Search tips
Search criteria 


Logo of nmcNeurologia medico-chirurgicaSubmissionsInstructions for AuthorsArchivesThe Japan Neurosurgical Society
Neurol Med Chir (Tokyo). 2017 February; 57(2): 82–93.
Published online 2017 January 20. doi:  10.2176/nmc.ra.2016-0191
PMCID: PMC5341344

Pediatric Traumatic Brain Injury: Characteristic Features, Diagnosis, and Management


Traumatic brain injury (TBI) is the leading cause of death and disability in children. Pediatric TBI is associated with several distinctive characteristics that differ from adults and are attributable to age-related anatomical and physiological differences, pattern of injuries based on the physical ability of the child, and difficulty in neurological evaluation in children. Evidence suggests that children exhibit a specific pathological response to TBI with distinct accompanying neurological symptoms, and considerable efforts have been made to elucidate their pathophysiology. In addition, recent technical advances in diagnostic imaging of pediatric TBI has facilitated accurate diagnosis, appropriate treatment, prevention of complications, and helped predict long-term outcomes. Here a review of recent studies relevant to important issues in pediatric TBI is presented, and recent specific topics are also discussed. This review provides important updates on the pathophysiology, diagnosis, and age-appropriate acute management of pediatric TBI.

Keywords: traumatic brain injury, pediatric, treatment, intensive care, intracranial pressure


Traumatic brain injury (TBI) is the leading cause of death and disability in children. TBI in children result in a range of traumatic injuries to the scalp, skull, and brain that are comparable to those in adults but differ in both pathophysiology and management. The differences are attributable to age-related structural change, mechanism of injuries based on physical ability of the child, and the difficulty in neurological evaluation of pediatric populations. The scalp is highly vascularized and a potential cause of lethal blood loss. Even a small loss of blood volume can lead to hemorrhagic shock in a newborn, infant, and toddler, which may occur without apparent external bleeding. Therefore, children are considered to exhibit a specific pathological response to brain injury and accompanying neurological symptoms. Advances in diagnostic imaging have improved the quality of care by assisting healthcare providers to evaluate and diagnose children with TBI. In addition, magnetic resonance imaging (MRI) has facilitated accurate diagnosis, appropriate selection of treatment, prevention of further complications such as higher brain dysfunction as well as post-traumatic seizures.


Unintentional injuries are the leading cause of death in children. Of all the types of traumatic injuries, brain injuries are the most likely to result in death or permanent disability. A large amount of data has emerged from studies by the U.S. Centers for Disease Prevention and Control regarding pediatric TBI. An estimated 475,000 people in U.S. in the age group of 0–14 years sustain TBI annually, of which up to 90% return home with mild injuries, 37,000 are hospitalized, and 2,685 die because of their injuries. A study with respect to age in the same year revealed that emergency consultations were most common among children aged 0–4 years (1,035 per 100,000 children), and of these, 80 per 100,000 children were hospitalized. The annual death rate from traumatic injury in children younger than 4 years is 5 per 100,000. The death rate is higher for children younger than 4 years than for those 5–14 years of age. The higher traumatic injury death rate in younger children may reflect the number of abusive injuries in infants and young children. 1) Hospitalization for TBI was most commonly observed in adolescents (129 per 100,000). More boys were found to undergo emergency consultation and hospitalization than girls. 2) The most common mechanisms of pediatric TBI vary according to age. Falls are the leading cause of TBI in children younger than 14 years of age. 3) Children younger than 4 years of age are injured mainly by falls but are also affected by abusive injuries and motor vehicle accidents. Children 4–8 years of age are injured in falls and motor vehicle accidents but also become more at risk for other transportation-related injuries such as bicycle-related incidents. 4) Abusive head trauma (AHT) is particularly common in young infants aged less than 2 years; approximately 30 of every 100,000 infants aged less than 1 year were hospitalized for AHT. 5)

Injury characteristics according to age and development

The clinical presentation of children with head injury is extremely variable depending on the severity of trauma. The Pediatric Glasgow Coma Scale (PGCS) is commonly used to assess consciousness and to define the severity of head injuries. Generally, neurological deficits are found at the time of injury, and newly appeared clinical signs may indicate further progression of pathological changes due to head injuries and should be carefully investigated. The evolving anatomy and age-specific properties of the skull, face, brain, and neck muscles make children susceptible for distinctive types of injuries that are not encountered in adults. (Table 1.)

Table 1
Injury characteristics according to age and development

There are unique biomechanical properties for pediatric brain injury due to a combination of higher plasticity and deformity, whereby external forces are absorbed in a different way compared to adults. The infant skull is less rigid, and open sutures function as joints, allowing for a small degree of movement in response to a mechanical stress.6) However, intra and extracranial injuries are also associated with a normal delivery and even intracranial hemorrhages can be seen in vaginal deliveries because of compression and traction exerted on the fetal head during its passage through the birth canal with the use of obstetric instruments. Neonates are prone to have conditions such as cephalic hematoma and subgaleal hematoma. Since it has been well known that a low birth weight and hypoxemia are risk factors for intraventricular hemorrhage in this age group, those factors should be differentiated from AHT and coagulopathy.7)

Shaking usually produces slight deformation of the skull, and high plasticity of the skull results in share forces between the skull and adjacent cortical vessels and brain. These share forces may result in stretching and sharing injuries of the vessels and brain parenchyma.8) Children have larger heads than adults in relation to their body size. Consequently, the likelihood of the head being hit in pediatric trauma is higher than that in adults. The relation between head and body size continuously declines with increasing age. Furthermore, the head is relatively heavy compared to the rest of the body making the head more vulnerable to TBI and results in different dynamics of head acceleration due to the external forces.

The cerebral white matter contains little myelin, and its distribution is very different in newborns compared with that in adults. The neonatal brain is watery, while the myelinated brain has a much higher density due to the progressing myelination and progressively lowering of the water content. Temporal differences between myelination of various brain areas are pronounced during progressing development. Myelination follows programmed patterns with a caudo-cranial and posterior-anterior predominance. The degree of myelination results in different absorption of traumatic forces, with increased susceptibility to TBI in the unmyelinated regions.9)

During development, more energy can be absorbed by the sinuses, with less energy directly transmitted to the skull and brain; hence, brain damage is limited with facial development and progressive development of the paranasal sinuses. In addition, the protruding forehead in young children increases the possibility that a force directly impacts the frontal skull and underlying cerebral parenchyma. Facial growth occurs in a forward and downward direction, which increases the chances of midfacial fractures with increasing age.

Young children have weaker neck muscles, and the head is relatively heavy. The cranio-cervical stability is more dependent on the ligaments and soft tissues than on the vertebrae. In severe trauma cases, cranio-cervical junction lesions are sometimes detected. Cervical spinal fractures and cervical vascular lesions need to be ruled out in the presence of acute, focal neurological deficits that cannot be explained by the forces that directly impacted the brain (Table 2).

Table 2
Structural consideration in pediatric population

Diagnosis and Clinical Features

In general, primary TBI includes extra-parenchymal injury (epidural hematoma, subdural hematoma, subarachnoid hemorrhage, and intraventricular hemorrhage), intra-parenchymal injury (intracerebral hemorrhage, diffuse axonal injury [DAI], and intracerebral hematoma) and vascular injury such as vascular dissection, carotid artery-cavernous sinus fistula, dural arteriovenous fistula, and pseudo-aneurysm. 10)

Primary TBI

1. Skull fracture

The majority of pediatric skull fractures can be managed conservatively. Frontal bone fractures are more likely to require repair, and cases of TBI associated with fracture are more likely to involve two or three bones. Linear fractures most commonly occur in the parietal bone, followed by the occipital, frontal, and temporal bones, in that order. 11) Those fractures can be distinguished from normal sutures by their anatomical configuration, signs of ossification along sutures, and the presence of complex serrations. Extracranial subcutaneous swelling is an important clinical feature to indirectly diagnose skull fractures. In a recent report, 2D+3D computed tomography (CT) in combination were shown to have high sensitivity in the diagnosis of linear skull fractures in all children and increased specificity in children less than 2 years of age, with concurrent intracranial lesions being detected in 15%–30% of these cases. 12) Hospitalization is not necessary for many children with non-displaced skull fractures but patients with mental status changes, additional injuries, or those suspected to be cases of AHT may require hospitalization. 13)

Among depressed fractures, simple type is more common in children and results from localized external force. Compound type accounts for 42%–66% of all fractures in children, and 9% of all fractures in children aged less than 1 year. Dural injury can be observed underneath fractures; approximately 11% of pediatric depressed fractures are accompanied by dural injuries that resulted in intracranial lesions. 14,15) When fractures were seen above dural sinuses, children needed to be observed in the intensive care unit (ICU) for progression of epidural hematoma and posttraumatic venous sinus thrombosis. The ping-pong ball fractures in newborns rarely damage the dura. Spontaneous reduction can be expected in cases of simple depressed fracture in newborns, but older children may require cranioplasty. The current guidelines for surgical management of TBI recommends surgical repair in the following cases: (1) Cerebrospinal fluid (CSF) leak is clearly recognized, (2) detection of foreign body, (3) debridement of the local wound is deemed necessary, (4) infected wounds, (5) evacuation of hematoma is required, and (6) for cosmetic reasons. 16) Depressed skull fracture was claimed to be an independent risk factor for post-traumatic seizures; however, several case reports appear to refute the reported correlation between the two. 17) Postoperative improvement of neurological function in cases of depressed fracture that overlie the superior sagittal sinus have been reported and may possibly be related to improvement in venous circulation. 18,19)

Basal skull fracture (BSF) is rarely seen in children. In age groups where facial bones are still developing, BSF can result in cranial nerve and vascular injuries. 20) Fractures may present as tardive meningitis. Careful evaluation of clinical signs and symptoms is mandated in all cases. 21) Alhelali et al. reported that BSFs occurred in 26% of their patients. The temporal bone was fractured in two thirds of the patients with BSFs, and cerebrospinal fluid leaks were observed in one-third of these patients. They concluded that BSFs are indicative of a significant linear blunt force and are independent predictors of mortality. 22)

1-1. Growing skull fracture

In developing infants or young children, a leptomeningeal cyst or herniated brain tissue through dura mater can result in enlargement of the fracture line. This is due to localized pulsatile pressure via lesions that are adhered to the inner table of the skull. Such pathological changes on the skull bone will facilitate nutritional deficiencies, especially at the bone edges. In most cases, cosmetic issues such as cranial depression or pulsatile swelling are diagnostic factors, whereas headache and seizures may be observed in some cases. Reconstructed CT images are quite useful for cranioplasty. Nowadays, more radical treatment for GSF is recommended based on better understanding of the lesion pathology with the use of advanced radiographic techniques, although spontaneous resolution of GSF has also been reported. 23)

2. Intracranial injury

2-1. Acute epidural hematoma

Acute epidural hematoma (AEDH) is relatively rare in young infants as the dura mater is strongly adhered to the inner surface of the skull, especially in the vicinity of the suture lines. In neonates, the middle meningeal artery is not contained within the skull, and the groove of arteries originating from extra-carotid artery is shallow and not likely to be damaged in TBI. 24,25) AEDH in infants is basically venous and often caused by injuries that overlie the dural venous sinus or by rupture of emissary veins in the vicinity of the fracture. Posterior fossa AEDH is commonly associated with occipital fracture overlying the region from the transverse to the sigmoid sinus. Other common sites of AEDH include the middle fossa, the parasagittal area, and the calvarium. However, the possibility of an arterial AEDH, which can rapidly grow and lead to cerebral herniation and death, should not be ignored. AEDH in neonates also commonly occurs in the posterior fossa as a type of birth-related head injury. It has been demonstrated that AEDH generally does not exceed the suture line. However, hematoma from venous sinus injury can extend beyond it and even to the opposite side; therefore, intensive care is required in such cases. 26) Recently, several groups have reported successful conservative management of pediatric AEDH attributed to absorption of blood through the fracture line to the adjacent subcutaneous layer.

2-2. Acute subdural hematoma

Acute subdural hematoma (ASDH) originates between the arachnoid membrane and dura mater and is thought to result not only from vascular rupture caused by direct external force but also due to the collision of a moving skull with a stationary object. A shearing force and rotational acceleration is inflicted due to the sudden deceleration thus causing vascular and cerebral parenchymal injury. 27) In particular, AHT is a relatively common cause of acute ASDH in children less than 2 years of age. Coexistence of multiple hematomas apparently sustained at different times (chronic and acute) in the absence of coagulopathy should be strongly suspected as a case of AHT.

Wide subdural space makes the bridging vein susceptible to traction and prone to rupture. 28) In patients with a history of cerebral atrophy, hydrocephalus following shunt placement, benign external hydrocephalus, and subdural effusion, the bridging vein can be easily extended and is eventually liable to rupture. 29) Compared to AEDH, there is a higher rate of concurrent cerebral contusions in such cases. Bilateral ASDHs are common, and hematomas are typically located on the tentorium, along the calvarium, interhemispheric fissure, falx cerebri, and tentorium cerebelli. ASDH is more likely to be thinner in pediatric population. Especially, in AHT, the extensive hypoxic-ischemic encephalopathy is usually present underneath the ASDH and may result in intracranial hypertension. In such cases, urgent craniotomy for evacuation of ASDH may sometimes lead to hypovolemic shock resulting in intraoperative cardiac arrest. Therefore, careful consideration of craniotomy is required to avoid unexpected operative complications.

2-2-1. Abusive head trauma

AHT has come to occupy an important place in severe pediatric TBI. The estimated incidence of AHT in children aged less than 1 year is between 14 and 40 in 100,000, which is comparable to that of neonatal meningitis (25–32 per 100,000 births) 30) and acute lymphocytic leukemia (28.7–36.6 per 100,000 children < 1 year of age). AHT has previously been referred to as inflicted TBI (ITBI), non-accidental head injury (NAHI), and shaken-impact syndrome. AHT is a generic term for head trauma including injury to the cranium, cerebral parenchyma, and cervical spinal cord. The mechanism of injury can be shaken, direct impact, or a combination of these, secondary brain injury due to hypoxia and/or hypotension, which is broader than syndromes such as shaken baby syndrome (SBS) that have a specific mechanism of injury. The diagnosis of SBS is contingent on observation of abnormal shaking behavior as the mechanism of injury and mandates close attention. 31) AHT is the most common cause of TBI in children less than 2 years of age; therefore, it is important to consider AHT in the differential diagnosis of children with traumatic injuries, including head injury. Clinical findings of AHT include impaired consciousness, seizures, vomiting, and delayed developmental milestones. On diagnostic imaging, ASDH is the most common finding (up to 77%–89% of all cases). 32,33) Up to 83%–90% of AHT cases have signs of ASDH on autopsy. 34,35) Other characteristic imaging findings include subarachnoid hemorrhage (SAH), Intracerebral hemorrhage (ICH), and cerebral contusion. AEDH, however, are rarely associated with AHT. Among physical findings, only “apnea” is specific to AHT, with a positive predictive value of 93%. 36) Rib fractures and retinal hemorrhage are important findings that have positive predictive values of 73% and 71%, respectively. Seizures are commonly observed in AHT. However, long bone fractures, skull fractures, and scalp injuries showed no significant association with AHT. Among ophthalmologic findings, retinal hemorrhage is observed in 74% of diagnosed AHT cases and 82% of autopsy cases. Retinal hemorrhages are often multilaminar and bilateral. 37) The absence of any superficial findings of trauma in cases of serious intracranial injury is suggestive of AHT.

2-2-2. Subdural fluid accumulation

Subdural fluid accumulation is a major subject of research linked to pediatric TBI. The accumulated fluid can vary from hematoma to a highly concentrated protein or a mixture of these. Most fluid accumulations are bilateral, and the symptoms are hard to differentiate from those generally seen in pediatric patients such as dysphoria, poor appetite, lethargy, excitability, and an enlarged head circumference. The subdural fluid collection is sometimes incidentally diagnosed on imaging. The treatment and natural course largely depend on the site of fluid accumulation (subdural or subarachnoid). 38,39) This is of interest considering its relevance to the applicability of subdural-peritoneal shunts. Y-shunt technique often successfully reduces the amount of subdural fluid collection over a period of 2–3 months. 40) Good prognosis can be expected in such cases. However, in cases of AHT, delayed enlargement of subdural space is more likely to involve the bifrontal area, but may also reflect compensated subdural fluid collection alongside extensive bilateral atrophic change in the cerebral hemispheres, an injury condition referred to as enceplalomalacia.

2-3. Traumatic subarachnoid hemorrhage

Traumatic SAH (tSAH) is caused by microvascular ruptures in the subarachnoid space or on the brain surface, circulation and redistribution of intraventricular hemorrhage, penetrated from intracranial hematomas and cerebral contusions and in the subarachnoid space. Hochstadter et al. retrospectively analyzed 171 severe TBI patients (pre-sedation Glasgow Coma Scale (GCS) ≤ 8 and head Maximum Abbreviated Injury Scale (MAIS) ≥ 4) who underwent CT head imaging within the first 24 h of hospital admission. tSAH was present in almost half of pediatric severe TBI patients, and it was indicative of TBI severity and a higher level of care required at discharge. tSAH in pediatric patients was not independently associated with increased risk of mortality. 41)

2-4. Intraventricular hemorrhage

Intraventricular hemorrhage (IVH) is often caused by intraventricular perforations of intracerebral hematomas located next to the cerebral ventricles. In addition, IVH can be observed in the event of subependymal vascular ruptures and damage to the paraventricular structures including the fornix, transparent septum, and corpus callosum. In some instances, tSAH flows back into the ventricle systems. In diffuse axonal injuries, shear and rotational forces can rupture subependymal and ventral corpus callosum blood vessels, causing IVH. In pediatric IVH, intensive care is required to monitor for signs of secondary hydrocephalus. Post-traumatic hydrocephalus is usually caused by either obstruction of the aqueduct or malabsorption of CSF due to subarachnoid granular obstruction. In addition, degradation products of red blood cells can cause chemical ependymitis. 42)

Evidence for treatment of IVH is rather deficient. Further research is required into the specific trauma-related phenomenon associated with IVH.

2-5. Cerebral contusions

Cerebral contusions are relatively common in pediatric TBI and tend to occur just below the site of impact of external force (coup injury). Contusions are seen usually on the gray matter, while the white matter is often relatively well preserved. Lesions tend to occur in the both frontal and temporal lobes because of the irregular surface of the cranial base, and the anatomical contiguity of the crista galli and the petrous bone to the cortex. 43) Lesions on the opposite site of the impacted area (contrecoup injury) are rarely seen in infants. However, cerebral swelling caused by primary contusion may quickly develop into extensive hypoxic lesion surrounding the original lesions. The progression of each focal hypoxic lesion may induce extensive secondary brain injury and influence the focal cerebral blood circulation as well. This may in turn aggravate cerebral ischemia at the site of primary lesion. Rapid increase in focal cerebral pressure in the limited compartments such as middle or posterior fossa can quickly progress to cerebral herniation and death.

2-6. Diffuse axonal injury

Classically, symptoms of DAI include coma with decorticate and decerebrate posturing. With recent advances in imaging technology and the development of new MRI sequences, the association between mild TBI and high cognitive function, especially in the pediatric population, has attracted much attention. Therefore, radiological evidence of DAI based on MRI findings may enable a more definitive diagnosis of DAI rather than relying only on clinical symptoms. 44) Recently, a case of axonal injury in the cervical spine was documented in an infant with AHT. Such patients tend to present complex pathological features due to repeated instances of external force applied throughout the brain from various motions. In DAI, blood vessels and nerve fibers are liable to be injured by shear force. Furthermore, changes are observed in the axons of the subcortical white matter of the frontal and parietal lobes as well as in the ampulla, basal ganglia, internal capsule, and the central corpus callosum. The diagnosis of DAI in pediatric TBI requires careful consideration as in the adult cases. 43)

2-7. Intracerebral hemorrhage

The intrinsic causes of intracerebral hemorrhage (ICH) may be difficult to determine, especially in children with congenital vascular abnormalities such as arterio-venous malformations. Traumatic ICH is commonly observed in the frontal and temporal white matter but may also be seen in the basal ganglia and the cerebellum due to disruption of perforators. Delayed traumatic intracerebral hemorrhage (DTICH) typically occurs in geriatric TBI patients who have multiple intraparenchymal contusions with possible coagulopathy. However, it should be considered in the differential diagnosis of children who develop sudden neurological deterioration and the condition requires urgent intervention. 4547)

Secondary TBI

1. Diffuse cerebral swelling

Diffuse cerebral swelling (DCS) is among the most life-threatening complications of TBI and commonly noted on CT of AHT patients. Based on a retrospective study of a series of 118 patients with DCS, Lang et al. reported that CT findings of DCS tend to develop more readily in children because of the relative lack of cerebrospinal fluid available for displacement. They also observed a relatively benign disease course in children as compared to that in adults, except in cases with severe primary injury or secondary hypotensive insult. 48) Due to an underdeveloped auto-regulatory mechanism for cerebral blood flow (CBF), children are particularly vulnerable to cerebral hyperemia, which can result in serious intracranial hypertension. 49) In preclinical studies, excessive exposure of immature brain tissue to excitatory neuro-transmitters was shown to enhance inflammatory response, vascular permeability, and accelerated pathological changes. In addition, infants have a low mean arterial pressure with little reserve capacity to counter low blood pressure and hypoxia, which renders them liable to develop a fatal decrease in CBF. 50) These mechanisms appear to play a key role in the pathogenesis of DCS. The typical CT findings of DCS include hemispheric extensive low density lesion with effacement of cerebral sulci and cisterns as well as ventricular system (Big Black Brain). 51,52)

Management of Severe Pediatric TBI

1. Intracranial Pressure monitoring

Use of intraparenchymal intracranial pressure (ICP) sensor is an invasive method but is the only scientifically proven method for early detection of increased ICP in children with severe TBI. In a recent report, use of ICP monitoring for this purpose was associated with reduced in-hospital deaths of children with severe TBI. 53) On the other hand, Alkhoury et al. analyzed patients’ data from the National Trauma Data Bank to determine the effect of ICP monitoring on survival in pediatric patients with severe TBI. They suggested that there is a survival advantage in patients who have ICP monitors and a GCS score of 3 with a longer hospital length of stay, longer ICU stay, and more ventilator days compared with those without ICP monitors. 54) The contribution of variable ICP monitoring rates to interhospital variation in pediatric TBI mortality was modest.

2. Cerebral perfusion pressure

The effect of ICP and cerebral perfusion pressure (CPP) on outcomes of TBI in adults is well acknowledged. 55,56) In adults, common practice is to augment arterial blood pressure in instances of raised ICP. However, not only marked elevations of CPP accelerate edema leading to secondary intracranial hypertension, 57,58) but they can frequently contribute to systemic insult. 59) This is more frequently observed in patients who present with a reduced GCS. 60) Although there is insufficient level I & II evidence to support the notion that uncontrolled ICP and CPP affects outcomes, joint management of ICP and CPP is considered a standard practice for management of children with severe TBI. 61) In some cohorts, strong association of high ICP with morbidity was well-demonstrated. However, Brady et al.62) found a significant correlation between outcomes and CPP, especially the deviation from optimal CPP. The concept of individualized CPP in the adult population has been around for over a decade 63) and has recently been proposed as an optional strategy in the current TBI guidelines. 64) While there have been no large studies to determine CPP in children, Chambers et al. 59) proposed age-stratified critical levels of CPP. Specifically, in the age groups 2–6, 7–10, and 11–16 years, CPP values of 43, 54, and 58 mmHg, respectively, were associated with good outcomes. 58) Using ΔCPP values, it was observed that deviation of values of CPP from optimum levels affected the association between pressure and outcomes. In particular, those who spent more time with CPP lower than optimal CPP appeared to have relatively poorer outcomes.

3. Treatment 61)

3-1. Therapeutic uses of sedatives, analgesics, and neuromuscular blockade

Sedatives and analgesics are required for general care of all TBI children to achieve a level of anesthesia needed for invasive procedures, such as airway management, ICP control, to synchronize respiratory efforts with the ventilator, and anxiety relief during diagnostic imaging. Mostly, combination of opioids and benzodiazepines for pain control and sedation are used in children with severe TBI. Continuous infusion of Propofol is prohibited to use for children due to propofol infusion syndrome. However, neuromuscular blockade is utilized in children with severe TBI to improve compliance with mechanical ventilation, reduce metabolic demand, and eliminate shivering. Sanfilippo et al. confirmed the lack of evidence on the effect of neuromuscular blockade on ICP and related outcomes in his recent systematic review. 65)

3-2. Hyperosmolar therapy

Intravenous mannitol and hypertonic saline are routinely used to control intracranial hypertension in children with severe TBI. Those osmotic agents are used after or concurrently with sedation, mild hyperventilation, and CSF drainage. Mannitol has been the traditional agent to use and a 20% of mannitol dose of 0.25–1.0 g/kg is often repeatedly administered. Treatment should be titrated to maintain plasma osmolality at ≤ 310 mOsm/L. Prevention of hypovolemia is another component of management of TBI. Recently, hypertonic saline has become one of the most popular options to treat intracranial hypertension in the North America. In a pediatric double-blind study, 3% saline resulted in a more significant reduction in ICP than 0.9% saline. Similarly, in a randomized controlled trial, 1.7% saline was superior to lactated Ringer’s solution in ICP reduction. Hypertonic saline may warrant consideration as the first-line drug for treating increased ICP, as it was associated with the most favorite cerebral hemodynamics and fastest resolution of intracranial hypertension in children with severe TBI. 66)

3-3. Cerebrospinal fluid drainage

Cerebrospinal fluid drainage is used to reduce the volume of the contents of the intracranial vault for the management of increased ICP. An external ventricular drain is commonly used to drain off the CSF. The addition of a lumbar drain may be considered in the case of refractory intracranial hypertension with a functioning external ventricular drainage (EVD), open basal cisterns, and no evidence of a mass lesion or shift on imaging studies. Therapy may be associated with an increased risk of complications from hemorrhage and infection.

3-4. Hyperventilation

Hyperventilation reduces ICP by lowering CBF by cerebral vasoconstriction of arterioles. A significant decrease in CBF is expected to occur within 48 h of injury, and hyperventilation may lead to subclinical cerebral ischemia and a reduction in cerebral oxygenation. Therefore, severe hyperventilation should be avoided. Mild hyperventilation (PaCO 2 , 30–35 mmHg) is recommended in patients who have refractory intracranial hypertension. Under such circumstances, arterial blood gas analysis or end-tidal carbon dioxide (ETCO 2 ) monitoring will be beneficial to monitor and prevent further reducing CBF.

3-5. Barbiturates

Barbiturates have been considered for the control of refractory intracranial hypertension after other medical therapies have failed. Pentobarbital has been found to be effective in lowering ICP in children with severe TBI. Concurrently, systemic hemodynamic parameters should be maintained stable with continuous monitoring, preferably in an ICU setting due to the potential risk of myocardial depression and hypotension.

3-6. Temperature control

It is recommended to at least avoid hyperthermia which increases metabolic demands, lipid peroxidation, inflammation, excitotoxicity, and lowering seizure thresholds. Those reactions can cause of extensive secondary brain injury. For the use of hypothermia (HT) to treat of refractory intracranial hypertension, the guidelines provide level II evidence for recommending moderate HT to treat severe TBI in children for duration of up to 48 h, followed by rewarming slowly prevent rebound intracranial hypertension over 12–24 h. 67) HT is effective in decreasing ICP as an adjunct to standard treatment but, so far, conveyed no functional outcome or increased mortality benefit at 6-months post-TBI.

3-7. Decompressive craniectomy

In pediatric cases, it has been reported that decompressive craniectomy (DC) is performed for controlling intracranial hypertension due to any causes such as TBI, hypoxic-ischemic encephalopathy, metabolic disease, CNS infection, or others, and was effective at ICP reduction. 68) Bifrontal craniotomy is more likely to be selected in children compared to adults. 69) In addition to the mortality, long-term outcome studies are required including the evaluation of various high cognitive functions. 70) The effectiveness of DC on AHT was also investigated, and it clearly reduced mortality; however, no answer has been obtained regarding functional outcomes. 71)

3-8. Corticosteroids

The routine use of corticosteroids to treat children with severe TBI is not recommended because the lack of evidence for benefit in children and potential harm from infectious complications. Significant suppression of endogenous cortisol levels was documented with dexamethasone treatment and trends toward increased incidence of pneumonia were observed. Steroid treatment is not associated with improved functional outcome, decreased mortality, reduced ICP.

3-9. Nutritional management

Nutritional support is very important for children with severe TBI. It is recommended that full nutritional replacement be instituted by day 7 post-injury because TBI patients lose sufficient nitrogen to reduce weight by 15% per week and support administration of 130-160% replacement of energy expenditure, which may reduce nitrogen loss.

3-10. Anticonvulsants

Children, particularly infants, have lower seizure thresholds and are at high risk for early seizures. Immediate prophylactic administration of anticonvulsant is recommended in children with severe TBI. There is a widespread opinion that prophylactic administration of anticonvulsant is ineffective to prevent the development of epilepsy. Risk factors for early onset of seizures in infants aged less than 2 years include concomitant hypotension, history of child abuse, and Glasgow Coma Scale score of ≤ 8. In such cases, prophylactic anticonvulsant is recommended. 72) No specific guidelines exist for the discontinuation of prophylactic anticonvulsant. If no further seizures occur more than 2 years after the last seizure, imaging studies, electroencephalogram (EEG), and CBF studies are recommended to decide potential reduction in dosage by half.

Outcomes 73,74)

Long-term follow-up is often required to evaluate both physical and intellectual disability outcomes. Kurihara et al. suggested a comprehensive, multidisciplinary rehabilitation protocol to promote recovery and facilitate a smooth transition to home and school activities. The importance of early and regular communication between rehabilitation specialists, family members, and educators is strongly recommended. Such collaboration permits a clear identification of functional abilities and increases the child’s potential for positive long-term outcomes.

In a cohort of TBI children who presented with GCS score of 3 or 4, 56.6% died within 1 year. However, approximately 15% of patients had good outcomes at 10 or more years. Pupillary response at admission, occurrence of hypothermia, and mechanism of injury were associated with survival and outcomes. 75)

Neuroimaging has an indispensable role in the management of pediatric TBI. Newer MRI-modalities such as diffusion weighted and diffusion tensor imaging, susceptibility weighted imaging, and (1) H-magnetic resonance spectroscopy allow for determination of several sensitive parameters that predict chronic function and possibly neuropsychological function. 76) They may also allow earlier identification of chronic sequelae of TBI in an individual child and, thereby, help tailor the rehabilitation services. 77)


The optimal care of an infant or child with TBI requires a multidisciplinary approach in each phase of management. After the initial evaluation, prompt diagnosis, multimodal monitoring, and titrated management of intracranial hypertension are necessary to minimize pathophysiological damage to the developing brain. Management of pediatric TBI provides challenges due to differences in the basic mechanisms of injury. Further additional medical evidences will be available on the aspects of the evolution of neuronal damage and repair in pediatric TBI near in the future.


I would like to thank A. Fuse for useful discussions. I would also like to thank S. Yokobori, K. Kuwamoto and H. Onda for years of collaboration and advice.


Conflicts of Interest Disclosure

The authors declare that they have no conflict of interest.


1) Centers for Disease Control and Prevention WISCARS. Leading Causes of Death Reports, National and Regional, 1999–2013, 2015. Access 2015.9.22
2) Langlois J, Rutland-Brown W, Thomas K.: Traumatic Brain Injury in the United States: Emergency Department Visits, Hospitalizations, and Deaths . Atlanta, Centers for Disease Control and Prevention, National Center for Injury Prevention and Control, 2004. Access 2015.9.22
3) Injury Prevention and Control : Traumatic Brain Injury, Centers for Disease Control and Prevention. Access 2015.9.22
4) Injury Prevention and Control : Traumatic Brain Injury, Centers for Disease Control and Prevention. Access 2015.9.22
5) Keenan HT, Runyan DK, Marshall SW, Nocera MA, Merten DF, Sinal SH.: A population-based study of inflicted traumatic brain injury in young children. JAMA 290: 621– 626, 2003. [PubMed]
6) Ghajar J, Hariri RJ.: Management of pediatric head injury. Pediatr Clin North Am 39: 1093– 1125, 1992. [PubMed]
7) Stark MJ, Hodyl NA, Belegar V KK, Andersen CC.: Intrauterine inflammation, cerebral oxygen consumption and susceptibility to early brain injury in very preterm newborns. Arch Dis Child Fetal Neonatal Ed 101: F137– F142, 2016. [PubMed]
8) Ommaya AK, Goldsmith W, Thibault L.: Biomechanics and neuropathology of adult and paediatric head injury. Br J Neurosurg 16: 220– 242, 2002. [PubMed]
9) Goldsmith W, Plunkett J.: A biomechanical analysis of the causes of traumatic brain injury in infants and children. Am J Forensic Med Pathol 25: 89– 100, 2004. [PubMed]
10) Silen ML, Kokoska ER, Fendya DG, Kurkchubasche AG, Weber TR, Tracy TF.: Rollover injuries in residential driveways: age-related patterns of injury. Pediatrics 104: e7, 1999. [PubMed]
11) Bonfield CM, Naran S, Adetayo OA, Pollack IF, Losee JE.: Pediatric skull fractures: the need for surgical intervention, characteristics, complications, and outcomes. J Neurosurg Pediatr 14: 205– 11, 2014. [PubMed]
12) Orman G, Wagner MW, Seeburg D, Zamora CA, Oshmyansky A, Tekes A, Poretti A, Jallo GI, Huisman TA, Bosemani T.: Pediatric skull fracture diagnosis: should 3D CT reconstructions be added as routine imaging? J Neurosurg Pediatr 16: 426– 431, 2015. [PubMed]
13) Arrey EN, Kerr ML, Fletcher S, Cox CS, Sandberg DI.: Linear nondisplaced skull fractures in children: who should be observed or admitted? J Neurosurg Pediatr 16: 703– 708, 2015. [PubMed]
14) Vitali AM, Steinbok P.: Depressed skull fracture and epidural hematoma from head fixation with pins for craniotomy in children. Childs Nerv Syst 24: 917– 23, 2008. [PubMed]
15) Erşahin Y, Mutluer S, Mirzai H, Palali I.: Pediatric depressed skull fractures: analysis of 530 cases. Childs Nerv Syst 12: 323– 331, 1996. [PubMed]
16) Steinbok P, Flodmark O, Martens D, Germann ET.: Management of simple depressed skull fractures in children. J Neurosurg 66: 506– 510, 1987. [PubMed]
17) Traumatic Epilepsy Research Committee Risk factors for traumatic epilepsy: A multicenter study. Japanese J Neurosurg 19: 1151– 1159, 1991. (Japanese)
18) Donovan DJ.: Simple depressed skull fracture causing sagittal sinus stenosis and increased intracranial pressure: case report and review of the literature. Surg Neurol 63: 380– 383, 2005. [PubMed]
19) Tamimi A, Abu-Elrub M, Shudifat A, Saleh Q, Kharazi K, Tamimi I.: Superior sagittal sinus thrombosis associated with raised intracranial pressure in closed head injury with depressed skull fracture. Pediatr Neurosurg 41: 237– 240, 2005. [PubMed]
20) Quayle KS, Jaffe DM, Kuppermann N, Kaufman BA, Lee BC, Park TS, McAlister WH. Diagnostic testing for acute head injury in children: when are head computed tomography and skull radiographs indicated? Pediatrics 99: E11, 1997. [PubMed]
21) Muhonen MG, Piper JG, Menezes AH.: Pathogenesis and treatment of growing skull fractures. Surg Neurol 43: 367– 372, 1995. [PubMed]
22) Alhelali I, Stewart TC, Foster J, Alharfi IM, Ranger A, Daoud H, Fraser DD.: Basal skull fractures are associated with mortality in pediatric severe traumatic brain injury. J Trauma Acute Care Surg 78: 1155– 61, 2015. [PubMed]
23) Prasad GL, Gupta DK, Mahapatra AK, Borkar SA, Sharma BS.: Surgical results of growing skull fractures in children: a single center study of 43 cases. Childs Nerv Syst 31: 269– 277, 2015. [PubMed]
24) Leggate JR, Lopez-Ramos N, Genitori L, Lena G, Choux M.: Extradural haematoma in infants. Br J Neurosurg 3: 533– 539, 1989. [PubMed]
25) Case ME.: Accidental traumatic brain injury in infants and young children. Brain Pathol 18: 583– 589, 2008. [PubMed]
26) Huisman TA, Tschirch FT.: Epidural hematoma in children: do cranial sutures act as a barrier?. J Neuroradiol 36: 93– 97, 2009. [PubMed]
27) Harn YS, Chyung C, Barthel MJ, Bailes J, Flannery AM, McLone DG.: Head injuries in children under 36 months of age. Demography and outcome. Childs Nerv Syst 4: 34– 40, 1988. [PubMed]
28) Duhaime AC, Christian CW, Rorke LB, Zimmerman RA.: Nonaccidental head injury in infants—the “shaken-baby syndrome.” N Engl J Med 338: 1822– 1829, 1998. [PubMed]
29) Loh JK, Lin CL, Kwan AL, Howng SL.: Acute subdural hematoma in infancy. Surg Neurol 58: 218– 224, 2002. [PubMed]
30) Hristeva L, Booy R, Bowler I, Wilkinson AR.: Prospective surveillance of neonatal meningitis. Arch Dis Child 69: 14– 18, 1993. [PMC free article] [PubMed]
31) Christian CW, Block R, Committee on Child Abuse and Neglect. American Academy of Pediatrics : Abusive head trauma in infants and children. Pediatrics 123: 1409– 1411, 2009. [PubMed]
32) Talvik I, Metsvaht T, Leito K, Põder H, Kool P, Väli M, Lintrop M, Kolk A, Talvik T.: Inflicted traumatic brain injury (ITBI) or shaken baby syndrome (SBS) in Estonia. Acta Paediatr 95: 799– 804, 2006. [PubMed]
33) Fanconi M, Lips U.: Shaken baby syndrome in Switzerland: results of a prospective follow-up study, 2002–2007. Eur J Pediatr 169: 1023– 1028, 2010. [PubMed]
34) Brennan LK, Rubin D, Christian CW, Duhaime AC, Mirchandani HG, Rorke-Adams LB.: Neck injuries in young pediatric homicide victims. J Neurosurg Pediatr 3: 232– 239, 2009. [PubMed]
35) Duhaime AC, Gennarelli TA, Thibault LE, Bruce DA, Margulies SS, Wiser R.: The shaken baby syndrome. A clinical, pathological, and biomechanical study. J Neurosurg 66: 409– 415, 1987. [PubMed]
36) Maguire S, Pickerd N, Farewell D, Mann M, Tempest V, Kemp AM.: Which clinical features distinguish inflicted from non-inflicted brain injury? A systematic review. Arch Dis Child 94: 860– 867, 2009. [PubMed]
37) Bhardwaj G, Chowdhury V, Jacobs MB, Moran KT, Martin FJ, Coroneo MT.: A systematic review of the diagnostic accuracy of ocular signs in pediatric abusive head trauma. Ophtalmology 117: 983– 992, 2010. [PubMed]
38) Morota N, Sakamoto K, Kobayashi N, Kitazawa K, Kobayashi S.: Infantile subdural fluid collection: diagnosis and postoperative course. Childs Nerv Syst 11: 459– 466, 1995. [PubMed]
39) Aoki N.: Chronic subdural hematoma in infancy. Clinical analysis of 30 cases in the CT era. J Neurosurg 73: 201– 205, 1990. [PubMed]
40) Yilmaz N, Kiymaz N, Yilmaz C, Bay A.: Surgical treatment outcomes in subdural effusion: a clinical study. Pediatr Neurosurg 42: 1– 3, 2006. [PubMed]
41) Hochstadter E, Stewart TC, Alharfi IM, Ranger A, Fraser DD.: Subarachnoid hemorrhage prevalence and its association with short-term outcome in pediatric severe traumatic brain injury. Neurocrit Care 21: 505– 513, 2014. [PubMed]
42) Lichenstein R, Glass TF, Quayle KS, Wootton-Gorges SL, Wisner DH, Miskin M, Muizelaar JP, Badawy M, Atabaki S, Holmes JF, Kuppermann N, Traumatic brain injury study group of the pediatric emergency care applied research network (PECARN) : Presentations and outcomes of children with intraventricular hemorrhages after blunt head trauma. Arch Pediatr Adolesc Med 166: 725– 731, 2012. [PubMed]
43) Graham DI.: Paediatric head injury. Brain 124: 1261– 1262, 2001. [PubMed]
44) Abu Hamdeh S, Marklund N, Lannsjö M, Howells T, Raininko R, Wikström J, Enblad P. Extended anatomical grading in diffuse axonal injury using MRI: Hemorrhagic lesions in the substantia nigra and mesencephalic tegmentum indicate poor long-term outcome. J Neurotrauma. 2016. July 25. [Epub ahead of print] [PMC free article] [PubMed]
45) Stein SC, Spettell CM.: Delayed and progressive brain injury in children and adolescents with head trauma. Pediatr Neurosurg 23: 299– 304, 1995. [PubMed]
46) Atluru V, Epstein LG, Zilka A.: Delayed traumatic intracerebral hemorrhage in children. Pediatr Neurol 2: 297– 301, 1986. [PubMed]
47) Matsumoto M, Sanpei K, Nishikawa H, Seki T, Shibata I, Terao H.: Characteristics of traumatic intracerebral hematomas in children. Neurol Med Chir (Tokyo) 28: 1081– 1088, 1988. [PubMed]
48) Lang DA, Teasdale GM, Macpherson P, Lawrence A.: Diffuse brain swelling after head injury: more often malignant in adults than children? J Neurosurg 80: 675– 680, 1994. [PubMed]
49) Bruce DA, Alavi A, Bilaniuk L, Dolinskas C, Obrist W, Uzzell B.: Diffuse cerebral swelling following head injuries in children: the syndrome of “malignant brain edema.” J Neurosurg 54: 170– 178, 1981. [PubMed]
50) Bruce DA, Raphaely RC, Goldberg AI, Zimmerman RA, Bilaniuk LT, Schut L, Kuhl DE.: Pathophysiology, treatment and outcome following severe head injury in children. Childs Brain 5: 174– 191, 1979. [PubMed]
51) Esparza J, M-Portillo J, Sarabia M, Yuste JA, Roger R, Lamas E.: Outcome in children with severe head injuries. Childs Nerv Syst 1: 109– 114, 1985. [PubMed]
52) Duhaime AC, Durham S.: Traumatic brain injury in infants: the phenomenon of subdural hemorrhage with hemispheric hypodensity (“Big Black Brain”). Prog Brain Res 161: 293– 302, 2007. [PubMed]
53) Alali AS, Gomez D, Sathya C, Burd RS, Mainprize TG, Moulton R, Falcone RA, de Mestral C, Nathens A.: Intracranial pressure monitoring among children with severe traumatic brain injury. J Neurosurg Pediatr 14: 1– 10, 2015. [PubMed]
54) Alkhoury F, Kyriakides TC.: Intracranial pressure monitoring in children with severe traumatic brain injury: national trauma data bank-based review of outcomes. JAMA Surg 149: 544– 548, 2014. [PubMed]
55) Lassen NA.: Cerebral blood flow and oxygen consumption in man. Physiol Rev 39: 183– 238, 1959. [PubMed]
56) Eker C, Asgeirsson B, Grande PO, Schalen W, Nordstrom CH.: Improved outcome after severe head injury with a new therapy based on principles for brain volume regulation and preserved microcirculation. Crit Care Med 26: 1881– 1886, 1998. [PubMed]
57) Nordström CH, Reinstrup P, Xu W, Gärdenfors A, Ungerstedt U.: Assessment of the lower limit for cerebral perfusion pressure in severe head injuries by bedside monitoring of regional energy metabolism. Anesthesiology 98: 809– 814, 2003. [PubMed]
58) Robertson CS, Valadka AB, Hannay HJ, Contant CF, Gopinath SP, Cormio M, Uzura M, Grossman RG.: Prevention of secondary ischemic insults after severe head injury. Crit Care Med 27: 2086– 2095, 1999. [PubMed]
59) Chambers IR, Stobbart L, Jones PA, Kirkham FJ, Marsh M, Mendelow AD, Minns RA, Struthers S, Tasker RC.: Age-related differences in intracranial pressure and cerebral perfusion pressure in the first 6 hours of monitoring after children’s head injury: association with outcome. Childs Nerv Syst 21: 195– 199, 2005. [PubMed]
60) Aries MJ, Czosnyka M, Budohoski KP, Steiner LA, Lavinio A, Kolias AG, Hutchinson PJ, Brady KM, Menon DK, Pickard JD, Smielewski P.: Continuous determination of optimal cerebral perfusion pressure in traumatic brain injury. Crit Care Med 40: 2456– 2463, 2012. [PubMed]
61) Kochanek PM, Carney N, Adelson PD, Ashwal S, Bell MJ, Bratton S, Carson S, Chesnut RM, Ghajar J, Goldstein B, Grant GA, Kissoon N, Peterson K, Selden NR, Tasker RC, Tong KA, Vavilala MS, Wainwright MS, Warden CR, American Academy of Pediatrics-Section on Neurological Surgery. American Association of Neurological Surgeons/Congress of Neurological Surgeons. Child Neurology Society. European Society of Pediatric and Neonatal Intensive Care. Neurocritical Care Society. Pediatric Neurocritical Care Research Group. Society of Critical Care Medicine. Paediatric Intensive Care Society UK. Society for Neuroscience in Anesthesiology and Critical Care. World Federation of Pediatric Intensive and Critical Care Societies : Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents—second edition. Pediatr Crit Care Med 13: S1– S82, 2012. [PubMed]
62) Brady KM, Shaffner DH, Lee JK, Easley RB, Smielewski P, Czosnyka M, Jallo GI, Guerguerian AM.: Continuous monitoring of cerebrovascular pressure reactivity after traumatic brain injury in children. Pediatrics 124: e1205– e1212, 2009. [PubMed]
63) Steiner LA, Czosnyka M, Piechnik SK, Smielewski P, Chatfield D, Menon DK, Pickard JD.: Continuous monitoring of cerebrovascular pressure reactivity allows determination of optimal cerebral perfusion pressure in patients with traumatic brain injury. Crit Care Med 30: 733– 738, 2002. [PubMed]
64) Le Roux P, Menon DK, Citerio G, Vespa P, Bader MK, Brophy G, Diringer MN, Stocchetti N, Videtta W, Armonda R, Badjatia N, Bösel J, Chesnut R, Chou S, Claassen J, Czosnyka M, De Georgia M, Figaji A, Fugate J, Helbok R, Horowitz D, Hutchinson P, Kumar M, McNett M, Miller C, Naidech A, Oddo M, Olson D, O’Phelan K, Provencio JJ, Puppo C, Riker R, Roberson C, Schmidt M, Taccone F.: The International Multidisciplinary Consensus Conference on Multimodality Monitoring in Neurocritical Care: Evidentiary Tables: A Statement for Healthcare Professionals from the Neurocritical Care Society and the European Society of Intensive Care Medicine. Neurocrit Care 21: S297– S361, 2014. [PubMed]
65) Sanfilippo F, Santonocito C, Veenith T, Astuto M, Maybauer MO.: The role of neuromuscular blockade in patients with traumatic brain injury: a systematic review. Neurocrit Care 22: 325– 34, 2015. [PubMed]
66) Shein SL, Ferguson NM, Kochanek PM, Bayir H, Clark RS, Fink EL, Tyler-Kabara EC, Wisniewski SR, Tian Y, Balasubramani GK, Bell MJ.: Effectiveness of pharmacological therapies for intracranial hypertension in children with severe traumatic brain injury—results from an automated data collection system time-synched to drug administration. Pediatr Crit Care Med 17: 236– 45, 2016. [PMC free article] [PubMed]
67) Hutchison JS, Ward RE, Lacroix J, Hébert PC, Barnes MA, Bohn DJ, Dirks PB, Doucette S, Fergusson D, Gottesman R, Joffe AR, Kirpalani HM, Meyer PG, Morris KP, Moher D, Singh RN, Skippen PW, Hypothermia Pediatric Head Injury Trial Investigators and the Canadian Critical Care Trials Group : Hypothermia therapy after traumatic brain injury in children. N Engl J Med 358: 2447– 2456, 2008.. [PubMed]
68) Riyaz M, Waqas M, Ujjan BU, Akhunzada NZ, Hadi YB, Javed G, Bari ME.: Decompressive craniectomy for infants: a case series of five patients. Childs Nerv Syst 31: 2117– 2122, 2015. [PubMed]
69) Polin RS, Shaffrey ME, Bogaev CA, Tisdale N, Germanson T, Bocchicchio B, Jane JA.: Decompressive bifrontal craniectomy in the treatment of severe refractory posttraumatic cerebral edema. Neurosurgery 41: 84– 92, 1997. [PubMed]
70) Pechmann A, Anastasopoulos C, Korinthenberg R, van Velthoven-Wurster V, Kirschner J.: Decompressive craniectomy after severe traumatic brain injury in children: complications and outcome. Neuropediatrics 46: 5– 12, 2015. [PubMed]
71) Oluigbo CO, Wilkinson CC, Stence NV, Fenton LZ, McNatt SA, Handler MH.: Comparison of outcomes following decompressive craniectomy in children with accidental and nonaccidental blunt cranial trauma. J Neurosurg Pediatr 9: 125– 132, 2012. [PubMed]
72) Liesemer K, Bratton SL, Zebrack CM, Brockmeyer D, Statler KD.: Early post-traumatic seizures in moderate to severe pediatric traumatic brain injury: rates, risk factors, and clinical features. J Neurotrauma 28: 755– 762, 2011. [PubMed]
73) Kurihara M, Shishido A, Yoshihashi M, Fujita H, Kohagizawa T.: Prognosis of posttraumatic epilepsy in children. J Jpn Epilepsy Soc 29: 460– 469, 2012. (Japanese)
74) Kurihara M, Araki H, editors. (Ed.): Pediatric head trauma: From the acute stage to rehabilitation. Ishiyaku Publishers, Tokyo, 2013. (Japanese)
75) Fulkerson DH, White IK, Rees JM, Baumanis MM, Smith JL, Ackerman LL, Boaz JC, Luerssen TG.: Analysis of long-term (median 10.5 years) outcomes in children presenting with traumatic brain injury and an initial Glasgow Coma Scale score of 3 or 4. J Neurosurg Pediatr 16: 410– 419, 2015. [PubMed]
76) Suskauer SJ, Huisman TA.: Neuroimaging in pediatric traumatic brain injury: current and future predictors of functional outcome. Dev Disabil Res Rev 15: 117– 123, 2009. [PMC free article] [PubMed]
77) Farmer JE, Clippard DS, Luehr-Wiemann Y, Wright E, Owings S.: Assessing children with traumatic brain injury during rehabilitation: promoting school and community reentry. J Learn Disabil 29: 532– 548, 1996. [PubMed]

Articles from Neurologia medico-chirurgica are provided here courtesy of Scientific Journal Publishing Dept., Medical Tribune, Inc.