Proper education and safety regarding high-risk behaviors can limit the incidence of TBI. By identifying populations and persons at high risk for TBI, appropriate prevention measures can be instituted. Most experts on the prevention of TBI recommend utilizing protective gear such as seatbelts while in motor vehicles, and helmets while bicycling or riding motorcycles. Participants and coaches for high-impact sports are urged to exercise caution and judgment (Cassidy et al. 2004). Alcohol has also been noted to play a role in increasing risk of TBI, and education about its use and abuse may also be helpful in the prevention of TBI.

The various definitions of TBI have complicated the surveillance and collection of epidemiologic data, and ambiguity exists with respect to classification of TBI. There are several different methods and scales available to measure the severity of TBI (Table 13.1). In general, most systems broadly define three categories of TBI: mild, moderate, and severe. Criteria used to categorize these patients include Glasgow Coma Scale (GCS) score, Abbreviated Injury Severity Scale (AISS), duration of LOC, and duration of posttraumatic amnesia (Corrigan et al. 2010). Within some of these scales, there exists even further variation, including initial GCS score plus GCS at 24 h postinjury vs. lowest overall GCS score within 24 h of injury (Hoffman et al. 2007).

Mild TBI comprises nearly 90% of all head injuries and approximately 75–85% of all forms of TBI (Khan et al. 2003; Thornhill et al. 2000). Mild brain injury is the most frequently studied of the three broad categories of TBI. Most studies define mild TBI as the presence of an initial GCS score of 13–15 with potential LOC of less than 30 min (Blyth and Bazarian 2010; Lahz and Bryant 1996; Uomoto and Esselman 1993). Other studies have alternatively included measurements such as LOC at time of trauma (Lahz and Bryant 1996) or duration of LOC less than 20 min with concurrent hospitalization of less than 48 h (Rimel et al. 1981b).

The CDC provides a standard definition of mild TBI, which states: “Mild TBI is an injury to the head (arising from blunt trauma or acceleration or deceleration forces) that results in 1 or more of the following: any period of confusion, disorientation, or impaired consciousness; any dysfunction of memory around the time of injury; LOC lasting less than 30 min; or the onset of observed signs or symptoms of neurological or neuropsychological dysfunction (National Center for Injury Prevention and Control 2003).”

Moderate TBI has been defined as a GCS score of 9–12, and severe TBI as a GCS score of 3–8 (Rimel et al. 1982). Some authors group moderate and severe TBI together, with various criteria such as a GCS score of 12 or less, greater than 30 min in a coma, or greater than 24 h of posttraumatic amnesia (Lahz and Bryant 1996; Walker et al. 2005). One study categorized general severe head injury as duration of LOC greater than 24 h, with concomitant cerebral contusion or intracerebral hemorrhage (Jensen and Nielsen 1990).

The mechanism of TBI is typically due to external blunt or penetrating trauma to the head, skull, dura, or brain (Kennedy et al. 2007). Other mechanisms include acceleration–deceleration injury (i.e., whiplash) or coup-contrecoup injury, which may lead to trauma without an actual external force of impact (Kennedy et al. 2007). TBI caused by blast injury (seen most often in military patients) is caused by brain over- or under-pressurization, which causes ultrastructural and biochemical alterations, most commonly in air-filled organs or at air–liquid interfaces (Kennedy et al. 2007; DePalma et al. 2005). The most vulnerable sites to blast injury are the tympanic membranes and the lungs. Military body armor has made great strides in protecting soldiers from penetrating injury, but it does not protect against the barotrauma of blast injury. Central nervous system damage due to blast injury may primarily occur as a result of diffuse axonal injury or due to acute gas embolism from pulmonary injury (DePalma et al. 2005).

Diffuse axonal injury, resulting from axonal strain, is the primary pathologic feature of TBI (Lux 2007). Increasing amounts of diffuse axonal injury generally correlate with increasing severity of TBI (Lux 2007). These injuries may eventually develop into pathologic neurophysiologic changes, such as altered levels of neurotransmitters, impaired axonal transport, synaptic loss, and disruption of neuronal circuits (Lux 2007; DeKosky et al. 2010). In some cases of mild TBI, axonal injury may be reversible, which may explain the complete or near-complete recovery (Lux 2007).

Other pathologic mechanisms of TBI are cerebral contusions, mechanical tissue damage, synaptic loss and neuronal dysfunction, and even ischemia (Khan et al. 2003; Lux 2007; DeKosky et al. 2010; Bryant 2008). The injuries may be due to immediate damage or secondary injury in the days immediately following the trauma (Khan et al. 2003). The anatomic distribution of injuries tends to involve the frontal and anterior temporal lobes (Lux 2007).

Mild TBI may be characterized by contusion and mild edema, leading to variable chronic cognitive or neuropsychiatric impairment (DeKosky et al. 2010). Mild repetitive TBI may result in alterations of the axonal and cytoskeletal structures, leading to abnormal protein aggregations and neurofibrillary tangles (DeKosky et al. 2010). Severe TBI may result in chronic impairment of neuronal homeostasis as well as protein aggregation (DeKosky et al. 2010).

The CDC and WHO definitions of TBI may be interpreted broadly, and thus may lead to overdiagnosis of TBI. A more clinically oriented assessment of TBI may involve taking a full history and physical, reviewing laboratory results, and possibly obtaining imaging studies such as MRI or CT. MRI has been shown to be more sensitive than CT at identifying TBI but is not necessary or sufficient for the diagnosis (Lux 2007). These studies, as well as other tests including electroencephalography, are frequently normal or nonspecific (Andary et al. 1993). Understanding a patient’s cognitive functioning prior to injury is an essential aspect of assessing TBI, and for this reason, neuropsychological assessment may be more clinically appropriate for evaluating TBI (Andary et al. 1993). Full classification of the severity of TBI is performed by using one of the metrics previously described (GCS, AISS, duration of LOC).

TBI typically presents with symptoms characteristic of a postconcussive state, including cognitive problems (difficulties with memory, attention, and concentration, slowed cognitive processing speed), physical problems (fatigue, headache, sleep disturbances), and affective problems (anxiety, depression) (Kennedy et al. 2007; Lux 2007; Bryant 2008). Current evidence favors both organic and psychological factors in contributing to the symptoms of TBI (Bryant 2008).

There are a wide variety of complications and comorbidities associated with TBI, including cognitive, physical, and emotional or social difficulties (Table 13.2). Mild TBI generally has a good prognosis, and most patients can expect to make a significant recovery (Warden 2006). Patients with mild TBI and cognitive and behavioral changes often experience recovery in as few as 4–12 weeks, or up to 3–6 months after injury (Khan et al. 2003; Kennedy et al. 2007; Mooney et al. 2005).

In a 2010 article, Cernich et al. provide a comprehensive, evidence-based review of cognitive rehabilitation of TBI. The authors recommend neuropsychological assessment to identify cognitive deficits (Cernich et al. 2010). Physical, occupational, and speech therapy were also recommended (Cernich et al. 2010). Pharmacological treatment may include psychostimulant medications such as methylphenidate (and to a lesser extent, cholinesterase inhibitors and dopaminergic agents) to help TBI patients that have attention or memory deficits, or impairment of executive function (Cernich et al. 2010).

Treatment includes both patient and family education, as well as psychological support. Inpatient rehabilitation is not usually needed for mild TBI, but may be required for more severe cases. Approximately 10–15% of patients with mild TBI report long-term symptoms associated with a persistent postconcussive syndrome (Khan et al. 2003). Some explanations for persistent symptoms include premorbid cognitive or psychiatric conditions that may complicate recovery, underestimation of injury severity, or financial or legal incentives for secondary gain (Mooney et al. 2005). Although most patients with mild TBI do not require chronic care, those who report persistent cognitive, emotional, and behavioral difficulties often do (Jennekens et al. 2010). There also appears to be a correlation between the length of time since the initial trauma and an increased need for care (Jennekens et al. 2010).

Increased age has been shown to have correlation with mortality and functional outcome in TBI (Gomez et al. 2000). Gender has also been shown to play a role. Male gender is associated with a higher risk of TBI. Female gender is associated with poorer functional outcomes following severe TBI (Lingsma et al. 2010). Ethnicity correlates with mortality after TBI. One study has shown that Asian patients with moderate to severe TBI have a higher mortality rate than African-American or white patients (Berry et al. 2010). Other studies have also noted that the greater the degree of clinical injury severity, the poorer the prognosis (Lingsma et al. 2010).

In general, patients with severe TBI tend to have poor outcomes, and nearly half of this population dies within 2 h of the injury (DeWall 2010). Willemse et al. conducted a review of prospective cohort studies in order to identify predictors for ongoing long-term (>1 year) disability following TBI, and found strong associations between older age, substance abuse, unemployment before the injury, and increased severity of disability at the time of discharge from rehabilitation (Willemse-van Son et al. 2009).

In the pediatric population, three original studies evaluated chronic pain as an outcome of TBI. Necajauskaite et al. conducted a cross-sectional study in Lithuania of children who had experienced a single mild TBI. The children were studied 1–5 years after the trauma. 47.1% reported headache prior to the trauma and 70.6% of the children had headache immediately after the trauma. 62.7% experienced chronic headache. In the children who had preexisting headache, there was a significant increase in the frequency of headaches after the trauma. 45.3% of the patients with mild TBI reported the presence of headaches 1–7 days per month. 29.7% stated that the headache was triggered by irregular sleep (Necajauskaite et al. 2005).

Overweg-Plandsoen et al. studied posttraumatic headache in the pediatric population in the Netherlands and found a prevalence of 45.5% (Overweg-Plandsoen et al. 1999). Lanzi et al. investigated the clinical characteristics of headache after brain injury in the Italian pediatric population. Twelve to 18 months after the trauma, 29.7% of the children reported chronic headache. In 41.5% of the patients, there appeared to be no correlation between the location of the head injury and the site of the headache. The study also reported that two of the pediatric subjects with preexisting diagnoses of migraines had remission of their headache symptoms after the trauma (Lanzi et al. 1985).

Timonen et al. noted that persons with TBI before the age of 15 were at higher risk for psychiatric hospitalization by age 31, and that males with both a psychiatric disorder and childhood history of TBI were at higher risk of having criminal activity (Timonen et al. 2002). McKinlay et al. reported that persons with TBI before the age of 5 were at increased risk of later developing attention-deficit/hyperactivity disorder, oppositional-defiant behavior, conduct disorder, substance abuse, and mood disorders (McKinlay et al. 2009).

According to the CDC, adults who are 75 years of age and older have the highest rates of hospitalization and death due to TBI (Faul et al. 2010). Falls are the most common cause of TBI in the geriatric population (Faul et al. 2010). The diagnosis of TBI may be complicated by various other comorbidities that are common in this population. Older patients typically have a higher prevalence of physical deconditioning. They may also have multiple medical comorbidities and polypharmacy. Each of these factors may confound the diagnosis and treatment of TBI in this population. Bhullar et al. performed a retrospective chart review of patients with TBI after blunt trauma and found that there was no significant difference in mortality between adults 65 and 80 years of age, and those above 80 years of age (Bhullar et al. 2010).

TBI among soldiers has been a major concern since World War I (when it was referred to as “shell shock”). In 1992, Congress formed the Defense and Veterans Brain Injury Center (DVBIC) to bring TBI care and research to the forefront of the military health care system (Jones et al. 2007; Schwab et al. 2007). The DVBIC has pioneered developments in the field of TBI care. Physicians at the Walter Reed Army Medical Center developed a screening process for TBI in the military population, which includes an initial interview and evaluation of cognitive function (Schwab et al. 2007). Those patients that are identified as having severe TBI are medically stabilized and transferred to an intensive rehabilitation center (Schwab et al. 2007).

Recently, TBI has increased in prominence within the military population. It is referred to as “the signature injury of the Iraq and Afghanistan conflicts (Jones et al. 2007; Hoge et al. 2008).” It has been estimated that approximately 20–25% of soldiers wounded in these recent conflicts have mild TBI, whereas the head injury rate was cited as less than 15% during the Vietnam War (Blyth and Bazarian 2010; Hoge et al. 2008; Okie 2005). Some have attributed this increase to the technological advances made in body armor and helmets, which are protecting soldiers from previously fatal injuries, and which may be artificially increasing the rate of TBI (Hoge et al. 2008; Okie 2005). In the military population with TBI, approximately 88% sustained closed TBI and 12% incurred penetrating TBI (Schwab et al. 2007). Of all cases of TBI in soldiers in this most recent conflict, 56% of cases were moderate or severe (Schwab et al. 2007).

Typically, these soldiers develop TBI following a blast injury, which causes rapid pressure shifts that can produce concussion or contusion. Up to 25% of people with severe blast injuries die as a result (Okie 2005). Survivors of these injuries who experience TBI may have persistent postconcussive symptoms such as headache and/or problems with memory or concentration (Hoge et al. 2008).

In 2008, Hoge et al. conducted a survey of 2,525 U.S. Army Infantry soldiers returning from a year-long deployment to Iraq, and reported that 15.2% of soldiers surveyed had sustained a mild TBI, defined as an injury with LOC or altered mental status (Hoge et al. 2008). They also reported that soldiers with mild TBI were more likely to be young, male, and junior in rank (Hoge et al. 2008). The authors then compared this cohort with mild TBI to those who reported other injuries. They found that 71.2% of the mild TBI group met criteria for posttraumatic stress disorder (PTSD), whereas only 16.2% of those with other injuries (excluding mild TBI) met the same criteria for PTSD (Hoge et al. 2008). It was also noted that, compared to the non-TBI group, the mild TBI group was more likely to report poor health, missed workdays, increased medical visits, and other physical and psychological complaints, including headache (Hoge et al. 2008). However, after adjusting for PTSD and depression, there was no longer a significant association between mild TBI and most of the aforementioned complaints (Hoge et al. 2008). This implies that these two conditions may be significant mediators of many of the physical and psychological problems associated with TBI (Hoge et al. 2008).

Patients with TBI may have a higher prevalence of disability than the general population. In one sample group of patients with mild TBI, nearly three-quarters reported disability associated with TBI (Mooney et al. 2005). The probability of disability related to TBI increases with age and is higher in women (Langlois et al. 2006). Data from 2003 reported an estimated 43.3% of hospitalized TBI survivors in the United States had injury-related disability 1 year after trauma (Selassie et al. 2008). The prevalence of Americans living with a disability related to TBI has been estimated to be 3.2 million (Corrigan et al. 2010; Zaloshnja et al. 2008).

In a European review, Tagliaferri et al. reported that persistent problems following severe TBI were described in selected studies, and included changes in employment, physical complaints, memory problems, and neuropsychological problems (Tagliaferri et al. 2006).

In a 2008 meta-analysis, Nampiaparampil reported that chronic pain is a common complication of TBI, independent of psychological disorders such as PTSD or depression (Nampiaparampil 2008). Described as a constant pain of at least 6 months’ duration, chronic pain has been reported by over half of all TBI patients (Lahz and Bryant 1996). Painful conditions are prevalent among patients with TBI and may include headaches, musculoskeletal conditions, complex regional pain syndrome (CRPS), spasticity, heterotopic ossification, and neuropathic pain (Lahz and Bryant 1996; Sherman et al. 2006).

Evaluating pain in patients with TBI can be complicated because of the higher prevalence of cognitive impairments in this population (Gellman et al. 1992). Interestingly, chronic pain was reported in 75.3% of mild TBI patients, 32.1% of severe TBI patients, and 43.1% of military TBI patients (Nampiaparampil 2008). It has been hypothesized that this disparity exists due to the fact that the more severely injured patients have an increased degree of cognitive impairment, which leads to decreased self-monitoring and reporting of pain (Young 2007). Bryant et al. noted that TBI patients generally manage chronic pain differently than do those without brain injury (Bryant et al. 1999).

One study reported that 95% of patients with mild TBI complained of pain that interfered with activities of daily living as opposed to 22% of patients with moderate or severe TBI (Andary et al. 1993). Another study found that over 85% of TBI patients with chronic pain reported pain on a daily basis (Lahz and Bryant 1996). Overall, studies have found that nearly three-quarters of all patients with TBI report some level of pain at 1 year postinjury, and over half of these patients report interference with activities of daily living (Hoffman et al. 2007).

In all cases, it has been emphasized that a complete, biopsychosocial approach be taken to evaluate the patient with TBI and chronic pain. Both conditions have overlapping symptoms such as pain behaviors, sleep disturbances, chronic fatigue, anxiety, and depression (Andary et al. 1993). Mistakenly identifying certain chronic pain symptoms as a consequence of brain injury may lead to improper or inadequate treatment (Uomoto and Esselman 1993). Failure to treat pain adequately in this population may eventually complicate rehabilitation and compromise recovery, as well as have a negative emotional impact on the individual (Sherman et al. 2006). However, effective treatment and prevention of chronic pain problems in this population may lower the incidence of disability (Uomoto and Esselman 1993).

Headache is the most common pain complaint in all TBI patients (with a reported incidence of 57.8%), and much of the research on TBI and pain has been focused on posttraumatic headache (Nampiaparampil 2008). In fact, headache is the most common sequelae of closed head injury, as well as the most common presenting symptom of mild TBI (Lane and Arciniegas 2002; Tyrer and Lievesley 2003). The prevalence of headache associated with TBI is as high as 57.8% (Nampiaparampil 2008). Patients with mild TBI reported a higher incidence of headaches (89%) than did patients with moderate or severe TBI (18%) (Uomoto and Esselman 1993).

Posttraumatic headache is a distinct classification, defined by the International Headache Society (IHS) as a headache that begins within 14 days of regaining consciousness after TBI (Walker et al. 2005). The IHS further categorizes posttraumatic headache by severity of injury: significant head trauma vs. minor head trauma, but it does not define the etiology of the headache (Branca and Lake 2004). Posttraumatic headache is defined as chronic when it persists for over 8 weeks postinjury (Branca and Lake 2004).

It is clinically impossible to differentiate posttraumatic headache from chronically recurrent headache, which may be present in TBI patients who had preinjury headaches (Jensen and Nielsen 1990). Posttraumatic headache is generally poorly characterized, and many TBI patients chronically complain of different types of headaches simultaneously (Young 2007; Sherman et al. 2006). Usually, these headaches are classified as migraines, are secondary to musculoskeletal complaints, or are related to rebound from analgesics (Sherman et al. 2006; Branca and Lake 2004).