Shear strain occurs when two layers slide on each other, moving in parallel in opposite directions (16). The injury from shearing or tearing is responsible for most lesions, especially in an infant or a young child, whose skull is more easily deformed than an adult’s. Deformation
absorbs much of the energy of impact, reducing the adverse effects of acceleration and deceleration but adding to the risk of tearing of blood vessels. Because of its elasticity and ability to undergo a greater degree of deformation, the skull of an infant absorbs the energy of the physical impact and protects the brain better than the skull of an older person.

The relationship between stress waves and deformity depends mainly on the momentum of the head and of the object at the instant of impact. In a child with intact reflexes, a free fall probably causes more injury to the brain than an aimed object striking the head with even greater speed. Approximately 70% of shear-strain deformation skull fractures are linear and single; the rest are depressed fractures. The faster moving the object delivering the blow, the more likely it is that a depressed fracture will result; a lower-velocity impact with the same momentum tends to produce deformity and linear fracture, sometimes distant from the point of impact but at a weak part of the cranial vault where distortion can occur. In addition, the size of the object that strikes the skull is important. Objects smaller than 5 cm² tend to produce a depressed fracture; larger objects tend to produce a linear fracture (16). A linear fracture is usually not important in management of the child because outcome of the injury and its complications are determined by damage to the intracranial contents at the moment of impact; an injury can be fatal in the absence of a fracture.

In an acceleration injury, in which the momentary compression is greatest, the effects of compression-rarefaction strains are usually maximal at the point of impact; at the same time, an area of low pressure or rarefaction occurs contralaterally, the site of the familiar contrecoup injury (13,14), Thus, a blow to the occiput can result in the major damage in the frontal and temporal regions. Contrecoup injuries generally occur on the undersurface and poles of the frontal and temporal lobes (16). They are relatively rare in infants and young children, presumably because skull distortion rather than pressure waves predominate (19). Contrecoup injuries are most likely to occur when the impact is to the occiput or to the side of the head (16). Distortion of the brainstem is particularly likely in deceleration injuries such as those that occur in falls; any resulting loss of function in this area is liable to have serious or fatal consequences.

Magnetic resonance imaging (MRI) has allowed a better understanding of the lesions that can result from head injury. These were grouped into primary and secondary lesions by Gentry and coworkers (20) (Table 9.2). The injuries expected from various accident mechanisms are depicted in Table 9.3.

The term diffuse axonal injury (DAI) refers to a clinical-pathologic-radiologic entity that clinically manifests itself by loss or impairment of consciousness.

The lesion usually is not the result of a fall, except when the fall occurs from a considerable height. Instead, it results from severe angular acceleration-deceleration forces (21) and is believed to induce coma through disconnection of the cortex from the lower centers. It is responsible for severe, irreversible, and potentially fatal brain damage occurring at the moment of injury. DAI is frequently unaccompanied by skull fracture, increased intracranial pressure, or cerebral contusion (21).

As viewed microscopically, the hallmark of DAI is the presence of axonal retraction balls identified by silver stains or, as in more recent studies, immunohistochemical staining for beta-amyloid precursor protein (16,22). Postmortem examinations have demonstrated axonal lesions in the inferior portion of the corpus callosum and the dorsolateral quadrant of the rostral brainstem, notably in the region of the superior cerebellar peduncles, and throughout the cerebral hemisphere and cerebellum (23,24,25). Damage to the superior cerebellar peduncles, which are particularly vulnerable to rotational injuries, is responsible for the ataxia commonly observed after major head injuries (26).

The microscopic picture of axonal lesions was first described by Strich (27), who proposed that the shearing forces sustained during injury cause stretching of axons, which might be sufficient to prevent them from functioning. The more subtle changes that precede this final state have been studied in animals by electron microscopy and through the use of immunocytochemical labeling techniques. Although the exact time course for humans has not been determined, in animals an alteration in the structure of the nodes of Ranvier occurs within 15 minutes of the injury (28). This is followed some 12 to 24 hours later by an interruption of antegrade and retrograde axonal transport, the loss of microtubules, and the gradual development of axonal swelling. When axonal swelling exceeds a certain critical level, effective transection of the axon occurs, although without evident tearing or damage to adjacent blood vessels. DAI is frequently accompanied by evidence of neuronal injury (29).

It is unclear how mechanical forces induce the instantaneous perturbation of the cell membrane that in turn initiates these axonal changes. Wolf and coworkers proposed that traumatic deformation of axons induces abnormal sodium influx through mechanically sensitive Na⁺ channels. This influx subsequently triggers an increase in intraaxonal calcium through the opening of the voltage-gated calcium channel (30). This can result in activation of calmodulin and an increase of extracellular potassium at the damaged node (31). Intracellular calcium, in turn, increases the activity of proteolytic enzymes that disrupt axonal cytoarchitecture. Over time, the swollen axons either degenerate or undergo regenerative changes, as shown by sprouting and growth cones (32).

On MRI, axonal damage is best visualized by diffusion tensor imaging (DTI) or high-spatial-resolution susceptibility-weighted imaging techniques (33,34). By these techniques diffuse axonal injury appears as small, oval, focal abnormalities in white matter tracts, usually adjacent to cortical gray matter, but sometimes in the splenium of the corpus callosum (20). Proton magnetic resonance spectroscopy can provide further information on the extent of axonal injury. A lowered ratio of N-acetylaspartate (NAA) to creatine is believed to be indicative of axonal injury, but there does not appear to be any elevation of tissue lactate (35).

The second-most-common type of brain injury visualized by MRI of patients with severe head trauma is cortical contusions, which tend to be multiple and represent bruises on the surface of the brain. As verified by both imaging and pathologic studies, points of predilection for contusions are the crests of gyri on the orbital surfaces of the frontal lobes and the inferolateral aspect of the temporal lobes. Contusions consist mainly of petechial hemorrhages in the superficial cortical layers occurring at the site of impact (coup injuries) or at contrecoup areas (Fig. 9.1). Impact on the forehead or vertex can send the initial pressure wave caudally, leading to downward displacement of the brain toward and into the tentorial opening. This
displacement can result in contusions of the hippocampal gyrus, particularly the uncus, the basal ganglia, and the upper part of the brainstem (36). The severity of brain damage caused by contusion depends on the extent of vascular injury. Damage tends to be less common in infants and small children than in older children or adults subjected to comparable trauma. Instead, contusions in infants consist of slitlike tears in the cerebral white matter of the frontal and temporal lobes (16,37). One of the major clinical issues in the management of contusions is their tendency to increase in size, coalesce, or cause a mass effect, especially after the first day following injury. Therefore, a follow-up imaging study is often useful.

Cerebral lacerations are usually the result of damage from penetrating wounds or depressed skull fractures, but they can occur without fracture in small children, whose skulls tend to become more grossly distorted at the moment of injury. Lacerations frequently involve the frontal and temporal poles and are associated primarily with tears of the dura and tears or other injuries of the major vessels and secondarily with thromboses, hemorrhages, or focal cerebral ischemia. Tears in the white matter are seen commonly in infants after blunt trauma even without fracture (38) (Fig. 9.2). They result from the soft consistency of the poorly myelinated cerebrum and from the pliancy of the immature skull.

MRI has demonstrated that macroscopic traumatic injuries to subcortical structures such as the thalamus and to the brainstem are rare. Instead, the pathologic change that results in the clinical picture generally attributed to primary brainstem damage is diffuse axonal injury.

The physical processes within the skull caused by trauma induce numerous changes within the brain. The most common is concussion. Although there is some disagreement with respect to the definition of concussion, the American Academy of Neurology defines it as a trauma-induced alteration in mental status with or without loss of consciousness (39). In addition, there also can be post-traumatic amnesia for the moment of injury and for a variable period before it (retrograde amnesia).

The pathogenesis of concussion is under debate. From a structural viewpoint, concussion is believed to result from minor degrees of diffuse axonal injury. With more severe concussive injuries, there is a massive release of excitatory neurotransmitters, notably glutamate (40). As a result, there is a synchronized depolarization of neuronal membranes with subsequent increase of extracellular potassium (41), resulting in a functional deafferentation of the cortex (42). Compounding the disruption of ionic homeostasis is an imbalance between energy demands and supply, a loss of cerebral autoregulation in a significant proportion of patients with minor head injuries (43),
the presence of vasospasm, and a global increase in intracranial pressure, which reduce the supply of substrates to the tissue.

From a clinical point of view, concussion is marked by the immediate loss of consciousness, a suppression of reflexes, a transient arrest in respiration, accompanied by bradycardia and a fall in blood pressure. Vital signs quickly stabilize, and there is a gradual return of consciousness. However, neuropsychologic testing will show deficits for as long as 15 minutes after the injury. With increasing injury, the loss of consciousness is prolonged and there is an increasing duration of post-traumatic amnesia (44). The clinical features of postconcussion syndrome are covered in another part of this chapter.

Secondary effects of trauma develop as a consequence of at least five factors: cerebrovascular dysregulation, excitotoxicity, free radical formation leading to oxidative stress, energy failure, and inflammation (Fig. 9.3; Table 9.4) (45). Cerebrovascular dysregulation, excitotoxicity, and energy failure are of primary importance in the evolution of cerebral swelling. This condition has been defined as an
increase in volume caused by an increase in brain water and sodium content. Brain swelling results from increased cerebral blood volume, cerebral edema, or a combination of the two (45).

Fishman distinguished three major categories of cerebral edema: vasogenic edema, cytotoxic or cellular edema, and interstitial edema (46). Vasogenic edema is characterized by increased permeability of brain capillary endothelial cells. This results from defects in the tight endothelial cell junctions and an increased number of pinocytic vesicles, which are responsible for the transport of macromolecules across the blood–brain barrier. Vasogenic edema fluid is extracellular and accumulates primarily in white matter because resistance to fluid flow is less in white matter than in gray matter. It occurs around brain tumors, notably glioblastomas and metastatic tumors, after cerebral infarction, and in lead encephalopathy. Cytotoxic edema is marked by swelling of all cellular elements of the brain with reduction in the volume of extracellular fluid. This last form of edema is characteristic of energy depletion such as occurs during the initial stages of cerebral hypoxia. Fishman postulated a third form of brain edema in which there is an increase in water and sodium content of periventricular white matter (46). This condition is seen in obstructive hydrocephalus.

In brain trauma, the prominence of astrocytic swelling, the integrity of the interepithelial tight junctions, and the relative paucity of protein-rich fluid suggest that edema is mainly cytotoxic (47), although massive swelling of perivascular astrocytic foot processes can compress the microvasculature and reduce tissue perfusion, inducing secondary vasogenic edema.

The importance of cytotoxic edema has been confirmed by diffusion-weighted MRI performed on experimental animals. These studies demonstrate that immediately after injury, there is predominantly vasogenic edema, which, over the next few hours to days, becomes superseded and overshadowed by cytotoxic edema (48).

A number of biochemical changes follow severe traumatic head injury (Fig. 9.3, Table 9.4). In both clinical and experimental settings, good correlation exists between the severity of traumatic brain injury and the amount of neuroexcitatory amino acids, such as glutamate and aspartate, that are released (40,49). As a result, neuronal membranes depolarize with subsequent increase of extracellular potassium (42). This is accompanied by the entry of calcium into nerve terminals and is followed by further glutamate release and potassium flux. At the same time, arachidonic acid is released, which in turn induces a cascade of reactions with the ultimate formation of free radicals (50). These changes are accompanied by increased energy demands as brain cells attempt to reinstate normal ionic membrane balance (51). With an increase in energy consumption there is a rapid decrease in adenosine triphosphate (ATP) and an increase in lactic acid (52). These biochemical alterations, which suggest impaired mitochondrial function, are confirmed by the electron microscopic observations of swollen neuronal mitochondria and an increased permeability of the organelles’ outer membranes (53). These factors all contribute to astrocytic swelling, as does an energy shortage–induced failure of the sodium pump (54). In addition, there is a local inflammatory response with complement and microglial activation and an increased release into cerebrospinal fluid (CSF) of a variety of cytokines (interleukin-1, interleukin-6, and interleukin-10) (56). These substances also contribute to the evolution of diffuse cerebral edema. The role of a trauma-induced upregulation of aquaporins, a family of transmembrane proteins that selectively allow the passage of water through the plasma membrane, in the formation of brain edema has not been fully clarified (56a).

The effects of traumatic brain injury on cerebral blood flow are critical to the development of cerebral edema. Early after severe traumatic brain injury, marked hypoperfusion develops with reduction in oxygen delivery and cerebral ischemia (57). Some 24 hours later cerebral blood flow increases, and there is uncoupling of cerebral blood flow and oxidative cerebral metabolism (1). Post-traumatic hyperemia is more common in infants and children than in adults and is probably the consequence of a loss of cerebral autoregulation (45). Hyperemia in turn contributes to massive brain swelling, which is not uncommon in infants and young children and has been termed malignant brain edema (58).

Anatomically, cerebral edema involves principally the subcortical white matter and the centrum semiovale. Less often, cerebral edema surrounds an area of contusion or an intracerebral hematoma. Brain swelling also can occur in response to the evacuation of a large extracerebral clot or after other major intracranial surgery (59).

When the additive effects of injury and brain swelling are severe, a self-perpetuating sequence develops, which can lead to further increases of intracranial pressure, with collapse of cerebral venules. This collapse in turn reduces cerebral perfusion and causes tissue hypoxia. This leads to further cerebral edema (60). A loss of selective permeability of cell membranes results, with increased loss of fluid from the vascular compartment into the parenchyma, thereby increasing cerebral swelling. Recovery has not been seen when intracranial pressure equals or exceeds mean systemic arterial pressure, at which point cerebral perfusion ceases.

Numerous changes occur secondary to cerebral edema. Herniation of the uncus over the tentorial edge compresses the midbrain and often occludes the posterior cerebral arteries. Edema and infarction of the occipital poles can occur, contributing further to supratentorial pressure and thus to herniation. Petechial hemorrhages develop in the midbrain and pons, with infarctions in the areas of the basal ganglia supplied by the anterior choroidal artery. A decrease in blood pressure, commonly seen with a severe injury, potentiates the vicious circle.

More than 90% of major pediatric head injuries are nonpenetrating and closed (i.e., no scalp wound exists). The clinical picture is highlighted by alterations in consciousness (14). As is the case for head injuries at all ages, boys are involved three times more often than girls.

Child abuse is the most common cause of head injury in infants younger than 2 years of age. In the experience of Duhaime and coworkers, in 24% of infants admitted to hospital with head injuries the injuries were presumed to have been inflicted, and in another 32% the injuries were suspicious for child abuse (68). Although the term “shaken baby” has been used in the past, pathologic data collected on a larger Scottish series has made it clear that a whiplash shaking injury could be documented in only 6% of cases (69). The hyperextension and hyperflexion whiplashing forces injure the brainstem or upper cervical spinal cord with consequent acute respiratory failure, hypoxia, and brain swelling. Subdural bleeding was generally trivial. These pathologic findings are commensurate with the clinical presentation of collapse or respiratory arrest (70). Shannon and Becker also stressed the frequency of brainstem and spinal cord injuries in infantile child abuse (71).

The more commonly encountered clinical picture is characterized by depressed consciousness, increased intracranial pressure, seizures, and subdural and retinal hemorrhages. These symptoms are frequently accompanied by other nonaccidental injuries and an inconsistent or unreliable medical history. This constellation of symptoms has been termed the shaken impact syndrome. The encephalopathy developed acutely in 53% of the Scottish cases, subacutely in 19%, and chronically in 22% (69). The less acute the presentation, the better is the outcome with respect to long-term morbidity. In the series of Bechtel and coworkers, the clinical picture of nonaccidental head injury could be distinguished from that seen in accidental head injury by more frequent bilateral retinal hemorrhages, a greater likelihood of presenting with an altered mental state and seizures, and a lesser incidence of scalp hematomas (71a).

Pathologic examination of the brain of infants subjected to nonaccidental head injury disclosed skull fractures in 36%, acute subdural bleeding in 72%, and retinal hemorrhages in 71% (70). Severe hypoxic brain damage was present in 77%, and the usual cause of death, seen in 82%, was increased intracranial pressure. Eighty-five percent of the children had signs of impact to the head at autopsy, and 51% had significant extracranial injuries (70). The clinical presentation of infants who showed no signs of impact was of collapse or respiratory arrest; the pathologic picture did not differ from the majority of infants who showed evidence of impact (72).

There is considerable uncertainty as to the mechanism of brain damage in shaken impact syndrome, and according to Donohoe there is inadequate scientific evidence to come to a firm conclusion on most aspects of causation (73). Geddes and Plunkett (74) shared this skepticism and stressed that although most infants do indeed show signs of inflicted violence, serious injury or death from a low-level fall is possible, and contrary to Harding and coworkers, who believed that retinal hemorrhages result from rotational acceleration and deceleration forces (75), they doubted that shaking can induce the characteristic retinal hemorrhages.

The combination of a subdural hematoma and retinal hemorrhages can also result from a variety of bleeding disorders. It is also encountered in Menkes disease and in type 1 glutaric aciduria (see Chapter 1) (76).

A recommended sequence consists of the following four steps: a rapid initial evaluation, resuscitation, a more extensive secondary evaluation including radiologic assessment, and definitive treatment (1,45,76a). In many instances of major closed head injury, diagnosis of the injury is performed in parallel with emergency treatment.

Because in children the clinical condition can change rapidly and frequently, a high degree of alertness and preparedness is required of both medical and nursing attendants.

The American Academy of Pediatrics issued guides for the management of minor head treauma in children older than age 2 years (120) and younger than age 2 years (121). These are summarized in Table 9.8. Considerable judgment is
required to avoid unnecessary hospitalization and expensive diagnostic studies, at the same time keeping in mind the possibility of post-traumatic complications that require emergency surgery. In general, children who have experienced only a momentary loss of consciousness are better managed at home. Parents are instructed to note at regular intervals the child’s state of alertness and ability to move his or her extremities. The parents should be told to contact the physician if diminished consciousness or limb weakness occurs.

The role of routine CT in the management of the child with minor head injuries continues to be controversial. As indicated in Tables 9.7 and 9.8, the infant younger than 2 years of age or the child who sustains loss of consciousness should undergo CT. The younger the child, the lower the threshold should be for imaging studies. In the small infant the incidence of significant intracranial injuries is greater, and there is a higher likelihood of asymptomatic intracranial injuries (121). The cost-effectiveness of CT as a screening for safe discharge as compared with hospitalization for observation has been affirmed in a number of centers both in the United States and Europe (122,123,124). These studies have not addressed the costs of follow-up visits for false-positive imaging studies or the costs of return visits and subsequent hospitalization for a youngster who is handled with observation only (120). The use of skull radiography as a screening device for children with minor head injuries has serious limitations and should no longer be used inasmuch as a CT with bone windows to show the presence of fractures is superior diagnostically (122). According to some authorities, the presence of a linear skull fracture should not influence the decision about whether to send the child home; others suggest that a child found to have a skull fracture is at increased risk for an extradural hematoma and therefore should be observed in the hospital (125). We believe that whenever the fracture line crosses the groove of the middle meningeal artery or crosses the path of the sagittal or other major venous sinus, the possibility of an extradural hemorrhage is increased, so that the child should be hospitalized for the initial 24 hours. If the fracture involves an air sinus, checking for the next 10 days for signs of intracranial infection is recommended even if the child is not hospitalized.

The rehabilitation of a child with a major head injury is summarized in Table 9.9. A more detailed discussion is presented in a book edited by Ylvisaker (126).

There has been continuing improvement in terms of mortality and ultimate neurologic status in the outcome of severely brain-injured infants and children as defined by a postresuscitation Glasgow coma score of 8 or less (127). The outlook for full intellectual function in children experiencing minor head injuries (i.e., head injuries without associated neurologic manifestations) is generally excellent (128). The prognosis for major head injuries, although less certain, is far better in children than in infants or adults. As a rule, prediction of outcome with respect to the severity of ultimate disability is accurate in only 70% by the end of the first week after the injury (129). In the experience of the Traumatic Coma Data Bank, children younger than age 4 years who have sustained a severe head injury have a cumulative mortality of 62% during the first year after their injury. This compares with a mortality during the same period of 22% in children aged 5 to 10 years and 48% in adults (130). In this series, only 1 in 5 infants had a favorable outcome. These figures, published in 1992, should be contrasted with a mortality of 10% in a cohort gathered in the years 1994 to 1996 (127). A low postresuscitation Glasgow coma score and the presence of cerebral swelling, particularly when it is accompanied by a shift of midline structures, are indices for a poor outcome. These indices have not changed in the last few decades. The poor outcome in infants in all series probably reflects the higher incidence of child abuse and multiple injuries during the first year of life. Keenan and colleagues, working in North Carolina, found that 53% of serious or fatal head injuries incurred by infants younger than 2 years of age were caused by child abuse (131).

In a series of children treated for major head injuries at the Johns Hopkins Hospital and reported in 1983, 29% were normal on follow-up and 53% had returned to school with mild behavioral or cognitive problems. In the latter group, however, 61% had shown evidence of significant language delay, minimal cerebral dysfunction, and learning problems before the accident (132). The outcome tended to be worse in children who sustained prolonged coma. When outcome is stratified according to age, all studies show that morbidity as well as mortality are greater when the injury is experienced in infancy or in early childhood.

Generally, children with only behavioral abnormalities during the early post-traumatic period later achieve normal functioning. No significant improvement in cognitive function can be expected after the first 6 to 12 months after injury. Improvement in speech and motor function, however, can continue for several years (133,134). Decerebrate rigidity during the early postinjury phase, although associated with an early mortality in 25% to 50% of patients, by itself does not preclude functional survival; approximately one-half of survivors have a fairly good quality of life (134). Excessive daytime sleepiness is fairly common after head trauma, especially in adolescents. In some of these, notably when there has been an associated whiplash injury, sleep apnea is responsible; in others, the condition resembles narcolepsy (see Chapter 15) (135). In the experience of Guilleminault and coworkers, daytime sleepiness
can persist for months to years, and its duration correlates with the severity of the initial head trauma (135). Methylphenidate or amphetamine appear to be the most effective medications. A significant postural and intention tremor affecting primarily the upper extremities has been observed in a substantial number of children recovering from a serious head injury. In the series of Johnson and Hall, the tremor appeared within 2 months of the injury in 49% of their patients and between 2 and 12 months of the injury in 40%. It subsided spontaneously in 54% (136). Hyperekplexia and myoclonic twitches have also been seen (137). The cause of this complication is not clear, but based on radiouptake studies, it probably reflects striatal dopaminergic denervation (138).

A substantial proportion of survivors from major head injuries experience subsequent emotional and psychiatric disorders. These are covered in another section of this chapter.

The immature and more flexible skull of the child can sustain a greater degree of deformation than that of an adult. Most skull fractures are linear and asymptomatic and, in the older child, are readily diagnosed by CT using bone windows. In infants, fractures tend to be irregular, so that on plain skull films they are sometimes confused with a suture or wormian bone (Fig. 9.5). In early childhood the fracture can be diastatic and usually involves the lambdoid suture. The separation of the bones indicates that the intracranial pressure increased at the moment of impact.

Often a subperiosteal or subgaleal hematoma, termed cephalhematoma, in the newborn infant accompanies a linear skull fracture. Palpation of the hematoma may falsely lead the examiner to think a depressed skull fracture exists. Imaging studies disclose the underlying linear fracture. A small number of these hematomas calcify (see Fig. 6.1). There rarely is an indication for aspiration of a traumatic hematoma, and insertion of a needle or drain only increases the risk of introducing an infection into the hematoma cavity (see Chapter 6 for further discussion of this complication).

Closed linear fractures generally heal in 3 to 4 months and, except for breaks crossing the path of major vessels or entering the paranasal sinuses, do not require special therapy or observations.

An infrequent complication of a closed head injury with a linear fracture in an infant is the diastatic or growing fracture (139). It occurs in less than 1% of all fractures and usually represents a complication of a serious head injury (140). It occurs when the fracture tears the dura causing the arachnoid to be trapped in the fracture (16). Rare after age 3 years, it is thought to be more common in victims of child abuse, but its appearance is not confined to victims of nonaccidental trauma (140). Dural tears responsible for a growing fracture occur mostly in the parietal area; their presence, unrecognized because the scalp is intact, leads to the development of a CSF-filled cyst between the cortex and the overlying bone. At the same time, the bone edges along the fracture do not unite, apparently prevented by their direct contact with fluid. The bone is resorbed, so that plain skull radiography or CT scans taken after an interval of several months show an irregular bone defect with scalloped edges that is an elliptical erosive cranial defect (139).