Pediatric Head Trauma: A Review and Update

Rose N. Gelineau-Morel, MD,* Timothy P. Zinkus, MD,† Jean-Baptiste Le Pichon, MD, PhD*
*Division of Neurology and †Division of Radiology, Children’s Mercy Hospital, Kansas City, MO

Practice Gaps
There is still a considerable amount of confusion when it comes
to managing concussions. An excessive number of head computed
tomographic scans are being obtained for concussions, resulting
in unnecessary exposure to ionizing radiation. Clinicians should be
aware of the most recent guidelines for the management of
concussion, including the need for imaging, and should be able
to differentiate mild from moderate and severe traumatic brain
injury.

Objectives After completing this article, readers should be able to:

1. Differentiate a mild from a moderate or severe traumatic brain injury

(TBI).
AUTHOR DISCLOSURE Drs Gelineau-Morel
2. Acutely manage a child with a TBI, including deciding when further and Zinkus have disclosed no financial
imaging is necessary. relationships relevant to this article. Dr Le
Pichon has disclosed that he has served as a
3. Manage a child with a postconcussion syndrome and identify when consultant for an AADC Deficiency Advisors
Forum and as a medical legal expert and
referral to a specialist is necessary.
that he currently serves as the chair of the
Subcommittee on Education for the American
Academy of Pediatrics Section on Neurology
Committee. This commentary does not
contain a discussion of an unapproved/
Traumatic brain injury (TBI) is the leading cause of death or severe disability in investigative use of a commercial product/
children older than 1 year. (1)(2) In a report to Congress published by the Centers device.
for Disease Control and Prevention (CDC) in 2018, (3) the CDC reported the
ABBREVIATIONS
public health burden of TBIs. They noted that 640,000 emergency department AAP American Academy of
visits and 18,000 hospital stays were directly related to TBI. The etiology of TBI Pediatrics
varies among age groups. In the 0- to 4-year-old age group, the most common AHT abusive head trauma
cause of TBI is falls. On the other hand, in the 15- to 24-year-old age group the CDC Centers for Disease Control
and Prevention
distribution of injuries caused by falls, assault, and motor vehicle events are nearly
Child SCAT5 Child Sport Concussion
equal. Epidemiologic studies have found that rates of TBI seen in the emergency
Assessment Tool
department have increased in all age groups since 2001, with children 0 to 24 CISG Concussion in Sport Group
years old having the highest rates of TBI of all age groups. Children 0 to 4 years old CT computed tomography
have almost twice the rate of TBI compared with the next highest age group (15–24 DAI diffuse axonal injury
years old), making pediatric traumatic brain injury an especially salient topic for FLAIR fluid-attenuated inversion
recovery
the modern-day pediatrician. (4) Moreover, 61% of children with moderate to
GCS Glasgow Coma Scale
severe TBI experienced a disability. Estimates conclude that at least 145,000 MRI magnetic resonance imaging
children aged 0 to 19 years are currently living with long-term symptoms due to a mTBI mild traumatic brain injury
TBI (likely an underestimate with underreporting of mild TBI [mTBI]), with TBI traumatic brain injury

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symptoms extending far beyond their initial hospital visit can be caused by any mechanical force on the brain, we
into the following months and years. (3) Even children focus on sports-related concussion because this is the focus
without overt neurologic deficits resulting from their TBI of most research and clinical guidelines and is the most
can demonstrate impairment in academic performance, common presentation of concussion for the general pedi-
attention and concentration, memory, and executive func- atrician. (7) Note that although sports-related concussions
tion, some of which only become apparent months or years have been studied most extensively, it is probable that most
after the initial injury. (4)(5)(6) The economic impact of of the recommendations made thereafter apply equally well
TBI is substantial, with estimates ranging from $77.9 to concussions related to other accidental and nonaccidental
million per year in direct costs to more than $1 billion per injuries. In fact, in their most recent recommendations, the
year for TBI-associated hospitalizations. (5) CDC (10) does not differentiate between these types of
With all the associated morbidity and mortality, it is vital concussions as it relates to diagnosis and management.
that pediatricians are educated in recognizing and treating
TBIs and their sequelae. In this article, we aim to provide Recognizing Concussion
current evidence on the recognition, treatment, and reha- The first step to treating concussion is recognition. The
bilitation of TBIs. We begin by discussing mTBI, typically clinical phenotype of concussion can vary between patients,
manifesting as a concussion, and then discuss moderate and it can be a challenge for the evaluating clinician to
and severe TBIs that are more often encountered in the consider all the possible manifestations of concussion. One
emergency department or hospital setting. useful acronym is COACH CV, which was developed by
Craton et al (12) and is based on the CISG guidelines. This
acronym includes the most common clinical phenotypes of
MILD TBI
concussion: Cognitive dysfunction, Oculomotor dysfunction,
mTBI commonly manifests as concussion, and this is the Affective disturbances, Cervical spine disorders, Headaches,
focus of our discussion. However, it is also worth noting that and Cardiovascular and Vestibular anomalies (Table 1).
even patients with more severe brain injury can exhibit signs Symptoms of concussion in these domains are broad and
and symptoms of concussion, and these should not be ignored. include impairment of memory or attention, blurred vision or
Concussion is a broad clinical diagnosis defined by the Amer- abnormal extraocular movements, fatigue, mood changes,
ican Academy of Neurology as “a clinical syndrome of bio- poor sleep, headaches, vestibular dysfunction, or heart rate
mechanically induced alteration of brain function, typically variability (see Table 1 for a more extensive list of potential
affecting memory and orientation, which may involve loss of concussion symptoms). Of note, a patient with a concussion
consciousness.” (6) Due to various mechanisms of action for may have 1 or more of these symptoms. There is no loss of
concussion, and the multiple disciplines involved, including consciousness required for a diagnosis of concussion.
neurology, sports medicine, rehabilitation medicine, and mil- In their recent recommendations for the diagnosis and
itary medicine, there are multiple diagnostic criteria and management of concussion, the CDC recommends using a
treatment recommendations in place, which can make it validated symptom rating scale in the evaluation of concus-
challenging for the primary care provider evaluating a patient sion. (10) The most commonly used tools include the Child
with a concussion. (7) Yet, concussion is a common complaint Sport Concussion Assessment Tool (Child SCAT5) devel-
in children, occurring in approximately 692 of 100,000 chil- oped by the CISG, (13) the Acute Concussion Evaluation
dren younger than 15 years, (8) indicating that an evidence- developed by the CDC, (9) the Postconcussion Symptom
based, comprehensive plan for concussion diagnosis and Scale, (14) and the Graded Symptom Checklist. (15)(16)
management is imperative. (7) These tools use a Likert scale completed by the patient
In this section, we aim to summarize current recom- and/or parent to assess symptom severity, with a higher
mendations on concussion evaluation and management for score indicating more severe symptoms. Although some of
the general pediatrician based on guidelines for concussion the scales, specifically the Child SCAT5, were developed for
management developed by the American Academy of Neu- sports-related concussion, the symptoms of concussion are
rology, (6) the CDC, (9)(10) and the Concussion in Sport generalizable to other concussion etiologies as well. Studies
Group (CISG), an international multidisciplinary group of have further analyzed these scales, attempting to identify the
clinicians and researchers focused on concussion diagnosis underlying symptom groups contributing to higher scores
and management. (11) The CDC recently published new in concussed patients (eg, neurocognitive, somatic, emo-
guidelines on concussion management, and these recom- tional), with mixed conclusions. (14)(15)(17) In practice, it is
mendations are reflected herein. (10) Although concussion best to choose a scale and get baseline testing, followed by

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 TABLE 1. Clinical Phenotypes of Concussion (COACH CV)
CLINICAL
PHENOTYPE SYMPTOMS SPECIFIC TESTING

C Cognitive function Memory impairment, decreased attention and Neuropsychological testing (in person or computer-
concentration, slowed processing speed based, such as ImPACT testing)
O Oculomotor Convergence insufficiency, blurred vision, abnormal Visual acuity testing
dysfunction saccades and/or smooth pursuit, photophobia King-Devick test (assess saccadic eye movements)
A Affective disturbances Fatigue, sadness, irritability, sleep disturbance, poor Depression screen
concentration, emotionality
C Cervical spine disorders Neck pain, headaches, dizziness, balance difficulty Neck range of motion
Palpation of bones and muscles of the neck
H Headaches Migrainous, tension-type, or cervicogenic headaches –
C Cardiovascular Exercise intolerance, heart rate variability or elevation, Orthostatic vital signs
anomaly postural orthostatic tachycardia syndrome, autonomic Exercise stress test
dysfunction Tilt table testing
V Vestibular dysfunction Dizziness, vertigo, balance difficulties Romberg test
Tandem gait
Vestibulo-ocular reflex
Balance Error Scoring System (see the Child Sport
Concussion Assessment Tool)

This table includes the common clinical phenotypes of concussion that patients may endorse on a symptom scale. Listed are the corresponding symptoms
of each phenotype, as well as further testing that can be considered to assess each symptom. See Craton et al. (12)

testing at the time of injury and repeated testing throughout evidence of skull fracture, or signs of clinical deterioration.
recovery to track changes in individual and total symptom (6) The Pediatric Emergency Care Applied Research Net-
scores. If symptoms in any 1 or more of the tested clinical work (PECARN) has established criteria that can be used in
domains are present, this suggests a diagnosis of concus- decision making for children presenting after a TBI. The
sion. (13) clinical criteria for children 2 years and older include
If further delineation of symptoms is required, additional normal mental status, no loss of consciousness, no vomit-
testing, either in the office or via a referral to the appropriate ing, nonsevere injury mechanism, no signs of basilar skull
provider, can be considered. Some toolkits, such as the Child fracture, and no severe headache. If all of these criteria are
SCAT5, include further testing that can be performed by the met, they demonstrate a negative predictive value of
provider to screen for certain concussion phenotypes. These 99.95% for clinically important TBI. Conversely, the pres-
include the Balance Error Scoring System, which assesses ence of any 1 of these predictors has sensitivity of 96.8%
postural stability, and the Sensory Organization Test, which in identifying clinically important TBI and indicates that
assesses the patient’s equilibrium with altering visual and further assessment with head CT is required. Criteria
somatosensory inputs. However, these methods are not as for children younger than 2 years are also included in
sensitive at concussion diagnosis as the previously men- the study. (18) Unfortunately, unnecessary head CT in
tioned Likert rating scales. (6) Other targeted testing could children remains a common concern, and further education
include visual acuity for oculomotor dysfunction, orthostatic of community providers can help reduce this unneeded
vital signs of cardiovascular dysfunction, or a detailed spinal radiation exposure. (19)
neuromuscular examination to evaluate for cervical spine Although clinical discretion is still required to make a
abnormalities (Table 1). (7) concussion diagnosis, the previously mentioned tools can
Of note, computed tomography (CT) cannot be used to help identify symptoms and track recovery, aiding the
diagnose concussion and should generally be avoided to clinician in decisions regarding return to play and when
prevent unnecessary ionizing radiation exposure, although to pursue referral or further testing. With the typical natural
it may be used to rule out a more severe TBI, especially in history of concussion, an athlete’s symptoms should return
patients with loss of consciousness, posttraumatic amnesia, to baseline in 2 weeks for adults and in 4 weeks for children.
persistent altered mental status, focal neurologic deficit, (20)

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Rest and Return to Play and progressing through graduated steps until full return to
Once a concussion is diagnosed it is imperative that the sport (Table 2). The child should take at least 24 hours for
patient is given the appropriate guidelines for rest and each step of the plan, with return to the previous step for any
return to play/school. Previous recommendations for com- worsening of symptoms. A similar progression can be used
plete rest until symptom resolution are now outdated and for return to school activities for children whose symptoms
likely stemmed from sports medicine literature in which are exacerbated by mental activities, beginning with a few
there was a concern for second impact syndrome. Although days of rest at home, followed by a gradual return to school
this remains a concern, strict rest is not required for this full time. (13) Nonessential cognitive activities, such as
entire period but rather guidelines now recommend com- playing video games, should be introduced as tolerated once
plete rest for 24 to 48 hours, after which patients have a a child is back to normal or near-normal physical routine.
gradual return to full activity. In fact, a recent study com- There is some evidence to suggest that the period for full
paring 2-day and 5-day strict rest periods in children with physiologic and metabolic recovery from concussion may
concussion demonstrated a slower resolution of symptoms extend beyond that for clinical symptom recovery and that a
in the group with a more prolonged rest. (21) After the initial repeat concussion during this period could further prolong
rest period, children can follow a gradual return-to-activity recovery. The NCAA Concussion Study on collegiate football
protocol, which is outlined further in available toolkits, players found that 11 of the 12 players with a repeat concussion
including the CDC Heads Up guidelines (9) and the Child in one season experienced their second concussion within 10
SCAT5. The general strategy includes gradually increasing days of their initial concussion, indicating that athletes are
physical activity, beginning with nonaerobic daily activities especially prone to recurrent concussion during this period.

TABLE 2. Return to Play Progression

GOAL OF EACH
EXERCISE STEP EXAMPLE ACTIVITIES ACTIVITY TIME STEP

No activity Complete physical and cognitive rest for 24–48 h

Nonaerobic Normal daily activities – Reintegrate into
activity that do not provoke work and school
symptoms activities
Light aerobic Exercise bike, walking, 5–10 min Light activities
activity light jogging at a leading to a mild
slow pace (no increase in heart
weight lifting, rate
jumping, or
running)
Moderate activity Jogging, brief running, Reduced from Limited body and
moderate-intensity normal routine head movement
stationary biking,
light resistance
activities
Heavy, noncontact Running, noncontact At or near normal Intense activity
activity drills, weight lifting, routine without contact
stationary biking Cognitive activity
during exercise
can be added
Full contact Normal full-contact Normal routine Return to full-
physical activities contact activities
Competitive Return to full Normal routine No further
activities competitive restrictions in
activities activity

The table is adapted from the Centers for Disease Control and Prevention Heads Up guidelines and the Child Sport Concussion Assessment Tool for
returning to play. Each step should take a minimum of 24 hours. During the above progression, the child, family, and health-care provider should pay
special attention to any new or worsening symptoms. If any symptoms worsen while exercising, the child should return to the previous step.

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 (22) However, further details of time to complete physiologic renamed “major or mild neurocognitive disorder due to
recovery are not known and, at this time, it is only recom- TBI.” It is up to the clinician to consider the severity and
mended that children have a “buffer” period of gradual return functional disability of the patient when assigning a diag-
to full activity after complete symptom resolution. (23) nosis. Postconcussive symptoms can be widely variable and
Although pharmacologic treatment has not been shown depend on preexisting comorbidities, including neurocogni-
to facilitate recovery from concussion, it may be considered tive disorders, vestibular dysfunction, affective symptoms,
in patients who have longer recovery periods or whose and medication/substance use. (27)
quality of life is significantly affected by their symptoms. Additional evaluation and therapy should be considered
In these cases, treatment should focus on symptom man- for children with persistent postconcussive symptoms. Al-
agement, including medications such as melatonin for sleep though most concussion patients will have normal cogni-
disturbance, nonopioid analgesics for acute headaches and tive function by 3 months after injury, some children could
amitriptyline or topiramate for headache prevention, and have cognitive deficits persisting up to 1 year, especially in
selective serotonin reuptake inhibitors or amantadine for the presence of a severe original injury, a history of previous
emotional or cognitive effects, respectively. (24) Of note, in concussions, and psychological risk factors. (29) These
patients using pharmacotherapy, this could mask the symp- children should be referred for formal neuropsychological
toms of concussion, and these medications should be testing. Magnetic resonance imaging (MRI) can be more
weaned or careful consideration should be given before sensitive at detecting certain types of brain injury, such as
returning to full play. (11) diffuse axonal injury (DAI) or petechial hemorrhages, which
are not detected in 25% to 30% of CT scans (see the
Referral "Management" subsection later herein). (30) Patients with
Occasionally, the situation will still arise in which children vestibular or oculomotor dysfunction should be referred to
do not have a complete recovery with the previously described the appropriate therapy for rehabilitation. Finally, the pos-
strategies. Children with symptoms persisting beyond 4 sibility of depression after concussion should not be ignored
weeks and adults with symptoms persisting beyond 2 weeks because it may often masquerade as cognitive or neurosen-
should be referred to a health-care provider specializing in sory dysfunction. (28)
concussion. (11) Studies have shown that higher symptom
scores on immediate postconcussive testing can indicate Risk Reduction
more severe or prolonged postcognitive effects with a longer General risk reduction for concussion centers around pre-
time for return to play. (25) ventive safety measures to decrease risk of head injury. This
Certain preexisting conditions may delay concussion includes the use of appropriate car seats, booster seats, or
recovery, including history of postural orthostatic tachycar- seat belts in automobiles; helmets while on bicycles or
dia syndrome, motion sickness, strabismus or ocular abnor- scooters; stair gates; and soft surfaces in play areas. (9)
malities, attention-deficit/hyperactivity disorder and learning However, the use of equipment in sports to protect
disabilities, and mood disorders. These children may require against concussions is a controversial topic. The use of
additional school accommodations to facilitate their return. mouth guards does not seem to provide protection from
(26) Other factors such as history of previous concussions, concussion. (6)(31) Helmets and headgear have been shown
more severe presenting or postconcussive symptoms, mem- to reduce the risk of concussion in skiing and snowboard-
ory problems, fatigue/fogginess, and disorientation may also ing, but the effect in full-contact sports such as hockey and
contribute to a more prolonged recovery. (6)(27) Some intrin- football has not been as conclusive. (31) This, in part, has led
sic factors, such as low socioeconomic status, Hispanic race, to the new rules for helmet contact implemented recently by
and high school age (especially in girls), also place children at the National Football League to reduce unnecessary risk of
risk for more prolonged symptoms compared with other head injury in its players. (32)
patient populations. (10)(11) Research on risk reduction for sports-related concussion
has also focused on analyzing age, level of competition, sex,
Residual Effects and type of sport to determine whether any individual factor
Unfortunately, approximately 10% to 15% of concussion can affect concussion symptoms and risk. A recent study
patients have persistent symptoms beyond the first few found that females with concussion are more likely to report
weeks. (28) As recently as 2014, the Diagnostic and Statistical a higher level of symptoms and to experience postconcus-
Manual of Mental Disorders criteria included a diagnosis sive headaches, whereas males are more likely to experi-
of postconcussion syndrome, although this has now been ence loss of consciousness, confusion, and amnesia with a

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concussion. (33) Although rates of concussion in males are agree on the importance of complete resolution of symp-
greater due to larger total numbers of athletes, concussion toms before return to play because this will decrease the risk
risk seems to be greater in female athletes playing soccer of prolonged postconcussive symptoms and the possibility
or basketball. In addition, for all athletes there seems to be of second impact syndrome. (31)
a higher risk of concussion with American football and
rugby compared with other sports, with baseball, softball,
MODERATE AND SEVERE TBI
volleyball, and gymnastics having the lowest risk. (6)
There is also evidence that children experiencing a first In this section we focus on moderate and severe TBI. Although
concussion before age 10 years have approximately twice the there are several scales that have been used to differentiate
risk of sustaining a subsequent concussion before age 18 mTBI from moderate and severe TBI, the most commonly
years compared with patients experiencing their first con- accepted classification relies on the Glasgow Coma Scale
cussion in adolescence. It is not known whether this is due (GCS), with moderate defined as a GCS score of 9 to 13
to the early concussion itself, the duration of participation and severe as a GCS score less than 8 (39) (Table 3). These
in contact sports, or intrinsic factors affecting an individu- more severe injuries are differentiated from mTBI by the fact
al’s concussion risk (eg, risk-taking behavior). (34) that they have clear imaging findings; mTBIs typically do not
Ultimately, health-care providers caring for amateur ath- have any MRI or CT findings. Although TBI remains one of
letes with a history of an early concussion, recurrent con- the leading causes of mortality and morbidity in children in
cussions, or persistent concussive symptoms may need to the United States, the management of this entity continues to
discuss the previously mentioned evidence as well as imple- be applied quite unevenly despite the existence of American
ment formal neurologic and neuropsychiatric assessments Academy of Pediatrics (AAP) recommendations. (40) The
to aid in the discussion of concussion risk management or epidemiology of TBI was reviewed in the Introduction.
possible retirement from play. (6)(35)
Pathophysiology of Pediatric Head Trauma
Second Impact Syndrome It is important to recognize that there are major differences
One of the greatest concerns of parents and clinicians between the pediatric brain and the adult brain in the
surrounding concussion is the threat of second impact pathophysiology of head trauma. Although it is generally
syndrome. Second impact syndrome is described as a true that the pediatric brain tends to be more resilient to
clinical syndrome of catastrophic cerebral edema that re- focal lesions (stroke, surgical excision) as a result of plas-
sults when a second concussion occurs before resolution ticity, the opposite seems to be true when it comes to TBI.
of symptoms from the initial concussion. (35) The second There is strong evidence that the younger a child is when
impact may be much less severe and not even a consequence experiencing a severe TBI, the longer he or she takes to
of a direct impact to the head. (35) It is thought to be due to a recover. (41) Furthermore, the morbidity from TBI seems to
failure of cerebral autoregulation coupled with a stress- be significantly higher in children than in adults. (42) This
induced catecholamine surge, leading to cerebral edema may be related to several factors, including incomplete
and consequent herniation, resulting in severe disability or myelination, the higher water content of the pediatric brain,
death. (36) Although it seems to be extremely rare, a recent and a critical period during development when synaptic
review of 17 cases reported in the literature from 1946 pruning depends on complex physiologic mechanisms.
through 2015 noted an age range of 13 to 23 years, indicating
that this is a syndrome that is particularly impactful in the Space-Occupying Traumatic Injuries
pediatric population. (37) Although cases seem to be most The most urgent clinical factor associated with TBI is the
common with repeated concussions within the first 2 weeks rapid expansion of space-occupying lesions, including
of the initial injury, children are considered to be at risk as bleeds and progressing edema. Interestingly, posttraumatic
long as they continue to be symptomatic from their initial hydrocephalus is much less common in children than in
concussion. This diagnosis has gained a lot of attention adults and can often be managed conservatively, obviating
in the medical literature owing to its devastating conse- the need for decompression or evacuation. (43)
quences, yet there remains some controversy around its
existence. It is known that diffuse cerebral swelling can Space-Occupying Lesions: Bleeds
occur after a single head injury, so the occurrence of a Bleeds caused by TBI can occur in several locations, includ-
second impact to create the clinical syndrome may not be ing potential or anatomical spaces formed by the meninges
required. (38) Nonetheless, all concussion practitioners and within the substance of the brain itself.

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 TABLE 3. Pediatric Glasgow Coma Scale
<1 Y >1 Y SCORE
Motor response Eye opening

Spontaneously Spontaneously 4
To shout To verbal command 3
To pain To pain 2
No response No response 1
Spontaneous Obeys 6
Localizes pain Localizes pain 5
Flexion withdrawal Flexion withdrawal 4
Decorticate Decorticate 3
Decerebrate Decerebrate 2
No response No response 1
0–23 mo 2–5 y >5 y
Verbal response

Smiles/coos Appropriate words Oriented 5

Cries, consolable Inappropriate words Disoriented, confused 4
Cries, inconsolable Cries, inconsolable Inappropriate words 3
Grunts, agitated Grunts Incomprehensible sounds 2
No response No response No response 1

Information from Teasdale G, Jennett B. Assessment of coma and impaired consciousness: a practical scale. Lancet. 1974;304:81–84.

Epidural Hematoma. Epidural hematomas tend to be the filled with cerebrospinal fluid (Fig 1). These bleeds are ex-
result of arterial bleeds associated with skull fractures. tremely common in the context of TBI and frequently cause
These bleeds result from the accumulation of blood in seizures because blood is an irritant to the cerebral cortex. CT
the potential space formed by the junction of the dura mater scans of an acute subarachnoid hemorrhage show hyperdense
and the skull (Fig 1). The classic example is a middle layering along the convexities of the cerebral cortex extending
meningeal artery tear in the context of a temporal or parietal into the sulci and often the basilar cisterns (Fig 2).
bone fracture. In this context, epidural bleeds can be cata-
strophic. Given the arterial nature of these bleeds they can Space-Occupying Lesions: Contusion and DAI
lead to a very rapid mass effect with resulting herniation of Contusions occur as a result of mechanical compression
the cerebral contents. However, it is important to recognize of the brain tissue, such as often occurs after a very rapid
that epidural bleeds in children are usually much more acceleration, and tend to have the greatest impact to the
forgiving than those in adults. (44) It is not completely clear orbital frontal region. These types of injuries frequently cause
why this might be, although in the study just cited smaller a corresponding injury in the diametrically opposite side of
clots tended to be more frequent in younger children. Acute the brain, likely a result of a low-pressure area of injury.
epidural bleeds are characterized by a hyperdense lens- These types of injuries are frequently referred to as coup
shaped lesion on CT (Fig 2). and contrecoup injuries (Fig 2). Interestingly, the contrecoup
Subdural Hematoma. Subdural hematomas result from injury is often more severe than the coup injury. (46)
the accumulation of blood in the potential space between the DAIs are deep white matter track injuries typically caused
dura mater and the arachnoid layers (Fig 1). These bleeds are by rapid rotational acceleration of the brain content. These
usually caused by the rupture of bridging veins that traverse injuries result in axonal damage and often axonopathy (axon
this space. They are quite frequent in infants, especially in disconnection). Technically, DAI can be diagnosed postmor-
the context of abuse. (45) They are also frequently caused by tem only. However, a patient presenting with a closed head
other forms of rapid shearing injuries to the brain, such as injury caused by a high-velocity impact and found to have a
motor vehicle accidents. Subdural bleeds typically layer in a GCS score less than 9 is highly likely to have sustained DAI.
crescentic shape that, when acute, appears hyperdense on (47) These lesions can have devastating morbidities, espe-
the CT scan of the brain (Fig 2). cially when they affect white matter tracts arising from the
Subarachnoid Hemorrhage. Subarachnoid hemorrhages frontal lobes and connecting to the limbic system. The frontal
result from the accumulation of blood in the subarachnoid lobes are the seat of important higher cognitive functions,
space. As opposed to the 2 previous types of bleeds, subarach- including premotor planning, executive function, motiva-
noid hemorrhages occur in an anatomical space normally tional states, and social behaviors. (48) It has been well

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Figure 1. Schematic representation of intracranial hemorrhages and associated herniations. Note that for the sake of clarity, intraparenchymal
hemorrhage, central herniation, and upward transtentorial herniation are not represented. (Illustration by Marie Le Pichon.)

established that subcortical injures in these regions can result Transtentorial Herniation
in significant neuropsychiatric impairments, including lack Transtentorial herniation is probably the most common herni-
of motivation, depression, disinhibition, aggressivity, and ation in the context of TBI. It occurs as a result of a mass effect
cognitive impairments, especially in the area of motor plan- in the supratentorial (above the tentorium cerebelli) region.
ning. Intraparenchymal hemorrhages as a result of head Transtentorial herniation can be unilateral (uncal herniation)
trauma also occur frequently in the context of DAI, either or bilateral (central herniation) (many authors refer to a bilat-
as microbleeds or as much larger hemorrhagic lesions (Fig 2). eral tentorial herniation as transtentorial).
Unilateral (Uncal) Herniation. If there is a unilateral
Herniation Syndromes compression from a bleed or hemispheric edema, there is
Herniation syndromes occur as a result of a rapidly grow- a risk of uncal herniation. In this case, the space-occupying
ing space-occupying lesion (over hours to days), such as a lesion forces a displacement toward the opposite side to the
hemorrhage or developing edema. Herniation of the brain lesion, resulting in compression of several critical structures
contents can occur around any of the major fixed intracra- below the tentorial incisura (ridge formed by the tentorium
nial structures, including the tentorium cerebelli (trans- cerebelli). Critical structures compromised in this syndrome
tentorial or uncal herniation), the falx cerebri (cingulate include the oculomotor nerve (CNIII) and the main motor
or subfalcine herniation), and the foramen magnum (ton- pathways (pyramidal tracts). As a result, one will observe a
sillar herniation). Each of these herniation syndromes has unilateral mydriasis that will be ipsilateral to the herniation
clinically distinct presentations (Fig 1 schematically illus- (compression of cranial nerve III) but contralateral to the lesion
trates each type of cerebral herniation; see also Table 4). It is and a hemiparesis that will be contralateral to the herniation
important to emphasize that the herniation itself is a con- (compression of the pyramidal tracts before the decussation of
sequence, not the cause, of the clinical symptoms observed. the pyramids) but ipsilateral to the lesion. A classic pathologic
The cause of the syndrome is in fact the downward pressure finding that has been described in this context is the Kernohan
on the individual anatomical structures of the cingulate notch, caused by compression of the cerebral peduncle against
gyrus, midbrain, and medulla. (49) the tentorium opposite to the side of the space-occupying

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 Figure 2. A. Computed tomographic (CT) scan, epidural hematoma, B. CT scan, subdural hematoma. C. CT scan, subarachnoid hemorrhage. D. Magnetic
resonance image (MRI), T2, coup and contrecoup injury, example of contusion. E. and F. MRI T2 and fluid-attenuated inversion recovery, subdural
hematoma (arrows). G-I. MRI T2, diffusion-weighted (DWI), and susceptibility-weighted (SWI) images, diffuse axonal injury (note the restricted diffusion
on the DWI sequence and the areas of hemorrhage on the SWI sequence).

lesion. It is important to recognize that anisocoria caused by toward the cortex, while decerebrate posturing is generally
transtentorial herniation is almost always accompanied by loss caused by injury below the red nucleus and the arms are
of consciousness as a result of a compression of the midbrain extended and pointing away from the cortex). The pupils will
(including the periaqueductal gray and other structures essen- initially be dilated and reactive. As the syndrome progresses
tial for maintaining consciousness). they will become fixed and upward eye movement will be
Bilateral (Central) Herniation. If there is diffuse cerebral compromised (resulting in a “sunsetting appearance”).
edema or a large bleed as a result of bilateral and severe
cerebral injury, transtentorial herniation may be bilateral, Cingulate Herniation
resulting from a downward compression force (aka central Cingulate herniation (or subfalcine herniation) occurs as a
herniation). In this case the patient will first develop decor- result of the brain contents being displaced under the falx
ticate posturing (arms flexed and legs extended) as a result of cerebri. This most often affects the frontal lobes as a result of a
midbrain compression, and as the herniation worsens, lateral rapidly growing mass lesion. The clinical signs of
decerebrate posturing (arms and legs extended) with exten- cingulate herniation are not as typical as those of the other
sion downward of the compression (a simple mnemonic is herniation syndromes. Because the cingulate gyrus is com-
to remember decorticate posturing is caused by injury above pressed under the falx, the anterior cerebral artery may become
the red nucleus and with the arms flexed and pointing compromised, with resultant ischemia of the medial motor

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TABLE 4. Summary of the Major Herniation Syndromes and Clinical
Manifestations
HERNIATION CLINICAL PRESENTATION ASSOCIATED CEREBRAL PATHOLOGY

Cingulate Symptoms secondary to anterior cerebral artery compression Cerebral lateral compressive mass such as epidural or
and stroke include contralateral foot paresis and subdural bleed.
numbness, abulia, and urinary incontinence. As the
syndrome progresses, uncal herniation may occur.
Uncal Ipsilateral pupillary dilation (cranial nerve III), contralateral Cerebral lateral compressive mass such as epidural or
hemiparesis (cerebral peduncles). Note that the mass subdural bleed compressing the cerebral peduncle
compressing the brain will often be contralateral to the against the tentorium toward the side opposite the mass
herniation. Always associated with altered consciousness. (will result in a Kernohan notch).
Central Initially bilateral fixed pupils, impaired upward eye Bilateral cerebral compressive mass such as diffuse TBI with
movements (sunsetting appearance), decorticate followed associated edema and/or ischemia resulting in
by decerebrate posturing as the syndrome progresses. downward compression of the midbrain.
Tonsillar Neck stiffness, cranial neuropathies, Cushing triad Rare in the context of TBI, brainstem mass.
(hypertension, bradycardia, and irregular breathing).

TBI¼traumatic brain injury.

cortex, leading to weakness of the contralateral lower extremity. absence of seizure activity, evidence of loss of consciousness
However, compression of the foramen of Monro will eventu- at the time of impact, or change in the level of consciousness
ally lead to increased intracranial pressure, and the patient will will all help guide the management of these children. In
develop symptoms typically associated with uncal herniation. addition, any child presenting with a decreased level of
consciousness or complaining of neck pain should immedi-
Tonsillar Herniation ately undergo cervical spine injury precautions with immo-
Tonsillar herniation is the least common type of herniation bilization of the spine. If the GCS score is less than 9 or if the
seen in the context of TBI (because the brain stem is much less child’s mental status is fluctuating, an airway should be
frequently involved in TBIs). Tonsillar herniation results from secured. The imaging modality of choice is CT because it
mass effect in the brain stem. As a result of the mass effect, the is ideal to show both bone fractures and hemorrhage. How-
cerebral contents will shift downward, forcing the cerebellar ever, DAI and contusion will not show as well on CT.
tonsils and the medulla through the foramen magnum. Ini-
tially the patient may complain of neck stiffness. On exami- MRI versus CT
nation cranial neuropathies may be evident. As the syndrome CT of the head is readily available in almost all emergency
progresses the children will often develop the Cushing triad: departments; it is a rapid study and is ideal to look for skull
hypertension, bradycardia, and slow and irregular breathing fractures or acute hemorrhages (acute hemorrhages will
from compression of the medulla oblongata. appear hyperdense on CT). In addition, if necessary, a CT of
the C-spine can be added to evaluate for spinal fractures. The
Evaluation of the Child with Moderate to Severe TBI CT will also reveal areas of edema as evidenced by hypo-
Evaluation of the child presenting with TBI depends largely dense lesions, although these changes can take some time to
on the initial assessment. The management will be radically become evident. It follows that a negative CT scan may
different depending on whether the child arrives with an require follow-up with MRI to fully characterize the lesion
mTBI (GCS score >13) or a moderate or severe TBI as depending on the clinical presentation. However, CT is a
evidenced by a GCS score less than 13 (for further details on poor study to evaluate for contusion or evidence of DAI.
the management of the child with an mTBI refer to the Furthermore, CT is associated with a significant amount of
Recognizing Concussion subsection). The child with a ionizing radiation. Note that the dose reduction techniques
decreased level of consciousness should be rapidly evaluated now commonly in use have resulted in significantly less
for symptoms of herniation while ensuring that airway, dose exposure (refer to the Recognizing Concussion sub-
breathing, and circulation measures are addressed. The section for further discussion of imaging in mTBI).
history in this case needs to be gathered rapidly but remains MRI offers a better evaluation of hemorrhage. T1, T2, and
essential. A description of the trauma, the presence or T2 fluid-attenuated inversion recovery (FLAIR) series are

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 best to evaluate for extra-axial hemorrhages. T1 and T2 syndrome. In 2009, the AAP recommended replacing all of
sequences are also useful in dating the age of the hemor- these terms with the nomenclature abusive head trauma
rhage. More subtle parenchymal injuries, shearing injuries, (AHT). (52) TBI inflicted on a child by an adult is unfor-
and microhemorrhage are better seen using susceptibility- tunately too frequent an occurrence. According to a recent
weighted imaging. T2 FLAIR images are considered the CDC publication on AHT, it is the leading cause of head
most sensitive MRI sequences to look for subarachnoid injury in infants. (53) Peak incidence occurs between the
hemorrhage, although CT is very sensitive for acute sub- ages of 2 and 3 months, and AHT is rare after 2 years of age.
arachnoid hemorrhage as well. Edema and ischemia are The mortality and morbidity of AHT are considerable, with
best evaluated with T2, FLAIR, diffusion-weighted imaging, up to 20% of children succumbing to their injuries and
and apparent diffusion coefficient sequences. In addition, two-thirds of the survivors having severe and permanent
diffusion- and susceptibility-weighted imaging will often reveal intellectual and physical impairments. The most common
evidence of shearing injury or DAI that may have been missed presentation of AHT is an infant or toddler with a decreased
on T1 or T2 sequences. Furthermore, MRI does not expose the level of consciousness and/or seizures. Frequently in such
children to ionizing radiation. However, MRI is time intensive situations there will be conflicting or vague histories from
and is not available in all hospitals 24 hours a day. the parents or guardians. In addition, there may be a clear
disconnect between the apparent severity of the injury and
Management the described mechanism (“fell off a chair and hit his/her
In 2012, the second edition of the guide for the acute medical head on the floor” would be a very uncommon cause of TBI).
management of severe TBI in infants, children, and adolescents One should also look for inappropriate affect in the adults
was published. (50) These guidelines were endorsed by mul- accompanying the child. The evaluation of the child with
tiple organizations, including the AAP, the Child Neurology suspected AHT should include an urgent CT scan of the
Society, and the American Association of Neurological Sur- head. Children with these types of injuries very frequently
geons. Although a detailed discussion of the management of have a combination of subdural hemorrhages (54) and
the child with severe TBI is beyond the scope of this review, it is significant DIA (as evidenced by hypodense lesions on
worth mentioning a few basic principles from these guidelines. the CTscan). (55) In addition, skull fractures may be observed,
First and foremost, children with TBI are at very high but it is important to emphasize that the absence of skull
risk for elevated intracranial pressure. This is especially fracture does not rule out AHT. Once there is suspicion of
notable in children with evidence of diffuse cerebral swelling AHT and the child is clinically stable one should obtain a
on CT, a finding noted to be 75% specific for the presence of skeletal survey to look for evidence of new or old bone
intracranial hypertension. Children with an altered level of fractures elsewhere and a dilated funduscopic examination
consciousness are also at markedly increased risk for ele- to look for evidence of retinal hemorrhages.
vated intracranial pressure. These children need urgent Of note, there are extremely rare metabolic disorders that
management in an ICU setting. are associated with spontaneous subdural hemorrhages. It is
Finally, a word must be said about the use of prophylactic important to keep these conditions in mind when consider-
antiepileptic medications. The guidelines cited previously ing the differential diagnosis of AHT. These conditions
herein note that the risk of posttraumatic seizures in the include coagulation disorders, galactosemia, and glutaric
pediatric patient is approximately 10%. Based on a single study aciduria. (56) Glutaric aciduria, galactosemia, and coagula-
the guideline states that prophylaxis with phenytoin may be tion disorders can all be ruled out with relatively simple
considered. However, although phenytoin and fosphenytoin laboratory studies. Another condition to consider is Menke
remain the most commonly used antiepileptic medications in disease because it has been associated with spontaneous
the prevention of posttraumatic seizures, there is accumulat- subdural hemorrhages. (57) However, this disorder should
ing evidence that levetiracetam is an excellent alternative. (51) be evident based on the child’s clinical appearance (severe
Levetiracetam is available in an intravenous formulation, does developmental delay, epilepsy, and unusual and brittle appear-
not have a significant protein-bound fraction (as opposed to ance of the hair). One should also recognize that spontaneous
phenytoin that is 90% protein bound), has essentially no liver subdural hemorrhages have been observed in children with
metabolism, and has very few significant drug interactions. benign extracerebral collections in infancy and minimal or no
evidence of trauma. (58) Benign enlarged extracerebral spaces
Special Considerations: Abusive Head Trauma have been referred to by many names, including benign
Inflicted TBIs have been labeled by a variety of different external hydrocephalus, benign communicating hydroceph-
names, including nonaccidental trauma and shaken baby alus, subdural hygroma, and others. It usually occurs in

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children with a head size larger than normal. The head size
typically crosses the 98% growth curve until approximately 10 is especially true of children presenting with altered
months of age and then stabilizes. These children are asymp- consciousness. (50)
tomatic, and the condition is benign and typically resolves • Abusive head trauma is the leading cause of head injury in infants.
spontaneously. The morbidity and mortality of abusive head trauma are
considerable, with up to 20% of the infants succumbing to their
injuries and two-thirds of the survivors having significant
CONCLUSION cognitive and/or physical impairments. (53)

TBI encompasses a broad spectrum of clinical presentations.

These injuries represent a major challenge for the primary care Suggested Quality Improvement Project
physician because the prognosis varies from excellent, with With the increasing numbers of children presenting to emer-
complete resolution in a few days to a few weeks with mTBI, to gency departments with TBIs, it is more important than ever
catastrophic, with severe morbidity and mortality in the case of that providers appropriately assess children to determine
moderate to severe TBIs. However, a systematic approach to whether head CT is needed and to avoid unnecessary and
the child who experiences a TBI should help in the proper harmful radiation exposure. Fortunately, there is a well-
clinical management. Guidelines exist for the management of validated set of clinical criteria developed by the PECARN
adult head injury (National Institute for Health and Care to assist in this decision-making process. (18) Previous
Excellence’s Head Injury: Assessment and Early Management efforts to implement these criteria in a community emer-
[https://www.nice.org.uk/guidance/cg176]). gency department have resulted in a reduction in rates of
These guidelines have been found to be highly reliable and head CT scan in children presenting with head trauma, (19)
easily adaptable to multiple environments, including low- and indicating that this is an excellent opportunity for further
middle-income countries. (59) The CDC has now published quality improvement projects.
guidelines for the diagnosis and management of mTBI in Project: Reduction of head CT scan rates in children
children. (10) The introduction and adoption of these guide- presenting with head injury.
lines will help resolve much of the guesswork that many Setting: Emergency department.
primary care providers have to consider when evaluating Prediction tool: PECARN prediction rule for clinically
children who have sustained some form of head trauma. (59) important TBIs.
Outcome Measure: Rate of pediatric head CTs in children
presenting with TBI.

Summary
• Traumatic brain injuries are the leading cause of death or severe To view teaching slides that accompany this article,
disability in children older than 1 year, and the incidence is visit http://pedsinreview.aappublications.org/
continuing to increase, making this topic especially relevant for content/40/8/468.supplemental.
the pediatrician.
• Based on a well-designed prospective cohort study, it
is not recommended that all children presenting with
head trauma obtain a head computed tomographic
scan. (18) Rather, this decision should be based on the
mechanism of injury and the signs and symptoms of the
patient.
• Based on multiple cohort studies and expert opinion, concussion
symptom checklists, such as the Child Sport Concussion
Assessment Tool, the Postconcussion Symptom Scale, or the
Graded Symptom Checklist, can be used to aid in concussion
diagnosis and tracking symptom resolution in determining
graduated return to play. (6)(11)(13)
• Children with moderate or severe traumatic brain injury
are at high risk for elevated intracranial pressure; this References for this article are at http://pedsinreview.aappub-
lications.org/content/40/9/468.

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 PIR Quiz
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C. Loss of Consciousness. must demonstrate a minimum
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5. A 14-year-old boy is being evaluated in the emergency department after a fall from a roof
(approximately 20 feet). His vital signs include heart rate of 55 beats/min, respiratory rate of
29 breaths/min, and blood pressure of 140/90 mm Hg. He has a large laceration to the
forehead and a bloody nose. He is minimally responsive, with occasional moans and no
purposeful movement of his extremities. On secondary survey you note that the left pupil
is larger than the right and poorly responsive. In addition, he has weakness of the left arm
and leg. Which one of the following findings would be expected on head imaging given
the clinical presentation?
A. Bilateral central herniation.
B. Cingulate herniation.
C. Diffuse axonal injury.
D. Tonsillar herniation.
E. Uncal herniation.

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 Pediatric Head Trauma: A Review and Update
Rose N. Gelineau-Morel, Timothy P. Zinkus and Jean-Baptiste Le Pichon
Pediatrics in Review 2019;40;468
DOI: 10.1542/pir.2018-0257

Updated Information & including high resolution figures, can be found at:
Services http://pedsinreview.aappublications.org/content/40/9/468
Supplementary Material Supplementary material can be found at:
http://pedsinreview.aappublications.org/content/suppl/2019/08/28/40
.9.468.DC1
References This article cites 52 articles, 12 of which you can access for free at:
http://pedsinreview.aappublications.org/content/40/9/468.full#ref-list
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ncy_medicine_sub
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 Pediatric Head Trauma: A Review and Update
Rose N. Gelineau-Morel, Timothy P. Zinkus and Jean-Baptiste Le Pichon
Pediatrics in Review 2019;40;468
DOI: 10.1542/pir.2018-0257

The online version of this article, along with updated information and services, is
located on the World Wide Web at:
http://pedsinreview.aappublications.org/content/40/9/468

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