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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: Aug 2022. | 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 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.

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. 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. 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].

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: Closed
head injury (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.)

Use of UpToDate is subject to the Terms of Use.

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78:1472.
Topic 4828 Version 27.0
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

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 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

Standardized assessment of concussion (SAC)

Orientation (1 point each) Delayed recall (Approximately 5

minutes after Immediate
Month
memory. 1 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
Delayed recall score: 5
each 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

Concentration
Reverse digits (Go to next string
length if correct on first trial. Stop
if incorrect on both trials. 1 point
each for each string length.)
between the Immediate memory
and Delayed recall portions of this
assessment when appropriate:
Neurologic screening
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 5 sit-ups

order (1 point for entire sequence 5 push-ups
correct)
5 knee bends
Dec-Nov-Oct-Sep-Aug-Jul

Jun-May-Apr-Mar-Feb-Jan
 Concentration score: 5

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

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.

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

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 Increase heart rate.

aerobic at slow to medium pace. No
exercise resistance training.

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

specific head impact activities.
exercise

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

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

5 Full Following medical clearance, Restore confidence and

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

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

Contributor Disclosures
Randolph W Evans, MD, FAAN Consultant/Advisory Boards: Lundbeck [Migraine]. Speaker's
Bureau: Abbvie [Migraine]; Amgen [Migraine]; Biohaven [Migraine]; Eli Lilly [Migraine]; Impel
[Migraine]; Teva [Migraine]. Other Financial Interest: Elsevier [Royalties]; Oxford University
Press [Royalties]; Medscape Neurology [Royalties]. All of the relevant financial relationships
listed have been mitigated. Christopher T Whitlow, MD, PhD, MHA No relevant financial
relationship(s) with ineligible companies to disclose. 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.

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