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Laskowitz D, Grant G, editors. Translational Research in Traumatic Brain Injury. Boca Raton (FL): CRC Press/Taylor and Francis Group; 2016.

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Translational Research in Traumatic Brain Injury.

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Chapter 19Neurocognitive and Psychiatric Symptoms following Mild Traumatic Brain Injury

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Traumatic brain injury (TBI) is associated with a wide variety of symptoms that impact cognition and emotional health. The vast majority of TBI incurred in the United States and across the world are of the mild severity (MTBI). Symptoms after MTBI are generally regarded as transient. Common symptoms include sensory and somatic symptoms (headache, blurred vision, dizziness, sleep problems), neurobehavioral and cognitive complaints (subjective memory problems, poor concentration, slowed information processing, and other cognitive difficulties), and neuropsychiatric complaints related to emotional difficulties (irritability, depression, anxiety).1,2

NEUROCOGNITIVE SYMPTOMS AND EXPECTED RECOVERY

Studies exploring self-reported neurobehavioral complaints after MTBI indicate that patients experience the most severe symptoms in the acute stage of injury (<72 hours after injury) and generally start improving over the next several days.3 The majority of patients experience full recovery within a couple of weeks to 3 months.1,3,4 However, well-designed prospective studies indicate a small percentage of patients continue to complain of symptoms 12 months after injury.5

Large-scale meta-analytical studies suggest that individuals with MTBI have good neurobehavioral and cognitive recovery.4,68 Specifically, recovery in cognitive functioning is found to have a similar trajectory to self-reported postconcussive symptoms. That is, after MTBI, disruptions in cognitive functioning may be observed within the first 6 days of injury with rapid improvement observed and patients becoming statistically indistinguishable from controls on cognitive tests at 1 month postinjury.9 In a meta-analysis, Belanger and colleagues6 investigated the long-term impact concussion has on specific cognitive domains. Within 90 days of injury, their analysis revealed a large impact on memory and verbal fluency with moderate impact on attention, language, and visuospatial ability. In patients more than 90 days from injury, the extent of cognitive impairment was dependent on their involvement in litigation as well as the sampling context (e.g., clinical setting versus prospectively studied individuals). The most methodologically sound studies (i.e., prospective) supported the conclusion that MTBI has no long-term impact on global cognitive functioning (d = 0.04) after 90 days. There was, however, evidence of an isolated impairment in verbal fluency (d = 0.98), though this finding was based on a single study.10 In contrast, studies that included litigants and studies that recruited participants from clinical settings both found moderate to large impacts in areas of attention, executive functioning, learning, and delayed memory.

In addition to neurocognitive symptoms, individuals sustaining a TBI of any level of severity are at higher risk of developing psychological distress, especially depression,11,12 anxiety, and post-traumatic stress disorder (PTSD).13 The prevalence rates of psychological distress after TBI have been reported as low as 4%–5%14 and as high as 49%–63%.15 The nature of the TBI as well as pre- and postinjury factors impact the presentation of subsequent psychological distress.

PERSISTENT POSTCONCUSSIVE SYMPTOMS (PPCS)

Though large-scale studies suggest individuals can expect complete recovery following MTBI, there is a subsample of individuals who appear to have persistent problems.1618 There has been criticism that the mainstream approaches to investigating MTBI substantiating the high recovery rate for the majority of patients (i.e., large group studies, meta analyses, etc.) obscure the minority of patients with persistent symptoms.1922 For example, Iverson19 demonstrated that statistical techniques relying on group analyses will not detect a hypothetical subgroup of individuals who are experiencing persistent symptoms. That is, there very well could be a subgroup of patients with persistent postconcussive symptoms (PPCS) who are veiled in traditional methodological and statistical approaches. Though the results of large-scale meta-analyses are extremely valuable in understanding MTBI, Iverson cautioned that the results should not be used to unequivocally state that MTBI cannot cause long-term problems in some individuals.

Estimates suggest 10% to 15% of patients who sustain an MTBI do not recover at 1 year postinjury,18 though it is important to mention this estimate has been criticized.23 The criticism is based primarily on methodological issues. Longitudinal studies indicate that presence or absence of clinically significant PPCS may vary over time. For example, Lange and colleagues24 assessed a group of service members with MTBI at 2 months and 12 months postinjury. They observed that more than half of participants had persistent symptoms at both time points. However, the individuals who had persistent symptoms at 2 months were not entirely the same group of participants who had persistent symptoms at 12 months. Specifically, approximately 20% of the sample with persistent symptoms at 2 months improved at 12 months, while almost 17% of the sample who did not have significant symptoms at 2 months reported increased and clinically significant PPCS at 12 months. Similar variability in symptom complaints following an MTBI has also been observed in civilian samples in which the specific type of symptoms reported changed over the course of a year.23,25,26

Studies on this topic continue to overcome methodological issues22,27 and account for confounding situational (e.g., secondary gain), social, psychological, and medical comorbidities28 that have limited previous work in this area. The prevalence of post-concussive symptoms, as well as its existence as a nosology, remains controversial.

Despite the ongoing debate, MTBI is known to have a substantial impact on disability in the United States, which indirectly speaks to the persistence of postcon-cussive symptoms. Employment issues represent a noteworthy indicator of overall disability and a sizeable number of patients (5%–20%) with MTBI, experience functional disability manifested by employment problems.2933 Given the extremely high incidence of MTBI, believed to be in excess of 100 to 600 per 100,000 people,34 even a relatively small percentage of patients with persistent disability represent a large societal and healthcare issue.

PSYCHOLOGICAL DISTRESS AND MILD TRAUMATIC BRAIN INJURY (MTBI)

A traumatic brain injury of any severity is by definition “traumatic,” and therefore indicates the individual sustaining the injury has experienced trauma. Thus, if there is emotional distress in response to the trauma sustained, and that distress persists, the individual may meet criteria for PTSD or some other psychiatric condition.35 In the military, as many as one-third of the service members who sustained an MTBI while on combat deployment reported post-traumatic stress symptoms.36 In those service members who had an MTBI with a loss of consciousness, 44% met criteria for PTSD, compared to only 9% of soldiers who did not sustain a concussion.

Post-traumatic symptoms (PTS) and PTSD after MTBI are also observed in civilians.37 Between 5% and 14% of civilians with MTBI will have “subthreshold” symptoms of acute stress disorder before being discharged from the hospital38,39 and 80% of these individuals will go on to develop PTSD.40 Overall, rates of PTS in civilians who suffered an MTBI is estimated to be between 13% and 40%.4145 Oddly, rates of PTSD appear to be higher after MTBI than moderate or severe TBI.46 There is evidence that individuals who experience longer post-traumatic amnesia (PTA) report less intrusive memories and are less likely to have subsequent PTSD or psychological distress.47 This suggests that loss of consciousness (LOC) or PTA surrounding injury may be a protective factor and could explain why PTSD rates are higher after MTBI than moderate or severe TBI, as more severe injuries are typically associated with longer LOC or PTA.46

Causal Links between TBI and Psychological Distress

The causal link between brain injury and psychological distress remains unclear. It has traditionally been thought that psychiatric responses after TBI are a reaction to persistent symptoms. That is, loss of functional abilities and independence, necessary lifestyle changes, or a loss of sense of self due to personality, mood, or cognitive changes resulting from the TBI contribute to feelings of depression, anxiety, or even PTSD. Other theories suggest PTSD is a learned response to trauma. That is, PTSD is hypothetically a classically conditioned response to the traumatic injury event.48 Therefore, it has been posited that, absent of LOC or PTA, the disorientation, confusion, or other alterations of consciousness that occurs after an injury may result in inaccurate or disorganized encoding of memories of the event, subsequently increasing the risk of developing PTS.35,49

Though a TBI is a “physical event” and PTSD or other psychiatric problems are a “psychological reaction” to an event, there is growing evidence supporting a link between biological and psychological processes and the subsequent physical and psychological recovery.37 As such, the injury could cause the psychological distress via physiological mechanisms. When directly linking biology and psychology, research has focused on the limbic regions and inferior frontal and medial temporal lobe structures.50,51 Langeland and Olff52 suggested PTS are related to an individual’s dysregulated biological response to stress, with direct implications for the hypothalamus-pituitary-adrenal (HPA) axis. Similarly, a limbic-frontal model has been implicated in the development of depression after TBI.53 Conversion disorder (i.e., psychological manifestation of physical symptoms) after TBI may also be related to injuries to the limbic, frontal, and temporal lobe structures.

There is an alternative viewpoint to the notion that psychological distress is caused by MTBI or persistent symptoms, with significant evidence building that psychological distress is independent of injury and even some evidence that PPCS may be better predicted by psychological distress rather than MTBI. Postconcussive symptoms are not specific to TBI, as many uninjured individuals report experiencing PPCS.54 Brenner and colleagues55 demonstrated that self-reported PPCS in service members returning from deployment were independently linked with either MTBI or PTSD.

As early as 1947, there were suggestions that a physical injury is not necessary for persistent injury symptoms.51 Miller, in 1961, described “accident neurosis” as a psychogenic manifestation of postinjury symptoms rather than being organically caused.56 Over 25 years ago, Lishman proposed that organic factors were more relevant in the acute injury phase, whereas psychological factors were more relevant during chronic stages of postinjury recovery.57 In 1996, McClelland suggested that symptoms in the first 3 months after injury were due to physical/biological reasons, and symptoms after this period were due to psychological reasons.58 More recently, Iverson and Lange13 state that if symptoms are actually due to TBI, they should be present in the first week after injury.

Growing evidence suggests that the causal link between injury, PPCS, and psychological distress may be in the opposite direction than expected. That is, psychological distress may be a better predictor of the presence of PPCS than an actual injury. Hoge and colleagues59 investigated the links between injury and subsequent symptoms, including psychological distress and PTSD, in service members returning from deployment. Their findings were somewhat controversial when first published, as they concluded that health problems reported by soldiers 3 to 4 months after sustaining MTBI were largely mediated by PTSD and not the actual injury. Since this publication, numerous other studies have demonstrated a similar effect. That is, non-TBI factors such as psychological distress contribute to the presence or worsening of symptoms in both military and civilian populations.45,6063 Specifically, psychological distress, notably depression and anxiety, present within the first 2 weeks postinjury, significantly increases the odds of displaying PPCS at 6 months postinjury.64

Premorbid Psychological Distress

Though psychological distress experienced in the acute stage of injury impacts recovery, this variable may not be as important as preinjury mental health. The presence of psychiatric issues, especially high levels of stress, prior to sustaining an injury is an important predictor for both psychological distress and PPCS after injury.6569 Ponsford and colleagues63 found that preinjury factors, notably physical or psychiatric problems, but not the actual MTBI, predicted PPCS. In a review of related civilian literature, McCauley and colleagues45 concluded that preinjury estimates of depressed mood and estimates of resilience were significant predictors of postinjury anxiety and PPCS, even after accounting for other potentially important factors such as age, gender, and education. However, they reported other preinjury factors predicted PPCS as well, including intelligence, demographics, poor social support, and personality factors.45

OTHER VARIABLES IMPACTING NEUROCOGNITIVE AND PSYCHIATRIC OUTCOMES

Demographic Variables

Other researchers in addition to McCauley and colleagues45 have indicated a variety of premorbid factors may impact an individual’s clinical presentation after injury. Several studies have indicated that women are more likely than men to experience PPCS,7072 though at least one study73 reported the opposite. With regard to age, some studies suggest that increased age is a risk factor for PPCS,71,73 while others have found little or no correlation between PPCS reporting and demographic factors such as age.74,75 These studies also found no relationship between level of education or socioeconomic status and PPCS.74,75 Overall, the research in this area can be contradictory and is still emerging, although it suggests that premorbid factors are important in considering an individual’s recovery after MTBI.

Blast-Related MTBI

Blast-related MTBI has unique pathophysiological mechanisms compared to blunt-force MTBI.76 MTBI, especially those related to blast overpressure exposure, has been a cardinal injury sustained by service members deployed to Operation Iraqi Freedom, Operation Enduring Freedom, and Operation New Dawn.59 Beyond the battlefield, blast-exposure to civilians through acts of terrorism (e.g., Boston Marathon bombing) and accidents (e.g., industrial plant explosions) presents a challenge to our medical community both in terms of response to mass causality incidents77,78 and proper treatment.79

Though mechanically and pathophysiologically unique, blast-related MTBI results in a similar behavioral presentation to nonblast-related MTBI during the acute stage. Luethcke and colleagues80 evaluated 39 individuals who sustained a blast-related MTBI and 38 individuals with a nonblast but combat-related MTBI within 72 hours of injury. The two groups were similar on measures of cognitive functioning, sleep, global mental health, and post-traumatic stress. The nonblast MTBI group reported more problems with balance, nausea, and vomiting, whereas the blast-related MTBI group reported more problems with hearing. In general, acute blast-related MTBI appears to result in similar clinical presentation to other causes of MTBI. Similarly, multiple studies have indicated that the long-term psychological and cognitive outcome of blast-related MTBI is no different than MTBI from other blunt force mechanisms.81,82

Though the clinical presentation of blast-related MTBI and blunt force trauma may be similar, Taber and colleagues83 recently observed that veterans with a prior history of blast-exposure had poorer white matter integrity compared to healthy controls. Interestingly, this relationship was observed in participants who had notable blast-exposure but who did not have any clinically significant symptoms following the event that would warrant a diagnosis of MTBI. However, the white-matter abnormalities in this blast-exposed group were related to poorer performance on cognitive tasks. The level of exposure to blast overpressure required to result in injury to the brain is not well delineated, and the impact of blast-exposure on neurological functioning may not be fully accounted for by current clinical diagnostic criteria for MTBI.

Repetitive Injuries

Repeated head injuries also impact recovery. Generally speaking, a history of repeated concussions (e.g., three or more) can be associated with greater vulnerability to subsequent injuries84 and greater memory impairment in the acute to subacute phase of injury.85 In a study of concussions in the National Hockey League, Benson86 observed that the time out of play (days) increased 2.25 times for every subsequent concussion. In a systematic review, Belanger and colleagues87 reported that the overall impact of repeated head injuries on neuropsychological outcome was statistically significant but not clinically meaningful (d = 0.06); this same study revealed that memory (d = 0.16) and executive functioning (d = 0.24) may be particularly vulnerable to multiple concussions.

There is early evidence to suggest repetitive “subconcussive” blows to the head can have neurological consequences that may have long-term neurobehavioral sequelae.88 These subconcussive events that do not result in a clinically diagnosable concussion are extremely common in contact sports such as rugby and American football. In the last 2 years advanced neuroimaging techniques have been used in investigations of repeated nonconcussive head injuries. These studies have typically evaluated individuals before and after periods of repetitive injury, such as an American football season. Abnormalities on neuroimaging using functional magnetic resonance imaging89,90 and diffusion tensor imaging83,91 in individuals exposed to frequent subconcussive events have both been reported. These changes on neuroimaging are correlated with head impact frequency and associated with cognitive and behavioral changes, as assessed by neuropsychological tests. This line of research on repeated subconcussive events dovetails with concerns about the longterm impact of multiple concussions on later cognitive and mental health problems as well as later development of neurodegenerative disease such as chronic traumatic encephalopathy (CTE).92,93

Medical Comorbidities

Polytrauma is common in individuals sustaining MTBI, and therefore concurrent physical injuries will play a role in the recovery from MTBI. However, research in the military indicates an inverse relationship between PPCS and other physical injuries sustained in the event. That is, the lowest levels of self-reported postconcussive symptoms are observed in those individuals who have the highest amount of physical injuries. Previous studies investigating combat-related TBI revealed that individuals with combat-related MTBI and bodily injuries tend to endorse fewer neurobehavioral and psychiatric symptoms than patients with only an MTBI.24,94,95 French and colleagues94 purported several explanations to account for this relationship. Primarily, the reduction of self-reported psychiatric and somatic symptoms may be a positive reaction to the tangible recovery that follows a physical injury. Recovery from MTBI, or at least perception of symptom severity, may be bolstered by the consistent and predictable recovery that often occurs with orthopedic injuries and wounds. In contrast, the recovery pattern and treatment response rate associated with “invisible wounds” such as MTBI and PTSD can be nebulous to patients and treatment providers. Those with overt injuries may receive more external sympathy from society that reacts strongly to overt combat injuries such as amputation.

METHODOLOGICAL ISSUES IN ASSESSING PPCS

The current literature suggests a complicated relationship between MTBI, PPCS, and psychological distress. Most studies are correlational in nature, and therefore the nature of causality between brain injury, PPCS, and psychological distress is not certain. Methodological issues in the assessment of PPCS and psychological distress further complicate the issue. Many assessments of PPCS and psychological distress rely on self-report of symptoms, which can be inherently flawed. Self-report can vary both between and within individuals, reducing test reliability and subsequently reducing test validity. Though clinicians would like to assume everyone is accurate, thorough, and objective in how they report symptoms, many individuals can be vague, emotional, and incomplete.28 Additionally, there are numerous biases, which have also been referred to as psychological responses to MTBI or a predisposition to PPCS,96 that can influence an individual’s accuracy in reporting symptoms after injury. These biases have been thoroughly reviewed by Iverson and colleagues,97 as well as several others, and are briefly reviewed here.

Individuals may be subject to overreporting of symptoms, and Iverson and colleagues liken this to “cognitive hypochondriasis and preoccupation.”97 This can manifest as reporting a previously resolved symptom as unresolved, exaggerating the extent and severity of current symptoms, or fabricating symptoms. Conversely, some individuals may underreport symptoms, which Iverson describes as “stoic.” This may occur in athletes or military personnel who do not want to be withheld from play or duty, respectively, or individuals who are minimizing ongoing symptoms and problems for other reasons.

Expectation as etiology or the “nocebo effect” may also impact the reliability of self-report assessment tools.98100 That is, the actual injury is not responsible for the development of symptoms. Rather the individual’s expectation that they should develop symptoms as a result of a negative event causes misperceptions of postinjury symptoms. In reality, individuals may be attributing benign, everyday events that are common to all people to a recent injury. This is similar to what others have described as the “good-old-days” bias. This results from people overestimating their preinjury levels of functioning, leading to a larger discrepancy between their perceptions of how they were before the injury and how they are after the injury. In studies looking at the accuracy of reporting preinjury functioning, researchers have found individuals with a TBI report fewer preinjury symptoms (i.e., higher levels of functioning) than populations of healthy, uninjured adults.99105

The final bias is referred to as diagnosis threat. This was first described by Suhr and Gunstad106 and results from the attention given to a diagnosis of head injury and its symptoms by medical professionals, family members, friends, or others. The message “you have a head injury” conveyed to the patient can lead to increased symptom reporting or worse performance on objective assessments, such as neurocognitive testing. This bias raises the concern for iatrogenic disorder, literally referring to disorder brought on by medical treatment. This is especially a concern when treating MTBI. Studies have demonstrated that the language used by medical professionals when treating individuals who recently sustained an MTBI can impact expected outcomes.107109 Terms that sound more medically serious such as “mild traumatic brain injury” can result in perceptions of a more serious injury and/or expectations of worse outcomes as compared to terms such as “concussion” or “mild head injury.”

Studies investigating outcome following MTBI are also impacted by the presence or absence of the potential for secondary gain by the individual with the injury. Individuals who have something to gain by being “disabled” or otherwise functionally impacted by the injury may exaggerate or fabricate symptoms or deliberately perform poorly on objective testing, such as neurocognitive assessment. Secondary gain can include financial incentives (e.g., disability payments, settlements from litigation), avoiding obligations (e.g., school, work, duty, punishment), or attention from others. In individuals involved in litigation or disability claims, as many as 40% are likely to be exaggerating symptoms on self-report measures and cognitive testing.110112 A growing body of literature suggests the participant’s effort on neurocognitive testing accounts for a significant portion of the variance in predicting testing outcomes.110,113116 Individuals with MTBI may even misrepresent their symptoms to the degree where they clinically resemble individuals with more serious injuries. In a study demonstrating this, Lange and colleagues117 found that individuals with MTBI who failed performance validity tests scored worse than individuals with severe TBI who had passed performance validity tests. Given such findings, it is a critical part of the clinical evaluation to determine the credibility of the patient’s symptom presentation before concluding that cognitive impairment or psychological distress is present.

BIOPSYCHOSOCIAL MODEL

The existent literature paints a complicated picture of the relationship between preinjury factors, the injury, physical symptoms and medical comborbidities, psychological distress, and PPCS. Trying to link PPCS to only physiological or only psychological reasons is an overly simplistic view. Rather, understanding PPCS requires a multifactorial conceptualization, taking into account biological, psychological, and social factors, as well as both pre- and postinjury variables, to adequately understand poor outcome following injury.28 Therefore, PPCS, including neurocognitive problems and psychological distress, are best understood within the context of a “biopsychosocial” model (Figure 19.1).

FIGURE 19.1. Biopsychosocial factors that influence symptom presentation after MTBI.

FIGURE 19.1

Biopsychosocial factors that influence symptom presentation after MTBI. (With kind permission from Springer Science+Business Media: The Little Black Book of Neuropsychology: A Syndrome Based Approach, M.R. Schoenberg and J.G. Scott, Editors, Post-concussion (more...)

Conceptualizing post-traumatic symptoms from a biopsychosocial perspective was first described by Symonds in 1937,118 and more recently by McLean and colleagues in 2005119 in the context of post-traumatic chronic pain, and Wood and colleagues120 as a “diathesis stress model” to describe the link between conversion and PPCS. Within the context of TBI, and especially MTBI, this model has been extensively expanded on by Iverson and colleagues.97,121 Approaching MTBI and PPCS from a biopsychosocial model provides a framework for assessment that has been described as the only “reasonable way to have a comprehensive, unbiased understanding of this disorder.”121

The biopsychosocial framework necessitates a multisystems, multimethod approach to assessment that extends well beyond neurocognitive and psychiatric evaluation. Iverson and colleagues121 describe PPCS as a “diagnosis of exclusion,” where clinicians should systematically rule out alternative explanations or diagnoses that may account for persistent symptoms. This requires an extensive history, careful documentation of the nature and course of symptoms, objective testing across multiple domains (e.g., neurological, cognitive, vestibular, vision), internal and external factors potentially influencing symptom presentation (e.g., secondary gain, malingering, iatrogenesis), consideration of preexisting conditions, and rule outs of coexisting medical or mental health conditions that may account for symptom presentation. The biopsychosocial approach to assessment is consistent with current recommended clinical guidelines and will more accurately guide clinicians to areas that should be the focus of treatment, aid in reducing the risk of iatrogenensis, decrease unnecessary burden on medical systems, and ideally improve long-term neurocognitive and psychiatric outcomes after MTBI.

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