It is likely that the mechanism and consequences of TBI in children differ from those in adults for both primary and secondary injuries. Children have a relatively large head and weak neck musculature, higher brain water content, and lack of myelination (15). Primary injuries related to impact and deceleration and rotational forces can be influenced by these factors. It has been suggested that forces could be more easily transmitted to deeper brain structures as a result of lack of myelination and higher brain water content (15). Primary injury related to mechanical forces includes contusions on the surface of the brain, where the brain can impact against the inner surfaces of the skull (usually focal gray matter injury) and the shearing-type injury that is associated with deceleration and rotational forces (usually diffuse white matter injury or at gray-white interfaces). Primary injury results from mechanical disruption of membranes and axons (16,17).

Secondary injuries occur due to complications or other events after the initial trauma. Potential causes of secondary injury include hypotension, hypoxia, vasospasm, infarction, prolonged seizure activity, and diffuse edema, resulting in increased intracranial pressure and a decrease in cerebral perfusion pressure (16,18). Early management of TBI has a goal of preventing secondary injury. Unfortunately, there are no guidelines concerning cerebral perfusion pressure and intracranial pressure targets for children with TBI. Values are thought to be age-dependent (19).

Contributing to both primary and secondary injury in TBI are cascades of biochemical events. Injury evolves as the cascade is initiated and progresses. Mechanisms initiating these cascades include cellular power failure, acidosis, overstimulation of excitatory neurotransmitter receptors, lipid membrane peroxidation, increase in intracellular calcium, and cellular damage by free radicals (2,16). With increasing knowledge about the biochemical processes involved, researchers are attempting to identify biomarkers in serum and cerebrospinal fluid (CSF) that will assist in diagnosis and prognostication regarding the outcome of TBI (19-22). Likewise, additional information is being sought utilizing magnetic resonance spectroscopy (MRS). In Suskauer and Huisman's review of MRS evidence, H-MRS data obtained shortly after TBI has predictive value for long-term behavioral and cognitive outcomes. Several studies have shown decreases in N-acetyl aspartate (NAA) after TBI and neurometabolite abnormalities also are predictive of overall outcome in pediatric TBI (23). Babikian and colleagues (24) found that NAA on MRS scans acquired 2 to 10 days after TBI correlated moderately to strongly with cognitive testing at 1 to 4 years postinjury. Also, mean NAA/creatinine ratio explained more than 40% of the variance in cognitive scores. They hypothesize that these values might be of assistance in predicting long-term outcome soon after injury when length of unconsciousness is not as yet known.


It is more common for children to experience diffuse cerebral swelling than adults (19,24,25). This could be due to increased diffusion of excitotoxic neurotransmitters through the immature brain, an increased inflammatory response in the developing brain, or increased blood-brain barrier permeability after injury in the immature brain (25). When a lucid interval is noted in children prior to deterioration in neurologic functioning post-TBI, it is likely due to the development of cerebral edema, in contrast to this phenomenon in adults being most commonly related to a focal mass lesion (2,26). This diffuse cerebral swelling is associated with a poor outcome (27). Children may experience impaired cerebral autoregulation after severe TBI (28,29). Cerebral blood flow varies with age, being approximately 24 cm/s in healthy newborns, 97 cm/s in children aged 6 to 9 years, and then decreasing to the adult value of approximately 50 cm/s (28). Some studies have suggested that children with TBI have a lower middle cerebral artery flow rate and therefore hypoperfusion is common (28).

Another phenomenon associated with cerebral swelling is called second impact syndrome, and is said to occur after repeated concussion in children and adolescents. Brain swelling can be severe, even fatal, and develops after seemingly minor head trauma in an athlete who is still symptomatic (though at times subclinically) from a previous concussion (30). Second impact syndrome is a theoretical condition with only a few case reports available. The theory describes an initial injury (the first concussion), which deranges the brain's autoregulatory and metabolic systems enough to produce vascular engorgement and poor brain compliance. This allows marked changes in intracranial pressure with small changes in intracranial volume (30). Second impact syndrome presumes that the brain cells are in a vulnerable state after the initial concussion. Minor changes in cerebral blood flow during the second concussion result in an increase in intracranial pressure and ultimately apnea due to herniation, cerebral ischemia, and brain death (31,32). Also, there have been reports of diffuse cerebral swelling after mild TBI in sports, usually occurring in male adolescents (32).


Nonaccidental TBI is a special subset of TBI in children. It has been described as having a clinical triad of subdural hemorrhage, retinal hemorrhage, and encephalopathy, and is commonly associated with the history given, being incompatible with the severity of the injuries, and the injuries being unwitnessed and inflicted by a solitary care provider (33). Classically, this so-called shaken baby syndrome has been described as being due to shaking alone causing tearing of bridging veins and rotational forces causing diffuse brain injury. More recent studies have indicated that there is most likely an impact in addition to the shaking episode(s). Often, nonaccidental brain injury in young children is also accompanied by a delay in seeking medical attention, potentially resulting in a hypoxic component to the mechanism of injury (18,21,33).


One must consider the effect of normal developmental activities of the immature brain on the mechanisms of developing damage after TBI. Apoptotic death of neurons is a part of plasticity and normal brain development. Does this result in the developing brain being more susceptible to activating the apoptotic cascade than the adult brain (15,25,34)? If so, this could help to explain the poorer prognosis for functional outcome for those injured at a very young age (34). In one animal study of post-trauma apoptosis, for a specific developmental age, the areas that had the highest density of programmed cell death were also noted to have high numbers of apoptotic cells in general (15). It may also be possible that excitatory neurotransmitter release could result in excessive stimulation of some pathways and stimulate the development of abnormal connections or that decreased excitatory activity could decrease connections (34). This implies that the relatively high plasticity of the developing brain could actually have a negative impact on the overall outcome after diffuse TBI and be at least partially responsible for the poorer outcomes seen in those injured at a very young age.

In a discussion of plasticity after early brain insult, Anderson and colleagues (35) conclude that neither plasticity nor vulnerability theories explain the range of functional outcomes seen and that multiple factors including the extent and severity of injury, age, and environmental influences such as family, sociodemographic factors, and interventions influence outcome as well. Evaluation at too young an age will prevent the identification of problems such as executive dysfunction as those skills do not emerge until later in life, supporting the need for long-term follow-up in children with TBI.


A rare complication of skull fracture in children is a growing skull fracture. It is reported to occur when a linear skull fracture in a child under age 3 is accompanied by a durai tear and a leptomeningeal cyst develops. Fluid pulsations result in bone erosion and a palpable skull defect that requires surgical repair (36-38). A series of eight children with growing skull fractures had MRI evidence of a zone of signal intensity similar to brain contusion or CSF through the margins of the fracture, leading to the conclusion that MRI can be useful in diagnosing growing skull fracture early after injury (38).

< Prev   CONTENTS   Next >