Children with concussion without subsequent neurologic deficits have a favorable long-term prognosis, and late sequelae are rare. Children with moderate contusions usually make good recoveries even when neurologic signs persist for weeks. Longterm sequelae may include poor memory, slowing of motor skills, generalized decrease in cognitive skills, behavioral alterations, or attention deficits. Language function, especially in a young child, frequently makes a good recovery. Rehabilitation programs with physical therapy, behavioral management, and appropriate education may be necessary. Poor prognostic signs include a Glasgow Coma Scale score of less than 4 on admission without improvement in 24 hours, absent pupillary light reflexes, and persistent extensor plantar reflexes.
Children with cerebral contusion who survive acute cerebral swelling may improve gradually or may remain vegetative. Extracranial trauma also contributes to the morbidity of these patients (aspiration pneumonia, acute respiratory distress syndrome, sepsis, emboli). Maximal recovery may take weeks or months. Coma lasting for weeks after head trauma may be compatible with a good outcome, although the risk of late sequelae is significant. Patients who remain in a vegetative state for months after head injury are unlikely to improve.
When the cranial sutures are fused, the skull becomes a rigid container enclosing a fixed volume, including the brain (80% to 85%), CSF (10% to 15%), and blood (5% to 10%). The exponential relationship between the volume within a closed container and pressure results in a massive increase in ICP as intracranial volume increases. The brain accommodates increased ICP initially by expelling CSF and blood from the intracranial compartment into the spinal subarachnoid space. When the limits of this accommodation are reached, the brain itself begins to shift in response to the continuing elevation of ICP. Brain shifts may cause herniations across the dural extensions or skull barriers (see Table 184-2).
The causes of increased ICP include mass lesion, hydrocephalus, cerebral edema due to trauma or infection and idiopathic intracranial hypertension (Tables 184-5, 184-6).
Mass lesions (brain tumor, abscess, hemorrhage) may produce increased ICP not only by virtue of large size, but by blockage of CSF pathways, blockage of venous outflow, or production of vasogenic cerebral edema. Brain abscesses usually present as mass lesions, producing focal neurologic signs and increased ICP. Symptoms of infection, including fever, malaise, anorexia, and stiff neck, may be subtle or absent. Brain edema around an abscess is usually severe and extends into the surrounding white matter. Children with chronic cardiac or pulmonary disease may embolize infected material to their brains, predisposing them to brain abscesses. Brain tumors in children are most often located in the posterior fossa and can result in elevated ICP due to obstruction of CSF flow through the cerebral aqueduct and fourth ventricle.