The Centers for Disease Control and Prevention (CDC) estimates that at least 2.4 million people sustained a traumatic brain injury (TBI) in 2009.1 However, the actual number of TBI cases is uncertain as many patients either receive care in the field or do not seek medical attention at all because approximately three-quarters of TBI are mild or concussions.2
The causes of TBI in all age groups combined are falls (35.2%), motor vehicle accident (17.3%), being struck by or running into an object (16.5%), assault (10%), and other or unknown causes (21%).3 Among all age groups, males have higher incidences of TBI and on average present with TBI about 1.4 times more frequently than females. The CDC identified three age groups—children (0–4 years), adolescents (15–19 years), and adults (65 years and older)—as most likely to sustain TBI.3 Children aged 0–4 years had the highest rate of TBI-related emergency department visits (1,256 per 100,000 population). However, the elderly (75 and older) had highest hospitalization (339 per 100,000 population) and death (57 per 100,000 population).3 TBI-related death rates have substantially declined in the past 30 years, and this can mostly be attributed to primary prevention. Motor vehicle–related TBI deaths declined 22% and firearm-related TBI deaths declined 14% between 1989 and 1998,4 but declines in death rates since that time have been more modest.5
The economic costs of TBI in 2010 was estimated at $76.5 billion, $11.5 billion from direct medical costs and the remaining $64.8 billion from indirect costs (e.g., lost wages, productivity). These data do not include the more than 31,000 military personnel who were seen in the Veterans Administration for TBI-related medical issues in 2010.6 An estimated 5.3 million Americans are living in with TBI-related physical, cognitive, or psychological impairments.7
An appreciation for the pathophysiologic mechanisms at work after TBI is important for the development and implementation of effective clinical therapeutic strategies. The injury due to TBI can be understood in terms of primary and secondary insults to neural tissue. Primary injury denotes the initial mechanical damage secondary to energy transmission during impact, whereas secondary injury results from the destructive tissue-intrinsic and body systemic response to primary injury. Primary injuries cannot be altered after the fact but can be reduced using primary prevention (seatbelts, helmets, etc.) and are the target of public health intervention.
Secondary injury includes edema and inflammation from the primary insult and the insults thereafter. Secondary injury can be caused by alterations in perfusion such as ischemia, hyperemia, or vasospasm, as well as by expanding hemorrhage, hypoxia, hypotension, seizures, and metabolic derangements such as hyper-/hypoglycemia and hyponatremia. Detailed accounts of the molecular and cellular mechanisms of TBI have been proposed.8–10 The foundation of TBI care is based in prevention and modification of secondary injury.11