Definition

Traumatic brain injury (TBI) is an insult to the brain from an external physical force and resulting in temporary or permanent impairment, functional disability, or psychosocial maladjustment. TBI occurs twice as frequently in males as in females. The incidence of TBI peaks among those 15 to 24 years old and again among those 75 years and older [1]. TBI usually is a consequence of motor vehicle accidents, falls, violence, and sports. Motor vehicle accidents and violence are more common in a younger population, and falls are more common in aging populations [2,3]. Recent trends have shown that TBI due to motor vehicle accidents is decreasing because of better traffic safety enforcement, whereas the percentage of TBI due to violence has increased, reported to be 7% to 10% [3]. These trends have consequences for the type of brain damage seen; contusion injury tends to be associated with falls, and diffuse injuries are more often seen in high-velocity traffic accidents [2].

In the United States, an average of 1.4 million TBIs occur each year, including 1.1 million emergency department visits, 235,000 hospitalizations, and 50,000 deaths [1,2,4,5]. The financial burden of TBI has been estimated at more than U.S. $60 billion per year [2]. However, routinely reported U.S. national data underestimate the true burden of TBI for several reasons. First, they do not include persons treated for TBI in other settings, including outpatient settings and physicians’ offices. Second, patients seen in military facilities both in the United States and abroad are not recorded. Finally, the number of those who receive medical care but for whom the TBI is not diagnosed or who sustain a TBI and do not seek care is not known [4,5].

The pathophysiologic process of brain injury is usually divided into primary injury, which is the injury to the brain that results at the time of the insult, and secondary injury, which can be thought of as the summation of the biochemical or physiologic damage that develops during a period of hours, days, weeks, and perhaps months after the primary injury. The primary injury is sustained from external forces as a result of direct impact, rapid velocity changes, penetrating injuries, or blast injuries. The resulting injuries include contusion, hematomas, and diffuse axonal injuries. These are often associated with superimposed hypoxic or ischemic injury, often as a result of systemic insult. In patients with mild TBI, there is often a disruption of the sodium channels on axons, which can result in a transient disruption in function and, with it, an increased state of vulnerability to additional trauma [6]. Secondary insults include intracranial hemorrhage, swelling, hypoxia, brain shift, herniation, and numerous neurochemical and cellular events [2]. Although many of the mechanisms of secondary TBI have yet to be elucidated, it is thought that the processes include neurotransmitter release, free radical generation, calcium-mediated damage, inflammatory responses, and mitochondrial dysfunction [2,7].

Symptoms

Symptoms may vary according to the severity of the injury and the stage of recovery. The patient’s history should include a detailed summary of the mechanism of injury, comorbid conditions, initial Glasgow Coma Scale score (Table 162.1), length of the coma (if any), and length of post-traumatic amnesia. Glasgow Coma Scale scores, however, can be obscured by confounders such as concurrent spinal cord injury, sedation, intubation, or other related injuries. Extracranial injuries (such as extremity fractures, thoracic or abdominal traumas), which have been reported to occur in about 35% of the cases, are associated with a higher incidence of secondary brain injuries [2,8].

Patients with severe injury and dramatically altered levels of arousal often can offer no subjective symptoms. After the acute phase of recovery, the clinician can expect symptoms to include seizures, contractures, spasticity, altered vision, vertigo or dizziness, and altered sense of smell. These may be the result of cranial nerve injuries or of central processing dysfunction. Symptoms of dysautonomia may still be seen at outpatient follow-up and may be characterized by increased body temperatures, tachycardia, tachypnea, increased posturing or tone, and profuse sweating [9]. Common late symptoms may include memory deficits, higher level executive dysfunction, headaches, difficulty with sleep-wake cycles, labile mood, depression, apathy, difficulty with attention, social disinhibition, sexual dysfunction, anxiety, impulsivity, fatigue, and difficulties with fine and gross motor control [10].

Physical Examination

A thorough neurologic examination, including a neuropsychological evaluation, is important to assess the consequences of a brain injury. The neurologic examination evaluates mental status, cranial nerve function, vision, hearing, deep tendon reflexes, and abnormal reflexes. The examination should also evaluate muscle strength, tone, and coordination and assess gait or mobility in a wheelchair. It is important to create a thorough neuropsychological profile with the assistance of a neuropsychologist. This should be done to determine both physical abilities and the cognitive and emotional issues that will affect the patient’s function. Cervical injury can be associated with TBI, especially in patients with a Glasgow Coma Scale score below 8 [11,12]. This must be recognized early to accurately assess injury severity and to determine treatment course.

Patients may have difficulty with mobility and self-care as a result of isolated motor weakness or coordination of either the upper or the lower extremities. Safe mobility may also be impeded by poor cognition, including deficits with planning and poor impulse control.

Behavior

Individuals often experience subtle or dramatic personality changes that alter relationships with others. These may include problems with the initiation of responses, verbal or physical aggression, altered emotional control, social disinhibition, depression, apathy, decreased sense of self-worth, and altered sexual function.

Social

Patients often are unable to return to work at their previous level of function. As a consequence, they may suffer significant economic strain and may have difficulty with their relationships, including their marriage. Studies have failed, however, to consistently show a significantly higher rate of divorce among those married at the time of injury [13]. Family members may be helpful in identifying issues of social isolation, depression, and anger.

Diagnostic Studies

Initial diagnostic studies can provide clues to the severity of the injury and will have prognostic implications. The IMPACT study suggests that in moderate to severe TBI, age, Glasgow Coma Scale motor scores, pupillary response, computed tomography characteristics, and the presence of subarachnoid hemorrhages are the most powerful independent prognostic factors for patient outcome. Other prognostic factors include hypotension, hypoxia, eye and verbal components of the Glasgow Coma Scale, glucose level, platelet number, and hemoglobin concentration [14].

Imaging Studies

The initial computed tomography scan has been shown to be useful as an outcome predictor with use of the Traumatic Coma Data Bank classification or the Rotterdam computed tomography score [15]. Previous studies and guidelines have recommended computed tomography scans for all TBI patients with a Glasgow Coma Scale score of 14 and of 15 in the presence of risk factors, such as emesis, advanced age, duration of amnesia, injury mechanism, neurologic deficits, or anticoagulation (Table 162.2) [2,15–17]. More sophisticated testing has been introduced, including single-photon emission computed tomography, functional magnetic resonance imaging, and positron emission tomography, but for the most part, these are of little use in assessing the functional limitations caused by the injury. In patients with otherwise normal findings on neuroimaging, diffusion tensor imaging is emerging as a potential diagnostic tool for mild brain injury as it can detect white matter microstructure changes (Fig. 162.1) [18,19]. Despite the potential of new imaging techniques, TBI remains primarily a clinical diagnosis [20,21].