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Official reprint from UpToDate®

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Acute mild traumatic brain injury (concussion) in adults

Authors: Randolph W Evans, MD, FAAN, Christopher T Whitlow, MD, PhD, MHA
Section Editors: Michael J Aminoff, MD, DSc, Maria E Moreira, MD
Deputy Editor: Janet L Wilterdink, MD

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Feb 2023. | 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

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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].

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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

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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].

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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'.)

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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

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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.

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.

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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].

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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
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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. 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-
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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. 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,
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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)
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● 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'.)

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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].

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].
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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.

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● 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".)

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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
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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.
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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
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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.

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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)

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• 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.)

Use of UpToDate is subject to the Terms of Use.

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87. Haydel MJ, Preston CA, Mills TJ, et al. Indications for computed tomography in patients with
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106. Douglas DB, Muldermans JL, Wintermark M. Neuroimaging of brain trauma. Curr Opin
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108. Shahim P, Tegner Y, Wilson DH, et al. Blood biomarkers for brain injury in concussed
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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
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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
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113. Menditto VG, Lucci M, Polonara S, et al. Management of minor head injury in patients
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115. Norlund A, Marké LA, af Geijerstam JL, et al. Immediate computed tomography or
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119. Kaen A, Jimenez-Roldan L, Arrese I, et al. The value of sequential computed tomography
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traumatic subarachnoid hemorrhage. J Trauma Acute Care Surg 2013; 74:581.
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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.
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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.

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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.
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the team physician: a consensus statement--2011 update. Med Sci Sports Exerc 2011;
43:2412.
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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 S
ociety, 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

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GRAPHICS

Glasgow Coma Scale (GCS)

Score

Eye opening

Spontaneous 4

Response to verbal command 3

Response to pain 2

No eye opening 1

Best verbal response

Oriented 5

Confused 4

Inappropriate words 3

Incomprehensible sounds 2

No verbal response 1

Best motor response

Obeys commands 6

Localizing response to pain 5

Withdrawal response to pain 4

Flexion to pain 3

Extension to pain 2

No motor response 1

Total

The GCS is scored between 3 and 15, 3 being the worst and 15 the best. It is composed of three
parameters: best eye response (E), best verbal response (V), and best motor response (M). The
components of the GCS should be recorded individually; for example, E2V3M4 results in a GCS score
of 9. A score of 13 or higher correlates with mild brain injury, a score of 9 to 12 correlates with
moderate injury, and a score of 8 or less represents severe brain injury.

Graphic 81854 Version 9.0

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Standardized assessment of concussion addendum [1,2]

Graded symptom checklist

Symptom (Likert scale 0 to 6) None Mild Moderate Severe

Headache 0 1 to 2 3 to 4 5 to 6

Nausea 0 1 to 2 3 to 4 5 to 6

Vomiting 0 1 to 2 3 to 4 5 to 6

Dizziness 0 1 to 2 3 to 4 5 to 6

Poor balance 0 1 to 2 3 to 4 5 to 6

Blurred/double vision 0 1 to 2 3 to 4 5 to 6

Sensitivity to light 0 1 to 2 3 to 4 5 to 6

Sensitivity to noise 0 1 to 2 3 to 4 5 to 6

Ringing in the ears 0 1 to 2 3 to 4 5 to 6

Poor concentration 0 1 to 2 3 to 4 5 to 6

Memory problems 0 1 to 2 3 to 4 5 to 6

Not feeling "sharp" 0 1 to 2 3 to 4 5 to 6

Fatigue/sluggish 0 1 to 2 3 to 4 5 to 6

Sadness/depression 0 1 to 2 3 to 4 5 to 6

Irritability 0 1 to 2 3 to 4 5 to 6

Amnesia

Post-traumatic amnesia Yes No Length:

Retrograde amnesia Yes No Length:

Strength
Right arm Normal Abnormal

Right leg Normal Abnormal

Left arm Normal Abnormal

Left leg Normal Abnormal

Sensation Normal Abnormal

Coordination of limbs/gait Normal Abnormal

The unscored portion of the Standardized Assessment of Concussion (SAC) includes a graded
symptom checklist, a brief neurologic examination, and records the presence of post-traumatic and

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retrograde amnesia.

References:
1. 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.
2. Guskiewicz KM, Bruce SL, Cantu RC, et al. National Athletic Trainers' Association Position Statement: Management of
Sport-Related Concussion. J Athl Train 2004; 39:280.

Graphic 67396 Version 6.0

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Standardized assessment of concussion (SAC)

Orientation (1 point each) Delayed recall (Approximately 5

minutes after Immediate memory. 1
Month
point each.)
Date
Word 1
Day of week
Word 2
Year
Word 3
Time (within 1 hr)
Word 4
Orientation score: 5
Word 5
Immediate memory (1 point for each
Delayed recall score: 5
correct, total over 3 trials)
Summary of total scores:
Trial 1 Trial 2 Trial 3
Orientation 5
Word 1
Immediate memory 15
Word 2
Concentration 5
Word 3
Delayed recall 5
Word 4
Total score 30
Word 5

Immediate memory score: 15

The following may be performed
between the Immediate memory and
Concentration Delayed recall portions of this
Reverse digits (Go to next string length assessment when appropriate:
if correct on first trial. Stop if incorrect
Neurologic screening
on both trials. 1 point each for each
string length.) Recollection of the injury

3-8-2 5-1-8 Strength

2-7-9-3 2-1-6-8 Coordination

5-1-8-6-9 9-4-1-7-5 Exertional maneuvers

6-9-7-3-5-1 4-2-8-9-3-7 1 40-yard sprint

Months of the year in reverse order (1 5 sit-ups

point for entire sequence correct) 5 push-ups

Dec-Nov-Oct-Sep-Aug-Jul 5 knee bends

Jun-May-Apr-Mar-Feb-Jan

Concentration score: 5

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Reproduced with permission from: McCrea M, Kelly JP, Kluge J, et al. Standardized assessment of concussion in football
players. Neurology 1997; 48:586. Copyright © 1997 Lippincott Williams & Wilkins.

Graphic 77142 Version 14.0

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Acute evaluation of an adult with mild head trauma

Mild head trauma is typically defined as head injury due to contact

and/or acceleration/deceleration forces and a score on the Glasgow
Coma Scale of 13 to 15.

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CT: computed tomography; NEXUS: National Emergency X-ray

Utilization Study; MRI: magnetic resonance imaging; MR: magnetic
resonance.

* Combined from Canadian CT head rule [1] , New Orleans criteria [2] ,
and NEXUS-II criteria [3] . Including all features will lead to a very high
sensitivity (>99%) and low specificity for identifying a patient with an
important brain injury. The features below the dashed line are
included in only one of the three validated criteria, while others are
included in at least two of them.

¶ If trauma occurred >7 days ago, head MRI without contrast, if

available, is more appropriate. If noncontrast images suggest a
vascular injury, intravenous contrast may be administered for CT or
MR angiography of the head and neck.

Δ These represent general guidelines for when neurosurgical

consultation is indicated. It may be prudent to obtain neurosurgical
consultation for less severe and other CT abnormalities.

◊ If there is no responsible caregiver at home, consider inpatient

observation or CT, if it has not been performed already.

References:
1. Stiell IG, Wells GA, Vandemheen K, et al. The Canadian CT Head Rule for
patients with minor head injury. Lancet 2001; 357:1391.
2. 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.
3. 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.

Graphic 50743 Version 5.0

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Graduated return-to-play protocol

Stage Aim Activity Goal of each step

1 Symptom- Daily activities that do not Gradual reintroduction of

limited provoke symptoms. work/school activities.
activity

2 Light Walking or stationary cycling at Increase heart rate.

aerobic slow to medium pace. No
exercise resistance training.

3 Sport- Running or skating drills. No Add movement.

specific head impact activities.
exercise

4 Non-contact Harder training drills, eg, passing Exercise, coordination and

training drills. May start progressive increased thinking.
drills resistance training.

5 Full contact Following medical clearance, Restore confidence and assess

practice participate in normal training functional skills by coaching staff.
activities.

6 Return to Normal game play.

sport

NOTE: An initial period of 24 to 48 hours of both relative physical rest and cognitive rest is
recommended before beginning the RTS progression. There should be at least 24 hours (or longer)
for each step of the progression. If any symptoms worsen during exercise, the athlete should go
back to the previous step. Resistance training should be added only in the later stages (stage 3 or 4
at the earliest). If symptoms are persistent (eg, more than 10 to 14 days in adults or more than 1
month in children), the athlete should be referred to a health care professional who is an expert in
the management of concussion.

RTS: return to sport.

From: McCrory P, Meeuwisse W, Dvořák J, et al. Consensus statement on concussion in sport—the 5th international
conference on concussion in sport held in Berlin, October 2016. Br J Sports Med 2017; 51:838. Reproduced with permission
from BMJ Publishing Group Ltd. Copyright © 2017.

Graphic 61318 Version 12.0

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Contributor Disclosures
Randolph W Evans, MD, FAAN Speaker's Bureau: Abbvie [Migraine]; Amgen [Migraine]; Biohaven
[Migraine]; Eli Lilly [Migraine]; Impel [Migraine]; Teva [Migraine]. Other Financial Interest: Elsevier
[Royalties]; Medscape Neurology [Royalties]; Oxford University Press [Royalties]. All of the relevant
financial relationships listed have been mitigated. Christopher T Whitlow, MD, PhD, MHA Patent Holder:
Application # 62425920 [Medical image analysis using mechanical deformation information].
Grant/Research/Clinical Trial Support: Michael J Fox Foundation [Parkinson disease]; National Institutes of
Health [TBI, Alzheimer disease, brain tumors, substance use/abuse]. Consultant/Advisory Boards: Biogen
[Alzheimer disease]; Genentech [Alzheimer disease]. All of the relevant financial relationships listed have
been mitigated. Michael J Aminoff, MD, DSc Consultant/Advisory Boards: Brain Neurotherapy Bio
[Parkinson disease]. All of the relevant financial relationships listed have been mitigated. Maria E Moreira,
MD No relevant financial relationship(s) with ineligible companies to disclose. Janet L Wilterdink, MD No
relevant financial relationship(s) with ineligible companies to disclose.

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must
conform to UpToDate standards of evidence.

Conflict of interest policy

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