Rudolph's Pediatrics, 22nd Ed.

CHAPTER 551. Trauma to the Nervous System

Magdi M. Sobeih

The statement that children are not small adults particularly applies when considering the developing nervous system. The nervous system is constantly changing throughout childhood. Thus the way trauma to the developing nervous system affects the child depends on where along the neuraxis the trauma occurs, at what age and developmental stage, and the mechanism of the trauma. These specifics are important to consider in the context of the most frequent causes of trauma, the implications, and the outcomes. Trauma usually results in acute deterioration in neurologic function but late sequelae or delayed effects must also be anticipated. In this section, discussion will focus on the most commonly encountered scenarios of trauma to the nervous system in pediatrics. This includes accidental traumatic brain injury, inflicted neurotrauma, spinal cord injury, and associated injury to adjacent tissues, such as bone in skull fractures and blood vessels in hemorrhage. The acute management of these injuries is further discussed in Chapter 104. Trauma to the brachial plexus during delivery will be briefly discussed.


Under normal circumstances, the skull protects the brain from minor trauma by cushioning the sensitive contents from external blows. The surrounding cerebrospinal fluid (CSF) assists in reducing any force by providing a fluid layer in which the brain may “float.” However, with more severe trauma, the differential rate of movement of the skull, brain, CSF, and blood vessels causes acute injury to the contents. Traumatic brain injury results from the sudden acceleration or deceleration of the brain relative to the skull or from penetrating injury. The degree of injury manifests along a spectrum from mild functional impairment without obvious visible injury (either on physical examination or neuroimaging) to severe, generalized, or focal/multifocal injury.

Head injury is one of the most common neurologic disorders in pediatrics. Millions of children and adolescents suffer an injury to the head each year but most do not seek medical attention or are seen by a primary physician well after the event. Thus, the incidence and characteristics of these head injuries are not fully known. Of those who seek care in a hospital-based setting, each year, approximately 475,000 traumatic brain injuries (TBIs) occur in children ages 0 to 14 years.1 More than 90% of these (435,000) present to emergency rooms for immediate care, 37,000 are hospitalized, and 2685 are fatal. The rate of TBI-related emergency room (ER) visits, hospitalizations and deaths is greater than 50% more common in boys than girls ages 0 to 14. Across all ages in children and adolescents, TBI is more common in males than in females. Falls are the most common cause of TBI from ages 0 to 14, accounting for 39% of all TBIs in that age range. After age 14, motor vehicle accidents become the most common cause, followed by assaults and falls. Most fall-related TBIs are evaluated in the emergency room and more than 90% of patients are released to their home. However, after age 4 years, motor vehicle accidents (usually as passenger but also as pedestrian or pedal-powered operator) increasingly account for TBI-related hospitalizations and deaths. These statistics have several implications for mechanisms and severity of injury, and prevention of TBI (discussed below).


It is clear from the statistics that the most common form of pediatric head injury results in mild traumatic brain injury (mTBI).2 Also known as concussion, minor head injury, minor head trauma, or minor TBI, mTBI had been diagnosed based on scores of 13 to 15 on the Glasgow Coma Scale. However, most recently, mTBI has been defined clinically by the brief presence of altered mental status after injury from impact or forceful linear or rotational motion of the head with or without loss of consciousness.3,4 This alteration in mental status is characterized by confusion or disorientation, trauma induced retrograde and/or anterograde amnesia, or loss of consciousness less than 30 minutes. By contrast, moderate or severe TBIs are associated with loss of consciousness longer than 30 minutes, amnesia longer than 24 hours, penetrating skull injury, or visible signs of focal/multifocal brain injury on physical examination or neuroimaging (see below).


Neurologic sequelae of mild traumatic brain injury (mTBI) are not the result of localization-related injury but of widespread neuronal metabolic dysfunction involving a cascade of subcellular ionic, metabolic, and local physiologic events. These involve neuronal depolarization with release of excitatory neurotransmitters, potassium release from the intracellular compartment, increased energy utilization by ion pumps to restore homeostasis, leading to increased glycolysis and lactate accumulation. This leads to changes in cerebral blood flow and axonal function (Fig. 551-1). During brain development, the excitatory neurotransmitter glutamate predominates, meaning there is an increased probability of excitotoxicity in the developing brain. The widespread activation of glutamate receptors also results in downregulation of the receptors and changes in inhibitory circuitry with increased the chance for seizures.5


Clinically, mild traumatic brain injury (mTBI) manifests as disruption of one or more of four domains: physical, cognitive, emotional, and sleep patterns. Acutely, children suffering mTBI may experience symptoms of vomiting, headache, emotional lability or inconsolability, restlessness, irritability, mental confusion, amnesia, dizziness, transient loss of vision (often confused with malingering), seizure, or change in personality. Physical signs are often lacking but should be considered as with any trauma-related injury. This includes monitoring of airway, breathing, and circulation. Further management depends on recovery of function and persistence of symptoms. Thus, immediate evaluation on site should document level of functioning after injury such as assessment of retrograde and anterograde amnesia and loss of consciousness. In school age children, mTBI often occurs in sports-related activities so that assessment on the field may be made by coaches or certified athletic trainers using standardized instruments such as the Standardized Assessment of Concussion. When a child is seen by a clinician, the Acute Concussion Evaluation (ACE) form available from the CDC4 helps to document and subsequently track symptoms thus assisting in planning recovery management. In preschool or pre-verbal children, clinicians must have a low threshold of suspicion for concussion after head injury because these individuals will not be able to report symptoms, even though they may have headache, crying, irritability, restlessness, dizziness, confusion, seizure, or change in personality. Emergency room evaluation is warranted if these symptoms worsen in a pre-verbal child.


Medical evaluation of any child with mild traumatic brain injury (mTBI) first documents the nature or cause and circumstances of the injury including type and strength of force and location on the head and position of the head at the time of impact. A greater force causing the injury correlates with greater potential for more severe symptoms. However, when the history suggests the symptoms are out of proportion to the force of the injury, malingering should not be assumed but increased susceptibility to mTBI (especially if there is a history of multiple mTBI) or other physical or psychological factors should be considered. Whiplash type injury occurs when a blow to the body or to a vehicle results in acceleration and deceleration forces on the brain, leading to coup and contrecoup injuries. Physical examination should first assess airway, breathing, and circulation. It is important to rule out any bleeding including hematoma or petechiae. Neuroimaging is not necessary in most cases of mTBI, particularly in children older than age 2 years. However, if there is a history of loss of consciousness longer than a few seconds, or deteriorating neurologic function, worsening of initial symptoms, or new symptoms, imaging should be considered. Head computed tomography (CT) is optimal for detecting skull fracture and intracranial blood; it is also ideal for rapid assessment and detection of brain edema.

Neuropsychologic testing using standardized tests establishes quantifiable measures of self-reported or observed impairments in the cognitive domain. This testing can be repeated over the subsequent 6 to 12 months in order to guide recommendations for return to full activity after mTBI.


After the initial symptoms of mild traumatic brain injury (mTBI), a child may continue to complain of headache, dizziness, and cognitive impairment, and exhibit behavioral disorders such as irritability for days, weeks, and even months. These symptoms constitute postconcussive syndrome and are treated symptomatically.

FIGURE 551-1. Neurometabolic cascade following traumatic injury. (1) Nonspecific depolarization and initiation of action potentials. (2) Release of excitatory neurotransmitters (EAAs). (3) Massive efflux of potassium. (4) Increased activity of membrane ionic pumps to restore homeostasis. (5) Hyperglycolysis to generate more adenosine triphosphate (ATP). (6) Lactate accumulation. (7) Calcium influx and sequestration in mitochondria leading to impaired oxidative metabolism. (8) Decreased energy (ATP) production. (9) Calpain activation and initiation of apoptosis. (A) Axolemmal disruption and calcium influx. (B) Neurofilament compaction via phosphorylation or sidearm cleavage. (C) Microtubule disassembly and accumulation of axonally transported organelles. (D) Axonal swelling and eventual axotomy. K+, potassium; Na+, sodium; Glut, glutamate; Mg2+, magnesium; Ca2+, calcium; NMDA, N-methyl-D-aspartate; AMPA, d-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid. (Source: Giza CC, Hovda DA: The neurometabolic cascade of concussion. J Athl Train. 2001; 36(3):228-235. Copyright © by the National Athletic Trainers’ Association, Inc.)


Most likely due to the general neuronal metabolic and physiologic dysfunction, during recovery from mTBI, symptoms may worsen or reemerge with physical or mental exertion. Thus treatment is symptomatic and preventive. Immediately after a concussion, rest is essential. There should be no physical exertion until there are no signs or symptoms of mTBI at rest. The decision to return to full activity should be guided and planned. Return to full activity should be gradual and graded as, for example, those involved in sports. The recommended return to sport guidelines6,7 include (1) complete rest, especially on the day of injury (thus removal from the competition); (2) light aerobic exercise, such as walking, without weight training; (3) sport-specific activity such as running with some weight lifting; (4) training drills without contact; (5) training drills with full contact; and (6) competitive game play. At each of these steps, physical and mental monitoring and comparison with initial Acute Concussion Evaluation status should guide ongoing and increasing level of activity.

Minimal TBI affects cognitive abilities and experience-dependent learning. For this reason, the child’s academic performance should be monitored and return to full academic participation should be gradual. Initially after concussion, lighter school and homework loads should be considered. If necessary, more formal Section 504 plans (designed to accommodate the unique needs of an individual with a disability) or Individualized Education Plans should be instituted.

Second Impact Syndrome

The risk of returning to full activity after mTBI is the possibility of further mTBI with resultant worsening of postconcussive symptoms. With the impairment in cognitive ability and reaction time after an initial mTBI, the risk of repeat injury is higher than baseline. A more dangerous, albeit less common occurrence with repeated mTBI, is second impact syndrome. If full recovery from the first impact has not occurred and cerebrovascular autoregulation is still impaired, a second episode of head trauma may trigger diffuse cerebral edema secondary to hyperemia, vasogenic edema, or cytotoxic edema. This may lead to increased intracranial pressure and brain herniation. Unrecognized after minor head trauma and untreated, this can be fatal.


Most children recover completely after mTBI and do not have lasting postconcussive symptoms. Treatment of any effects of concussion should be symptomatic with rest, over-the-counter analgesics for headaches and medication for attention deficit symptoms or other behavioral problems. Effects of mTBI may be slightly worse for the younger child. For example, some evidence suggests longer times to recover from the cognitive deficits after concussions in high school athletes compared with college athletes.

Because the mechanisms of mTBI involve direct force on the brain, measures to avoid or dissipate potential forces on the head decrease the likelihood of mTBI. This involves the use of appropriate car seats and seatbelts in motor vehicles to decrease the chance of whiplash injuries, and the use of helmets during sporting and physical activities such as bicycle and scooter riding or winter snow and ice activities. For parents of toddlers, anticipatory guidance against use of walkers is warranted.


Clinically, moderate traumatic brain injury (TBI) has been classified based on Glasgow Coma Scale (GCS) score of 9 to 12 and severe TBIs with scores less than 8. These somewhat artificial distinctions are meant to reflect severity of injuries causing unconsciousness longer than 30 minutes, amnesia longer than 24 hours, or penetrating skull injuries. In pediatric patients with severe TBI, lower GCS scores correlate with worse outcome. There may also be associated intracranial injuries based on neuroimaging. These may include skull fractures, brain contusions, and intracranial hemorrhages (see below).


With child development, muscles strengthen, skull thickness and tensile strength increase, and the motor repertoire expands and becomes more adept. The mechanisms of injury and implications of accidental injury change with the age of the child. Infants tend to suffer accidental injury most frequently due to low-level falls (ie, less than 3–4 feet), for example from cribs and beds. Skull thickness increases with age from 1 mm in infants to 4 mm in a young child and 10 mm in adults.8 With impact injury, the skull of an infant is more likely to fracture compared with that of an adult, particularly in the thinnest part of the calvarium—the parietal region. The infant skull is able to deform and absorb a significant amount of the energy of the fall thus protecting the brain from more severe injury. Much more energy is required to cause intracranial injury (ie, bleeding) and axonal damage in the infant and young child compared with the adult. Still, intracranial injury may occur (see below) even without any clinical signs and symptoms. As the child begins to ambulate, falls from heights, such as off furniture or down stairs, become more common.

The neurometabolic cascade discussed above also operates after a more forceful head injury. Additionally, diffuse axonal injury from shear forces, disconnection, and necrotic and apoptotic cell death may occur. The resultant effects on the developing brain have delayed and lasting implications for prognosis and outcome (see below). Other than the initial TBI, second insults such as hypoxia and hypotension exacerbate brain injury and are associated with poorer outcome. Diffuse cerebral edema, which may lead to decreased cerebral perfusion, is more common in infants and children compared with adults, after severe TBI.9


After stabilizing and securing the airway, breathing, and circulation, the diagnostic evaluation of a child with moderate to severe TBI begins with physical examination for associated injuries and neurologic examination followed by neuroimaging. In infants in whom specific symptoms are difficult to elicit early, imaging of the cranium for signs of skull fracture must be included. Underlying intracranial bleeding is quickest and best seen using computed tomography (CT scanning). If magnetic resonance imaging (MRI) is available, sequences to detect blood can be used. An advantage of MRI is the ability to detect signs of brain edema early and without exposure to radiation. Also, any child with a change in level of consciousness or focal neurologic deficit on examination should undergo neuroimaging using brain MRI.


Hospital-based treatment of acute moderate to severe TBI in children aims to reduce the likelihood of second insult and maintain adequate cerebral perfusion pressure and tissue oxygenation. Thus, management of airway, breathing, and circulation is paramount, as is decreasing brain edema to guard against increased intracranial pressure. There is no clear treatment standard but algorithms for tiered management of acute TBI exist (Fig. 551-2).10 Strategies including prophylactic use of antiepileptics and antipyretics are instituted to decrease metabolic demand of the brain and possible second insult. Hypothermia therapy is another means of reducing the metabolic demands of the brain. Observations of improved survival and recovery after cold water drowning have led to trials of therapeutic brain cooling after TBI. However, speed of initiation of hypothermia, degree of cooling, length of cooling time, and rapidity of rewarming have yet to be established. The most recent multicenter trial of hypothermia for pediatric TBI initiated within 8 hours and lasting for 24 hours failed to show any improvement in either neurologic outcome or survival benefit.11 Further large-scale trials to establish standards for hypothermia in pediatric TBI are needed.


Children who suffer focal brain lesions often show remarkable neurologic recovery because of developmental plasticity. In fact, the earlier in development a lesion is acquired, the better the neurologic outcome will be. However, this same capacity for plasticity and reorganization may belie a propensity for worse outcome after the more global insult of TBI in children compared with adults. Because a majority of cognitive and adaptive behavior neural systems continue to develop throughout childhood to young adulthood, injury to these frontal, subcortical, distributed systems leads to significant developmental and cognitive delay and behavioral impairment. In one study12 children who suffered accidental TBI prior to age 2 on average performed at least one standard deviation below the mean on standardized cognitive developmental testing at age 3. Those with nonaccidental TBI fared worse (see below). Posttraumatic headaches and seizures may also occur. Seizures occurring within 7 days of injury are termed acute and are the result of immediate effects of the injury such as glutamate release, stretch induced neuronal depolarization, and local irritation from blood products. Late seizures (occurring after 7 days postinjury) may be secondary to infection, neuronal death, gliosis, and aberrant neuronal circuit development.

The same physical protective measures described for mild traumatic brain injury (mTBI) (vehicle safety and helmet use) apply for more serious TBI.


Physical abuse of children by adults results in many types of injury (see also Chapter 35). The most severe and fatal injuries affect the nervous system, especially the brain and cervical spinal cord. Over the past few decades, various terminologies have been used to describe the method of injury including battered child syndrome, shaken baby syndrome, shaken impact syndrome, trauma X, nonaccidental trauma, inflicted TBI, and inflicted childhood neurotrauma. An adult or older child may inflict injury on an infant or younger child by shaking, hitting, throwing down onto the floor or against a wall, or asphyxiation in attempts to quiet by smothering or strangulating. Each of these mechanisms causes significant and multifocal injuries to the child’s neuraxis.

FIGURE 551-2. Tiered management algorithm for traumatic brain injury. CPP, cerebral perfusion pressure; CT, computerized tomography; EVD, external ventricular drain; HOB, head of bed elevation; ICP, intracranial pressure monitor. (Source: From Mazzola CA, Adelson PD. Crit Care Med 2002;30:S393-401.)


Traumatic brain injury due to child abuse is the leading cause of infant death secondary to accidental injury. It is also a leading cause of moderate to severe traumatic brain injury (TBI) in children. Accurate estimates of the incidence of abuse are difficult to obtain and represent only those with physical injuries serious enough to come to medical attention. These statistics are likely underestimates of head injuries from abuse. In a population-based study of inflicted childhood neurotrauma,13 the incidence of inflicted moderate to severe TBI of children under age 2 years was 17.0 per 100,000 person-years. Infants were almost 10 times more often affected than children age 1 to 2 years and boys over 50% more likely than girls to suffer inflicted TBI. Young maternal age (≤ 21 years old) and limited social support were identified risk factors for inflicted neurotrauma.14


The larger head-to-body ratio, undeveloped shoulder and neck musculature, and laxity of the atlanto-occipital joints of infants compared with adults lead to greater impulsive or rotational forces on the infant head during periods of shaking. Force exerted through the held torso during shaking causes repeated acceleration/deceleration of the head leading to significant shear force on the brain, resulting in axonal damage and intracranial bleeding. Shaking alone does not account for the severity of most injuries. Accompanying impact and/or suffocation (as from restriction on the thoracic cage) are often necessary to explain the intracranial pathology of inflicted neurotrauma.

Head injury associated with inflicted neurotrauma includes skull fractures, subgaleal hematoma, subdural hematoma, subdural effusions, subarachnoid hemorrhage, cerebral contusions, and cerebral edema. These injuries are not unique to child abuse but, if present, consideration of child abuse in the differential diagnosis is warranted (see below).


Although neurotrauma is the most frequent cause of fatality in child abuse, injury may have been inflicted on other parts of the body and signs of injury should be sought elsewhere. Facial injury is associated with inflicted neurotrauma especially around the mouth and teeth. Retinal hemorrhages frequently occur with repeated shaking. Scalp and soft tissue hematoma and bruising, ruptured ear drums, long and rib bone fractures, and pattern bruising (indicating a mechanism of holding or impact, as with an open hand or object) may also be seen.


Children suffering abusive head injuries are usually first brought to medical attention with relatively minor and nonspecific symptoms such as vomiting and irritability. In fact, in one study of cases of abusive head trauma not initially diagnosed, symptoms at first presentation included facial injury, seizures, altered mental status, abnormal respiratory pattern, vomiting, and irritability.15 Suspicion of inflicted neurotrauma should be raised when no explanation or history of trauma is given.16 Also, if the given history frequently changes from caregiver to caregiver or from the same caregiver, or if the history given is inconsistent with the developmental level of the child, the possibility of inflicted neurotrauma should be considered.

With suspicion of inflicted neurotrauma, there should be a thorough documentation of the history provided, not only of the events leading up to symptoms or injury, but also birth history and family medical history. Physical examination should include thorough evaluation of all skin surfaces to document any bruising, especially pattern bruising. Assessment of Glasgow Coma Scale or the equivalent for infants should be documented. Because abused infants and children may also be neglected, laboratory evaluation and assessment of fluid balance or signs of dehydration should be obtained. Clotting defects and bleeding may lead to anemia and thus should be evaluated. There are promising laboratory measures suggestive of inflicted neurotrauma. Elevated serum and/or cerebrospinal fluid (CSF) levels of the neuronal and CNS glial markers, neuron specific enolase (NSE), and myelin basic protein (MBP) may serve as screening markers of inflicted neurotrauma.17 Further evaluation by neuroimaging starts with a head computed tomography (CT) scan, which can be performed immediately and can assess skull fracture and intracranial bleeding. Subsequently magnetic resonance imaging (MRI) may possibly be indicated for more accurate assessment of injuries and dating of intracranial bleeding.

There is often concern for false accusation of child abuse, but the safety of the child is of paramount importance. The primary caregiver or accompanying adult may not have perpetrated the abuse or even be aware of it. The observation that households with young, single mothers are most often associated with child abuse may simply reflect the difficulty in finding suitable care-givers.13 Missed cases of inflicted neurotrauma often represent within a week to months of the first episode with more serious injury.15 Thus, erring on the side of caution to consider and investigate suspicious injuries in an infant or child may be lifesaving. Investigation of accidental injuries may also reveal deficiencies in the home or childcare setting. Investigations should not be pursued as punitive but as a means of offering assistance and guidance so that further accidents do not occur.

The differential diagnosis of nonaccidental neurotrauma includes accidental injury such as falls and susceptibility to injury secondary to genetic or metabolic disorder. Falls are distinguished based on height as a surrogate for force of impact. Short, low impact falls of less than 4 feet may lead to skull fracture in infants but rarely to intracranial pathology. Falls from heights greater than 4 feet may lead to more serious skull and intracranial injury. However, the pattern of brain injury differs from that of abusive injury. Additionally, with inflicted neurotrauma, there is often associated cervical spinal cord and nerve root injury. Multiple bone fractures and subdural effusions or hematoma from abuse must be distinguished from injuries that are secondary to rare genetic syndromes such as osteogenesis imperfecta or glutaric aciduria type I.


Treatment of inflicted neurotrauma is supportive care with monitoring for posttraumatic seizures. Longer-term, careful follow-up is important as children suffering abusive head injury are at greatly increased risk of cognitive and behavioral difficulties. Family- and school-based support with appropriate accommodations should be anticipated.


The range of subsequent difficulties and sequelae following inflicted TBI is similar to accidental TBI. However, inflicted TBI results in more severe injury than injuries caused by accident. Overall, children with inflicted TBI have a worse prognosis than do those with TBI caused by accidents. Estimates of mortality from inflicted neurotrauma range from 15% to 38% and neurologic morbidity up to 68%. The range of morbidity following inflicted TBI includes motor deficits, visual deficits, epilepsy, speech and language impairment, and behavioral problems.18 Most victims of inflicted neurotrauma have only mild disability by age 2 years with 45% functioning at age appropriate levels.19

Adults rarely inflict serious injury on infants and children in a premeditated fashion. These unfortunate events often occur at times of emotional upset, stress, and anger over unexpected and uncontrollable situations, such as crying and toileting accidents. Prevention of abuse in specific situations is difficult but assistance and guidance to help prepare for these unexpected times is needed. Social intervention and child-care assistance need to be made available to those at risk. If pediatric neurotrauma does occur, the child will need ongoing monitoring of development, academic abilities, and behavior so that assistance may be provided at school to prevent significant and long-lasting effects.



Trauma to the head may result in skull fractures which may be (1) simple linear or dia-static, causing abnormal suture separation; (2) simple depressed; (3) comminuted; or (4) ping-pong (pond). More than 80% of skull fractures are simple linear and usually occur in the parietal region. In infants the cranium is not well calcified, allowing for displacement without fracture. This results in a ping-pong or pond fracture. Skull-base fractures are associated with bilateral orbital or retroauricular ecchymoses (Battle sign). Skull fracture with accompanying otorrhea or rhinorrhea is of concern because it suggests basilar fracture with associated risk of infection. This can be detected by testing the fluid for the presence of glucose, which is found in cerebrospinal fluid (CSF) but not in nasal secretions.

Skull fracture are evaluated by skull radiograph or computed tomography (CT) scan with bone windows. In infants, a skeletal survey should be strongly considered to search for other signs of injury. In children under age 8 years, cervical spine films are also recommended, particularly if there is neck pain or tenderness.

No treatment is required for uncomplicated simple linear skull fracture or pond fracture. Healing should occur within 6 to 12 months. However, migration of the meninges through the fracture site with brain herniation may give rise to an expanding leptomeningeal cyst and bony erosion. Repeat skull radiograph at 3-month intervals to demonstrate union is recommended.


Head trauma may lead to the acute collection of blood in the potential space between the skull and dura, causing an epidural hematoma. With trauma and fracture of the temporal bone, the source of this blood may be the middle meningeal artery. However, in young children bleeding is often from the bridging veins; because venous pressure is low, blood accumulates slowly. The loss of blood may lead to anemia, which may be the first indication of pathology. However, faster accumulation from arterial bleeding leads to compression of underlying brain tissue and more acute presentation. Prompt detection of this blood by CT or MRI scan allows for surgical evacuation and complete recovery without residual deficit.


Subdural hematomas (SDH) result from the tearing of cortical bridging veins. They are commonly seen after accidental and inflicted head trauma. Appearance on CT imaging is of a crescent shaped hyperdensity beneath the skull. Subdural hematoma may develop with apparent neurologic symptoms within 3 days of trauma—acute subdural hematoma. Symptoms may develop within 4 to 20 days (subacute) or after 20 days (chronic). Surgical treatment by evacuation is sought for acutely symptomatic SDH. The child should also be monitored for any signs of increased intracranial pressure. Cerebrospinal fluid (CSF) removal (10–20 mL per day) relieves this pressure and also helps to reduce the size of the hematoma. Removal of larger amounts may lead to reaccumulation of the hematoma. Outcome after treatment of traumatic SDH is good if there are no other parenchymal injuries; up to 75% of infants achieve normal developmental milestones.


Cerebral contusions occur when the surface of the brain directly affects the bony surface of the skull. This is rare in children but may occur in the frontal or temporal regions, usually along gyri. Treatment is usually unnecessary unless bleeding or edema become symptomatic.




Isolated traumatic spinal cord injury (SCI) in children is rare, with approximately 1000 pediatric SCI annually in the United States. Sixty to eighty percent of pediatric SCI affects the cervical spinal cord.20The incidence of pediatric spinal cord injury was 18.2 per million among those ages 1 to 12 year in one population-based study. Motor vehicle accidents and falls are the two most frequent causes of pediatric SCI. Motor vehicle accidents usually involve young children as pedestrians or on bicycles, whereas older children suffer SCI as passengers in motor vehicle accidents. Sports-related injuries increase in frequency in adolescence.

Obstetrical trauma is the most common cause of SCI in infancy occurring in approximately 1 in 60,000 births. Most injuries result from breech presentations and usually involve the cervical or cervicothoracic region. Birth-related spinal cord injuries after cephalic presentation most frequently involve the upper cervical region.


The infant and child’s head to body ratio is approximately 25% compared with an older child’s and adult’s ratio of 10%. The change in this ratio occurs gradually, reaching the adult ratio at about 8 to 10 years of age. Additionally, the undeveloped shoulder and neck musculature, ligamentous laxity, C2 weakness, and shallowness and horizontal orientation of the facet joints of infants and young children compared with adults and older children place the upper cervical spine at relatively greater risk for injury. In infants, abuse leads to fracture of the upper and lower cervical and upper thoracic vertebral bodies by the mechanisms of hyperflexion/hyperextension from shaking. Thus 80% of spine injuries in children under age 8 years occur in the cervical spinal cord. In children under age 3 years, 50% of those injuries occur in the C1-2 region.

The spinal cord is well protected by the spinal column. However, trauma to the spine may result in spinal cord injury when there is (1) spinal fracture; (2) fracture with subluxation; (3) subluxation alone; and (4) hyperflexion, hyperextension, or rotation without obvious radiographic features. After pediatric spinal trauma, spinal cord injury without radiographic abnormalities (SCIWORA) has been described21potentially associated with significant morbidity. However, consensus on the use of the term has not been reached.22 With more advanced MRI techniques such as diffusion weighted imaging, and spinal cord abnormalities are more frequently detected.23 Clinical spinal cord injury without neuroimaging accompaniment may be similar to minimal traumatic brain injury in which functional change occurs secondary to neuronal metabolic dysfunction involving subcellular ionic, metabolic, and local physiologic events.


In the neonatal period, clinical features of spinal cord injury (SCI) after birth trauma may be subtle. Signs include apnea, intercostal paralysis, a weak cry, and flaccid paralysis. The latter is evidenced by a flaccid, abducted, and motionless limb. Decreased sensation is evident as decreased response to pain. A Gallant reflex, in which the infant is held suspended in the palm in a prone position and the paraspinal region is scratched, leads to reflex curvature of the spine toward the stimulus. Absence of this reflex at a position along the back helps determine the cord level of injury. The differential diagnosis of SCI in the neonatal period includes neonatal asphyxia, intracranial injury, congenital defects, or progressive infantile spinal muscular atrophy.

In the infant who has been subjected to inflicted neurotrauma, it is important to recognize that SCI (particularly of the cervical and upper thoracic spinal cord) may also occur. In the older child with a history of trauma, the diagnosis of SCI is self-evident. Pain and tenderness are typical presenting features. Physical examination should delineate the spinal cord level based on motor, sensory, and deep tendon reflex function.


In the case of suspected birth injuries, spinal radiographs are often normal. Fractures and subluxation may be detected but radiographs are best interpreted by those familiar with the normal variations of the cervical spine in infancy. Spine MRI will allow detection of soft tissue and ligamentous injury, as well as myelopathy.

In the older child with suspected spine injury from blunt trauma, particularly with altered mental status, antero-posterior and lateral radiographs will quickly assess the bony elements for fracture or dislocation. Whereas radiographs are a minimum requirement for suspected spinal trauma, the addition of MRI is useful for detection of ligamentous injury, bleeding, disc herniation, and myelopathy.


Spinal cord injury in the neonatal period often involves the upper cervical cord and thus diaphragmatic control may be compromised. Careful and immediate attention to ensure adequate and safe ventilation is essential. Mask ventilation may be sufficient and effective so as to avoid intubation with manipulation of the neck and worsening of spinal cord injury.

Children involved in trauma with suspected spinal cord injury must have complete stabilization of the entire spine by immobilization. At the scene of injury, the child should be placed on a rigid board, which can accommodate the occiput and maintain the child’s head in neutral position without cervical flexion. Rolls placed under the shoulders can help achieve this.24

After stabilization and acute care, subsequent treatment is supportive. Whereas trials of intravenous methylprednisolone have demonstrated some recovery of motor and sensory function, the degree of functional recovery has been minimal. Furthermore, complications from high-dose steroid administration should be anticipated and avoided. If steroid therapy is used, an intravenous bolus of 30 mg/kg of methylprednisolone is given no later than 8 hours after the injury followed by maintenance intravenous infusion of 5.4 mg/kg per hour. If steroid therapy is begun within 3 hours of injury, total steroid therapy is recommended for 24 hours; if begun 3 to 8 hours after injury, it is recommended for 48 hours.


Injury to the cervical spine and spinal cord, especially in the first year of life, may lead to ligamentous laxity and development of a syrinx. After spinal cord injury, pain spasms and autonomic dysfunction may develop and are treated symptomatically. The sequelae of spinal cord injury depend on the level at which injury occurs and the functions affected. Motor and sensory function of the lower extremities is often impacted significantly with resultant paralysis and anesthesia. Without proper care, this may lead to decubitus ulcers and serious infection. Bowel and bladder function are also affected, requiring catheterization. This introduces a lifelong risk of infection. The psychologic impact of the loss of independent mobility is difficult for the child and adolescent and may be mitigated by ensuring that support networks and counseling are provided.


With rapid immobilization and appropriate traction, infants and children may recover from spinal cord injury. After the initial recovery period, long-term care and rehabilitation are needed. The child should be cared for at an established pediatric rehabilitation center with expertise in spinal cord injury. During recovery, efforts focus on reestablishing bowel and bladder function or teaching bowel, bladder, and skin care.

As with all accidental injuries, prevention of injury by protective means is paramount. Because children under age 10 years are at increased risk of cervical cord trauma as a result of the anatomical differences described above, it is appropriate to restrict their participation in contact sports, which may lead to head trauma with forces transmitted to the cervical spinal column. Additionally, the use of proper restraints in motor vehicles (car seats and seat belts) and headgear in sporting activities should be recommended at every opportunity.


During birth, injuries to the brachial plexus may occur. Incidence has ranged from 0.38 to 3 per 1000 deliveries.25 Obstetric brachial plexus lesions may result in root syndromes affecting the upper root (C5-6 +/– C7) in 70 to 90% of brachial plexus palsy (BPP) lesions, global brachial plexus injuries (C5-T1) in approximately 20%, or rarely lower root (C8-T1) in less than 1% of patients. Risk factors include increasing birth weight, assisted delivery, macrosomia, breech presentation, and shoulder dystocia. Most (70–90%) upper root injuries recover full function by 3 months of age. The remainder may have some functional recovery of antigravity movement of biceps, triceps, and deltoid by 6 months. Surgical evaluation and repair at a center with experience in obstetrical brachial plexus injury should be sought.