Clinical Considerations in the Evaluation and Management of Patients Following Traumatic Brain Injury
Abstract
Traumatic brain injury (TBI) is one of the most common causes of injury and disability, affecting about 1.7 million individuals annually in the U.S. Furthermore, TBI is also recognized as the “signature wound” for military personnel in recent wars. Both civilian and military TBIs result in individual, family, and societal economic and health costs. Even mild TBIs (i.e., concussions) can produce persistent difficulties in mental and physical well-being (e.g., problems with sleep, fatigue, pain, and cognitive functioning), which may be compounded by psychiatric comorbidities. Current treatment and management of the TBI patient typically involves case-by-case use of pharmacologic and/or cognitive-behavioral approaches that individually address post-TBI symptoms. We review the current literature on TBI diagnosis and treatment strategies and note areas where clinical controversies exist. It is hoped that through continued research (and discussion) of these important issues, a greater consensus on the science of treatment of TBI will be achieved.
The Diagnostic and Statistical Manual of Mental Disorders (DSM [1]) provides a limited set of criteria for diagnosing traumatic brain injury (TBI). According to the DSM, a diagnosis of postconcussional disorder requires: A) a history of head trauma causing cerebral concussion, B) objective evidence of difficulty in attention or memory, and C) three or more symptoms (fatigue, sleep disturbance, headache, vertigo/dizziness, irritability/aggression, anxiety, depression, affective instability, personality change, and/or apathy) occurring shortly after the trauma and lasting for at least 3 months. The symptoms in criteria B and C must follow the head trauma or represent a worsening of preexisting symptoms and must cause significant social or occupational impairment, representing a significant decline from previous functioning. A recent consensus group has more concisely defined TBI as “an alteration in brain function, or other evidence of brain pathology, caused by an external force” (2). Alterations in brain functioning may include a period of loss of consciousness or alteration of consciousness, posttraumatic amnesia (a deficit in encoding new memories), global or specific neurologic deficits, and/or evidence of brain pathology (e.g., abnormalities detected in neuroimaging assessments). TBIs may result from external force, sudden acceleration/deceleration of the head, any forces to the head caused by blasts or explosions, and/or a foreign body penetrating the head (2). The type, direction (e.g., angular, rotational, shear, and translational forces), intensity, and duration of forces all contribute to the characteristics and severity of TBI. Damage may occur directly under the site of impact, on the side opposite the impact (coup and contrecoup injuries, respectively [3]), or may be diffuse.
TBI represents a serious public health problem in the United States. The Center for Disease Control and Prevention estimated that 1.7 million people sustain a TBI annually in the U.S., which leads to 52,000 deaths, 275,000 hospitalizations, and 1.4 million emergency department visits (4). TBI is a contributing factor in 30.5% of all injury-related deaths in the United States (4). Overall, direct and indirect medical costs from TBIs were $60 billion in the US in 2000 (5). Of those hospitalized, 70,000 to 90,000 people per year sustain substantial injuries that will necessitate long-term or lifetime care (6, 7). Additionally, TBI is a risk factor for other medical conditions, including depression, substance abuse, and posttraumatic stress disorder (PTSD), which entail additional costs (8–11). The costs are even higher when considering lost productivity and earnings for patients and their caregivers, diminished tax revenue, and the burden on social programs (7, 11, 12). Of course, financial costs cannot capture the effects of TBI on family members and caregivers, who report increased stress and major disruptions in family functioning (13–15).
Approximately 75% of TBIs are concussions, also termed mild TBI (mTBI), characterized by alteration of consciousness or loss of consciousness for no more than 30 minutes (6). Falls are the most common cause of TBI (32.5%), followed by motor vehicle injuries (17.3%), being struck against the head (16.5%), assaults (10%), and other causes (21%) (4). Falls result in the greatest number of emergency department visits and hospitalizations, but motor vehicle injuries account for the most TBI-related deaths, especially for adults aged 20–24 (4). Children up to 4 years of age, adolescents 15–19 years old, and adults over age 65 are most likely to sustain a TBI, although adults 75 years and older experience the highest rates of TBI-related hospitalization and death (4). Across all age groups, TBI rates are higher for males than for females (4). Additionally, TBI incidence rates appear to be increasing. From 2002–2006, fall-related TBIs in children younger than 14 increased 62%, and in adults over 65, there was a 46% increase in emergency department visits, 34% increase in hospitalizations, and 27% increase in TBI-related deaths (4). Across all age groups, TBI-related emergency department visits increased by 14% and hospitalizations increased by 20% during this time period (4).
TBIs can be classified as mild, moderate, and severe. Commonly used diagnostic guidelines include ratings of injury severity on the Glasgow Coma Scale (GCS) and criteria that include duration of posttraumatic amnesia and loss of consciousness (see Table 1). Additionally, several scales have been used or are proposed for diagnosing and grading concussion (see Tables 2 and 3). It has been suggested that grading the severity of TBI may be improved through wider use of neuroimaging technologies (16). Because the vast majority of TBIs are in the mild-to-moderate range and because those with mild-to-moderate injuries are more likely to consult a psychiatrist, this review will focus on the evaluation and treatment of mild-to-moderate TBI.
| Severity | Glasgow Coma Scale Score | Posttraumatic Amnesia | Loss of Consciousness |
|---|---|---|---|
| Mild | 13–15 | <1 day | 0–30 minutes |
| Moderate | 9–12 | >1 to <7 days | >30 min to <24 hours |
| Severe | 3–8 | >7 days | >24 hours |
a
Adapted from VA/DoD Clinical Practice Guideline for Management of Concussion/Mild Traumatic Brain injury (117).
| Organization | Loss of Consciousness | Posttraumatic Amnesia | Mental Status | Neurological Signs |
|---|---|---|---|---|
| American Congress of Rehabilitation Medicine (151) | ≤ 30 minutes | ≤ 24 hours | Any alteration in mental status at time of injury | May or may not be transient |
| American Academy of Pediatrics (152) | ≤ 1 minute | Not specified | Normal mental status at time of initial evaluation | None at exam, but may have seizures or other signs immediately following injury |
| World Health Organization (153) | ≤ 30 minutes | ≤ 24 hours | Confusion and disorientation | Transient neurological abnormalities |
| Guidelines | Grade I | Grade II | Grade III |
|---|---|---|---|
| Cantu, 1992 (154) | PTA<30 minutes, no LOC | LOC<5 minutes or PTA lasting 30 minutes–24 hours | LOC>5 minutes or PTA>24 hours |
| Ruff Concussion Grades (155) | Altered mental state or transient LOC, 1–60 seconds of PTA, one or more neurological symptoms | Definite LOC with time unknown or<5 minutes, 60 seconds to 12 hours of PTA, one or more neurological symptoms | 5–30 minutes of LOC, more than 12 hours of PTA, one or more neurological symptoms |
| Colorado Medical Society (156) | Confusion, no loss of consciousness | Confusion, PTA, no LOC | Any LOC |
| American Academy of Neurology (157) | Confusion, symptoms last<15 minutes, no LOC | Symptoms last>15 minutes, no LOC | LOC (IIIa, LOC lasts seconds, IIIb, LOC lasts minutes) |
a
LOC=Loss of consciousness; PTA=Posttraumatic amnesia
What Happens During and After a TBI?
TBIs occur due to trauma involving focal and/or diffuse injuries to the brain. Focal injuries include contusions, lacerations, and intracranial hemorrhage or hematoma. Diffuse injuries tend to result from subtle stretching and tearing of brain tissue that is less observable, yet still problematic for recovery (17). Evaluation of the TBI patient can incorporate clinical observation/interview, neuropsychological testing, and/or neuroimaging, which is showing potential to enhance evaluation of TBIs (especially more mild forms of TBI). There are now two instruments designed for immediate assessment of concussion in sports, the Sport Concussion Assessment Tool (SCAT2) (18), designed for athletes 10 years and older, and the computerized Immediate Post-Concussion Assessment and Cognitive Testing (ImPACT) (19) device, which is both sensitive and specific for the neurocognitive and neurobehavioral sequelae of concussion (20). Other technologies such as magnetic resonance spectroscopy may be useful in detecting metabolic changes; diffusion tensor imaging (DTI) may help detect subtle structural damage; functional magnetic resonance imaging (fMRI) and magnetic resonance perfusion can identify changes in functional networks; and susceptibility-weighted imaging can detect microhemorrhaging (21). Use of combined magnetoencephalography (MEG) and DTI may also detect subtle neuronal injury in mTBI not identified by traditional CT or MRI (22).
Symptoms of TBI vary depending on the location and extent of the damage to the brain. In more severe forms of TBI, impairments observed in the postinjury evaluation generally align well with the location and severity of the injury. A person with a moderate-to-severe TBI may experience persistent headaches, vomiting or nausea, convulsions or seizures, an inability to awaken from sleep, dilation of one or both pupils, slurred speech, weakness or numbness in the extremities, loss of coordination, and/or increased confusion, restlessness, or agitation (23). More serious brain injuries may result in stupor, coma, or a persistent vegetative state. However, even mTBIs often result in a complex set of postconcussive symptoms that may result from neurochemical changes that occur due to the injury (24). mTBI can result in damage to neuronal and axonal cell membranes while sparing the function of cell bodies and myelin sheaths (25). Damage to the cell membranes precipitates changes in ionic (potassium and calcium) equilibrium, resulting in release of excitatory neurotransmitters, particularly glutamate (26). In an effort to reestablish ionic equilibrium, the cells become more active, thereby increasing glucose metabolism. Increased metabolism may in turn result in depletion of energy stores in the cells, eventually leading acidosis and edema (24, 27). These biological changes that occur following mTBI may result in headaches, confusion, lightheadedness, dizziness, blurred vision, tinnitus, fatigue, sleep disturbance, behavioral or mood changes, and cognitive difficulties.
The most commonly reported postconcussive symptoms are sleep disturbance, fatigue, and pain. Sleep disturbances, especially insomnia (28), following TBI are extremely common, occurring in 30%−70% of patients (29). Additionally, a recent meta-analysis determined that some form of sleep disturbance was reported in 25%−29% of individuals following a TBI, and that TBI patients were 2–4 times more likely than individuals in the general population to experience problems with sleep maintenance, sleep efficiency (percentage of time asleep out of time in bed), nightmares, excessive sleepiness, early awakenings, and sleepwalking (30). Fatigue also represents a major problem for many patients, occurring in 45%−73% of TBI patients and reported as the primary symptom for 43% of patients (31). Fatigue may last for years after the injury (32), resulting in persistent and disabling feelings of mental, physical, and psychological exhaustion, tiredness, weariness and/or lack of energy. Lastly, pain (especially headache and neck pain) is a major problem for many TBI patients (33). A recent review found that rates of chronic pain ranged from 43% in studies of Veteran patients to 52% in civilian studies. Chronic pain may be more prevalent in patients with mTBI (75%) compared with those with moderate or severe TBI (32%) (34).
TBIs may damage any part of the brain or multiple parts of the brain, so neuropsychological deficits following TBI can vary in both type and severity. Impairments in attention, processing speed, learning, memory, prospective memory, and executive functioning may be present (8, 35–41). Evidence suggests, however, that mTBI may only have short-term impact on neuropsychological functioning, which should return to baseline within three months in most cases (42). Research in individuals with sports-related concussions (43), for example, suggests that following mTBI, most cognitive symptoms resolve within days to three months, however, some individuals have persistent cognitive problems beyond several months (8, 44–46). Recent studies have highlighted poor neuropsychological outcomes even among individuals with mild-to-moderate TBI (33). These impairments can hinder functional recovery, including cognitive readiness for work, school, and independent living (12, 47).
Cognitive dysfunction following TBI is often exacerbated by other biological, psychological, or social characteristics of the individual. For example, previous studies have reported increased sleep disturbances among TBI patients (48, 49) (especially among those with comorbid PTSD [50]), which may be related to attention and memory deficits (51). Variations in cognitive recovery rates may also be attributable to individual characteristics such as premorbid illness perception, educational background, and life stress (9, 36, 52–57).
What Predicts Outcome Following TBI?
Injury severity is generally the best predictor of TBI outcomes. Individuals with moderate-to-severe TBIs tend to have extended recovery periods and significant long-term impairment. Recovery may vary depending on the aspect of functioning assessed, with 65% of patients achieving preinjury functioning in basic self-care and only 40% showing full recovery in areas of cognitive competency, major activities, and leisure and recreation (58). Length of posttraumatic amnesia appears to be the strongest predictor of functional outcomes at 6 and 12 months postinjury (59). Other predictors of poor outcome following moderate-to-severe TBI include older age, motor deficits, impaired pupillary reactivity, history of subarachnoid hemorrhage, and lower GCS (60, 61).
With regard to mTBI, symptoms tend to be the most severe immediately after an injury, with gradual improvement over several hours up to 90 days (62). About 10% of individuals with mTBI have persistent postconcussive symptoms, including headache, dizziness, fatigue, insomnia, difficulty concentrating, irritability, anxiety, depression, and sensitivity to light and noise. These symptoms may lead to social and/or vocational difficulties out of proportion to the severity of the initial injury, a condition termed persistent postconcussive syndrome (63).
In addition to injury severity, several other factors have been studied as predictors of TBI outcomes, including the timing of the TBI within the lifespan, the setting of the TBI, the type of TBI, and the presence of more than one TBI. We discuss these factors below.
Child Versus Adult TBIs
It is commonly held that, given injuries of equal severity, children will recover better than will adults due to the plasticity of the brain at younger ages (64, 65). However, recent animal and human research is challenging this assumption. For example, studies now indicate that a developmentally immature brain may be less capable of recovering from TBI (66). There may also be critical periods of development during which the diffuse injuries caused by TBIs will result in lost functioning only observable at later stages of brain maturation (66). Additionally, studies have found important complications for the younger brain following TBI, including an increased propensity for apoptosis, age-dependent parameters for cerebral blood flow and metabolism, development-specific biomarkers, increased likelihood of early posttraumatic seizures, differential sensitivity to commonly used neuroactive medications, and altered neuroplasticity during recovery from injury (67). Therefore, differences in outcomes for older adults may reflect reductions in the ability to acquire new skills rather than reduction in plasticity, per se. In younger adults, outcomes following TBI may be more dependent on multiple factors including the severity, nature, and age at time of injury, as well as environmental influences during the recovery period (68).
Civilian Versus Military TBIs
Although TBI is common in the general population, there is increased clinical and research interest in TBI due to its high incidence in military personnel involved in recent wars. TBI has been identified as the “signature wound” of the Iraq and Afghanistan Wars, with increased rates of TBI attributed to blast-related injuries emanating from artillery, mortar, rocket shells, mines, bombs, grenades, and improvised explosive devices (69). Blast injuries differ from injuries related to blunt-force trauma (most frequently observed in civilian populations) in several unique ways. Blast injuries are more complicated, as the head may be exposed to multiple insults during the same event. Brain injury may be primary (from exposure to the blast pressure wave), secondary (from shrapnel or projectiles from the blast), tertiary (from being thrown to the ground or against a solid object), or quaternary (from blood loss associated with bodily injuries or inhalation of toxic gases). Therefore, diagnosis and management of individuals with blast injuries may require greater understanding of factors such as the type of blast, size of the blast, distance from the blast, and postblast trauma(s).
Despite the severity and complexity of blast-related head injuries, researchers have found few differences between blast-injured and blunt-force-injured individuals with mTBI in terms of postconcussive symptoms, psychiatric symptoms, and neurocognitive performance (70, 71). Recent research examining postmortem brains from blast-exposed Veterans found evidence for tau neuropathology that appeared identical to the tau neuropathology, neuroinflammation, and neurodegeneration observed in brains of athletes with histories of repeat concussive injury (72). However, studies using DTI in military personnel with blast-related mTBI have found abnormalities in regions (e.g., middle cerebellar peduncles and orbitofrontal white matter) not known to be commonly injured in civilian cases of mTBI but that are predicted to be sensitive to blast injuries (73). Taken together, these results suggest that short- and long-term impact of blast injuries is not yet fully understood.
Effect of Repeated TBIs, Even Without Loss of Consciousness
Long-term outcome resulting from exposure to multiple concussions or mTBIs has not been well-studied and is not currently well understood. Recent studies suggest that repeated mTBI can lead to an increased risk of cognitive impairment and neurodegenerative disease later in life (74, 75). Repeated injury appears to impact structural, functional, metabolic, and behavioral responses in the brain, and the impact of repeated injuries is most severe when the second injury occurs within hours to 1 month following the first injury (76). It is unknown whether vulnerability to the effects of a second injury is mediated by age, gender, severity and intensity of injury, length of time between injuries, and/or related to observed metabolic and neuroimaging alterations (76). Nonetheless, it is well-documented that repeated concussions can result in a condition now termed chronic traumatic encephalopathy (CTE). CTE is believed to result in a decline in memory and cognition over time, as well as increased risk for depression, suicide, aggressiveness, Parkinsonism, and dementia (77), and may be associated with persistent abnormalities in visual motor and motor cortex functioning (even after recovery of other neuropsychological performance) (78). CTE has been well-studied in boxing (79, 80), and is now being studied in other sports, especially football (75, 81–84). Slower recovery rates have also been observed in patients with more than one concussion (85). These findings suggest that repetitive head injury has significant short- and long-term ramifications that require understanding of both the severity of the initial injury and the duration between injuries as probable predictors of increased morbidity in this population (76).
Common Psychiatric Comorbidities in TBI Patients
Individuals with a history of TBI are more likely to have psychiatric disorders, including those related to mood, anxiety, and substance abuse (86, 87). Among TBI survivors, 43% have at least one psychiatric diagnosis, compared with only 20% of those without a TBI (86). Psychiatric comorbidities may be even more common in veterans: about 7% of recent veterans using VA healthcare have persistent postconcussive symptoms and higher utilization of healthcare services due to high rates of PTSD (comorbid in 73% of veterans with TBI), depression (comorbid in 47%), and back/neck/headache pain (comorbid in 72%) (88). Veterans may be more susceptible to psychiatric illness following TBI due to exposure to blasts, which may selectively impact the prefrontal cortex, leading to disinhibition of regions that regulate fear and anxiety (89). As well, inflammation caused by TBI may also lead to increased risk for psychiatric illness (89). Psychiatric comorbidities not only complicate the course of the injury but impede both the emotional and physical recovery from TBI (90, 91). These comorbidities can also further contribute to cognitive impairment (8–10).
Mood disorders are some of the most common psychiatric complications of TBI (92, 93). Major depression is the most prevalent, affecting at least 25% of those who have experienced a TBI (89). The risk of developing depression is not limited to the acute stages of TBI but exists even decades after the injury (90). The prevalence of depression within the first year following TBI ranges from 33%−42%, and rises to as high as 61% within the first 7 years (87). Those with more severe TBI are more vulnerable to depression in the first 12 months postinjury, whereas those with milder TBI show a more prolonged onset and persistent risk of incidence (90, 94). Despite efforts to uncover a biological basis for the development of post-TBI depression, a consistent pattern of localized lesions associated with the development of depression remains elusive (95). In addition to major depression, those who suffer a TBI are also more likely to suffer from dysthymia and bipolar disorder (96).
Anxiety disorders after TBI also occur at a much greater frequency than in the general population, with an overall prevalence of 29% (56). Of the range of anxiety disorders associated with TBI, PTSD is very common (97), with a large increase relative to the general population (90, 98). PTSD is arguably the most expected of psychiatric sequelae, given the sometimes violent and life-threatening nature of TBI. Prevalence estimates of PTSD are highly variable, ranging from 1%−50% across studies (96, 99, 100). Much of this variability is probably due to differences in diagnostic criteria, populations, and time postinjury. Military service members seem to be particularly susceptible to PTSD in the context of TBI (101). Among veterans, those who screen positive for TBI are three times more likely to be diagnosed with PTSD (102). Comorbid substance abuse and depression appear to increase vulnerability to PTSD following TBI (103). Longer loss of consciousness and posttraumatic amnesia appear to decrease vulnerability to PTSD due decreased memory for the traumatic event, explaining why comorbid PTSD is more common in those who experience milder brain injuries (104–106, but also see 107). In addition to PTSD, there are increased rates of generalized anxiety disorder, panic disorder, and OCD in TBI patients (86, 90).
Substance abuse and dependence rates are elevated for those who experience TBI, with incidence rates ranging from 28%−32% (91, 108). Those who suffer a TBI tend to have higher preinjury substance use and abuse (109, 110). Comorbid substance abuse and TBI is even more prevalent in the military population; in a study of veterans, those who screened positive for a TBI were twice as likely to have a substance-related disorder (102). Substance abuse after TBI hampers recovery, increases risk of other psychiatric disorders, and increases rates of reinjury (111, 112). Poor medical, neurobehavioral, vocational, and quality of life outcomes have also been linked with postinjury substance abuse (110). Evidence suggests that some TBI patients decrease their drug and alcohol abuse in the short term following TBI, but this abstinence may be short-lived, with substance abuse increasing in the years following TBI (110, 112).
Treatments
Pharmacological
There is an undoubted need to treat the cognitive, behavioral, and psychiatric symptoms following TBI. However, most comprehensive reviews in this field have concluded that pharmacological treatment of TBI does not produce substantial clinical benefit (113). The published literature offers inadequate evidence to refute or support pharmacological treatment or to offer comprehensive standards or guidelines of such treatment following TBI (114). Despite this, there is limited evidence (see Table 4) suggesting that certain medications may be helpful in treating TBI sequelae and supporting recovery (114, 115). Treatment of comorbid psychiatric conditions according to practice guidelines is recommended, but it should also be noted that TBI patients may be more susceptible to adverse effects of many drugs, making it especially important to monitor for interactions and toxicity (116, 117). It has also been recommended that TBI patients avoid medications that lower seizure thresholds, cause confusion, or contribute to cognitive slowing or fatigue (117).
| Mood symptoms | Neurocognitive sequelae | Neurobehavioral sequelae |
|---|---|---|
| selective serotonin reuptake inhibitors | methylphenidate (attention, processing speed, memory deficits) | amantadine (agitation, anxiety) |
| valproic acid | amantadine (attention, concentration, alertness, mobility deficits) | selective serotonin reuptake inhibitors (anxiety, agitation) |
| donepezil (attention, memory deficits) | methylphenidate (agitation, impulsivity) | |
| modafinil (memory, motor, attention deficits) | beta-blockers (agitation, aggression) | |
| bromocriptine (initiation, speech deficits) | amitriptyline (agitation) | |
| selective serotonin reuptake inhibitors (motor speed, recent memory deficits) | bromocriptine (restlessness) | |
| valproic acid (problem solving, recent memory deficits) | bupropion (restlessness) | |
| valproic acid (agitation, impulsivity, restlessness) | ||
| antiandrogens (inappropriate sexual behavior) |
Note. Table adapted from Talsky et al, 2000 (115)
Nonpharmacological
Nonpharmacological interventions for TBI are usually focused on symptom management, recovery of function, and community reintegration into the least restrictive living, educational, vocational, and social settings. Cognitive and postconcussive symptoms are likely to require different approaches, and there is consensus that treatment of mTBI should involve psychoeducation regarding TBI, emphasizing the expectation of full recovery (9).
Cognitive rehabilitation.
Cognitive rehabilitation has been used in TBI, psychiatric disorders (118, 119), and memory disorders such as Alzheimer’s disease (120), and is generally classified as restorative or compensatory (121). Restorative treatments use drills and practice, either paper and pencil or computer-assisted, to restore cognitive abilities, whereas compensatory interventions focus on teaching strategies to work around cognitive impairments and using spared cognitive functions to develop alternative ways to carry out activities of daily living. Compensatory strategies can be internal to the person (e.g., using visualization to remember to carry out a task) or external (e.g., using calendars, alarms, or smart devices). Interventions may also be combined with environmental approaches, which decrease the cognitive demands of the environment (e.g., simplifying a work space). Most of the extant research on cognitive rehabilitation for TBI has investigated interventions for individuals with strokes or severe brain injuries (101, 121–123), so little is known about rehabilitation for those with mild-to-moderate TBI (124), especially those with chronic symptoms—the very population most likely to come to the attention of mental health professionals. Less than a handful of randomized controlled trials of cognitive rehabilitation for individuals with mild-to-moderate TBI have been conducted (125, 126), and systematic reviews have had to rely on small, poorly designed, or uncontrolled trials (124, 127, 128). Due to the limited research available, the VA/Department of Defense Clinical Practice Guideline for Management of Concussion/Mild TBI (117) did not make recommendations in favor of or against cognitive rehabilitation but did recommend psychoeducation and family education regarding TBI and interventions to promote return to work and community reintegration (117). The literature on cognitive rehabilitation in severe mental illness has demonstrated that cognitive interventions have larger effects when delivered in the context of a broader psychiatric/psychosocial rehabilitation program (119). Along these lines, compensatory strategies have been combined with supported employment for individuals with TBI (129).
VA researchers are currently evaluating interventions such as Cognitive Symptom Management and Rehabilitation Therapy (CogSMART) and Compensatory Cognitive Training (CCT) for veterans with mild-to-moderate TBIs. CogSMART is a 12-week, multimodal compensatory cognitive training intervention emphasizing habit learning and compensatory strategies in prospective memory, attention, learning/memory, and executive functioning. Compensatory strategies appear to be useful regardless of the etiology of the impairment (e.g., TBI, sleep disturbance, comorbid PTSD/depression). There are also modules on psychoeducation regarding TBI and strategies to improve postconcussive symptoms (sleep disturbance, fatigue, headaches, and tension). Borrowing from Mittenberg and colleagues’ seminal work on psychoeducation (9), the intervention sets the expectation of full recovery from postconcussive symptoms. The treatment manual was developed in consultation with the Acquired Brain Injury program at Mesa College in San Diego and other cognitive rehabilitation researchers. Similar strategies had positive effects on cognition, psychiatric symptoms, functional capacity, and quality of life in a schizophrenia sample (130). CCT is a 10-week intervention combining elements of CogSMART with Cognitive Strategy Training, which had been developed in parallel (131). CCT is currently being evaluated in a randomized controlled trial, as is SMART-CPT, a combination of Cognitive Processing Therapy for PTSD and CogSMART strategies, for individuals with both PTSD and TBI.
Supported employment.
Rates of return to work following TBI range from 12%−70%, mainly depending on injury severity, emotional and neuropsychological functioning, self-awareness, and community support (12, 52, 129, 132, 133). Even in mTBI patients, return to previous level of employment is not guaranteed. One study of motor vehicle accident survivors with mTBI showed that 42% of the patients returned to work, and only 12% regained employment at their premorbid level (134). Those who return to work tend to earn less than they did prior to the TBI (7, 135). The consequences of unemployment in this population are not merely financial but also include social isolation, low self-esteem, and increased substance abuse (12).
Supported employment is the evidence-based practice to assist people with TBI in returning to work (12, 129, 132) and is cost-effective (135). Supported employment is an individualized approach to work rehabilitation based on the client’s interests and abilities and emphasizing rapid job searching for competitive work in the community (129, 132). Employment specialists develop relationships with local employers and provide clients and employers with follow-up support as long as necessary after job placement (133, 136). Studies show that return to work depends more on early intervention than initial injury severity (136), indicating that successful outcomes are possible across the TBI severity spectrum.
Controversies
Several controversies regarding TBI are noteworthy. Some researchers have suggested that the term “mTBI” is over-used and favor the term “concussion” in order to help set the expectation for recovery and avoid making the event sound more serious than it is (137). Although some have used the label “post-concussive syndrome,” others prefer “post-concussive symptoms.” There is no evidence that the symptoms typically reported following mTBI represent a syndrome, as they do not cluster in any reliable manner, nor does resolution of any particular symptom predict resolution of other symptoms (138). Additionally, postconcussive symptoms typically vary in duration and often require separate treatments to be adequately addressed. Moreover, there is little consensus on the diagnostic criteria for concussion, with multiple scales having been published in recent decades (see Tables 2 and 3).
The majority of those who experience mTBI will fully recover within 3 months, but a significant minority report continued postconcussive symptoms (139), with symptoms reported to last as long as 15 years after mTBI (8, 140, 141). There is much disagreement as to whether these persistent symptoms are due to psychiatric cormorbidies or the TBI itself (140–146). Recent studies have found that most postconcussive symptoms (except headache) can best be attributed to psychiatric illness (e.g., PTSD, MDD), especially in military personnel (145). Evidence shows that anxiety, notably PTSD, mediates the relationship between TBI history and subjective measures of health and psychosocial functioning (141, 143). It has also been demonstrated that PTSD and depression are more reliable predictors of emotional and cognitive symptoms than is TBI itself (140, 141). Conversely, other investigations have found that comorbid conditions do not mediate this relationship entirely. After controlling for other psychiatric conditions, mTBI may still be significantly associated with headaches, sleep problems, and memory difficulties, even in the chronic phase years after injury (140). This disagreement in the literature has led some to conclude that pathology and psychology may interact to influence the generation, reinforcement, and perpetuation of symptoms following TBI (90). It has proven difficult to disentangle the TBI from its comorbid psychiatric conditions, suggesting that each of these conditions has its own additive properties, with each disorder serving to hinder recovery from the other (142, 147; see also Figure 1).
Figure 1. Traditional Interpretation and Revised Model of Relationship Between mTBI and Development of Postconcussive Symptomsa
aThe revised model emphasizes the role of psychiatric illness in the onset and maintenance of symptoms except for pain (adapted from Hoge et al., 2008 [145]).
The validity of neuropsychological testing following TBI is another topic of vigorous discussion. In light of multiple potential sources of secondary gain (e.g., litigation, disability benefits) measures of test-taking effort are included in neuropsychological evaluations to ensure the validity of test results (148). Effort test scores signifying suboptimal effort do not necessarily equate to malingering, and may reflect other factors, such as fatigue, apathy, pain, psychiatric symptoms, substance use, or conversion disorder. Malingering is the intentional exaggeration or fabrication of deficits in the context of external incentives; intentionality may be difficult to prove because it is not an observable behavior (148, 149), and the presence of external incentives is not always known. Delis and Wetter developed the term “cogniform disorder” to explain the unintentional exaggeration of cognitive symptoms (149). In contrast to research demonstrating that postconcussive symptoms and cognitive performance normalize within the first 3 months following mTBI (8, 45–47), evidence suggests that individuals in litigation tend to report continued postconcussive symptoms and cognitive difficulties over time (41). It is estimated that 40% of concussion cases involving litigation are associated with invalid test results, reflecting a range of possible explanations from unconscious symptom exaggeration to outright malingering (32). One study (150) found that after controlling for suboptimal effort, the cognitive performance of veterans with mTBI was indistinguishable from those who had never sustained a TBI, validating previous research that effort can account for a significant portion of the variance seen in neuropsychological testing (148, 150).
Future Directions
Development of biomarkers for mTBI are urgently needed, and such biomarkers will be invaluable for assisting with assessment of events involving unwitnessed or unclear loss of consciousness, posttraumatic amnesia, and GCS. Biomarkers of mTBI would also be useful as outcome measures as well as predictors of outcome. With regard to treatment, despite the imprecise etiology of the cognitive and postconcussive symptoms following mTBI, it is clear that many patients presenting with these symptoms require treatment and rehabilitation to achieve their optimal functioning. Behavioral treatment modalities may be similar to those used for individuals with more severe injuries. Future research is likely to examine the effects of combination treatments, for example, the combination of restorative cognitive rehabilitation (the “bottom-up” approach that trains basic cognitive skills) and compensatory cognitive approaches (those that focus on “top-down” training of more complex cognitive and functional skills). Another combination of interest is that of pharmacological treatment with cognitive rehabilitation. Drugs that enhance specific cognitive domains (e.g., attention, working memory, learning), particularly if those cognitive domains are subserved by healthy neural circuitry, might synergistically enhance the benefits of cognitive rehabilitation. Research on combining pharmacologic and cognitive rehabilitation approaches would be further enhanced by establishing biomarkers that predict sensitivity to medication or training effects and can be used as an index of treatment outcome. Finally, taking a cue from the literature on cognitive rehabilitation in severe mental illness, we expect that cognitive rehabilitation interventions for TBI will increasingly be studied and delivered in a broader rehabilitation context that emphasizes school/work functioning and community reintegration.
References
1.
American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th ed., text revision. Washinton, DC, American Psychiatric Publishing, 2000
2.
Menon DK, Schwab K, Wright DW, Maas AIDemographics and Clinical Assessment Working Group of the International and Interagency Initiative toward Common Data Elements for Research on Traumatic Brain Injury and Psychological Health: Position statement: definition of traumatic brain injury. Arch Phys Med Rehabil 2010; 91:1637–1640
3.
Drew LB, Drew WE: The contrecoup-coup phenomenon: a new understanding of the mechanism of closed head injury. Neurocrit Care 2004; 1:385–390
4.
Faul M, Xu L, Wald MM, Coronado VG: Traumatic brain injury in the United States: emergency department visits, hospitalizations, and deaths, 2002-2006. Atlanta, GA, Centers for Disease Control and Prevention, National Center for Injury Prevention and Control, 2010
5.
Finkelstein E, Corso P, Miller T: The Incidence and Economic Burden of Injuries in the United States. New York, Oxford University Press, 2006, pp 12–159
6.
National Center for Injury Prevention and Control (US): Report to Congress on mild traumatic brain injury in the United States: Steps to prevent a serious public health problem. Centers for Disease Control and Prevention, 2003
7.
Johnstone B, Mount D, Schopp LH: Financial and vocational outcomes 1 year after traumatic brain injury. Arch Phys Med Rehabil 2003; 84:238–241
8.
Binder LM: Persisting symptoms after mild head injury: a review of the postconcussive syndrome. J Clin Exp Neuropsychol 1986; 8:323–346
9.
Mittenberg W, DiGiulio DV, Perrin S, Bass AE: Symptoms following mild head injury: expectation as aetiology. J Neurol Neurosurg Psychiatry 1992; 55:200–204
10.
Cicerone KD, Kalmar K: Persistent postconcussion syndrome: the structure of subjective complaints after mild traumatic brain injury. J Head Trauma Rehabil 1995; 10:1–1
11.
Langlois JA, Rutland-Brown W, Wald MM: The epidemiology and impact of traumatic brain injury: a brief overview. J Head Trauma Rehabil 2006; 21:375–378
12.
Wehman P, Targett P, West M, Kregel J: Productive work and employment for persons with traumatic brain injury: what have we learned after 20 years? J Head Trauma Rehabil 2005; 20:115–127
13.
Hall KM, Karzmark P, Stevens M, Englander J, O’Hare P, Wright J: Family stressors in traumatic brain injury: a two-year follow-up. Arch Phys Med Rehabil 1994; 75:876–884
14.
Anderson MI, Parmenter TR, Mok M: The relationship between neurobehavioural problems of severe traumatic brain injury (TBI), family functioning and the psychological well-being of the spouse/caregiver: path model analysis. Brain Inj 2002; 16:743–757
15.
Kreutzer JS, Marwitz JH, Kepler K: Traumatic brain injury: family response and outcome. Arch Phys Med Rehabil 1992; 73:771–778
16.
Lee B, Newberg A: Neuroimaging in traumatic brain imaging. NeuroRx 2005; 2:372–383
17.
Andriessen TMJC, Jacobs B, Vos PE: Clinical characteristics and pathophysiological mechanisms of focal and diffuse traumatic brain injury. J Cell Mol Med 2010; 14:2381–2392
18.
McCrory P, Meeuwisse W, Johnston K, Dvorak J, Aubry M, Molloy M, Cantu R: Consensus statement on Concussion in Sport–the 3rd International Conference on Concussion in Sport held in Zurich, Nov 2008. South African Journal of Sports Medicine 2009; 21:36–46
19.
Lovell MR, Collins MW, Podell K, Powell J, Maroon J: ImPACT: Immediate post-concussion assessment and cognitive testing. Pittsburgh, PA, NeuroHealth Systems, LLC, 2000
20.
Schatz P, Pardini JE, Lovell MR, Collins MW, Podell K: Sensitivity and specificity of the ImPACT Test Battery for concussion in athletes. Arch Clin Neuropsychol 2006; 21:91–99
21.
Van Boven RW, Harrington GS, Hackney DB, Ebel A, Gauger G, Bremner JD, D’Esposito M, Detre JA, Haacke EM, Jack CR, Jagust WJ, Le Bihan D, Mathis CA, Mueller S, Mukherjee P, Schuff N, Chen A, Weiner MW: Advances in neuroimaging of traumatic brain injury and posttraumatic stress disorder. J Rehabil Res Dev 2009; 46:717–757
22.
Huang MX, Theilmann RJ, Robb A, Angeles A, Nichols S, Drake A, D’Andrea J, Levy M, Holland M, Song T, Ge S, Hwang E, Yoo K, Cui L, Baker DG, Trauner D, Coimbra R, Lee RR: Integrated imaging approach with MEG and DTI to detect mild traumatic brain injury in military and civilian patients. J Neurotrauma 2009; 26:1213–1226
23.
National Institute of Neurological Disorders and Stroke (US): Traumatic Brain Injury Information Page [internet]. National Institute of Health; [Cited Oct 2012]. Available from: http://www.ninds.nih.gov/disorders/tbi/tbi.htm
24.
Barkhoudarian G, Hovda DA, Giza CC: The molecular pathophysiology of concussive brain injury. Clin Sports Med 2011; 30:33–48, vii–iii
25.
Spain A, Daumas S, Lifshitz J, Rhodes J, Andrews PJ, Horsburgh K, Fowler JH: Mild fluid percussion injury in mice produces evolving selective axonal pathology and cognitive deficits relevant to human brain injury. J Neurotrauma 2010; 27:1429–1438
26.
Blennow K, Hardy J, Zetterberg H: The neuropathology and neurobiology of traumatic brain injury. Neuron 2012; 76:886–899
27.
Giza CC, Hovda DA: The Neurometabolic Cascade of Concussion. J Athl Train 2001; 36:228–235
28.
Orff HJ, Ayalon L, Drummond SP: Traumatic brain injury and sleep disturbance: a review of current research. J Head Trauma Rehabil 2009; 24:155–165
29.
Ouellet MC, Savard J, Morin CM: Insomnia following traumatic brain injury: a review. Neurorehabil Neural Repair 2004; 18:187–198
30.
Mathias JL, Alvaro PK: Prevalence of sleep disturbances, disorders, and problems following traumatic brain injury: a meta-analysis. Sleep Med 2012; 13:898–905
31.
Belmont A, Agar N, Hugeron C, Gallais B, Azouvi P: Fatigue and traumatic brain injury. Ann Readapt Med Phys 2006; 49:283–288, 370–374
32.
Olver JH, Ponsford JL, Curran CA: Outcome following traumatic brain injury: a comparison between 2 and 5 years after injury. Brain Inj 1996; 10:841–848
33.
Sherman KB, Goldberg M, Bell KR: Traumatic brain injury and pain. Phys Med Rehabil Clin N Am 2006; 17:473–490, viii
34.
Nampiaparampil DE: Prevalence of chronic pain after traumatic brain injury: a systematic review. JAMA 2008; 300:711–719
35.
Halbauer JD, Ashford JW, Zeitzer JM, Adamson MM, Lew HL, Yesavage JA: Neuropsychiatric diagnosis and management of chronic sequelae of war-related mild to moderate traumatic brain injury. J Rehabil Res Dev 2009; 46:757–796
36.
Larson EB, Kondiles BR, Starr CR, Zollman FS: Postconcussive complaints, cognition, symptom attribution and effort among veterans. J Int Neuropsychol Soc 2013; 19:88–95
37.
Bogdanova Y, Verfaellie M: Cognitive sequelae of blast-induced traumatic brain injury: recovery and rehabilitation. Neuropsychol Rev 2012; 22:4–20
38.
Kinsella G, Murtagh D, Landry A, Homfray K, Hammond M, O’Beirne L, Dwyer L, Lamont M, Ponsford J: Everyday memory following traumatic brain injury. Brain Inj 1996; 10:499–507
39.
Vanderploeg RD, Crowell TA, Curtiss G: Verbal learning and memory deficits in traumatic brain injury: encoding, consolidation, and retrieval. J Clin Exp Neuropsychol 2001; 23:185–195
40.
Vanderploeg RD, Curtiss G, Belanger HG: Long-term neuropsychological outcomes following mild traumatic brain injury. J Int Neuropsychol Soc 2005; 11:228–236
41.
Belanger HG, Curtiss G, Demery JA, Lebowitz BK, Vanderploeg RD: Factors moderating neuropsychological outcomes following mild traumatic brain injury: a meta-analysis. J Int Neuropsychol Soc 2005; 11:215–227
42.
Vasterling JJ, Brailey K, Proctor SP, Kane R, Heeren T, Franz M: Neuropsychological outcomes of mild traumatic brain injury, post-traumatic stress disorder and depression in Iraq-deployed US Army soldiers. Br J Psychiatry 2012; 201:186–192
43.
Binder LM, Rohling ML, Larrabee GJ: A review of mild head trauma. Part I: Meta-analytic review of neuropsychological studies. J Clin Exp Neuropsychol 1997; 19:421–431
44.
Iverson GL: Outcome from mild traumatic brain injury. Curr Opin Psychiatry 2005; 18:301–317
45.
Schretlen DJ, Shapiro AM: A quantitative review of the effects of traumatic brain injury on cognitive functioning. Int Rev Psychiatry 2003; 15:341–349
46.
Dawson DR, Schwartz ML, Winocur G, Stuss DT: Return to productivity following traumatic brain injury: cognitive, psychological, physical, spiritual, and environmental correlates. Disabil Rehabil 2007; 29:301–313
47.
Belanger HG, Vanderploeg RD: The neuropsychological impact of sports-related concussion: a meta-analysis. J Int Neuropsychol Soc 2005; 11:345–357
48.
Castriotta RJ, Wilde MC, Lai JM, Atanasov S, Masel BE, Kuna ST: Prevalence and consequences of sleep disorders in traumatic brain injury. J Clin Sleep Med 2007; 3:349–356
49.
Parcell DL, Ponsford JL, Rajaratnam SM, Redman JR: Self-reported changes to nighttime sleep after traumatic brain injury. Arch Phys Med Rehabil 2006; 87:278–285
50.
Calhoun PS, Wiley M, Dennis MF, Means MK, Edinger JD, Beckham JC: Objective evidence of sleep disturbance in women with posttraumatic stress disorder. J Trauma Stress 2007; 20:1009–1018
51.
Bloomfield ILM, Espie CA, Evans JJ: Do sleep difficulties exacerbate deficits in sustained attention following traumatic brain injury? J Int Neuropsychol Soc 2010; 16:17–25
52.
Doctor JN, Castro J, Temkin NR, Fraser RT, Machamer JE, Dikmen SS: Workers’ risk of unemployment after traumatic brain injury: a normed comparison. J Int Neuropsychol Soc 2005; 11:747–752
53.
Gunstad J, Suhr JA: Perception of illness: nonspecificity of postconcussion syndrome symptom expectation. J Int Neuropsychol Soc 2002; 8:37–47
54.
Snell DL, Siegert RJ, Hay-Smith EJC, Surgenor LJ: Associations between illness perceptions, coping styles and outcome after mild traumatic brain injury: preliminary results from a cohort study. Brain Inj 2011; 25:1126–1138
55.
Hannay HJ, Howieson DB, Loring DW, Fischer JS, Lezak MD: Neuropathology for neuropsychologists. Neuropsychological Assessment 2004; 4:157–194
56.
Moore EL, Terryberry-Spohr L, Hope DA: Mild traumatic brain injury and anxiety sequelae: a review of the literature. Brain Inj 2006; 20:117–132
57.
Ponsford J, Willmott C, Rothwell A, Cameron P, Kelly AM, Nelms R, Curran C, Ng K: Factors influencing outcome following mild traumatic brain injury in adults. J Int Neuropsychol Soc 2000; 6:568–579
58.
Dikmen SS, Machamer JE, Powell JM, Temkin NR: Outcome 3 to 5 years after moderate to severe traumatic brain injury. Arch Phys Med Rehabil 2003; 84:1449–1457
59.
Katz DI, Alexander MP: Traumatic brain injury. Predicting course of recovery and outcome for patients admitted to rehabilitation. Arch Neurol 1994; 51:661–670
60.
Steyerberg EW, Mushkudiani N, Perel P, Butcher I, Lu J, McHugh GS, Murray GD, Marmarou A, Roberts I, Habbema JD, Maas AI: Predicting outcome after traumatic brain injury: development and international validation of prognostic scores based on admission characteristics. PLoS Med 2008; 5:e165-, discussion e165
61.
Perel P, Arango M, Clayton T, Edwards P, Komolafe E, Poccock S, Roberts I, Shakur H, Steyerberg E, Yutthakasemsunt SMRC CRASH Trial Collaborators: Predicting outcome after traumatic brain injury: practical prognostic models based on large cohort of international patients. BMJ 2008; 336:425–429
62.
McCrea M, Iverson GL, McAllister TW, Hammeke TA, Powell MR, Barr WB, Kelly JP: An integrated review of recovery after mild traumatic brain injury (MTBI): implications for clinical management. Clin Neuropsychol 2009; 23:1368–1390
63.
Willer B, Leddy JJ: Management of concussion and post-concussion syndrome. Curr Treat Options Neurol 2006; 8:415–426
64.
Aram DM, Eisele J: Plasticity and recovery of higher cortical functions following early brain injury. Handbook of Neuropsychology: Child Neuropsychology. Amsterdam, Elsevier, 1992
65.
Vargha-Khadem F, Isaacs E, Muter V: A review of cognitive outcome after unilateral lesions sustained during childhood. J Child Neurol 199; 9(Supp. 2):67-73
66.
Giza CC, Prins ML: Is being plastic fantastic? Mechanisms of altered plasticity after developmental traumatic brain injury. Dev Neurosci 2006; 28:364–379
67.
Giza CC, Mink RB, Madikians A: Pediatric traumatic brain injury: not just little adults. Curr Opin Crit Care 2007; 13:143–152
68.
Anderson V, Spencer-Smith M, Wood A: Do children really recover better? Neurobehavioural plasticity after early brain insult. Brain 2011; 134:2197–2221
69.
Gondusky JS, Reiter MP: Protecting military convoys in Iraq: an examination of battle injuries sustained by a mechanized battalion during Operation Iraqi Freedom II. Mil Med 2005; 170:546–549
70.
Luethcke CA, Bryan CJ, Morrow CE, Isler WC: Comparison of concussive symptoms, cognitive performance, and psychological symptoms between acute blast-versus nonblast-induced mild traumatic brain injury. J Int Neuropsychol Soc 2011; 17:36–45
71.
Cooper DB, Chau PM, Armistead-Jehle P, Vanderploeg RD, Bowles AO: Relationship between mechanism of injury and neurocognitive functioning in OEF/OIF service members with mild traumatic brain injuries. Mil Med 2012; 177:1157–1160
72.
Goldstein LE, Fisher AM, Tagge CA, Zhang XL, Velisek L, Sullivan JA, Upreti C, Kracht JM, Ericsson M, Wojnarowicz MW, Goletiani CJ, Maglakelidze GM, Casey N, Moncaster JA, Minaeva O, Moir RD, Nowinski CJ, Stern RA, Cantu RC, Geiling J, Blusztajn JK, Wolozin BL, Ikezu T, Stein TD, Budson AE, Kowall NW, Chargin D, Sharon A, Saman S, Hall GF, Moss WC, Cleveland RO, Tanzi RE, Stanton PK, McKee AC: Chronic traumatic encephalopathy in blast-exposed military veterans and a blast neurotrauma mouse model. Sci Transl Med 2012; 4:34ra60
73.
Mac Donald CL, Johnson AM, Cooper D, Nelson EC, Werner NJ, Shimony JS, Snyder AZ, Raichle ME, Witherow JR, Fang R, Flaherty SF, Brody DL: Detection of blast-related traumatic brain injury in U.S. military personnel. N Engl J Med 2011; 364:2091–2100
74.
Plassman BL, Havlik RJ, Steffens DC, Helms MJ, Newman TN, Drosdick D, Phillips C, Gau BA, Welsh-Bohmer KA, Burke JR, Guralnik JM, Breitner JC: Documented head injury in early adulthood and risk of Alzheimer’s disease and other dementias. Neurology 2000; 55:1158–1166
75.
Guskiewicz KM, Marshall SW, Bailes J, McCrea M, Cantu RC, Randolph C, Jordan BD: Association between recurrent concussion and late-life cognitive impairment in retired professional football players. Neurosurgery 2005; 57:719–726, discussion 719–726
76.
Povlishock JT: The window of risk in repeated head injury. J Neurotrauma 2013; 30:1–1
77.
Stern RA, Riley DO, Daneshvar DH, Nowinski CJ, Cantu RC, McKee AC: Long-term consequences of repetitive brain trauma: chronic traumatic encephalopathy. PM R 2011; 3(Suppl 2):S460–S467
78.
Matser EJ, Kessels AG, Lezak MD, Jordan BD, Troost J: Neuropsychological impairment in amateur soccer players. JAMA 1999; 282:971–973
79.
Corsellis JAN, Bruton CJ, Freeman-Browne D: The aftermath of boxing. Psychol Med 1973; 3:270–303
80.
Roberts AH: Brain damage in boxers: A study of the prevalence of traumatic encephalopathy among ex-professional boxers. London, Pitman Medical & Scientific Publishing Co, Ltd, 1969
81.
Cantu RC: Chronic traumatic encephalopathy in the National Football League. Neurosurgery 2007; 61:223–225
82.
Daneshvar DH, Nowinski CJ, McKee AC, Cantu RC: The epidemiology of sport-related concussion. Clin Sports Med 2011; 30:1–17, vii
83.
Gavett BE, Stern RA, McKee AC: Chronic traumatic encephalopathy: a potential late effect of sport-related concussive and subconcussive head trauma. Clin Sports Med 2011; 30:179–188, xi
84.
Guskiewicz KM, Marshall SW, Bailes J, McCrea M, Harding HP, Matthews A, Mihalik JR, Cantu RC: Recurrent concussion and risk of depression in retired professional football players. Med Sci Sports Exerc 2007; 39:903–909
85.
Daniel JC, Olesniewicz MH, Reeves DL, Tam D, Bleiberg J, Thatcher R, Salazar A: Repeated measures of cognitive processing efficiency in adolescent athletes: implications for monitoring recovery from concussion. Neuropsychiatry Neuropsychol Behav Neurol 1999; 12:167–169
86.
Silver JM, Kramer R, Greenwald S, Weissman M: The association between head injuries and psychiatric disorders: findings from the New Haven NIMH Epidemiologic Catchment Area Study. Brain Inj 2001; 15:935–945
87.
Fann JR, Hart T, Schomer KG: Treatment for depression after traumatic brain injury: a systematic review. J Neurotrauma 2009; 26:2383–2402
88.
Taylor BC, Hagel EM, Carlson KF, Cifu DX, Cutting A, Bidelspach DE, Sayer NA: Prevalence and costs of co-occurring traumatic brain injury with and without psychiatric disturbance and pain among Afghanistan and Iraq War Veteran V.A. users. Med Care 2012; 50:342–346
89.
Hoffman SW, Harrison C: The interaction between psychological health and traumatic brain injury: a neuroscience perspective. Clin Neuropsychol 2009; 23:1400–1415
90.
Rogers JM, Read CA: Psychiatric comorbidity following traumatic brain injury. Brain Inj 2007; 21:1321–1333
91.
Rosenthal M, Christensen BK, Ross TP: Depression following traumatic brain injury. Arch Phys Med Rehabil 1998; 79:90–103
92.
Jorge R, Robinson RG: Mood disorders following traumatic brain injury. Int Rev Psychiatry 2003; 15:317–327
93.
Dikmen SS, Bombardier CH, Machamer JE, Fann JR, Temkin NR: Natural history of depression in traumatic brain injury. Arch Phys Med Rehabil 2004; 85:1457–1464
94.
Fann JR, Burington B, Leonetti A, Jaffe K, Katon WJ, Thompson RS: Psychiatric illness following traumatic brain injury in an adult health maintenance organization population. Arch Gen Psychiatry 2004; 61:53–61
95.
Levin HS, Brown SA, Song JX, McCauley SR, Boake C, Contant CF, Goodman H, Kotrla KJ: Depression and posttraumatic stress disorder at three months after mild to moderate traumatic brain injury. J Clin Exp Neuropsychol 2001; 23:754–769
96.
Taylor CA, Jung HY: Disorders of Mood After Traumatic Brain Injury. Semin Clin Neuropsychiatry 1998; 3:224–231
97.
Stein MB, McAllister TW: Exploring the convergence of posttraumatic stress disorder and mild traumatic brain injury. Am J Psychiatry 2009; 166:768–776
98.
van Reekum R, Cohen T, Wong J: Can traumatic brain injury cause psychiatric disorders? J Neuropsychiatry Clin Neurosci 2000; 12:316–327
99.
Hiott DW, Labbate L: Anxiety disorders associated with traumatic brain injuries. NeuroRehabilitation 2002; 17:345–355
100.
Koponen S, Taiminen T, Portin R, Himanen L, Isoniemi H, Heinonen H, Hinkka S, Tenovuo O: Axis I and II psychiatric disorders after traumatic brain injury: a 30-year follow-up study. Am J Psychiatry 2002; 159:1315–1321
101.
IOM (Institute of Medicine): Cognitive Rehabilitation Therapy for Traumatic Brain Injury: Evaluating the Evidence. Washington, DC, The National Academies Press, 2011
102.
Carlson KF, Nelson D, Orazem RJ, Nugent S, Cifu DX, Sayer NA: Psychiatric diagnoses among Iraq and Afghanistan war veterans screened for deployment-related traumatic brain injury. J Trauma Stress 2010; 23:17–24
103.
Feinstein A, Hershkop S, Jardine A, Ouchterlony D: The prevalence and neuropsychiatric correlates of posttraumatic stress symptoms following mild traumatic brain injury. Brain Cogn 2000; 44:78–82
104.
Sbordone RJ, Liter JC: Mild traumatic brain injury does not produce post-traumatic stress disorder. Brain Inj 1995; 9:405–412
105.
Mayou R, Bryant B, Duthie R: Psychiatric consequences of road traffic accidents. BMJ 1993; 307:647–651
106.
Zatzick DF, Rivara FP, Jurkovich GJ, Hoge CW, Wang J, Fan MY, Russo J, Trusz SG, Nathens A, Mackenzie EJ: Multisite investigation of traumatic brain injuries, posttraumatic stress disorder, and self-reported health and cognitive impairments. Arch Gen Psychiatry 2010; 67:1291–1300
107.
McMillan TM: Errors in diagnosing post-traumatic stress disorder after traumatic brain injury. Brain Inj 2001; 15:39–46
108.
Hibbard MR, Uysal S, Kepler K, Bogdany J, Silver J: Axis I psychopathology in individuals with traumatic brain injury. J Head Trauma Rehabil 1998; 13:24–39
109.
Sparedo F, Gill D: Effects of prior alcohol use on head injury recovery. J Head Trauma Rehabil 1989; 4:75–82
110.
Taylor LA, Kreutzer JS, Demm SR, Meade MA: Traumatic brain injury and substance abuse: A review and analysis of the literature. Neuropsychol Rehabil 2003; 13:165–188
111.
Ruff RM, Marshall LF, Klauber MR, Blunt BA: Alcohol abuse and neurological outcome of the severely head injured. J Head Trauma Rehabil 1990; 5:21–31
112.
Kolakowsky-Hayner SA, Gourley EV, Kreutzer JS, Marwitz JH, Meade MA, Cifu DX: Post-injury substance abuse among persons with brain injury and persons with spinal cord injury. Brain Inj 2002; 16:583–592
113.
Marklund N, Bakshi A, Castelbuono DJ, Conte V, McIntosh TK: Evaluation of pharmacological treatment strategies in traumatic brain injury. Curr Pharm Des 2006; 12:1645–1680
114.
Warden DL, Gordon B, McAllister TW, Silver JM, Barth JT, Bruns J, Drake A, Gentry T, Jagoda A, Katz DI, Kraus J, Labbate LA, Ryan LM, Sparling MB, Walters B, Whyte J, Zapata A, Zitnay GNeurobehavioral Guidelines Working Group: Guidelines for the pharmacologic treatment of neurobehavioral sequelae of traumatic brain injury. J Neurotrauma 2006; 23:1468–1501
115.
Talsky A, Pacione LR, Shaw T, Wasserman L, Lenny A, Verma A, Hurwitz G, Waxman R, Morgan A, Bhalerao S: Pharmacological interventions for traumatic brain injury. B C Med J 2010; 53:26–31
116.
Rao V, Lyketsos C: Neuropsychiatric sequelae of traumatic brain injury. Psychosomatics 2000; 41:95–103
117.
Management of Concussion/mTBI Working Group: VA/DoD clinical practice guideline for management of concussion/mild traumatic brain injury. J Rehabil Res Dev 2009; 46:703–716
118.
Twamley EW, Jeste DV, Bellack AS: A review of cognitive training in schizophrenia. Schizophr Bull 2003; 29:359–382
119.
Wykes T, Huddy V, Cellard C, McGurk SR, Czobor P: A meta-analysis of cognitive remediation for schizophrenia: methodology and effect sizes. Am J Psychiatry 2011; 168:472–485
120.
Sitzer DI, Twamley EW, Jeste DV: Cognitive training in Alzheimer’s disease: a meta-analysis of the literature. Acta Psychiatr Scand 2006; 114:75–90
121.
Carney N, Chesnut RM, Maynard H, Mann NC, Patterson P, Helfand M: Effect of cognitive rehabilitation on outcomes for persons with traumatic brain injury: A systematic review. J Head Trauma Rehabil 1999; 14:277–307
122.
Cicerone KD, Langenbahn DM, Braden C, Malec JF, Kalmar K, Fraas M, Felicetti T, Laatsch L, Harley JP, Bergquist T, Azulay J, Cantor J, Ashman T: Evidence-based cognitive rehabilitation: updated review of the literature from 2003 through 2008. Arch Phys Med Rehabil 2011; 92:519–530
123.
NIH Consensus Development Panel on Rehabilitation of Persons With Traumatic Brain Injury: Consensus conference. Rehabilitation of persons with traumatic brain injury. JAMA 1999; 282:974–983
124.
Comper P, Bisschop SM, Carnide N, Tricco A: A systematic review of treatments for mild traumatic brain injury. Brain Inj 2005; 19:863–880
125.
Tiersky LA, Anselmi V, Johnston MV, Kurtyka J, Roosen E, Schwartz T, Deluca J: A trial of neuropsychologic rehabilitation in mild-spectrum traumatic brain injury. Arch Phys Med Rehabil 2005; 86:1565–1574
126.
Cicerone KD: Remediation of “working attention” in mild traumatic brain injury. Brain Inj 2002; 16:185–195
127.
Borg J, Holm L, Peloso PM, Cassidy JD, Carroll LJ, von Holst H, Paniak C, Yates DWHO Collaborating Centre Task Force on Mild Traumatic Brain Injury: Non-surgical intervention and cost for mild traumatic brain injury: results of the WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury. J Rehabil Med 2004; 43(Suppl):76–83
128.
Snell DL, Surgenor LJ, Hay-Smith EJC, Siegert RJ: A systematic review of psychological treatments for mild traumatic brain injury: an update on the evidence. J Clin Exp Neuropsychol 2009; 31:20–38
129.
Kreutzer JS, Wehman P, Morton MV, Stonnington HH: Supported employment and compensatory strategies for enhancing vocational outcome following traumatic brain injury. Brain Inj 1988; 2:205–223
130.
Twamley EW, Vella L, Burton CZ, Heaton RK, Jeste DV: Compensatory cognitive training for psychosis: effects in a randomized controlled trial. J Clin Psychiatry 2012; 73:1212–1219
131.
Huckans M, Pavawalla S, Demadura T, Kolessar M, Seelye A, Roost N, Twamley EW, Storzbach D: A pilot study examining effects of group-based Cognitive Strategy Training treatment on self-reported cognitive problems, psychiatric symptoms, functioning, and compensatory strategy use in OIF/OEF combat veterans with persistent mild cognitive disorder and history of traumatic brain injury. J Rehabil Res Dev 2010; 47:43–60
132.
Shames J, Treger I, Ring H, Giaquinto S: Return to work following traumatic brain injury: trends and challenges. Disabil Rehabil 2007; 29:1387–1395
133.
McNamee S, Walker W, Cifu DX, Wehman PH: Minimizing the effect of TBI-related physical sequelae on vocational return. J Rehabil Res Dev 2009; 46:893–908
134.
Ruffolo CF, Friedland JF, Dawson DR, Colantonio A, Lindsay PH: Mild traumatic brain injury from motor vehicle accidents: factors associated with return to work. Arch Phys Med Rehabil 1999; 80:392–398
135.
Wehman P, Kregel J, Keyser-Marcus L, Sherron-Targett P, Campbell L, West M, Cifu DX: Supported employment for persons with traumatic brain injury: a preliminary investigation of long-term follow-up costs and program efficiency. Arch Phys Med Rehabil 2003; 84:192–196
136.
Malec JF, Moessner AM: Replicated positive results for the VCC model of vocational intervention after ABI within the social model of disability. Brain Inj 2006; 20:227–236
137.
Hoge CW, Goldberg HM, Castro CA: Care of war veterans with mild traumatic brain injury—flawed perspectives. N Engl J Med 2009; 360:1588–1591
138.
Arciniegas DB, Anderson CA, Topkoff J, McAllister TW: Mild traumatic brain injury: a neuropsychiatric approach to diagnosis, evaluation, and treatment. Neuropsychiatr Dis Treat 2005; 1:311–327
139.
Macciocchi SN, Barth JT, Alves W, Rimel RW, Jane JA: Neuropsychological functioning and recovery after mild head injury in collegiate athletes. Neurosurgery 1996; 39:510–514
140.
Vanderploeg RD, Belanger HG, Curtiss G: Mild traumatic brain injury and posttraumatic stress disorder and their associations with health symptoms. Arch Phys Med Rehabil 2009; 90:1084–1093
141.
Pietrzak RH, Johnson DC, Goldstein MB, Malley JC, Southwick SM: Posttraumatic stress disorder mediates the relationship between mild traumatic brain injury and health and psychosocial functioning in veterans of Operations Enduring Freedom and Iraqi Freedom. J Nerv Ment Dis 2009; 197:748–753
142.
Nelson LA, Yoash-Gantz RE, Pickett TC, Campbell TA: Relationship between processing speed and executive functioning performance among OEF/OIF veterans: implications for postdeployment rehabilitation. J Head Trauma Rehabil 2009; 24:32–40
143.
Hoge CW, McGurk D, Thomas JL, Cox AL, Engel CC, Castro CA: Mild traumatic brain injury in U.S. Soldiers returning from Iraq. N Engl J Med 2008; 358:453–463
144.
O'Neil ME, Carlson KF, Storzbach D, Brenner LA, Freeman M, Quiñones A, Motu'apuaka M, Ensley M, Kansagara D: Complications of Mild Traumatic Brain Injury in Veterans and Military Personnel: A Systematic Review. VA-ESP Project #05-225, 2012
145.
Rutherford WH: Postconcussion symptoms: relationship to acute neurological indices, individual differences, and circumstances of injury. Mild head injury 1989; 217-228
146.
Bohnen N, Jolles J: Neurobehavioral aspects of postconcussive symptoms after mild head injury. J Nerv Ment Dis 1992; 180:683–692
147.
Vasterling JJ, Verfaellie M, Sullivan KD: Mild traumatic brain injury and posttraumatic stress disorder in returning veterans: perspectives from cognitive neuroscience. Clin Psychol Rev 2009; 29:674–684
148.
Carone D: Mild Traumatic Brain Injury: Symptom Validity Assessment and Malingering . New York, Springer, 2012
149.
Delis DC, Wetter SR: Cogniform Disorder and Cogniform Condition: proposed diagnoses for excessive cognitive symptoms. Arch Clin Neuropsychol 2007; 22:589–604
150.
Armistead-Jehle P: Symptom validity test performance in U.S. veterans referred for evaluation of mild TBI. Appl Neuropsychol 2010; 17:52–59
151.
Mild Traumatic Brain Injury Committee, ACoRM Head Injury Interdisciplinary Special Interest Group: Definition of mild traumatic brain injury. J Head Trauma Rehabil 1993; 8:86–87
152.
Halstead ME, Walter KDCouncil on Sports Medicine and Fitness, American Academy of Pediatrics: Clinical report—sport-related concussion in children and adolescents. Pediatrics 2010; 126:597–615
153.
World Health Organization: International Statistical Classification of Diseases and Related Health Problems, Tenth Revision. Geneva, WHO, 1992
154.
Cantu RC: Cerebral concussion in sport: management and prevention. Sports Med 1992; 14:64–74
155.
Ruff RM, Jurica P: In search of a unified definition for mild traumatic brain injury. Brain Inj 1999; 13:943–952
156.
Department of Labor and Employment: Traumatic brain injury medical treatment guidelines. Denver, Colo, Division of Workers’ Compensation, 2005
157.
Report of the Quality Standards Subcommittee: Practice parameter: the management of concussion in sports (summary statement). Neurology 1997; 48:581–585
Information & Authors
Information
Published In
History
Published online: 1 July 2013
Published in print: Summer 2013
Authors
Funding Information
Author Information and CME Disclosure
Henry J. Orff, Ph.D., Center of Excellence for Stress and Mental Health, VA San Diego Healthcare System; and Department of Psychiatry, University of California, San Diego
Chelsea C. Hays, Research Service, VA San Diego Healthcare System
Ashlee A. Heldreth, B.A., B.S., School of Speech, Language, and Hearing Sciences, San Diego State University
Murray B. Stein, M.D., M.P.H., Department of Psychiatry, University of California, San Diego; Department of Family and Preventive Medicine, University of California, San Diego; and Psychiatry Service, VA San Diego Healthcare System
Elizabeth W. Twamley, Ph.D., Center of Excellence for Stress and Mental Health, VA San Diego Healthcare System; Psychiatry Service, VA San Diego Healthcare System; Department of Psychiatry, University of California, San Diego
All authors report no competing interests.
The authors acknowledge grant support from the VA Rehabilitation Research and Development Service (D7217-R to EWT) and the Department of Defense (W81XWH-08-2-0159, INTRuST Clinical Consortium, to MBS).Metrics & Citations
Metrics
Citations
Export Citations
If you have the appropriate software installed, you can download article citation data to the citation manager of your choice. Simply select your manager software from the list below and click Download.
For more information or tips please see 'Downloading to a citation manager' in the Help menu.
View Options
View options
PDF/EPUB
View PDF/EPUBGet Access
Login options
Already a subscriber? Access your subscription through your login credentials or your institution for full access to this article.
Personal login Institutional Login Open Athens loginNot a subscriber?
PsychiatryOnline subscription options offer access to the DSM-5-TR® library, books, journals, CME, and patient resources. This all-in-one virtual library provides psychiatrists and mental health professionals with key resources for diagnosis, treatment, research, and professional development.
Need more help? PsychiatryOnline Customer Service may be reached by emailing [email protected] or by calling 800-368-5777 (in the U.S.) or 703-907-7322 (outside the U.S.).