acute setting. Ann Emerg Med 2002; 40:231.
  129. Schneider KJ, Iverson GL, Emery CA, et al. The effects of rest and treatment following sport-related concussion: a systematic review of the literature. Br J Sports Med 2013; 47:304.
  130. Thomas DG, Apps JN, Hoffmann RG, et al. Benefits of strict rest after acute concussion: a randomized controlled trial. Pediatrics 2015; 135:213.
  131. Meehan WP 3rd, Bachur RG. The recommendation for rest following acute concussion. Pediatrics 2015; 135:362.
  132. Makdissi M, Cantu RC, Johnston KM, et al. The difficult concussion patient: what is the best approach to investigation and management of persistent (>10 days) postconcussive symptoms? Br J Sports Med 2013; 47:308.
  133. Guskiewicz KM, McCrea M, Marshall SW, et al. Cumulative effects associated with recurrent concussion in collegiate football players: the NCAA Concussion Study. JAMA 2003; 290:2549.
  134. Gronwall D, Wrightson P. Cumulative effect of concussion. Lancet 1975; 2:995.
  135. Collins MW, Lovell MR, Mckeag DB. Current issues in managing sports-related concussion. JAMA 1999; 282:2283.
  136. Herring SA, Cantu RC, Guskiewicz KM, et al. Concussion (mild traumatic brain injury) and the team physician: a consensus statement--2011 update. Med Sci Sports Exerc 2011; 43:2412.
  137. Harmon KG, Drezner JA, Gammons M, et al. American Medical Society for Sports Medicine position statement: concussion in sport. Br J Sports Med 2013; 47:15.
  138. Guidelines for the management of concussion in sports. Rev May 1991. Colorado Medical Society, Denver 1991.
  139. Echemendia RJ, Iverson GL, McCrea M, et al. Advances in neuropsychological assessment of sport-related concussion. Br J Sports Med 2013; 47:294.
  140. Halstead ME, Walter KD, Moffatt K, Council on Sports Medicine and Fitness. American Academy of Pediatrics. Clinical report--sport-related concussion in children and adolescents. Pediatrics 2018; 142:e20183074.
  141. Triebel KL, Martin RC, Novack TA, et al. Treatment consent capacity in patients with traumatic brain injury across a range of injury severity. Neurology 2012; 78:1472.
Topic 4828 Version 27.0

References

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