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.^4,6–8 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.^16–18 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.^19–22 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 issues^22,27 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.^29–33 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 hospital^38,39 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%.^41–45 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

OTHER VARIABLES IMPACTING NEUROCOGNITIVE AND PSYCHIATRIC OUTCOMES

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.^98–100 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.^99–105

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.^107–109 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.^110–112 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.^{110,113–116} 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. (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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