Chronic morbidities after traumatic brain injury: an update for the advanced practice nurse.
Emerging data suggest that traumatic brain injury (TBI) is a disease process with considerable long-range morbidities requiring lifelong monitoring and treatment. Multiple chronic morbidities develop across the life span after TBI, including mental health disorders, headaches, seizures, and neuroendocrine imbalances as well as chronic diseases. Still, there has been limited focus on effective guides and strategies for helping persons with TBI meet their chronic health needs as they live with the consequences of TBI. The advanced practice nurse is well positioned to participate collaboratively in practices that promote health screening and chronic disease management after TBI to ameliorate distress and enhance quality of life as persons with TBI live with lifelong consequences.
Keywords: chronic, disability, morbidity, mortality, rehabilitation, traumatic brain injury, treatment
Worldwide, traumatic brain injury (TBI) affects an estimated 10 million people (Institute of Medicine, 2011). It is an "alteration in brain function or other evidence of brain pathology, caused by an external force" (Menon, Schwab, Wright, & Maas, 2010, p. 1637). Resulting from a blow to the head or a force impacting the brain, it is associated with injuries from motor vehicle crashes, sports injuries, falls, assaults, or blast injuries (Centers for Disease Control [CDC], 2013). Most of those injured are ages 18-25 years as well as those over 75 years (CDC, 2013). Every year, nearly 1.7 million emergency department visits occur, and about 25% of these visits require hospitalization for TBI (Faul, Xu, Wald, & Coronado, 2010). Furthermore, the annual sum of direct and indirect costs associated with hospitalizations and recovery related to TBI are estimated to exceed $76 billion (Finkelstein, Corso, Miller, & Associates, 2006).
Recovery from TBI occurs in various health settings and phases. Key difficulties are associated with each phase. For example, the acute phase emphasizes prevention and acute treatments, whereas the subacute and chronic phases focus on rehabilitation, psychosocial adjustments, and community integration. However, many individuals with milder TBI tend to deviate from these phases by delaying help-seeking and not participating in any or all phases of recovery (Shah, Bazarian, Mattingly, Davis, & Schneider, 2004).
Those hospitalized for TBI may have to undergo multiple healthcare transitions across their life span. For example, the acute event may warrant a critical care admission with transfers to an acute rehabilitation setting, then an outpatient setting, followed by multiple outpatient visits to specialists. Others might have a brief hospitalization for TBI, return to their preinjury lifestyle, and find themselves seeing their primary care provider about bothersome symptoms or reduced quality of life months or years later. Moreover, those with multiple TBIs may experience difficulties as they age, such as cognitive decline or neuroendocrine imbalances (Testa, Malec, Moessner, & Brown, 2005).
Because persons with TBI articulate their past and present unique clinical problems, current status, and personal goals to a myriad of health providers, the plan for disease prevention and management of chronic conditions and morbidities can lack personal tailoring. However, advanced practice nurses (APNs), because of their expertise in individualized acute and chronic disease management, are well suited to guide this vulnerable population through their care transitions. With increased focus on personal and system factors impacting recovery from the TBI event, APN-guided transition care within any healthcare setting can promote healthy living and management of chronic diseases or conditions.
The purpose of this article is three-fold. First, we provide background information in support of the chronic implications of TBI as a disease with characteristics of reduced life span and chronic lifelong comorbidities that require management. Then, we describe the screening and treatment recommendations put forth by the Department of Defense Special Task Force on chronic disorders after mild TBI (MTBI; Defense Centers of Excellence, 2011) as well as offer applications for the person with civilian injury who may be seen in the outpatient setting. Finally, we present a care guide for the APN, which describes approaches and psychosocial interventions that may be used to promote improved chronic conditions and disease management.
Background and Significance TBI: A Disease Process
To date, there is emerging evidence that TBI is a disease (Masel & DeWitt, 2010). This is because, afterward, numerous chronic morbidities or conditions arise and contribute to disease development (Bazarian, Cernak, Noble-Haeusslein, Potolicchio, & Temkin, 2009), increased mortality, (Harrison-Felix et al., 2009; Ventura et ah, 2010), and likely acceleration of the aging process (Marquez de la Plata et ah, 2008). The public health impact of this is particularly relevant in light of an increased prevalence of TBI in our military, aging processes of persons with TBI, and the high number of TBI from falls sustained by older adults. This review of the classification, pathophysiology, mortality, and morbidity issues throughout the TBI recovery process provides a backdrop for the excellent work that has been put in place by the Department of Defense and that could be applied to our civilians.
TBI has been classified by severity as severe, moderate, or mild, most likely depending on the force of the acceleration/deceleration injury. Severity has been associated with outcomes. More than 75% of all injuries are classified as MTBI without clearly defined biomarkers, transitions, trajectories, or help-seeking patterns (CDC, 2003). Those with moderate levels of injury typically do enter the acute hospital setting because of notable unconsciousness and abnormal imaging results, whereas those with more severe TBI enter the health setting because of critical injury or the need for neurosurgical interventions and rehabilitation. Still, severity is not always associated with the evolving difficulties and symptoms that have been clustered into major domains: physical, cognitive, sleep, and emotional.
The 3- to 12-month disability outcomes for those with mild-to-moderate TBI are, in general, expected to be good (Belanger, Curtiss, Demery, Lebowitz, & Vanderploeg, 2005; Belanger, Spiegel, & Vanderploeg, 2010; Skandsen et al., 2010). However, the disability outcomes for those with more severe TBI are more dependent on their duration of coma, lesion location, and pupillary response to the acute injury (Skandsen et al., 2011). In the case of those with MTBI, nearly 20%-30% will go on to develop chronic symptoms termed postconcussion syndrome (PCS; Sayegh, Sandford, & Carson, 2011). Thus, most of those with less than severe TBI will not have a long-term disability.
Nonetheless, these broad disability outcomes do not portray the entire clinical picture of TBI recovery. For example, those with more severe TBI who show improvements in cognitive function (information processing speed) may have improved functional outcomes (Cicerone et al., 2011; Rassovsky et al., 2006). Furthermore, it still remains unclear why, in general, there are worse functional outcomes for those with behavioral or emotional challenges versus those with more severity (Hudak, Hynan, Harper, & Diaz-Arrastia, 2012). The answer to variability in disability outcomes may lie in the underlying pathophysiology of the disease process.
Complex cellular-molecular and neurometabolic events that contribute to the chronic difficulties are currently being examined within basic science and imaging fields. The events begin with disruption to neuronal cell membranes and axonal stretching and persists with widespread inflammation (Ramlackhansingh et al., 2011) and movement of neurotransmitters. This may cause energy stores to be quickly depleted and cerebral hypo-function to occur. These changes, in the case of milder injuries, are generally time limited, unless there are repeated injuries (Guskiewicz, Marshall, & Bailes, 2005). After dismptions in ionic balance, there is glycolysis and mitochondrial dysfunction, which may compromise cerebral blood flow and can result in hypoperfusion, hyperemia, and cerebral vasospasm. In cases of severe injury, traumatic axonal injury may be present resulting in disconnection and significant disruption of axonal transport (Barkhoudarian, Hovda, & Giza, 2011). Even in the case of MTBI, magnetic or diffusion tensor imaging sequences depict evidence of axonal damage (Matsushita, Hosoda, Naitoh, Yamashita, & Kohmura, 2011; Zhou et al., 2013) or chronic structural deficits associated with person-tailored connectomics (mapping of the neural connections in the nervous system; Irimia et al., 2012).
Along with inflammation and axonal stretching in the initial days of the injury, acute activation of the hypothalamic pituitary adrenal axis (HPA-axis) occurs (Griesbach, Hovda, Tio, & Taylor, 2011). In animals with experimentally induced TBI, compared with sham, there is a heightened physiological stress response to experimentally induced acute stress for 2 weeks (Griesbach et al., 2011). Furthermore, there seems to be severity-related differences in the stress response over time (Taylor et al., 2008).
These results suggest that heightened stress responses to situational stressors in the acute phase of recovery may contribute to chronic changes in the HPA-axis and subsequent stress dysregulation and psychosocial dysfunction (Bay, Sikorskii, & Gao, 2009). Stress hormone dysregulation or hypocortisolemia, in persons not exposed to TBI, have been associated with chronic diseases, including depression, dementia, posttraumatic stress disorder (PTSD), and cardiovascular disease (CVD; Heim, Ehlert, & Hellhammer, 2000; McEwen, 2008), and may play a role in chronic disease development and mortality after TBI. Perhaps, by counteracting the negative effects of inflammation and HPA dysregulation, key foci for interventions in healthy aging within the general population (Davidson & McEwen, 2012), we may be able to interrupt the pathway toward chronic disease development after TBI. Thus, psychosocial therapies, delivered by the APN and directed toward inflammatory pathways and preventing chronic stress, may have the potential to promote neuroplastic changes after TBI and lessen chronic disease development (Davidson & McEwen, 2012).
Mortality and TBI
Mortality data indicate that, compared with the general population, TBI confers increased risk for death decades after the injury (Harrison-Felix et al., 2009; Harrison-Felix, Whiteneck, DeVivo, Hammond, & Jha, 2004; McMillan & Teasdale, 2007; McMillan, Teasdale, Weir, & Stewart, 2011; Ventura et al., 2010). Factors contributing to the overall 2.5 times increased risk for mortality include increased morbidity for those older people (age of >40 years; Ventura et al., 2010), seizures, mental health disorders, stroke, digestive disorders, sepsis, and dementia. Of lesser significance were circulatory system problems, neoplasms, and respiratory diseases. After 1 year, persons with TBI were 49 times more likely to die of aspiration pneumonia or 22 times more likely to die of seizures compared with the general population (Harrison-Felix et al., 2009). Neurosurgical outcome studies indicate that those with traumatic subdural hematoma, typically viewed as moderateto-severe level of injury, were 60 times more likely to die when there were more than three comorbidities (Kalanithi, Schubert, Lad, Harris, & Boakye, 2011). Together, these findings suggest a critical need to limit mortality in this vulnerable population through early screening and treatment of chronic diseases/conditions.
TBI has been shown to reduce life expectancy by 7 years in a prospective cohort study. Indeed, population studies indicate that, when hospitalized for the TBI, those younger than age 55 years were seven times more likely to die compared with the general population death rate of that country. Similarly, when patients with TBI were prospectively followed and compared with a noninjured comparison group, increased mortality was more likely in those younger, unless they were older when they experienced the TBI. Deaths at the 7-year mark were often associated with postinjury lifestyle, such as living alone, substance abuse, or general health decline. These data were not associated with injury severity. Thus, even with MTBI, mortality rates are higher than the general population (5.6% death rate during year 1 and an average of 35% death rate for cases with mild, moderate, or severe injury; McMillan et al., 2011; McMillan & Teasdale, 2007). Mortality may be reduced through early lifestyle interventions for those hospitalized with TBI. Similarly, these interventions may benefit those with chronic morbidities, but research supporting this hypothesis is lacking.
Chronic Morbidities After TBI: Neuroendocrine Changes
Recent reviews indicate that as many as 80% of persons with TBI have neuroendocrine disorders (e.g., gonadotropin or cortisol deficiency and vasopressin abnormalities; Behan, Phillips,Thompson, & Agha, 2008). In a large meta-analysis involving persons with all levels of TBI severity, even those with MTBI were estimated to have nearly a 17% chance of hypopituitarism. Such dysregulation has been associated with the direct effects of the trauma, hypoxia, or indirect declines in blood supply to the hypothalamus or HPA-axis (Schneider, Kreitschmann-Andermahr, Ghigo, Stalla, & Agha, 2007).
Clinical consequences of neuroendocrine dysregulation are vast and may contribute to mortality or morbidity (Behan et al., 2008). Growth hormone deficiencies result in reductions in bone mineral density, exercise capacity, and/or cardiac function. Furthermore, sex and thyroid hormone deficiencies can affect exercise tolerance and muscle strength as well as physical and emotional recovery (Behan et al., 2008). Thus, neuroendocrine screening is recommended for those with moderate-to-severe TBI and may be required in those with MTBI who have persistent symptoms (Tanriverdi, Unluhizarci, & Kelestimur, 2010).
Chronic Morbidities After TBI: Neuropsychiatric
There is emerging evidence that neuroendocrine dysregulation can contribute to cognitive difficulties, reduced quality of life, and neuropsychiatric manifestations (Cuneo, Salomon, & McGauley, 1992; Kelly et al., 2006; Rothman, Arciniegas, Filley, & Wierman, 2007). Major depression, a neuropsychiatric disorder linked with stress and HPA dysregulation, is present in nearly a third of those with TBI. Furthermore, nearly 50% will experience some form of post-TBI depression (Bombardier et al., 2010; Vreeburg et al., 2009). The impact of depression on healthcare costs, cognition, everyday functioning, health service utilization, and psychosocial functioning cannot be underestimated (Rockhill et al., 2012). Risk factors for depression include female gender, younger age, premorbid depression, and substance abuse (Malec, Brown, Moessner, Stump, & Monahan, 2010; Whelan-Goodinson, Ponsford, Johnson, & Grant, 2009).
Viewed as a complex biopsychosocial phenomenon, depression has been linked with organic lesions (Jorge et al., 2004), preinjury and postinjury chronic stress conditions (Bay, Kirsch, & Gillespie, 2004; Ponsford et al., 2000), and poor psychosocial outcomes (Teasdale & Engberg, 2001; Whelan-Goodinson et al., 2009). Depression can be detected in the early (Levin et al., 2005) or more chronic phases of recovery from TBI (Flibbard et al., 2004; Jorge et al., 1993). Prevention of post-TBI depression has not been examined.
Current evidence on best practices for treatment of depression is sparse. According to a recent systematic review, there is little support for tricyclic antidepressants because of their cognitive, sedative, and "risk for seizure" side effects. Rather, it is recommended that pharmacotherapies, if required, be started in low-range doses and titrated slowly. Current best evidence suggests that sertraline may be helpful while having a positive effect on cognitive symptoms (Fann, Hart, & Schomer, 2009). At this time, biofeedback, magnetic stimulation, and acupuncture remain experimental therapies. There is also a lack of sufficient and compelling evidence for traditional psychotherapies such as cognitive-behavioral therapies (CBTs), problem solving, and activity scheduling (Fann et al., 2009).
Other mental health conditions are associated with TBI and include anxiety disorders, PTSD, and substance abuse, with risk for these rising in the first 12 months after injury (Deb, 2003; Fann et al., 2004). In general, those less than age 65 years or with milder injuries are more likely to develop a psychiatric disorder compared with those over age 65 years (Deb & Burns, 2009). Although there seems to be an initial decline in substance use disorders soon after TBI, this pattern does not persist over time. Comorbid psychiatric disorders are also common. For example, anxiety has been associated with depression (Jorge et al., 2004) as well as PTSD (Schneiderman, Braver, & Kang, 2008). Intervention studies are limited, but for those with anxiety or PTSD, it appears that CBT shows some benefit (Soo & Tate, 2009).
Mental health conditions present before or after the injury have been associated with the persistence of post-concussion symptoms or PCS. Its causal pathway remains unclear (Silverberg & Iverson, 2011). Regardless of premorbid mental health conditions, it seems that the presence of emotional distress soon after injury contributes to the presentation of PCS (Meares et al., 2006, 2008). This suggests that mitigating emotional distress early after injury may pave the way for complete recovery. Although no published results from clinical control trials aimed on therapies for PCS, CBTs or mindfulness-based meditation may be beneficial (Sayegh et al., 2011).
Chronic Conditions and TBI: Chronic Pain, Insomnia, and Fatigue
Persistent emotional distress may also contribute to the development of other chronic conditions following TBI such as chronic pain, insomnia, and fatigue. Chronic pain after TBI has a high incidence, specifically 75.3% for those with MTBI and nearly 58% incidence for anyone with TBI (Nampiaparampil, 2008). Predominately, chronic pain results from sustained headaches. Persons injured in combat compared with injured civilians seem to have higher rates of chronic pain. Furthermore, chronic pain is comorbid with depression (Hibbard et al, 2004). The regular assessment and treatment of pain for persons with TBI has not been systematically studied. According to Bazarian and associates, interventions directed to pain management after TBI are not consistent and evidence based (Bazarian, McClung, Cheng, Flesher, & Schneider, 2005). The management of pain after TBI is complicated by intentions to avoid sedatives or platelet-altering agents.
Posttraumatic headache (PTH), also referred to as cephalgia, is the most common symptom after TBI (Neely, Midgette, & Scher, 2009), developing in 60%-90% of patients (Watanabe, Bell, Walker, & Schomer, 2012). According to the second edition of the International Classification of Headache Disorders (ICHD), PTH is categorized as a type of secondary headache specifically related to head trauma occurring within 7 days of injury or revival of consciousness (Watanabe et al., 2012). In most cases, PTH resolves within 6-12 months; however, 18%-33% of patients experience PTH for more than 1 year after injury (Lew, Lin, Wang, Clark, & Walker, 2006). Pain from PTH often interferes with patients' participation in work and functional activities and interacts with other posttraumatic symptoms and recovery processes (Watanabe et al., 2012). Determinants of PTH include a prior history of headaches, gender, and severity of TBI, with PTH being more prevalent in women and those with MTBI (Hoffman et al., 2011).
The epidemiology and treatment of PTH remains unclear. Proposed mechanisms involved in PTH include musculoskeletal and soft tissue damage, dural bleeding, intracranial pressure, intracranial hypotension, and/or posttraumatic venous sinus thrombosis (Neely et al., 2009). Emotional distress has been shown to increase PTH, suggesting that psychosocial therapies aimed at emotional self-regulation may be helpful. Pharmacotherapies involved in treating PTH include the following categories: nonsteroidal anti-inflammatories, tricyclics, muscle relaxants, serotonin inhibitors anticonvulsants, and caffeine or vasoconstrictors used to abort the presence of migraines. Careful use of medications is needed because, if the medication is overused, the headaches can worsen in intensity.
After TBI, difficulties with fatigue and sleep abound. As many as 30%-70% of persons with TBI experience some form of sleep disorder, whereas up to 29% had a diagnosed disturbance, for example, insomnia, hypersomnia, or apnea (Orff, Ayalon, & Drummond, 2009). This prevalence exceeds that of the general population and most likely contributes to complaints of fatigue, reduced quality of life, and limitations in the rehabilitation process (Mathias & Alvaro, 2012). Post-TBI sleep disorders have been attributed to disruption in circadian rhythms and psychological disturbances (e.g., depression and/or PTSD) as well as neuroendocrine disturbances (e.g., hypocretin-1 decreases or HPA-axis dysregulations; Orff et al., 2009). Sleep-wake disturbances after TBI seem to persist with nearly 67% displaying some form of disturbance for up to 3 years, although a control comparison group is needed to confirm these assertions (Kempt, Werth, Kaiser, Bassetti, & Baumann, 2010).
To date, treatment for these sleep disorders has not been systematically studied. Although Larson and Zollman (2010) offer recommendations for pharmacotherapies for sleep disorders, caution is advised in prescribing therapies that impact cognitive functioning, such as benzodiazepines and atypical GAGA agonists.
Chronic Diseases and TBI: Multiple Sclerosis, Epilepsy, Parkinson Disease, Stroke, and Dementia
Other diseases/conditions have been linked to TBI. These include multiple sclerosis (MS), epilepsy, Parkinson disease, stroke, and dementia. No common pathophysiological processes have been found to explain their onset. Their development may begin soon after injury (e.g., epilepsy) or years later when causal linkages to the injury are unclear (MS and dementia). Regardless, early recognition and treatment of these diseases/conditions may prevent worsening disability.
There is good evidence that seizures soon after TBI contribute to the development of postinjury epilepsy. In a large population cohort study that considered persons with all levels of TBI severity who were hospitalized, epilepsy was associated with rising severity and increased onset over time. Specifically, the prevalence was 4 of 100 cases for those hospitalized with MTBI, 7.6 of 100 for those with moderate TBI, and 13.6 of 100 for those with severe TBI. Risk factors for epilepsy include those with more severe TBI and/or penetrating injury, posttraumatic seizures before hospital discharge, and depression disorders. Although some of these factors are unmodifiable, the data suggest that early depression treatment may be beneficial in reducing the incidence of epilepsy (Ferguson et al., 2010). Furthermore, a randomized, single-blinded comparison study revealed that, when TBI was associated with a subarachnoid hemorrhage (N = 52), levetiracetam compared with phenytoin for seizure prophylaxis may lead to better neurological outcomes at 3 and 6 months (Szaflarski, Sangha, Lindsell, & Shutter, 2010). In persons who are refractory to seizure control with anti-epileptic medications, vagal nerve stimulation may be beneficial (Englot et al., 2012).
Direct causal linkages between MS and TBI remain unclear. Older studies examining this relationship have relied on population data without clearly defined definitions of TBI and found no associations (Goldacre, Abisgold, Yeates, & Seagroatt, 2006). Still, a more recent report of a population-based study with more clearly defined TBI parameters and randomization showed that patients hospitalized with TBI had a higher risk for subsequent MS with the 6-year follow-up period (Kang & Lin, 2012). Although these more recent findings are statistically significant, they do not provide generalizable data because the sample was largely Chinese.
Comparison studies suggest an association between TBI and Parkinson disease, determined with neurological examination and TBI history; yet the study designs were not established to detect causal relationships, so results should be interpreted cautiously (Bower et al., 2003; Goldman et al., 2006; Taylor et al., 1999). Some have suggested that the combination of TBI with environmental toxins known to increase dopaminergic neurodegeneration (e.g., pesticides) may increase risk for Parkinson' disease (Lee, Bordelon, Bronstein, & Ritz, 2012). Others claim that associations between TBI and Parkinson disease are spurious and only suggest the development of a movement disorder (Rugbjerg, Ritz, Korbo, Martinussen, & Olsen, 2008). Thus, findings remain inconclusive for establishing causal linkages between TBI and Parkinson disease.
Emerging data suggest that moderate-to-severe TBI confers increase risk for dementia and stroke (Plassman, Havlik, & Steffens, 2000). These findings were recently supported in a large retrospective cohort population study when persons with TBI had a higher prevalence of stroke, CVD, and dementia during the 5-year follow-up period. Even when controlling for comorbid diagnoses, there was still increased risk for dementia and stroke in those with TBI compared with a matched non-TBI cohort. These authors speculate that potential mechanisms may include chronic inflammation or similar risk factors known to contribute to stroke and CVD (Burke et al., 2013; Wang et ah, 2012).
TBI is not just an event but also a developing disease characterized by a number of chronic conditions and diseases that require management across a variety of settings. Following acute care management and rehabilitation, persons with TBI transition to a chronic disease management phase, requiring multiple specialists and therapies. A consistent provider is necessary to guide the long-term management of persons with risk for these chronic conditions and diseases so that personal factors, including health risks, chronic diseases, and new chronic diseases, can be well managed or even prevented. The APN is well positioned to provide the health screenings, chronic disease management, and psychosocial support that could facilitate optimal community living and quality of life. The following section describes the Defense Centers for Excellence chronic morbidity management guidelines with applications to the civilians with TBI (Table 1).
Chronic Condition/Disease Management: Applications From the Defense Centers for Excellence
In 2011, the Defense Special Task Force on chronic disorders after MTBI (Defense Centers for Excellence, 2011) published a toolkit for health professionals involved in assessing and treating persons in the ambulatory care setting with MTBI-related chronic conditions. This toolkit provides useful screening guides and suggestions for pharmacy and psychosocial therapies for those working with persons in the outpatient setting who experienced MTBI. It does not describe patient-specific cognitive rehabilitation therapies. According to recent findings from the Institute of Medicine experts, the effectiveness of cognitive rehabilitation therapies on various aspects of cognitive function is yet to be determined following refinements in the standardization, design, and conduct of these studies (Institute of Medicine's Committee on Cognitive Rehabilitation Therapy for TBI, 2011). The following provides a summary of this toolkit.
According to the toolkit, specific approaches are recommended for the initial visit when a person with MTBI seeks help for chronic difficulties, including sleep or mood disorder, pain, or cognitive impairment. Their recommendations focus on communication styles for the office visit and setting priorities for the assessment process. In general, communication styles are focused on interactions appropriate for someone who has mild cognitive impairment. These include keeping the sentences short and simple and the environment quiet and calm, providing both written and verbal communication, and using summarization. At the time of a first visit, not only should the provider establish trust, personal goals, and acceptance, but there also should be priority screenings for substance misuse and abuse, medication adherence, and suicide and violence potential.
Assuming that the initial visit provides effective provider-patient communication, symptom assessment and self-management strategies should also be addressed. Often, pain (headache) and sleep or mood disturbance co-occur, so management of one clinical condition may lead to improvements in other difficulties. Of course, assessing the overall physical integrity of every system is important and serves as a basis to determine whether biological imbalances, such as neuroendocrine disorders, are contributing to the presenting clinical complaints. Pharmacotherapies and treatment suggestions are offered for common chronic conditions associated with MTBI; these typify best practices known to date, but scientific study of these recommendations is lacking.
TBI Chronic Condition and Disease Management: The Role of the APN
Overall, principles for chronic disease management have been explicated in models depicting best processes, such as case management, preventive home visits, proactive rehabilitation, and transitional care (Boult et al., 2009). Such models of care are without clear support for effectiveness in the case of TBI and may shift with the healthcare reforms soon to come. Models of care focused on chronic disease management have focused on engaging patients and their families in self-regulation and have the potential to impact quality of life and functional autonomy (Boult & Wieland, 2010). Processes include comprehensive assessment, practicing care that is evidence based, and coordinating with other providers. Yet, these models remain untested in the case of TBI and chronic disease management.
Futuristic models of care designed to assist persons with TBI and their family as they make healthcare transitions are needed (Buck et al., 2012). In these models, efforts directed toward the following are required:
(a) regular planned health screenings for chronic conditions and early referral to specialists;
(b) partnered, goal-centered care with the person with TBI and their advocate;
(c) focus on the best community context for daily living that has full social engagement potential; and
(d) structured health promotion screenings and education as the person transitions across the life span.
After an initial health assessment, which includes a review of systems, presenting complaints, and updates on preventive care practices, the provider may decide to assess the person for common comorbidities, if warranted and new symptoms are present. For example, a decline in word finding or information processing speed is not expected for someone with MTBI at a 1-year assessment. Still, if present, further investigation might include depression screening, a speech therapy, or neuroendocrine evaluation. In addition, the APN could assess whether additional TBIs have occurred and obtain precise information about sleep patterns, caffeine, menopause, exercise, and the presence of other new comorbidities. In addition, each visit should provide regular psychosocial interventions and determine the extent to which the person maintains or engages in social connections.
To promote brain health throughout the life span, the injured person and family should be instructed on the health benefits of social support and community engagement as methods to promote brain neuroplasticity and positive behavioral outcomes. Although the mechanisms remain elusive concerning how social behaviors contribute to neuroplasticity, there is a growing body of evidence that social service programs, meditation, and physical exercise improve brain plasticity (Davidson & McEwen, 2012). The family and injured person should be informed of the benefits of community engagement, friendships, and social relationships as well as, reducing stress through cognitive reframing or meditation practices. Furthermore, these psychosocial interventions can prevent or reduce the negative effects of emotional distress and depression, which are both known to contribute to the inhibition of neural activity.
The following case study illustrates proper accommodation for the office visit and determination of a realistic plan for an initial outpatient assessment and symptom self-management visit.
Case Study Exemplar
Lativa is a 48-year-old woman who experienced a mild-to-moderate TBI 4 months ago. At that time, she received an emergency department assessment and screening and was told to follow up with her primary care physician for symptom management. At this visit, she reports increasing difficulty at work where she is the school office secretary. She is increasingly intolerant of loud noise and experiences regular headaches by mid-afternoon. She is frustrated and irritable and claims to have early morning awakening. Although she does not experience vertigo or dizziness, occasionally, her coordination seems unbalanced. Cognitively, she is improving and claims she does well with organizing her computer files, short-term memory, and word finding. She does say that her concentration remains poor and has to frequently refocus herself.
You have scheduled her for 15 minutes before the office visit for her to complete the required "initial visit" paper work as well as several screening tools (Patient Health Questionnaire 9, the Alcohol Use Disorder Identification Tool, the Primary Care Posttraumatic Screening Disorder tool, the Pittsburgh Sleep Quality Inventory, and a pain assessment tool). During the office visit, you find her overall physical health to be within normal limits and note no discernible balance or coordination challenges. She is negative for PTSD and substance misuse. She overuses caffeinated beverages, and her sleep quality is impaired. In general, she has mild depressive symptoms, is not suicidal, and has no intentions of being violent toward others. At work, she is kind and patient with the children but, at, home is reclusive.
You discuss your treatment plan with her in simple terms and in writing and suggest a 2-week follow-up visit if the symptoms persist. Priority 1 is to improve her sleep quality by decreasing her caffeine intake, improving her nutrition and exercise, and establishing good sleep hygiene practices. It is possible that these simple interventions will improve sleep quality, enhance focus, and lessen depression and headaches. However, it is possible that reducing caffeine intake will contribute to the headaches unless the caffeine is tapered, so suggestions were offered for over-the-counter medications for relief of headache. The educational focus was on lessening depression through better sleep, nutrition, and exercise while providing education about positive thinking and avoiding stress and prolonged isolation. Your office notes suggest possible PCS, but without having good sleep patterns and specific cognitive testing by a neuropsychologist or rehabilitation specialist, the diagnosis cannot be confirmed.
It is also possible that Lativa may reenter the health system years later for new onset difficulties, such as fatigue, depression, or neuroendocrine disorders. Education about the chronic difficulties that can potentially develop may be helpful for family members and the injured person, so that early assessment and treatment are provided should these conditions arise.
TBI is a significant worldwide public health problem characterized as a disease process with long-lasting consequences and economic and social burdens. It is clear that multiple phases occur within the recovery process, and multiple healthcare utilizations can potentially occur as the person seeks treatment. Science, to date, is clear that multiple systems are affected by the TBI and that there is most likely a reduced life span. Viewing TBI as a chronic disease with longstanding consequences requires new assessment, screening, and treatment models. Comprehensive and regular screenings for neuroendocrine, psychiatric, and chronic pain issues are suggested, and chronic conditions, such as insomnia; chronic symptom management; and prevention or management of epilepsy, stroke, Parkinson disease, and dementia could be improved with health promotion strategies and psychosocial interventions. These therapies are best delivered by a consistent care provider who has an established relationship with the patient and their family and who can advocate for goal-focused therapies that can be accomplished by this vulnerable group. Most suited to this role is the APN, educated and skilled in the assessment and treatment of chronic conditions and diseases that affect this vulnerable population. Chronic disease models of care are needed that allow for regular assessments, early interventions, and reduction of risky behaviors, while increasing health promotion lifestyle changes. With these models of care, empirical study can begin that will allow us to promote quality of life for persons with TBI across the life span.
In conclusion, most persons with less than severe TBI can expect good outcomes and quality of life. Yet, population studies, morbidity and mortality data, and studies on aging with TBI suggest that there are still major public health concerns. These concerns rest on the limited knowledge we have gained related to therapies for the prominent chronic diseases and conditions, such as depression, neuroendocrine imbalance, epilepsy, chronic pain, sleep, and PCS. Pharmacotherapies, a traditional mainstay of Western medicine, may offer some benefit but are not without challenges in side-effect management and medication adherence. Currently, there is a lack of a guiding framework on which to base intervention science for persons with TBI. These authors suggest that chronic condition and disease management must be guided by the APN and focus on self-regulated symptom management, holistic and comprehensive health screenings and healthy living, and prevention of chronic conditions after TBI.
Barkhoudarian, G., Hovda, D., & Giza, C. (2011). The molecular pathophysiology of concussive brain injury. Clinical Sports Medicine, 30, 33-48.
Bay, E., Kirsch, N., & Gillespie, B. (2004). Chronic stress conditions do explain post-TBI depression. Research and Theory for Nursing Practice: An International Journal, 18(2/3), 213-228.
Bay, E., Sikorskii, A., & Gao, F. (2009). Functional status, chronic stress, and cortisol response after mild-to-moderate TBI. Biological Research in Nursing, 10(3), 213-225.
Bazarian, J., Cernak, I., Noble-Haeusslein, L., Potolicchio, S., & Ternkin, N. (2009). Long-term neurologic outcomes after TBI. Journal of Head Trauma Rehabilitation, 24(6), 439-451.
Bazarian, J. J., McClung, J., Cheng, Y. T., Flesher, W., & Schneider, S. M. (2005). Emergency department management of mild traumatic brain injury in the USA. Journal of Emergency Medicine, 22, 473-477.
Behan, L. A., Phillips, J., Thompson, C. J., & Agha, A. (2008). Neuroendocrine disorders after traumatic brain injury. Journal of Neurology, Neurosurgery and Psychiatry, 79(7), 753-759.
Belanger, H., Curtiss, G., Demery, J. A., Lebowitz, B. K., & Vanderploeg, R. D. (2005). Factors moderating neuropsychological outcomes following mild traumatic brain injury: A meta-analysis. Journal of International Neuropsychological Society, 11(3), 215-227.
Belanger, H. G., Spiegel, E., & Vanderploeg, R. D. (2010). Neuropsycholigcal performance following a history of multiple self-reported concussions: A meta-analysis. Journal of International Neuropsychological Society, 16(2), 262-267.
Bombardier, C., Fann, J., Ternkin, N., Esselman, P., Barber, J., & Dikmen, S. (2010). Rates of major depressive disorder and clinical outcomes following traumatic brain injury. Journal of the American Medical Association, 303(19), 1938-1945.
Boult, C., Green, A., Boult, L., Pacaola, J., Snyder, C., & Leff, B. (2009). Successful models of comprehensive care for older adults with chronic conditions: Evidence for the IOM's "Retooling for an Aging America" report. Journal of the American Geriatric Society, 57, 2328-2337.
Boult, C., & Wieland, G. D. (2010). Comprehensive primary care for older patients with multiple chronic conditions. Journal of the American Medical Association, 304(11), 1936-1943.
Bower, J. H., Maraganore, D. M., Peterson, B. J., McDonnell, S. K., Ahlskog, J. E., & Rocca, W. A. (2003). Head trauma preceding Parkinson's disease: A case-control study. Neurology, 60(1), 65-72.
Buck, H., Meghani, S., Bettger, J., Byun, E., Fachko, M., O'Connor, M., ... Naylor, M. (2012). The use of comorbidities among adults experiencing care transitions: A systematic review and evolutionary analysis of empirical literature. Chronic Illness, 3(4), 278-295.
Burke, J., Stulc, J., Skolarus, L., Seares, E. D., Zahuranec, D. B., & Morgenstern, L. B. (2013). Traumatic brain injury may be an independent risk factor for stroke. Neurology, 81, 33-39.
Centers for Disease Control. (2003). Report to Congress on mild traumatic brain injury in the United States: Steps to prevent a serious public health problem (pp. 1-37). Atlanta, GA: Author.
Centers for Disease Control. (2013). Traumatic brain injury facts. Atlanta, GA. Retrieved from http://cdc.gov/traumaticbraininjury/ statistics.html
Cicerone, K., Langenbah, D., Braden, C., Malec, J., Kalmar, K., Fraas, M., ... Ashman, T. (2011). Evidence-based cognitive rehabilitation: Updated review of the Literature from 2003 through 2008. Archives in Physical Medicine and Rehabilitation, 92, 519-530.
Cuneo, R. C., Salomon, F., & McGauley, G. A. (1992). The growth hormone deficiency syndrome in adults. Clinical Endocrinology, 37, 387-397.
Davidson, R. J., & McEwen, B. S. (2012). Social influences on neuroplasticity: Stress and interventions to promote well-being. Nature Neuroscience, 15(5), 689-695.
Deb, S. (2003). Almost half of people suffering traumatic brain injury may later be diagnosed with Axis I disorders. Evidenced Based Mental Health, 6(2), 59.
Deb, S., & Burns, J. (2009). Neuropsychiatric consequences of TBI: A comparison between two age groups. Brain Injury, 21(3), 301-307.
Defense Centers of Excellence. (2011). Co-occurring conditions toolkit: Mild traumatic brain injury and psychological health (2nd ed.). Retrieved from http://dcoe.health.mil
Englot, D. J., Rolston, J. D., Wang, D. D., Hassnain, K. H., Gordon, C. M., & Chang, E. F. (2012). Efficacy of vagus nerve stimulation in posttraumatic versus nontraumatic epilepsy. Journal of Neurosurgery, 117(5), 970-977.
Fann, J., Hart, T., & Schomer, K. (2009). Treatment for depression after TBI: A systematic review. Journal of Neurotrauma, 26, 2383-2402.
Fann, J. R., Burington, B. E., Leonetti, A., Jaffe, K., Katon, W. J., & Thompson, R. (2004). Psychiatric illness 1 year after traumatic brain injury in an adult health maintenance organization population. Archives in General Psychiatry, 61, 53-61.
Faul, M., Zu, L., Walk, M. M., & Coronado, V. G. (2010). Traumatic brain injury in the US: Emergency department visits, hospitalizations, and deaths 2002-2006. Retrieved from http:// www.cdc.gov/traumaticbraininjury/pdq/bluebook.pdf
Ferguson, P., Smith, G., Wannamaker, B., Thurman, D. J., Pickelsimer, E., & Selassie, A. (2010). A population-based study of risk of epilepsy after hospitalization for traumatic brain injury. Epilepsia, 51(5), 891-898.
Finkelstein, E., Corso, P., Miller, T., & Associates. (2006). The incidence and economic burden of injuries in the US. New York, NY: Oxford University Press.
Goldacre, M. J., Abisgold, J. D., Yeates, D. G. R., & Seagroatt, V. (2006). Risk of multiple sclerosis after head injury: Record linkage study. Journal of Neurology, Neurosurgery, and Psychiatry, 77(3), 351-353.
Goldman, S. M., Tanner, C. M., Oakes, D., Bhudhikanok, G. S., Gupta, A., & Langston, J. W. (2006). Head injury and Parkinson's disease risk in twins. Annals of Neurology, 60(1), 65-72.
Griesbach, G. S., Hovda, D. A., Tio, D. L., & Taylor, A. (2011). Heightening of the stress response during the first weeks after a mild TBI. Neuroscience and Biobehavioral Reviews, 178, 147-158.
Guskiewicz, K. M., Marshall, S. W., & Bailes, J. (2005). Association between recurrent concussion and late-life cognitive impairment in retired professional footfall players. Neurosurgery, 57(4), 719-726.
Harrison-Felix, C., Whiteneck, G., DeVivo, M., Hammond, F. M., & Jha, A. (2004). Mortality following rehabilitation in the traumatic brain injury model systems of care. NeuroRehabilitation, 79(1), 45-54.
Harrison-Felix, C., Whiteneck, G., Jha, A., DeVivo, M., Hammond, F., & Hart, D. (2009). Mortality over four decades after traumatic brain injury rehabiitation: A retrospective cohort study. Archives in Physical Medicine Rehabilitation, 90(9), 1506-1513.
Heim, C., Ehlert, U., & Hellhammer, D. (2000). The potential role of hypocortisolism in the pathophysiology of stress-related bodily disorders. Psychoneuroendocrinology, 25, 1-35.
Hibbard, M. R., Ashman, T. A., Spielman, L. A., Chun, D., Charatz, H. J., & Melvin, S. (2004). Relationship between depression and psychosocial functioning after traumatic brain injury. Archives in Physical Medicine Rehabilitation, 85(4), S43-53.
Hoffman, J. M., Lucas, S., Dikmen, S., Braden, C. A., Brown, A. W., Brunner, R., ... Bell, K. R. (2011). Natural history of headache after TBI. Journal of Neurotrauma, 28(9), 1719-1725.
Hudak, A., Hyman, S., Harper, C. R., & Diaz-Arrastia, R. (2012). Association of depressive symptoms with functional outcome after traumatic brain injury. Journal of Head Trauma Rehabilitation, 27(2), 87-98.
Institute of Medicine's Committee on Cognitive Rehabilitation Therapy for TBI, 2011Institute of Medicine's Committee on Cognitive Rehabilitation Therapy for TBI. (2011). Cognitive rehabilitation therapy for traumatic brain injury: Evaluating the evidence. Editors: R. Koehler, E. Wilhelm, & R. Shoulson. National Academies Press. Retrieved from http://www.nap .edu/catalog
Irimia, A., Chambers, M. C., Torgerson, C. M., Filippou, M., Hovda, D. A., Alger, J. R., ... Van Horn, J. D. (2012). Patient-tailored connectomies visualization for the assessment of white matter atrophy in TBI. Frontiers in Neurology, 3(10), epub 2/6/2012.
Jorge, R., Robinson, R., Arndt, S., Forrester, A., Geisler, F., & Starkstein, S. (1993). Comparison between acute-and delayed onset depression following traumatic brain injury. Journal of Neuropsychiatry, 5(1), 43-49.
Jorge, R., Robinson, R., Moser, D., Tateno, A., Crespo-Facorro, B., & Arndt, S. (2004). Major depression following traumatic brain injury. Archives of General Psychiatry, 61(1), 42-50.
Kalanithi, P., Schubert, R., Lad, S., Harris, O., & Boakye, M. (2011). Hospital costs, incidence, and inhospital mortality rates of traumatic SDH in the US. Journal of Neurosurgery, 115, 1013-1018.
Kang, J.-H., & Lin, H.-C. (2012). Increased risk of multiple sclerosis after TBI: A nationwide population based study. Journal of Neuro trauma, 29, 90-95.
Kelly, D. E., McArthur, D. L., Levin, H. S., Swimmer, S., Dusick, J. R., Cohan, P., ... Swerdloff, R. (2006). Neurobehavioral and quality of life changes associated with growth hormone insufficiency after complicated mild, moderate, or severe traumatic brain injury. Journal of Neurotrauma, 23(6), 928-942.
Kempt, J., Werth, E., Kaiser, P., Bassetti, C. L., & Baumann, C. (2010). Sleep-wake disturbances 3 years after TBI. Journal of Neurology Neurosurgery and Psychiatry, 81, 1402-1405.
Larson, E., & Zollman, F. (2010). The effect of sleep medications on cognitive recovery from TBI. Journal of Head Trauma Rehabilitation, 25(1), 61-67.
Lee, R C., Bordelon, Y., Bronstein, J., & Ritz, B. (2012). Traumatic brain injury, paraquat exposure, and their relationship to Parkinson disease. Neurology, 79(20), 2061-2066.
Levin, H. S., McCauley, S., Josic, C., Boake, C., Brown, S., Goodman, H., ... Brundage, S. (2005). Predicting depression following mild traumatic brain injury. Archives in General Psychiatry, 62(5), 523-528.
Lew, H. L., Lin, F., Wang, S. J., Clark, D. J., & Walker, W. C. (2006). Characteristics and treatment of headache after TBI. American Journal of Physical Medicine Rehabilitation, 85(7), 619-627.
Malec, J., Brown, A., Moessner, A., Stump, T., & Monahan, P. (2010) . A preliminary model for posttraumatic brain injury depression. Archives in Physical Medicine Rehabilitation, 91, 1087-1097.
Marquez de la Plata, C., Hart, T., Hammond, F., Frol, A., Hudak, A., Harper, C., ... Diaz-Arrastia, R. (2008). Impact of age on long-term recovery from traumatic brain injury. Archives in Physical Medicine and Rehabilitation, 89(5), 896-903.
Masel, B. E., & DeWitt, D. (2010). Traumatic brain injury: A disease process, not an event. Journal of Neurotrauma, 27, 1529-1540.
Mathias, J. L., & Alvaro, P. K. (2012). Prevalence of sleep disturbances, disorders, and problems following TBI: A meta-analysis. Sleep Medicine, 13, 898-905.
Matsushita, M., Hosoda, K., Naitoh, Y., Yamashita, H., & Kohmura, E. (2011). Utility of diffusion tensor imaging in the acute stage of mild to moderate traumatic brain injury for detecting white matter lesions and predicting long-term cognitive function in adults. Journal of Neurosurgery, 115(1), 130-139.
McEwen, B. S. (2008). Central effects of stress hormones in health and disease: Understanding the protective and damaging effects of stress and stress mediators. European Journal of Pharmacology, 583, 174-185.
McMillan, T. M., & Teasdale, G. M. (2007). Death rate is increased for at least 7 years after head injury: A prospective study. Brain Injury, 130, 2520-2527.
McMillan, T. M., Teasdale, G. M., Weir, C. J., & Stewart, E. (2011) . Death after head injury: The 13 year outcome of a case control study. Journal of Neurology, Neurosurgery and Psychiatry, 82, 931-935.
Meares, S., Shores, E. A., Batchelor, J., Baguley, I. J., Chapman, J., Gurka, J., & Marosszeky, J. E. (2006). The relationship of psychological and cognitive factors and opioids in the development of the postconcussion syndrome in general trauma patients with mild traumatic brain injury. Journal of the Neuropsychological Society, 12, 792-801.
Meares, S., Shores, E. A., Taylor, A. J., Batchelor, J., Bryant, R. A., Baguley, I. J., ... Marosszeky, J. E. (2008). Mild traumatic brain injury does not predict acute postconcussion syndrome. Journal of Neurology, Neurosurgery and Psychiatry, 79(3), 300-306.
Meares, S., Shores, E. A., Taylor, A. J., Batchelor, J., Bryant, R. A., Baguley, I. J., ... Marosszeky, J. E. (2011). The prospective course of postconcussion syndrome: The role of mild TBI. Neuropsychology, 25(4), 454-465.
Menon, D., Schwab, K., Wright, D., & Maas, A. (2010). Position statement: Definition of traumatic brain injury. Archives In Physical Medicine and Rehabilitation, 91, 1637-1640.
Nampiaparampil, D. (2008). Prevalence of chronic pain after traumatic brain injury: A sytematic review. Journal of the American Medical Association, 300(6), 711-719.
Neely, E., Midgette, L., & Scher, A. (2009). Clinical review and epidemiology of headache disorders in US Service members: Emphasis on post-traumatic headache. Headache, 7, 1089-1096.
Orff, H., Ayalon, L., & Drummond, S. (2009). Traumatic brain injury and sleep disturbance: A review of current research. Journal of Head Trauma Rehabilitation, 24(3), 155-165.
Plassman, B. L., Havlik, R., & Steffens, D. (2000). Documented head injury in early adulthood and risk of Alzheimer's disease and other dementias. Neurology, 55(8), 11158-11166.
Ponsford, J., Willmott, C., Rothwell, A., Cameron, P., Kelly, A.-M., Nelms, R., ... Ng, K. (2000). Factors influencing outcome following mild traumatic brain injury in adults. Journal of the International Neuropsychological Society, 6(5), 568-579.
Ramlackhansingh, A., Brooks, D., Greenwood, R. J., Bose, S., Turkheimer, F. E., Kinnunen, K, ... Sharp, D. (2011). Inflammation after trauma: Microglial activation and traumatic brain injury. Annals of Neurology, 70, 374-383.
Rassovsky, Y., Satz, P., Alfano, M., Light, R., Zaucha, K., McArthur, D., & Hovda, D. (2006). Functional outcome in TBI.I: Neuropsychological, emotional, and behavioral mediators. Journal of Clinical and Experimental Neuropsychology, 25(4), 567-580.
Rockhill, C., Jaffe, K., Zhou, C., Fan, M., Katon, W., & Fann, J. R. (2012). Health care costs associated with TBI and psychiatric illness in adults. Journal of Neurotrauma, 29, 1-11.
Rothman, M., Arciniegas, D., Filley, C., & Wierman, M. (2007). The neuroendocrine effects of traumatic brain injury. Journal of Neuropsychiatry in Clinical Neuroscience, 19(4), 363-372.
Rugbjerg, K., Ritz, B., Korbo, L., Martinussen, N., & Olsen, J. (2008). Risk of Parkinson's disease after hospital contact for head injury: Population based case-control study. British Medical Journal, 337, 2494.
Sayegh, A. M., Sandford, D., & Carson, A. (2011). Psychological approaches to treatment of postconcussion syndrome: A systematic review. Journal of Neurology, Neurosurgery, and Psychiatry, 81, 1128-1134.
Schneider, H., Kreitschmann-Andermahr, I., Ghigo, E., Stalla, G., & Agha, A. (2007). Hypothalamopituitary dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage. Journal of the American Medical Association, 295(12), 1429-1438.
Schneiderman, A., Braver, E., & Kang, H. (2008). Understanding sequelae of injury mechanisms and mild traumatic brain injury incurred during the conflicts in Iraq and Afghanistan: Persistent postconcussive symptoms and posttraumatic stress disorder. American Journal of Epidemiology, 767(12), 1446-1452.
Shah, M., Bazarian, J., Mattingly, A., Davis, E., & Schneider, S. (2004). Patient with head injuries refusing emergency medical services transport. Brain Injury, 18(%), 765-773.
Silverberg, N., & Iverson, G. (2011). Etiology of the post-concussion syndrome: Physiogenesis and psychogenesis revisited. Neurorehabilitation, 29(4), 317-329.
Skandsen, T., Finnanger, T., Andersson, S., Lydersen, S., Brunner, J., & Vik, A. (2010). Cognitive impairment 3 months after moderate and severe traumatic brain injury: A prospective follow-up study. Archives in Physical Medicine and Rehabilitation, 91, 1904-1913.
Skandsen, T., Kvistad, K. A., Solheim, O., Lydersen, S., Strand, I. H., & Vik, A. (2011). Prognostic value of magnetic resonance imaging in moderate and severe head injury: A prospective study of early MR1 findings and one-year outcome. Journal of Neurotrauma, 28(5), 691-699.
Soo, C., & Tate, R. L. (2009). Psychological treatment for anxiety in people with TBI. Cochrane Database of Systematic Reviews, (3), CD005239.
Szaflarski, J., Sangha, K., Lindsell, C., & Shutter, L. (2010). Prospective, randomized, single-blinded comparative trial of intravenous Levetiracetam versus Phenytoin for seizure prophylaxis. Neurocritical Care, 12, 165-173.
Tanriverdi, F., Unluhizarci, K., & Kelestimur, F. (2010). Pituitary function in subjects with mild traumatic brain injury: A review of literature and proposal of a screening strategy. Pituitary, 13, 146-153.
Taylor, A., Rahman, S., Sanders, N., Tio, D., Prolo, P, & Sutton, R. (2008). Injury severity differentially affects short-and long-term neuroendocrine outcomes of traumatic brain injury. Journal of Neurotrauma, 25, 311-323.
Taylor, C. A., Saint-Hilaire, M. H., & Cupples, L. A. (1999). Environmental, medical and family history risk factors for Parkinson's disease: A New England-based case control study. American Journal of Genetics, 88(6), 742-749.
Teasdale, T., & Engberg, A. (2001). Suicide after TBI: A population study. Journal of Neurology, Neurosurgery, & Psychiatry, 71, 436-440.
Testa, J., Malec, J., Moessner, A., & Brown, A. (2005). Outcome after traumatic brain injury: Effects of aging on recovery. Archives in Physical Medicine Rehabilitation, 86, 1815-1823.
Ventura, T., Harrison-Felix, C., Carlson, N., DiGuiseppi, C., Gabella, B., Brown, A., ... Whiteneck, G. (2010). Mortality after discharge from acute care hospitalization with TBI: A population-based study. Archives in Physical Medicine and Rehabilitation, 91, 20-29.
Vreeburg, S., Hoogendijk, J. G., van Pelt, J., DeRijk, R., Verhagen, J., van Dyck, R., ... Penninx, B. (2009). Major depressive disorder and hypothalamic-pituitary-adrenal axis activity: Results from a large cohort study. Archives in General Psychiatry, 66(6), 617-626.
Wang, H., Lin, S., Sung, P., Wu, M., Hung, K., Wang, L., ... Tsai, K. J. (2012). Population based study on patients with traumatic brain injury suggests increased risk of dementia. Journal of Neurology, Neurosurgery and Psychiatry, 83, 1080-1085.
Watanabe, T., Bell, K., Walker, M. D., & Schomer, M. A. (2012). Systematic review of interventions for post-traumatic headache. Physical Medicine and Rehabilitation, 4(2), 129-140.
Whelan-Goodinson, R., Ponsford, J., Johnson, L. G., & Grant, F. (2009). Psychiatric disorders following traumatic brain injury: Their nature and frequency. Journal of Head Trauma Rehabilitation, 24(5), 324-332.
Zhou, Y., Kierans, A., Kenul, D., Ge, Y., Rath, J., Reaume, J., ... Lui, Y. W. (2013). Mild TBI: Longitudinal regional brain volume changes. Radiology, 267, 880-890.
Questions or comments about this article may be directed to Esther H. Bay, PhD ACNS-BC, at email@example.com. She is a Clinical Associate Professor, School of Nursing, University of Michigan, Ann Arbor, MI.
Kattlynn S. Chartier, BSN(c), is a Senior Honors Student, University of Michigan, Ann Arbor, MI.
This manuscript was authored collaboratively by Esther H. Bay and Kattlyn S. Chartier.
The authors declare no conflicts of interest.
TABLE 1. Comorbidities Following Traumatic Brain Injury Condition/Disease Prevalence Depression 33%-50% PTSD 10%-20% Anxiety 18%-60% Postconcussion disorder 20%-30% Chronic pain 58%-73% Neuroendocrine disorders 17%-80% Headache 58%-90% Sleep disorders 30%-70% Note. PTSD = posttraumatic stress disorder.
|Printer friendly Cite/link Email Feedback|
|Author:||Bay, Esther H.; Chartier, Kattlynn S.|
|Publication:||Journal of Neuroscience Nursing|
|Date:||Jun 1, 2014|
|Previous Article:||Screening, diagnosis, and treatment of post-stroke depression.|
|Next Article:||Clinical outcomes of patient mobility in a neuroscience intensive care unit.|