Considerations for return to work following traumatic brain injury

Handbook of Clinical Neurology, Vol. 131 (3rd series) Occupational Neurology M. Lotti and M.L. Bleecker, Editors © 2015 Elsevier B.V. All rights reserved

Chapter 26

Considerations for return to work following traumatic brain injury DEBORAH M. LITTLE1,2*, ANDREW J. COOK2,3, SANDRA B. MORISSETTE2,3, AND JOHN W. KLOCEK4 1 Baylor Scott and White Healthcare, Temple, TX, USA 2

Neuroscience Institute, Texas A&M Health Science Center College of Medicine, Temple, TX, USA 3 4

Central Texas Veterans Healthcare System, Temple, TX, USA

Department of Psychology and Neuroscience, Baylor University, Waco, TX, USA

Traumatic brain injury (TBI) is a significant public health concern, with annual costs at nearly $17 billion each year in healthcare costs and lost productivity in the USA (Finkelstein et al., 2006). In the USA alone, almost 1.7 million new cases of TBI present to emergency departments or require hospitalization each year (Langlois et al., 2006). The gross majority (
75%) of these TBI cases are classified as mild in severity, with infants and young children and individuals in late adolescence and early adulthood as the most prevalent group (Langlois et al., 2005). Within the range of mild TBI, it is reported that the gross majority will fully recover (Bigler and Maxwell, 2012; Eierud et al., 2014), while 10–20% will not have symptom resolution following a single event (Bazarian and Atabaki, 2001). The risk of incomplete recovery (as evidenced by sustained symptoms) may be increased by genetic loading (McAllister, 2010), affected by gender (Niemeier et al., 2014), and influenced by acute management and adherence to safety regulations for prevention and return-to-play and return-to-work standards following the injury (for example, Harmon et al., 2013). Importantly, TBI severity, which is a classification made based on acute TBI variables, is only grossly predictive of outcome (e.g., those who sustain milder injuries tend to show better recovery and less long-term impairment than those with severe injuries) and not by itself directly predictive of chronic outcomes within each severity grade (Dikmen and Levin, 1993; Hoofien et al., 2001). Impairment, in this chapter, is used to describe sustained alterations in cognition, behavior, and mood, as all of these variables

contribute to lifetime disability, degree of independence, and return to the workforce. In addition, because TBI is a traumatic insult to the central nervous system that can and does co-occur with other physical trauma, other factors including development of chronic pain and chronic headache must also be considered. Further complicating the multifactorial relationship between TBI and return to work is an age-dependent increase in risk for TBI. Across the lifespan, those at greatest risk for TBI are children from birth to age 4 (2193 per 100 000), who present most commonly with TBI due to falls and abuse (Centers for Disease Control and Prevention (CDC), The National Institutes of Health (NIH), The Department of Defense (DoD), and The Department of Veterans Affairs (VA) Leadership Panel, 2013). The second most prevalent age group to suffer from TBI are those approaching the legal age of motor vehicle operation (982 per 100 000) (Centers for Disease Control and Prevention (CDC) et al., 2013). In these populations one must consider both direct impacts on independence and the indirect relationship between age of injury, scholastic performance, and the effects of scholastic performance on highest degree of formal education later in life, as all have been associated with occupational attainment. Multiple longitudinal studies are ongoing with a focus on further defining these relationships. In addition to age-related increases in TBI presentation, one must also consider groups at higher risk for TBI due to occupational exposure. It is this group that is the focus of this chapter, as the occupation is not only

*Correspondence to: Deborah M. Little, PhD, Neuroscience Institute, Baylor Scott and White Healthcare, 5701 Airport Road, MS AR D120, Temple TX 76508, USA. E-mail: [email protected]

466

D.M. LITTLE ET AL.

the cause for TBI exposure but also requires an almost immediate consideration of the effect of that injury on return to work, demands efforts to optimize the workplace for the injured party, and raises disability benefit considerations. The occupations at greatest risk for TBI include professional drivers (taxi cab drivers, truck drivers), construction workers, first responders, professional athletes, and those in the military. For both first responders and veterans, extreme stress at the time of injury and in the period following injury must also be considered. In this chapter we provide first a definition of TBI and brief introduction to the pathophysiology of TBI as well as considerations for return to work and risk of premature return. We then provide a detailed review of the most commonly impaired domains, methods to assess these domains, and discussion of the comorbid and co-occurring conditions that affect recovery and a successful return to work. We also provide a brief review of the current state of the literature on long-term health outcomes for which TBI is a risk factor.

TRAUMATIC BRAIN INJURY Although multiple definitions and criteria exist, we, for the purposes of this chapter, use the definition issued by the US Assistant Secretary of Defense for Health Affairs (2007), which is: a traumatically induced structural injury and/or physiological disruption of brain function as the result of an external force that is indicated by new onset or worsening of at least one of the following clinical signs, immediately following the event: any period of loss of or decreased level of consciousness; any loss of memory for events immediately before or after the injury; neurologic deficits; intracranial lesion. Within the range of TBI injuries, we further subspecify as a function of injury severity based upon acute injury variables, including duration of loss of consciousness (LOC), Glasgow Coma Score (GCS), and duration of posttraumatic amnesia (PTA) (Levin et al., 1979). Mild TBI, which requires a LOC of less than 30 minutes, a GCS of 13–15, and period of PTA not to exceed 24 hours, is the most common severity, with a recent World Health Organization taskforce reporting that 70–90% of all treated TBI fell into this category (Holm et al., 2005). Those who exceed the thresholds for mild TBI are then graded as either moderate or severe based upon a cutoff of 24 hours of LOC and 7 days of PTA. These standards are consistent with the National Institute of Neurological Disorders and Stroke common data elements, the

American Congress on Rehabilitation Medicine (1993), the American Academy of Neurology practice guidelines on concussion grading (1997) and the report on definition of TBI and TBI severity from the US Assistant Secretary of Defense for Health Affairs. Positive neuroimaging is also commonly included but, with the exception of the more severe injuries, not predictive of outcome.

MECHANISMS OF TBI Common civilian mechanisms of injury include, in order of frequency, falls, being struck by or against an object (excluding motor vehicle accidents), motor vehicle accidents, and assaults. In terms of specific at-risk populations, sports-related concussions are believed to represent anywhere from 1.6 to 3.8 million new cases per year in the USA alone. The final mechanisms that require identification are TBIs due to military service and are associated with a blast. Of these mechanisms of injury, recovery patterns are generally similar. Those who suffer injuries secondary to assaults, those with injuries that co-occur with other major trauma, and those sustained in the combat theater of operations appear to have, based upon the limited information available, different degrees of recovery and impairment. Sports-related concussions are also commonly identified in the media but do not appear unique in outcome data. Patients with sports-related concussions, as with occupational risk, are more likely to report multiple lifetime TBIs and are at a greater risk for repeated injuries. It is for this reason, and not based upon the pathophysiology, that these mechanisms are commonly separated from discussion. With the exception of blast-related injuries, most TBIs are acceleration–deceleration injuries. The primary mechanism of injury in acceleration–deceleration injury is from the movement of brain within the skull with or without focal injuries, including contusions. Of course, many acceleration–deceleration injuries also involve rotational components. This rotational component may explain damage to the optic nerve and self-reports following head trauma of visual defects (Gutierrez et al., 2001). Severe rotational injury also can result in damage to the cranial nerves, damage to cerebral vasculature resulting in bleeds, and damage to the hippocampus (Gutierrez et al., 2001). The specific deformations of the brain during acceleration and deceleration were investigated in vivo in humans using magnetic resonance imaging (MRI) techniques. Four volunteers had MRI data acquired during acceleration and deceleration impact (Bayly et al., 2005). First, the head was lifted off the table by a small amount. The subject then initiated a release of the head

CONSIDERATIONS FOR RETURN TO WORK FOLLOWING TRAUMATIC BRAIN INJURY on to the table. Using optic triggers, MRI data collection was initiated as the head was released. The data showed a shortening or compression of tissues in the anterior and frontal tissue and a lengthening in the posterior and inferior tissue (Bayly et al., 2005). How well these data describe the actual acceleration–deceleration forces needed to cause alteration in consciousness is unknown, but the study does demonstrate that the shear strain on tissue is not homogeneous. Confirmatory evidence for an acceleration–deceleration model more selective of diffuse axonal injury (DAI, which is more common in certain regions) has been reported as part of retrospective chart and literature review. This damage is likely worse near the contrecoup injury because of the greater deformation observed away from the injury (Drew and Drew, 2004). It is this selective finding of a common location that distinguishes human from animal models in TBI and calls the validity of these models into question, because many animal models of DAI do not show this same pattern of damage (Maxwell et al., 1997). However, differences in skull shape may account for such differences. Indeed, the best model appears to be with primates but, due to cost and other factors, these studies are uncommon. One of the few primate models of DAI not only demonstrates a similar preference for these selective DAI locations observed in human studies, but also provides a timeline for components of DAI (Gennarelli et al., 1982). In contrast to acceleration–deceleration injury, blastrelated TBI offers a number of additional concerns, including that the blast itself can affect central nervous system function (Moore et al., 2009) and can result in alterations in intracranial pressure as well as direct shear and strain injury due to mechanical forces (Chafi et al., 2010). Similar to acceleration–deceleration TBI, blast TBI is associated with damage to axons, cerebral edema, and small hemorrhages in white matter, the cerebellum, and brainstem (Dennis and Kochanek, 2007). The specific pathophysiology of damage due to blast is uncertain, but at least three main mechanisms have been proposed. The first is that the blast waves travel directly through the brain, rapidly increasing and decreasing intracranial pressure and shearing tissue (DePalma et al., 2005; Taber et al., 2006; Chavko et al., 2007; Dennis and Kochanek, 2007). Second, blast-wave overpressure forces the skull away from the blast, leaving the brain to lag behind and then impact the side of the skull (Levi et al., 1990). This is then followed by negative pressure, which pulls the skull back toward the direction of blast again, with the brain lagging behind. The initial blast effects are proposed to be similar to acceleration– deceleration injury. However, how these effects interact with the second force of returning the skull toward the blast is unknown. Finally, it has also been proposed that

467

blast wave energy in the torso and neck forces organs to constrict and relax, thus producing a surge of blood into the brain (Cernak et al., 1999). Although the specific mechanism is unknown, it is likely that brain injury secondary to blast wave involves at least two of these components, if not all. It has also been suggested that, in addition to primary brain injury from blast, the biochemical cascade that follows acute injury impairs the ability of the cerebral vascular system to compensate, making it more susceptible to additional damage such as from the effects of acceleration–deceleration injury resulting from the blast (DeWitt and Prough, 2009). As with civilian injury, brain injury due to blast includes significant shear and strain injury, DAI, hematomas, and hemorrhage (Hicks et al., 2010). Primary blast-related injury (barotrauma) is commonly followed by an acceleration–deceleration injury due to objects striking the individual or due to the individual striking an object. Blast-related TBI shares significant pathophysiology with nonblast TBI, including DAI, oxidative stress, and excitotoxic cell damage. The acute sequelae, including retrograde amnesia, compromised executive function, headache, confusion, amnesia, difficulty concentrating, mood disturbance, alterations in sleep patterns, and anxiety, also appear similar to civilian TBI (Ling et al., 2009). In chronic TBI, early investigations also report similar patterns of cognitive function between civilian and veteran populations (Belanger et al., 2009).

PATHOPHYSIOLOGY OF TBI Certain aspects of the pathophysiology of TBI may be especially pertinent to the risk for neurobehavioral sequelae. There are several important components that can contribute to neurobehavioral outcome, including the location and severity of the injury, diffuse effects, and secondary biochemical mechanisms of injury. Primary neurologic injury due to TBI can be direct and/or indirect. Contusions are common following TBI, and can directly disrupt function in a specific area. Certain areas of the brain may be more vulnerable to contusion following trauma, such as the frontal and anterior temporal cortices, due to their position within the skull. (Adams et al., 1980; Levin et al., 1992). Importantly, disruption of function can also result from direct and indirect damage to white-matter fiber tracts, the links in neural networks. The primary pathophysiology in head injury is DAI and appears to be the most common in parasagittal white matter, the corpus callosum, brainstem, and any gray-matter–white-matter junction (Gentry et al., 1988; Meythaler et al., 2001). We define DAI in this chapter to include both increased microglia

468

D.M. LITTLE ET AL.

as a marker of degeneration of white matter and Wallerian-type axonal degeneration. This damage is not necessarily shearing of the axon itself, but instead is a marker of a pathophysiologic process that damages the integrity of the axon. Maxwell and colleagues (1993) demonstrated that there is shearing to axons acutely following injury, but that axonal membranes seal themselves within the first hour. Following this, axons also demonstrate swelling, which results in disconnection of the axon. It is likely this secondary process that leads to the effects we observe in humans. The degree of damage and/or depth of damage in the brain following acceleration–deceleration injury may serve as an independent marker of severity of acceleration–deceleration forces (Levin et al., 1997). Secondary processes, including inflammation and free radical formation, also contribute to white-matter damage (Bandak, 1995). DAI can disrupt critical cortical-subcortical pathways (Gennarelli et al., 1982; Povlishok, 1992), as these white-matter fiber tracts are particularly susceptible to the shearing forces that often occur with TBI, especially at gray–white-matter junctions like the thalamus (Graham et al., 2002). Brain edema and shift can also compromise blood supply and lead to secondary infarction in the corpus callosum and deep gray matter, and elevated intracranial pressure can cause damage to the brainstem and optic nerve in TBI (Graham et al., 1987). Although the diagnosis of DAI can only be definitively confirmed by microscopic examination, it may be inferred from specific neuroimaging findings, such as hemorrhages in the corpus callosum or areas of rostral brainstem (Geddes, 1997; Geddes et al., 1997). DAI may be the only significant pathology found in certain cases of TBI, and has been identified via direct pathologic studies as well as on both standard clinical neuroimaging in severe cases and in high-resolution imaging of the white matter in mild to moderate injury (Povlishock et al., 1983; Graham et al., 1989; Blumbergs et al., 1994, 1995; Goodman, 1994; Mittl et al., 1994; Aihara et al., 1995; Gennarelli, 1996; Inglese et al., 2005b). Changes in cerebral white matter have been shown, even in mild TBI (Inglese et al., 2005a, b), and in both acute and chronic phases of recovery. Regions reported to have been affected include the corpus callosum, internal capsule, and centrum semiovale (Inglese et al., 2005b). Another issue is the specificity of the types of lesion found in mild TBI. Kurca et al. (2006) reviewed MRI results on 30 patients with reported mild TBI within 96 hours postinjury, and 30 matched controls. They divided MRI findings into traumatic and nonspecific, but were not only looking at white matter. They found that the group with the defined traumatic lesions showed significantly greater impairment on neuropsychologic

evaluations and subjective reports of postconcussion syndrome-type symptoms. However, it is not entirely clear that the lesion types that the authors define as nontraumatic are actually nontraumatic. In addition, this is also another study on an acute, not chronic population. In moderate to severe injuries, white-matter abnormalities have been more clearly demonstrated, as would be expected. Mathias et al. (2004) studied a group of 25 moderate and severe TBI patients and 25 controls, all receiving the same neuropsychologic test battery. The average time out from injury for the group was 212.9 days (SD ¼ 86.6). Of the TBI group, 18 underwent MRI on a 1.5 T scanner. They acquired 5-mm-thick axial proton density and T2-weighted turbo spin echo, fluidattenuated inversion recovery (FLAIR), and T2*weighted gradient echo images. Quantitative MRI analysis for whole-brain white-matter volume, hippocampal volume, and corpus callosum area was performed. The primary outcome was the level of corpus callosum atrophy in the TBI group. The corpus callosum measurements for the TBI group were found to be smaller than the comparison group, except for the splenium. They also found that reaction time data from the neuropsychologic tasks they chose correlated negatively with the total white-matter volume, but the correlations did not reach significance. The controls were not imaged; rather, they used normative data previously collected from a different healthy control group. It is not clear how the authors selected or even matched these groups.

NEUROBEHAVIORAL OUTCOMES FOLLOWING TBI Neurobehavioral sequelae of TBI often underlie functional disability and include disorders of cognition, mood, and behavior (CDC, 2003). The most common of these behavioral and psychologic concerns are presented in Table 26.1. Cognitive deficits after TBI are common and well documented across severities. Disorders of mood are also common following TBI, and results of epidemiologic studies have typically demonstrated high prevalence rates for major depression, bipolar disorder, and generalized anxiety in patients with a coexisting history of TBI (van Reekum et al., 1996). Of these, apathy and depressive symptoms are the most prevalent following TBI, with estimates extending to greater than 50% (Dikmen et al., 2004). These deficits are logical given the nature of the neuropathology following TBI (Levin et al., 1992; Levin and Kraus, 1994), and they are often the primary source of disability that prevents the patient from successful social and occupational reintegration (Levin et al., 1992; Levin and Kraus, 1994) The observed cognitive changes that can follow TBI include impairments in attention and

CONSIDERATIONS FOR RETURN TO WORK FOLLOWING TRAUMATIC BRAIN INJURY Table 26.1 Most common behavioral diagnoses following traumatic brain injury Diagnosis

Frequency

Apathy Depression Agitation Posttraumatic stress disorder Psychosis

60%1 10–50%2 25%3 11–18%4 7–10%5

1

Kant et al. (1998). McAllister (1992); National Institute of Mental Health (2001); Holsinger et al. (2002); Dikmen et al. (2004); Guskiewicz et al. (2007). 3 Nott et al. (2006). 4 Fedoroff et al. (1992); Jorge et al. (1993, 2004); Jorge and Robinson (2003). 5 Davison and Bagley (1969). 2

executive functions, such as decreased mental flexibility, and trouble shifting sets (Levin and Kraus, 1994; Miller, 2000; Godefroy, 2003). Patients also demonstrate additional executive functioning deficits, including poor planning, lack of organization, problems with sequencing, impaired judgment, deficits in verbal fluency, problems with working memory, as well as impulsivity errors (Levin and Kraus, 1994; Miller, 2000; Godefroy, 2003). Mood and behavioral disturbances are also common, including various symptoms of depression, irritability, impulsivity, apathy, and amotivation (Levin et al., 1992, 2005; McAllister, 1992; van Reekum et al., 1996; Hoofien et al., 2001; Dikmen et al., 2004; Jorge et al., 2004; Moldover et al., 2004). Neurobehavioral deficits often persist and can even result in long-term problems for patients with mild TBI (Gronwall and Wrightson, 1974; Rimel et al., 1981; Bohnen et al., 1994, 1995; Ruff et al., 1994; Alexander, 1995; Roberts et al., 1995; Binder et al., 1997; Ashman et al., 2006; Marsh and Kersel, 2006). Importantly, while an older CDC report (CDC, 2003) emphasizes that there are numerous studies demonstrating neuropsychologic deficits in mild TBI, it underscores that there is controversy as to how long these problems persist. It is this interindividual variability in longer-term outcomes that needs to be studied further, especially to discern the differences between those with good recovery and those with persistent disability. In a combat-injured sample of TBI patients treated at Walter Reed Medical Center between 2003 and 2005, approximately 90% reported postconcussive symptoms, including over 40% with reported problems in memory, attention and concentration, and irritability, as well as other behavioral disturbances (Warden, 2006). Even when variables such as age, litigation, substance abuse,

469

and prior psychiatric history are controlled for, there is still unexplained variability in mild TBI, as well as in more severe injuries. Depression is often poorly conceptualized following TBI, and may be underrecognized and undertreated in acute care and rehabilitation models and must be considered in a return-to-work setting (National Institute of Mental Health, 2001). There are likely multiple etiologic pathways that converge to a common clinical presentation of disturbed mood with a myriad of features (McAllister, 1992). A 2007 study of professional athletes in the National Football League showed that those players who had had at least three concussions were three times as likely to develop depression (Guskiewicz et al., 2007). Those employees for whom the TBI is not the first lifetime injury should be monitored more closely for depression in the years following a TBI. Additionally, it is reasonable to posit that those with depression prior to the injury may have poorer outcomes. Dikmen and colleagues (2004) conducted a 3–5-year prospective study examining the rates and risk factors associated with depression in moderate to severe TBI at a Level I trauma hospital. The Center for Epidemiological Studies Depression (CES-D) scale was used as the primary outcome measure. The authors found that rates of moderate to severe depression ranged from 31% at 1 month to 17% at 3–5 years, suggesting a timedependent decline in depression rates from the time of injury. The rates of depression did not appear dependent upon the severity of injury (Dikmen et al., 2004). Premorbid depression and psychosocial factors were predictive of worsening depression following TBI, which suggests a strong need to screen this vulnerable group after head trauma (Dikmen et al., 2004). Beyond the impact of depression on quality of life, it has also been well documented to impede the achievement of optimal functional outcome in both acute and chronic stages (Rapoport et al., 2003). As emphasized previously, TBI commonly results in disturbances in mood and in changes in cognition and behavior. Additionally, other issues, such as chronic pain (e.g., headaches), which are relatively common in TBI, can play a significant role in the extent of neurobehavioral symptoms. As such, these other factors must also be characterized and addressed. All of these features may interact with each other. Outside of the neurobehavioral symptoms described above, there are three additional comorbid and co-occurring conditions that affect return to the workplace. These are potential issues not only with successful return to work but as conditions that may limit the patient from return to prior duties. These include chronic posttraumatic headache (PTH) and chronic pain.

470

D.M. LITTLE ET AL.

CHRONIC POSTTRAUMATIC HEADACHE

Table 26.2

Headache is the most common symptom after TBI, often one of a constellation of symptoms of postconcussive syndrome. There is an inverse relationship between the severity of TBI and prevalence of PTH, with the highest rates found for mild TBI (Branca, 2006). The incidence of chronic PTH (CPTH) after mild head injury is between 30% and 90%, and varies between countries (Ramadan and Keidel, 2000; Lane and Arciniegas, 2002). Headache is the most common residual impairment 5 years following TBI (Hillier et al., 1997). The most common form of CPTH by a large margin is tension-type headache, followed by migraine, occipital neuralgia, and other headache presentations (e.g., mixed, cluster) (Chibnall and Duckro, 1994; Seifert and Evans, 2010). The pathophysiology of PTH associated with mild TBI is thought to involve DAI and neurometabolic processes (e.g., excitatory neurotransmitters such as aspartate, glutamate, and acetylcholine) (Branca, 2006; Seifert and Evans, 2010). Adaptive gray-matter changes in pain-processing centers have been identified in patients with CPTH (Obermann et al., 2009). CPTH is a common complaint among returning military service members due to the prevalence of mild TBI. More than 90% of those reporting blast injuries have headaches, mostly of the migraine type (Seifert and Evans, 2010). In the original 1988 edition of the International Classification of Headache Disorders (ICHD: Headache Classification Committee of the International Headache Society, 1988), persistence of PTH beyond 8 weeks was classified as chronic. In the second ([The International Classification of Headache Disorders: 2nd edition], 2006) and third (World Health Organization, 2013) editions of ICHD, CPTH is characterized by persistence beyond 3 months, and resulting from either mild or moderate to severe head injury (World Health Organization, 2013). These classifications are presented in Table 26.2. Due to the episodic nature of headache and variations in its course, both within and between individuals, measurement of functional disability from chronic headache is difficult (Andrasik et al., 2011). Many of the validated self-report headache instruments use a 1–3-month reporting period to provide a representative assessment. There are many self-administered instruments for assessing headache-related functional impairment and disability (Borkum, 2005; Andrasik et al., 2011), including the Headache Impact Test (Kosinski et al., 2003), Headache Impact Questionnaire (Stewart et al., 1998), and the Henry Ford Hospital Headache Disability Inventory (Jacobson et al., 1994). Though no standardized criteria exist for impairment ratings in CPTH, a systematic ratings system has been proposed (Packard and Ham, 1993).

ICHD-III classification of headache. (From the International Classification of Headache Disorders, 3rd edition, 2013, with permission from Sage Publications Ltd.) 5.1 Acute headache attributed to traumatic injury to the head 5.1.1 Acute headache attributed to moderate or severe traumatic injury to the head 5.1.2 Acute headache attributed to mild traumatic injury to the head 5.2 Persistent headache attributed to traumatic injury to the head 5.2.1 Persistent headache attributed to moderate or severe traumatic injury to the head 5.2.2 Persistent headache attributed to mild traumatic injury to the head 5.3 Acute headache attributed to whiplash 5.4 Persistent headache attributed to whiplash 5.5 Acute headache attributed to craniotomy 5.6 Persistent headache attributed to craniotomy

Important information related to functioning and treatment is also obtained by assessment of cognitive status and psychosocial constructs such as stress, locus of control (i.e., the degree to which an individual perceives his or her headaches to be under personal or external control), self-efficacy (i.e., perceived ability to achieve a desired action or outcome), and catastrophizing (i.e., a pattern of thinking characterized by hopelessness and helplessness) (Andrasik et al., 2011); these are common assessments done in patients with depression as well. Though most patients experiencing PTH recover within a few months, chronic problems are experienced by a significant minority. CPTH affects almost 25% of patients at 4 years (Seifert and Evans, 2010). Factors hypothesized to contribute to poor recovery include insufficient treatment, analgesic rebound headache due to excessive use of analgesics, and/or psychosocial comorbidities such as anxiety, depression, insomnia, or substance abuse (Lane and Arciniegas, 2002; Lipton et al., 2003; Walker et al., 2006). Posttraumatic stress disorder (PTSD) is a common comorbidity in some CPTH subpopulations due to co-experienced psychologic and physical trauma (Chibnall and Duckro, 1994; Borkum, 2005). Though there has been active debate about the association between accident-related CPTH and presence of litigation and/or potential for financial gain (Sheftell et al., 2007; Obermann et al., 2010; Seifert and Evans, 2010), there is evidence for its persistence beyond time of legal settlements (Packard, 1992) and some have cautioned against premature oversimplification of potentially complex etiologic factors (Obermann et al., 2010). Of greatest relevance to the present discussion, chronic headache produces a high level of occupational

CONSIDERATIONS FOR RETURN TO WORK FOLLOWING TRAUMATIC BRAIN INJURY disability. For chronic tension-type headache, 12% of sufferers report missed work days, with a very significant average annual absenteeism of 27 days (Borkum, 2005). Traumatic onset is known to be associated with higher levels of reported disability in clinical samples, believed to be due to the commonly comorbid symptoms such as postconcussive syndrome, PTSD, and depression (Borkum, 2005). CPTH is associated with greater reductions in activity level, more complete disability, and lower physical function than nontraumatic chronic headache (Marcus, 2003). Though a clear understanding of predictors of vocational rehabilitation is lacking, identified factors from past research include age at injury, severity and duration of posttraumatic amnesia, types of persisting impairments, and premorbid occupation and characteristics. The often slow and challenging course of treatment can be demoralizing to patients and their families, who can be inadequately prepared with strategies for long-term coping (Barnat, 1986). Self-awareness and acceptance of limitations are important to vocational rehabilitation (Branca, 2006). Cognitive symptoms (e.g., difficulties with memory, concentration, and/or information processing) are common among CPTH sufferers, especially females (Packard et al., 1993), with high potential for impact on occupational function. Age and performance on cognitive tests have been found to predict work status in a majority of military service members with mild TBI (Branca, 2006). The affective component of CPTH should also be considered in occupational rehabilitation for workers with CPTH. Depression predicts functional disability in CPTH, partially mediated by anger (both suppressed and expressed) (Duckro et al., 1995). When CPTH sufferers return to work, they may experience improvements in psychosocial domains, such as less depression and reduced likelihood of substance abuse (Branca, 2006). Making the return to work and treatment more complex is the absence of randomized, placebo-controlled studies to demonstrate efficacy for CPTH treatments. As such, treatment recommendations are based on expert opinion and evidence-based guidelines for specific primary headache phenotypes, such as migraine and tension-type (Vargas and Dodick, 2012). As with rehabilitation for other chronic pain disorders, there is general consensus that multimodal and interdisciplinary, or at least multidisciplinary, treatment is most effective for CPTH, especially when early resolution is not achieved. Complex comorbid conditions, such as chronic pain, TBI, and PTSD, also warrant an interdisciplinary approach (Otis et al., 2011). Medical management (prophylactic, abortive, physical) (Bell et al., 1999) and cognitive-behavioral therapy (Gurr and Coetzer, 2005) can be effective components of multimodal treatment.

471

Management of stress in the workplace is critical to effective employee functioning (von Onciul, 1996) and can play an important role in successful return to work for workers with CPTH. Neuropsychologic assessment can provide valuable input on current cognitive status as well as premorbid level of functioning (Branca, 2006). Behavioral treatment that is anchored in the biopsychosocial model, that is, multimodal treatment, has been shown to be effective for treatment of CPTH following occupational trauma (Duckro et al., 1985). Successful reintegration for workers with CPTH is supported by the presence of health insurance, effective tailoring of work duties, supported employment (SE), and a socially inclusive work environment (Branca, 2006). It has been suggested that the costs of occupational rehabilitation may be influenced more by the relative decline from an individual’s premorbid functioning than by the absolute level of neuropsychologic impairment (Branca, 2006). General modalities and principles of TBI rehabilitation and chronic headache management (e.g., Whyte et al., 2010) typically provide a foundation for successful treatment of CPTH and work reintegration.

NONHEADACHE-RELATED CHRONIC PAIN As with TBI, it is critical to start any discussion on the topic of chronic pain with a definition. In this chapter we use the definition provided by the International Association for the Study of Pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” (Merskey and Bogduk, 1994). The taxonomy of chronic pain conditions is extensive and beyond the scope of this chapter. Reference here will be limited to the broad classifications of chronic pain utilized by the various studies assessing the presence and role of nonheadache-related chronic pain following TBI. Further complicating the relationship between TBI and nonheadache-related chronic pain is the lack of an obvious etiologic connection between the brain injury and the painful region (except in the case of TBI with concurrent other physical trauma). The literature investigating the prevalence and role of nonheadache-related chronic pain following TBI is limited, as the majority of studies are inclusive of both headache and nonheadache-related chronic pain. Nevertheless, an emerging body of research indicates that nonheadache-related chronic pain is a significant challenge to individuals following TBI. While not as prevalent as CPTH, nonheadacherelated chronic pain is common following TBI (Nampiaparampil, 2008), with estimates ranging from 24% among individuals with severe brain injury

472

D.M. LITTLE ET AL.

(Bryant et al., 1999) to 75% among individuals with mild TBI (Alfano et al., 2000). Lahz and Bryant (1996) found similar rates of chronic neck and shoulder pain among individuals with moderate to severe TBI (n ¼ 79; 24%) and mild TBI (n ¼ 53; 28%). They also found similar rates of chronic low-back pain among individuals with moderate to severe TBI (n ¼ 79; 16%) and mild TBI (n ¼ 53; 19%). Pain can complicate recovery from TBI. In a sample of 67 adults studied, 9% were found to have pain as a significant barrier to recovery following a mild TBI (Mooney et al., 2005). Of note, they also found that 49% showed mild TBI, pain, and a psychiatric diagnosis as the factors which substantially interfered with recovery. As is true with chronic headache, nonheadacherelated chronic pain also results in significant impairment in occupational function and increased healthcare costs (Pizzi et al., 2005). Return to work in non-CTPHrelated chronic pain has been found to be impacted by over 100 distinct factors (Krause et al., 2001). These include factors that are both subject to modification with treatment and those which are not subject to change through treatment. For example, demographic variables such as older age, lower education, lower income, and blue-collar or labor-related profession were negatively associated with return to work (Krause et al., 2001). However, other authors have noted that variables such as an individual’s prediction of when s/he may be able to return to work, ability to change professions or jobs, and active participation in a return-to-work treatment program can be modified – and have successfully been the target of interventions (Hamer et al., 2013).

LONG-TERM CONSIDERATIONS FOLLOWING TBI What is known is that the best predictor of future concussion is past concussion. As discussed, TBI and repeated TBI have been associated with increased risk of depression (O’Connor et al., 2012; Rapoport, 2012; Reeves and Laizer, 2012; Scheibel et al., 2012; Vasterling et al., 2012; Bryan et al., 2013), increased impairments in memory (Vasterling et al., 2012), increased postconcussive symptoms (van der Horn et al., 2013), increased sleep disturbance (Bryan, 2013), and decreased quality of life (Williamson et al., 2013). Repeated concussion risk can however be partially mitigated, as is the case with robust and comprehensive concussion identification. The challenge is that there are few validated measures to allow an accurate lifetime history to be obtained. This is critical in an occupational setting where risk for TBI exposure is part of an employee’s job duties. At present, one of the best measures is the Ohio State University TBI Identification tool (Corrigan and

Bogner, 2007), which was initially validated in part on a prison population (Bogner and Corrigan, 2009). However, this is a lengthy assessment tool that might exceed time available outside of a research setting. Beyond these concerns that present in the acute to chronic stages following TBI, repeated concussions are also a risk factor for long-term health concerns, specifically, neurodegenerative diseases. Epidemiology data show increased risk for chronic traumatic encephalopathy, Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. However, unlike for depression, pain, and cognitive impairment, there is little convincing evidence that a history positive for a single uncomplicated concussion increases risk for these neurodegenerative diseases. However, although there is public concern for the risk of neurodegenerative disease, it is critical to remember that the bounding conditions for this increased risk are not known in any detail beyond presence of multiple injuries. For example, the threshold for the minimum number of lifetime TBIs, effects of time between TBIs for increased risk, or factors such as age at first or last TBI are still unknown. Multiple large-scale studies supported by federal grants are ongoing on these topics. The reasonable person judgment should be followed when considering risk and potential disability due to repeated injuries. In this case, a reasonable person (or employer) should put forth effort to ensure the employee has recovered and is safe to return to work after a period of rest. This rest period is believed to be critical in facilitating recovery and should help limit lost productivity and costs associated with disability. Although no data on rest and repeated concussion exist to inform long-term risk for neurodegenerative disease, it seems prudent to ensure return to work occurs only after that period of rest. Informal reports from the combat theater also support the positive effects of rest as it relates to full recovery. Early position papers from the field of sports medicine also support this approach. One unique challenge for occupational safety is that, unlike sports and the military, baseline testing is generally not used but may be of benefit for those occupations at the greatest risk for head injury, such as firefighters. Wider use of baseline testing would provide critical tools for those assessing return to work. Factors that influence successful return to work and available interventions to assist with return to work following injury are discussed below.

RE-ENTRY TO THE WORKFORCE The International Classification of Functioning, Disability and Health (ICF), created by the World Health Organization (2002), recognizes that return to work is

CONSIDERATIONS FOR RETURN TO WORK FOLLOWING TRAUMATIC BRAIN INJURY a central component to successful reintegration. Those who are employed report greater sense of wellbeing, health status, and quality of life (Corrigan et al., 2001; Steadman-Pare et al., 2001). Reciprocally, failure to return to work can create tremendous psychosocial and financial strain for both the person with TBI and his/her family. Although a significant proportion of individuals with severe TBI successfully return to work, rates vary widely (12–70%) and are usually contingent upon a comprehensive medical and psychosocial rehabilitation approach (Shames et al., 2007). In a review of 49 studies, Van Velzen and colleagues (2009a) found that 40% of those with traumatic or nontraumatic brain injury returned to work after 1–2 years. Evaluation of successful return, however, is often complicated by how success is defined (i.e., return to previous job/ premorbid levels of functioning, degree of job modification, full- vs part-time). Myriad factors influence functional recovery and return to work following brain injury, including severity and area of the injury, educational and occupational background prior to the injury, and age of injury (Wehman et al., 2005). Data on injury severity are mixed, likely due to varying definitions, with some studies indicating that patients with more severe injuries have difficulty returning to work (Brooks et al., 1987) and others finding no effect (Van Velzen et al., 2009b). Further, a significant proportion of those with mild TBI experience lingering postconcussive symptoms that can interfere with work functioning, such as dizziness (Chamalian and Feinstein, 2004) and tiredness (van Velzen et al., 2011). In turn, persistent postconcussive symptoms are further complicated by commonly co-occurring mental health disorders, such as PTSD and depression (Morissette et al., 2011), which also can negatively impact work functioning (Zivin et al., 2011). Problematically, deficits related to mild TBI can be hard to detect during formal neuropsychologic testing, and testing situations do not reflect challenges related to real-world work settings in which environments are less structured, have distractions, and require longer performance times (Sbordone, 2001). In terms of prior education and work history, skilled professionals and those with higher education are more likely than manual workers to return to work (Greenspan et al., 1996; Gollaher et al., 1998; Walker et al., 2006). Moreover, age over 40 negatively predicts return to work, which could be related to physiologic factors associated with neurologic recovery along with cultural influences regarding age and re-employment (Ponsford et al., 1995; Keyser-Marcus et al., 2002). Finally, a particularly important factor influencing return to work is selfawareness, impairments in which may curtail motivation and ability to set reasonable goals (Ben-Yishay and

473

Lakin, 1989; Sherer et al., 1998). For this reason, selfawareness is often a key component of rehabilitation treatment. With respect to rehabilitation treatment programs for work re-entry, approaches are generally cognitive or cognitive-behavioral in nature, although content, length, and intensity vary considerably based on funding and availability of trained professionals.

INTERVENTIONS FOR RETURN TO WORK One of the most widely studied interventions is called supported employment or SE, which aims to increase competitive employment rates among those with TBI (Wehman et al., 1993). SE involves job placement that is supported by job coaches who advocate for the patient and facilitate training and work accommodations. In addition to making physical adaptations, SE includes behavioral and skills training, social adjustment, and development of cognitive strategies. Coordination between rehabilitation specialists and employers is a critical component. Wehman and colleagues demonstrated job retention rates of more than 70%. Further, the SE approach has been found to be effective in obtaining and maintaining employment for individuals with a wide variety of mental health conditions (e.g., Bond et al., 2001; Rogers et al., 2006; Davis et al., 2012). Adjunctive cognitive rehabilitation treatment has also been successfully added to SE to address cognitive impairments that might limit effectiveness (McGurk et al., 2007). Finally, approximately 15–30% of military personnel serving in the current wars in Iraq and Afghanistan report TBI (Hoge et al., 2007, 2008), making this a key concern to the Veterans Health Administration, US Department of Defense, and public health initiatives. Ability to return to work following head injury can be a critical piece of the reintegration process for service members who are trying to reset for future missions or find their next “mission” as civilians. To that end, in a randomized controlled trial of two acute inpatient rehabilitation approaches (integrated cognitive-didactic versus functional-experiential rehabilitation therapy) for TBI in active duty and veterans, Vanderploeg and colleagues (2008) did not find group differences in return to work. However, within exploratory subgroup analyses, younger participants who engaged in the cognitive-didactic therapy returned to work/school at higher rates than same-aged participants receiving functional-experiential therapy. In contrast, those who were over 30 years of age and had higher educational level had greater rates of independent living at 1-year follow-up when receiving functional therapy compared to those in the cognitive treatment. These findings are

474

D.M. LITTLE ET AL.

particularly important in the context of military demographics, in which 42.7% of all active duty service members are aged 25 years or younger, whereas 43.8% of officers are 36 years or older. Clearly, future research is needed to determine whether different strategies may be needed for differing military demographics to assist them with recovery.

CONCLUSIONS TBI presents many challenges, whether the injury is a function of the job duties or if a person with a previous injury is returning to or entering the workplace. In the case of occupational injury, return to work, after a period of rest, should be considered relative to a resolution of symptoms. In the case of milder injuries, this may be sufficient for optimizing the return and for reducing the risk of long-term disability. In the case of complicated mild injuries, mild injuries that result in sustained impairments, or more severe injuries, then an assessment of those impairments and limitations, relative to job duties, should be considered proactively. The literature is clear that factors such as frustration related to challenges in performing previous duties that had been easy result in poorer long-term outcomes. Similarly, one should be aware of areas of greatest challenge, including multitasking and learning new skills. A prospective approach and involvement of the injured employee in this process will be beneficial to all parties. In the cases where cognitive impairment is present, options for interventions should be considered as early in the return-towork process as possible. For occupations where work is associated with risk of repeated injury, additional concern is warranted not only to optimize acute recovery but for reduction in long-term risk. Patient and staff education is also helpful at optimizing return to work. TBI is associated with behavioral changes, including frustration, anger, impulsivity, anxiety, and depression. These can have a negative impact on the workplace and should be monitored early in the process. Employee health should also re-examine medication use if warranted by the job duties, as many medications can impact employee safety. These are of greatest concern in populations that exhibit the most common comorbid diagnoses, including chronic pain and chronic headache. Special consideration should be given to those who must seek other employment when brain injury makes return to the same occupation unsafe. These cases are most common among military veterans and first responders. For these populations, consideration must go beyond ratings of disability and include plans for identification of new careers and training to support these careers.

ACKNOWLEDGMENTS We would like to thank Dr. Suzy B. Gulliver and Dr. Sara L. Dolan for their contribution to this chapter.

REFERENCES Adams HJ, Graham DI, Scott G et al. (1980). Brain damage in fatal non-missile head injury. J Clin Pathol 33 (12): 1132–1145. Aihara N, Hall J, Pitts L et al. (1995). Altered immunoexpression of microglia and macrophages after mild head injury. J Neurotrauma 12: 53–63. Alexander M (1995). Mild traumatic brain injury: pathophysiology, natural history, and clinical management. Neurology 45: 1253–1260. Alfano D, Asmundson G, Larsen D (2000). MTBI and chronic pain: preliminary findings. Arch Clin Neuropsychol 15: 831–832. American Academy of Neurology (1997). Practice Parameter: The management of concussion in sports (summary statement). Report of the Quality Standards Subcommittee. Neurology 48: 581–585. American Congress on Rehabilitation Medicine (1993). Definition of mild traumatic brain injury. J Head Trauma Rehabil 8: 86–87. Andrasik F, Buse D, Lettich A (2011). Assessment of headaches (D Turk, R Melzack Eds.), Guildford Press, New York. Ashman T, Gordon W, Cantor J et al. (2006). Neurobehavioral consequences of traumatic brain injury. Mt Sinai J Med 73 (7): 999–1005. Assistant Secretary of Defense for Health Affairs (2007). Health Affairs Memorandum. Traumatic Brain Injury: Definition and Reporting. Bandak FA (1995). On the mechanics of impact neurotrauma – a review and critical synthesis. J Neurotrauma 12 (4): 635–649. Barnat MR (1986). Post-traumatic headache patients I: Demographics, injuries, headache and health status. Headache 26 (6): 271–277. Bayly P, Cohen T, Leister E et al. (2005). Deformation of the human brain induced by mild acceleration. J Neurotrauma 22 (8): 845–856. Bazarian JJ, Atabaki S (2001). Predicting postconcussion syndrome after minor traumatic brain injury. Acad Emerg Med 8 (8): 788–795. Belanger HG, Kretzmer T, Yoash-Gantz R et al. (2009). Cognitive sequelae of blast-related versus other mechanisms of brain trauma. J Int Neuropsychol Soc 15 (1): 1–8. Bell KR, Kraus EE, Zasler ND (1999). Medical management of posttraumatic headaches: pharmacological and physical treatment. J Head Trauma Rehabil 14 (1): 34–48. Ben-Yishay Y, Lakin P (1989). Structured group treatment for brain injury survivors, Kluwer Academic, Boston. Bigler ED, Maxwell WL (2012). Neuropathology of mild traumatic brain injury: relationship to neuroimaging findings. Brain Imaging Behav 6 (2): 108–136.

CONSIDERATIONS FOR RETURN TO WORK FOLLOWING TRAUMATIC BRAIN INJURY Binder L, Rohling M, Larrabee J (1997). A review of mild head trauma, part I: meta-analytic review of neuropsychological studies. J Clin Exp Neuropsychol 19: 421–431. Blumbergs P, Scott G, Manavis J et al. (1994). Staining of amyloid precursor protein to study axonal damage in mild head injury. Lancet 344: 1055–1056. Blumbergs P, Scott G, Manavis J et al. (1995). Topography of axonal injury as defined by amyloid precursor protein and the sector scoring method in mild and severe closed head injury. J Neurotrauma 12: 565–572. Bogner J, Corrigan JD (2009). Reliability and predictive validity of the Ohio State University TBI identification method with prisoners. J Head Trauma Rehabil 24 (4): 279–291. Bohnen NI, Van Zutphen W, Twinjstra A (1994). Late outcome of mild head injury: results from a controlled postal survey. Brain Inj 8 (8): 701–708. Bohnen NJ, Wijnen G, Twijnstra A et al. (1995). The constellation of late posttraumatic symptoms of mild head-injury patients. J Neurol Rehabil 9 (1): 33–39. Bond GR, Becker DR, Drake RE et al. (2001). Implementing supported employment as an evidence-based practice. Psychiatr Serv 52 (3): 313–322. Borkum J (2005). Predicting disability from headache. In: I Schultz, R Gatchel (Eds.), Handbook of complex occupational disability claims: early risk identification, intervention and prevention. Springer, New York. Branca B (2006). Neuropsychologic aspects of post-traumatic headache and chronic daily headache. Curr Pain Headache Rep 10 (1): 54–66. Brooks N, McKinlay W, Symington C et al. (1987). Return to work within the first seven years of severe head injury. Brain Inj 1 (1): 5–19. Bryan CJ (2013). Repetitive traumatic brain injury (or concussion) increases severity of sleep disturbance among deployed military personnel. Sleep 36 (6): 941–946. Bryan CJ, Clemans TA, Hernandez AM et al. (2013). Loss of consciousness, depression, posttraumatic stress disorder, and suicide risk among deployed military personnel with mild traumatic brain injury. J Head Trauma Rehabil 28 (1): 13–20. Bryant RA, Marosszeky JE, Crooks J et al. (1999). Interaction of posttraumatic stress disorder and chronic pain following traumatic brain injury. J Head Trauma Rehabil 14 (6): 588–594. CDC (2003). Report to Congress on Mild Traumatic Brain Injury in the United States: Steps to Prevent a Serious Public Health Problem. Centers for Disease Control, Atlanta, GA. Centers for Disease Control and Prevention (CDC), The National Institutes of Health (NIH), The Department of Defense (DoD), The Department of Veterans Affairs (VA) Leadership Panel (2013). Report to Congress on Traumatic Brain Injuries in the United States: Understanding the Public Health Problem among Current and Former Military Personnel. Available online at: http://www.cdc.gov/traumaticbraininjury/pdf/Report_to_ Congress_on_Traumatic_Brain_Injury_2013-a.pdf.

475

Cernak I, Savic J, Ignjatovic D et al. (1999). Blast injury from explosive munitions. J Trauma 47: 96–104. Chafi M, Karami G, Ziejewski M (2010). Biomechanical assessment of brain dynamic responses due to blast pressure waves. Ann Biomed Eng 38: 490–504. Chamalian l, Feinstein A (2004). Outcome after mild to moderate TBI: the role of dizziness. Arch Phys Med Rehabil 85: 1662–1666. Chavko M, Koller W, Prusaczyk W et al. (2007). Measurement of blast wave by a miniature fiber optic pressure transducer in the rat brain. J Neurosci Meth 159 (2): 277–281. Chibnall JT, Duckro PN (1994). Post-traumatic stress disorder in chronic post-traumatic headache patients. Headache 34 (6): 357–361. Corrigan JD, Bogner J (2007). Initial reliability and validity of the Ohio State University TBI Identification Method. J Head Trauma Rehabil 22 (6): 318–329. Corrigan JD, Bogner JA, Mysiw WJ et al. (2001). Life satisfaction after traumatic brain injury. J Head Trauma Rehabil 16 (6): 543–555. Davis LL, Leon AC, Toscano R et al. (2012). A randomized controlled trial of supported employment among veterans with posttraumatic stress disorder. Psychiatr Serv 63 (5): 464–470. Davison K, Bagley C (1969). Schizophrenia-like psychosis associated with organic disorder of the CNS. Br J Psychiatry 4: 113–184. Dennis A, Kochanek P (2007). Pathobiology of blast injury. Intensive Care Med 21. DePalma R, Burris D, Champion H et al. (2005). Blast injuries. N Engl J Med 352: 1335–1342. DeWitt D, Prough D (2009). Blast-induced brain injury and post-traumatic hypotension and hypoxemia. J Neurotrauma 26: 1–11. Dikmen S, Levin H (1993). Methodological issues in the study of mild head injury. J Head Trauma Rehabil 8 (3): 30–37. Dikmen SS, Bombardier CH, Machamer JE et al. (2004). Natural history of depression in traumatic brain injury. Arch Phys Med Rehabil 85 (9): 1457–1464. Drew L, Drew W (2004). The contrecoup-coup phenomenon: a new understanding of the mechanism of closed head injury. Neurocrit Care 3: 385–390. Duckro PN, Tait R, Margolis RB et al. (1985). Behavioral treatment of headache following occupational trauma. Headache 25 (6): 328–331. Duckro PN, Chibnall JT, Tomazic TJ (1995). Anger, depression, and disability: a path analysis of relationships in a sample of chronic posttraumatic headache patients. Headache 35 (1): 7–9. Eierud C, Craddock RC, Fletcher S et al. (2014). Neuroimaging after mild traumatic brain injury: review and meta-analysis. Neuroimage Clin 4: 283–294. Fedoroff JP, Starkstein S, Forrester AW et al. (1992). Depression in patients with acute traumatic brain injury. Am J Psychiatr 149: 918–923. Finkelstein E, Corso P, Miller T (2006). The Incidence and Economic Burden of Injuries in the United States. Oxford University Press, New York.

476

D.M. LITTLE ET AL.

Geddes J (1997). What’s new in the diagnosis of head injury? J Clin Pathol 50 (4). Geddes J, Vowles G, Beer T et al. (1997). The diagnosis of diffuse axonal injury: implications for forensic practice. Neuropathol Appl Neurobiol 23 (4): 339–347. Gennarelli T (1996). The spectrum of traumatic axonal injury. Neuropathol Appl Neurobiol 22: 509–513. Gennarelli TA, Thibault LE, Adams JH et al. (1982). Diffuse axonal injury and traumatic coma in the primate. Ann Neurol 12 (6): 564–574. Gentry L, Godersky J, Thompson B (1988). MR imaging of head trauma: review of the distribution and radiopathologic features of traumatic lesions. AJR Am J Roentgenol 150: 663–672. Godefroy O (2003). Frontal syndrome and disorders of executive functions. J Neurol 250 (1): 1–6. Gollaher K, High W, Sherer M et al. (1998). Prediction of employment outcome one to three years following traumatic brain injury (TBI). Brain Inj 12 (4): 255–263. Goodman J (1994). Pathologic changes in mild head injury. Semin Neurol 14: 19–24. Graham D, Lawrence A, Adams J et al. (1987). Brain damage in non-missile head injury secondary to high intracranial pressure. Neuropathol Appl Neurobiol 13: 209–217. Graham D, Lawrence A, Adams J et al. (1989). Pathology of mild head injury. In: Mild to Moderate Head Injury, Blackwell Scientific, Boston, pp. 63–75. Graham D, Gennarelli T, McIntosh T (2002). Trauma. In: D Graham, P Lantos (Eds.), Greenfield’s Neurpathology. Vol. 2. Arnold, Hodder Headline Group, London. Greenspan AI, Wrigley JM, Kresnow M et al. (1996). Factors influencing failure to return to work due to traumatic brain injury. Brain Inj 10 (3): 207–218. Gronwall D, Wrightson P (1974). Delayed recovery of intellectual function after minor head injury. Lancet 2 (7881): 605–609. Gurr B, Coetzer BR (2005). The effectiveness of cognitivebehavioural therapy for post-traumatic headaches. Brain Inj 19 (7): 481–491. Guskiewicz K, Marshall S, Bailes J et al. (2007). Recurrent concussion and risk of depression in retired professional football players. Med Sci Sports Exerc 39 (6): 903–909. Gutierrez E, Huang YC, Haglid K et al. (2001). A new model for diffuse brain injury by rotational acceleration: I model, gross appearance, and astrocytosis. J Neurotrauma 18 (3): 247–257. Hamer H, Gandhi R, Wong S et al. (2013). Predicting return to work following treatment of chronic pain disorder. Occup Med (Lond) 63 (4): 253–259. Harmon KG, Drezner J, Gammons M et al. (2013). American Medical Society for Sports Medicine position statement: concussion in sport. Clin J Sport Med 23 (1): 1–18. Headache Classification Committee of the International Headache Society (1988). Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Cephalalgia (8 Suppl 7): 1–96. Hicks R, Fertig S, Desrocher R et al. (2010). Neurologic effects of blast injury. J Trauma 68: 1257–1263.

Hillier SL, Sharpe MH, Metzer J (1997). Outcomes 5 years post-traumatic brain injury (with further reference to neurophysical impairment and disability). Brain Inj 11 (9): 661–675. Hoge CW, Terhakopian A, Castro CA et al. (2007). Association of posttraumatic stress disorder with somatic symptoms, health care visits, and absenteeism among Iraq war veterans. Am J Psychiatr 164: 150–153. Hoge CW, McGurk D, Thomas JL et al. (2008). Mild traumatic brain injury in US soldiers returning from Iraq. N Engl J Med 358: 453–463. Holm L, Cassidy JD, Carroll LJ et al. (2005). Neurotrauma task force on mild traumatic brain injury of the WHO Collaborating Centre. Summary of the WHO Collaborating Centre for Neurotrauma Task Force on Mild Traumatic Brain Injury. J Rehabil Med 37 (3): 137–141. Holsinger T, Steffens DC, Phillips C et al. (2002). Head injury in early adulthood and the lifetime risk of depression. Arch Gen Psychiatry 59 (1): 17–22. Hoofien D, Gilboa A, Vakil El et al. (2001). Traumatic brain injury (TBI) 10–20 years later: a comprehensive study of psychiatric symptomatology, cognitive abilities and psychosocial functioning. Brain Inj 15 (3): 189–209. Inglese M, Bomsztyk E, Gonen O et al. (2005a). Dilated perivascular spaces: hallmarks of mild traumatic brain injury. Am J Neuroradiol 26 (4): 719–724. Inglese M, Makani S, Johnson G et al. (2005b). Diffuse axonal injury in mild traumatic brain injury: a diffusion tensor imaging study. J Neurosurg 103 (2): 298–303. Jacobson GP, Ramadan NM, Aggarwal SK et al. (1994). The Henry Ford Hospital Headache Disability Inventory (HDI). Neurology 44 (5): 837–842. Jorge R, Robinson RG (2003). Mood disorders following traumatic brain injury. Int Rev Psychiatry 15 (4): 317–327. Jorge R, Robinson RG, Arndt SV et al. (1993). Comparison between acute-and delayed-onset depression following traumatic brain injury. J Neuropsychiatr 5 (1): 43–49. Jorge RE, Robinson RG, Moser D et al. (2004). Major depression following traumatic brain injury. Arch Gen Psychiatry 61 (1): 42–50. Kant R, Duffy J, Pivovarnik A (1998). Prevalence of apathy following head injury. Brain Inj 12: 87–92. Keyser-Marcus LA, Bricout JC, Wehman P et al. (2002). Acute predictors of return to employment after traumatic brain injury: a longitudinal follow-up. Arch Phys Med Rehabil 83 (5): 635–641. Kosinski M, Bayliss MS, Bjorner JB et al. (2003). A six-item short-form survey for measuring headache impact: the HIT-6. Qual Life Res 12 (8): 963–974. Krause N, Frank J, Dasinger L et al. (2001). Determinants of duration of disability and return-to-work after work-related injury and illness: challenges for future research. Am J Ind Med 40: 464–484. Kurca E, Sivak S, Kucera P (2006). Impaired cognitive functions in mild traumatic brain injury patients with normal and pathologic magnetic resonance imaging. Neuroradiology 48 (9).

CONSIDERATIONS FOR RETURN TO WORK FOLLOWING TRAUMATIC BRAIN INJURY Lahz S, Bryant RA (1996). Incidence of chronic pain following traumatic brain injury. Arch Phys Med Rehabil 77 (9): 889–891. Lane JC, Arciniegas DB (2002). Post-traumatic headache. Curr Treat Options Neurol 4 (1): 89–104. Langlois JA, Rutland-Brown W, Thomas KE (2005). The incidence of traumatic brain injury among children in the United States: differences by race. J Head Trauma Rehabil 20 (3): 229–238. Langlois JA, Rutland-Brown W, Wald MM (2006). The epidemiology and impact of traumatic brain injury: a brief overview. J Head Trauma Rehabil 21 (5): 375–378. Levi L, Borovich B, Guilburd J (1990). Wartime neurosurgical experience in Lebanon, 1982–1985. Israel J Med Sci 26: 555–578. Levin H, Kraus M (1994). The frontal lobes and traumatic brain injury. J Neuropsychiatry Clin Neurosci 6: 443–454. Levin HS, O’Donnell VM, Grossman RG (1979). The Galveston Orientation and Amnesia Test: a practical scale to assess cognition after head injury. J Nerv Ment Dis 167 (11): 675–684. Levin HS, Williams DH, Eisenberg HM et al. (1992). Serial magnetic resonance imaging and neurobehavioral findings after mild to moderate closed head injury. J Neurol Neurosurg Psychiatry 55 (4): 255–262. Levin H, Mendelsohn D, Lilly M et al. (1997). Magnetic resonance imaging in relation to functional outcome of pediatric closed head injury: a test of the Ommaya-Gennarelli model. Neurosurgery 40: 432–441. Levin HS, McCauley SR, Josic CP et al. (2005). Predicting depression following mild traumatic brain injury. Arch Gen Psychiatry 62 (5): 523–528. Ling G, Bandak F, Armonda R et al. (2009). Explosive blast neurotrauma. J Neurotrauma 26: 1–11. Lipton RB, Silberstein SD, Saper JR et al. (2003). Why headache treatment fails. Neurology 60 (7): 1064–1070. Marcus DA (2003). Disability and chronic posttraumatic headache. Headache 43 (2): 117–121. Marsh N, Kersel D (2006). Frequency of behavioural problems at one year following traumatic brain injury: correspondence between patient and caregiver reports. Neuropsychol Rehabil 16 (6): 684–694. Mathias J, Bigler E, Jones N et al. (2004). Neuropsychological and Informational processing performance and its relationship to white matter changes following moderate and severe traumatic brain injury: a preliminary study. Appl Neuropsychol 11 (3): 134–152. Maxwell WL, Watt C, Graham DI et al. (1993). Ultrastructural evidence of axonal shearing as a result of lateral acceleration of the head in nonhuman-primates. Acta Neuropathol 86 (2): 136–144. Maxwell W, Povlishock J, Graham D (1997). A mechanistic analysis of nondisruptive axonal injury: a review. J Neurotrauma 14: 419–440. McAllister TW (1992). Neuropsychiatric sequelae of head injuries. Psychiatr Clin North Am 15 (2): 395–413. McAllister TW (2010). Genetic factors modulating outcome after neurotrauma. PM R 2 (12 Suppl 2): S241–S252.

477

McGurk SR, Mueser KT, Feldman K et al. (2007). Cognitive training for supported employment: 2–3 year outcomes of a randomized controlled trial. Am J Psychiatry 164: 437–441. Merskey H, Bogduk N (1994). Part III: Pain Terms, A Current List with Definitions and Notes on Usage. In: Classification of Chronic Pain, 2nd edn. In: IASP Task Force on Taxonomy. IASP Press, Seattle, pp. 209–214. Meythaler J, Peduzzi J, Eleftherious E et al. (2001). Current concepts: diffuse axonal injury associated traumatic brain injury. Arch Phys Med Rehabil 82: 1461–1471. Miller E (2000). The prefrontal cortex and cognitive control. Nat Rev Neurosci 1 (1): 59–65. Mittl R, Grossman R, Hiehle J et al. (1994). Prevalence of MR evidence of diffuse axonal injury in patients with mild head injury and normal head CT findings. AJNR Am J Neuroradiol 15: 1583–1589. Moldover JE, Goldberg KB, Prout MF (2004). Depression after traumatic brain injury: a review of evidence for clinical heterogeneity. Neuropsychol Rev 14 (3): 143–154. Mooney G, Speed J, Sheppard S (2005). Factors related to recovery after mild traumatic brain injury. Brain Inj 19 (12): 975–987. Moore D, Jerusalem A, Nyein M et al. (2009). Computational biology – modeling of primary blast effects on the central nervous system. Neuroimage 47 (Suppl 2): T10–T20. Morissette SB, Woodward M, Kimbrel NA et al. (2011). Deployment-related TBI, persistent postconcussive symptoms, PTSD, and depression in OEF/OIF veterans. Rehabil Psychol 56 (4): 340–350. Nampiaparampil DE (2008). Prevalence of chronic pain after traumatic brain injury: a systematic review. JAMA 300 (6): 711–719. National Institute of Mental Health (2001). The numbers count: mental disorders in America: a summary of statistics describing the prevalence of mental disorders in America. Retrieved from, http://www.nimh.nih.gov/publicat/ numbers.cfm. Niemeier JP, Perrin PB, Holcomb MG et al. (2014). Gender differences in awareness and outcomes during acute traumatic brain injury recovery. J Womens Health (Larchmt) 23 (7): 573–580. Nott M, Chapparo C, Baguley I (2006). Agitation following traumatic brain injury: an Australian sample. Brain Inj 20: 1175–1182. Obermann M, Nebel K, Schumann C et al. (2009). Gray matter changes related to chronic posttraumatic headache. Neurology 73 (12): 978–983. Obermann M, Keidel M, Diener HC (2010). Post-traumatic headache: is it for real? Crossfire debates on headache: pro. Headache 50 (4): 710–715. O’Connor SS, Zatzick DF, Wang J et al. (2012). Association between posttraumatic stress, depression, and functional impairments in adolescents 24 months after traumatic brain injury. J Trauma Stress 25 (3): 264–271. Otis JD, McGlinchey R, Vasterling JJ et al. (2011). Complicating factors associated with mild traumatic brain injury: impact on pain and posttraumatic stress disorder treatment. J Clin Psychol Med Settings 18 (2): 145–154.

478

D.M. LITTLE ET AL.

Packard RC (1992). Posttraumatic headache: permanency and relationship to legal settlement. Headache 31 (10): 496–500. Packard RC, Ham LP (1993). Impairment ratings for posttraumatic headache. Headache 33 (7): 359–364. Packard RC, Weaver R, Ham LP (1993). Cognitive symptoms in patients with posttraumatic headache. Headache 33 (7): 365–368. Pizzi L, Carter C, Howell J et al. (2005). Work loss, healthcare utilization, and costs among US employees with chronic pain. Dis Manag Health Outcome (13): 201–208. Ponsford JL, Olver JH, Curran C et al. (1995). Prediction of employment status 2 years after traumatic brain injury. Brain Inj 9 (1): 11–20. Povlishock J, Becker D, Cheng C et al. (1983). Axonal change in minor head injury. J Neuropathol Exper Neurol 42: 225–242. Povlishok JT (1992). Traumatically induced axonal injury: pathogenesis and pathobiological implications. Brain Pathol 2 (1): 1–12. Ramadan N, Keidel M (2000). Chronic posttraumatic headache. In: J Olesen, P Tfelt-Hansen, K Welch (Eds.), The Headaches, 2nd edn. Lippincott Williams and Wilkins, Philadelphia, pp. 771–780. Rapoport MJ (2012). Depression following traumatic brain injury: epidemiology, risk factors and management. CNS Drugs 26 (2): 111–121. Rapoport MJ, McCullagh S, Streiner D et al. (2003). The clinical significance of major depression following mild traumatic brain injury. Psychosomatics 44 (1): 31–37. Reeves RR, Laizer JT (2012). Traumatic brain injury and suicide. J Psychosoc Nurs Ment Health Serv 50 (3): 32–38. Rimel RW, Giordani B, Barth JT et al. (1981). Disability caused by minor head injury. Neurosurgery 9 (3): 221–228. Roberts MA, Manshadi FF, Bushnell DL et al. (1995). Neurobehavioural dysfunction following mild traumatic brain injury in childhood: a case report with positive findings on positron emission tomography (PET). Brain Inj 9 (5): 427–436. Rogers E, Anthony W, Lyass A et al. (2006). A randomized clinical trial of vocational rehabilitation for people with psychiatric disabilities. Rehabil Counsel Bull 49: 143–156. Ruff RM, Crouch JA, Troster AI et al. (1994). Selected cases of poor outcome following a minor brain trauma: comparing neuropsychological and positron emission tomography assessment. Brain Inj 8 (4): 297–308. Sbordone RJ (2001). Limitations of neuropsychological testing to predict the cognitive and behavioral functioning of persons with brain injury in real-world settings. Neurorehabilitation 16 (4): 199–201. Scheibel RS, Newsome MR, Troyanskaya M et al. (2012). Altered brain activation in military personnel with one or more traumatic brain injuries following blast. J Int Neuropsychol Soc 18 (1): 89–100. Seifert TD, Evans RW (2010). Posttraumatic headache: a review. Curr Pain Headache Rep 14 (4): 292–298. Shames J, Treger I, Ring H et al. (2007). Return to work following traumatic brain injury: trends and challenges. Disabil Rehabil 29 (17): 1387–1395.

Sheftell FD, Tepper SJ, Lay CL et al. (2007). Post-traumatic headache: emphasis on chronic types following mild closed head injury. Neurol Sci 28 (Suppl 2): S203–S207. Sherer M, Bergloff P, Levin E et al. (1998). Impaired awareness and employment outcome after traumatic brain injury. J Head Trauma Rehabil 13 (5): 52–61. Steadman-Pare D, Colantonio A, Ratcliff G et al. (2001). Factors associated with perceived quality of life many years after traumatic brain injury. J Head Trauma Rehabil 16 (4): 330–342. Stewart WF, Lipton RB, Simon D et al. (1998). Reliability of an illness severity measure for headache in a population sample of migraine sufferers. Cephalalgia 18 (1): 44–51. Taber KH, Warden DL, Hurley RA (2006). Blast-related traumatic brain injury: What is known? J Neuropsychiatry Clin Neurosci 18 (2): 141–145. [The International Classification of Headache Disorders: 2nd edition] (2006). Neurol Neurochir Pol 40(2 Suppl 1): S7– S41. van der Horn HJ, Spikman JM, Jacobs B et al. (2013). Postconcussive complaints, anxiety, and depression related to vocational outcome in minor to severe traumatic brain injury. Arch Phys Med Rehabil 94 (5): 867–874. van Reekum R, Bolago I, Finlayson MA et al. (1996). Psychiatric disorders after traumatic brain injury. Brain Inj 10 (5): 319–327. Van Velzen J, Van Bennekom C, Edelaar M et al. (2009a). How many people return to work after acquired brain injury? A systematic review. Brain Inj 23: 473–488. Van Velzen J, Van Bennekom C, Edelaar M et al. (2009b). Prognostic factors of return to work after acquired brain injury: a systematic review. Brain Inj 23: 385–395. van Velzen J, van Bennekom C, van Dormolen M et al. (2011). Factors influencing return to work experienced by people with acquired brain injury: a qualitative research study. Disabil Rehabil 33: 23–24. Vanderploeg RD, Schwab K, Walker WC et al. (2008). Rehabilitation of traumatic brain injury in active duty military personnel and veterans: defense and Veterans Brain Injury Center randomized controlled trial of two rehabilitation approaches. Arch Phys Med Rehabil 89: 2227–2238. Vargas BB, Dodick DW (2012). Posttraumatic headache. Curr Opin Neurol 25 (3): 284–289. Vasterling JJ, Brailey K, Proctor SP et al. (2012). Neuropsychological outcomes of mild traumatic brain injury, post-traumatic stress disorder and depression in Iraq-deployed US Army soldiers. Br J Psychiatry 201 (3): 186–192. von Onciul J (1996). ABC of work related disorders. Stress at work. Br Med J 313 (7059): 745–748. Walker WC, Marwitz JH, Kreutzer JS et al. (2006). Occupational categories and return to work after traumatic brain injury: a multicenter study. Arch Phys Med Rehabil 87 (12): 1576–1582. Warden D (2006). Military TBI during the Iraq and Afghanistan wars. J Head Trauma Rehabil 21 (5): 398–402.

CONSIDERATIONS FOR RETURN TO WORK FOLLOWING TRAUMATIC BRAIN INJURY Wehman P, Kregel J, Sherron P et al. (1993). Critical factors associated with the successful supported employment placement of patients with severe traumatic brain injury. Brain Inj 7 (1): 31–44. Wehman P, Targett P, West M et al. (2005). Productive work and employment for persons with traumatic brain injury: what have we learned after 20 years? J Head Trauma Rehabil 20 (2): 115–127. Whyte J, Ponsford J, Watanabe T et al. (2010). Traumatic brain injury. In: W Frontera (Ed.), Delisa’s Physical Medicine and Rehabilitation: Principles and Practice, 5th edn. Lippincott, Williams & Wilkins, Philadelphia, PA.

479

Williamson ML, Elliott TR, Berry JW et al. (2013). Predictors of health-related quality-of-life following traumatic brain injury. Brain Inj 27 (9): 992–999. World Health Organization (2002). International classification of functioning, disability and health. ICF: World Health Organization, Geneva. World Health Organization (2013). The International Classification of Headache Disorders, 3rd edition (beta version). Cephalalgia 33 (9): 629–808. Zivin K, Bohnert AS, Mezuk B et al. (2011). Employment status of patients in the VA health system: implications for mental health services. Psychiatr Serv 62 (1): 35–38.