Introduction: Traumatic Brain Injury (TBI) remains a significant public health burden in the United States. Persons afflicted with more severe TBIs are usually admitted to an ICU, where they are at risk for a number of complications throughout their hospitalization. Recent literature has attempted to describe such complications from a cardiovascular perspective as part of a “cardio-cerebral syndrome.” We described the frequency of cardiac complications in the ICU among patients with a TBI and compared patients with and without measured cardiac dysfunction. We investigated the potential impact of cardiac dysfunction on in-hospital mortality. Methods: This was a retrospective review of a prospective cohort study in adult ICU patients with moderate-to-severe TBI (GCS≤12). We measured cardiac dysfunction using initial EKG echocardiography findings and peak serum troponin levels during hospitalization. Primary outcome was in-hospital mortality for patients with and without cardiac dysfunction using multivariable adjusted Cox Proportional Hazards Regression. Secondary outcomes examined the relationship between severity of brain injury and degree of cardiac dysfunction. Results: Ordinal logistic regression showed patients with more indicators of cardiac injury were significantly more likely to have greater brain injury as reflected by lower GCS scores (OR 0.76; 95%CI 0.58-0.99). There was a significantly increased multivariable adjusted risk of dying for each increase in measured cardiac injury (HR 2.41; 95% CI 1.29-4.53). Conclusions: Cardiac dysfunction was frequently observed in patients with TBI and we showed an association between increasing TBI severity and development of cardiac injury. Cardiovascular dysfunction was associated with an increased risk of in-hospital death. Adverse outcomes from TBI could potentially be mediated by cardiac injury, which could be used as a target for therapeutic intervention.

Includes bibliographical references / South Africa has a high incidence of injury-related disorders, such as traumatic brain injury (TBI) as a result of motor vehicle accidents and assault. Dysphagia is a common sequela of TBI, which may result in malnutrition or aspiration pneumonia. There is limited epidemiological data available for TBI and dysphagia in South Africa which is important for health care planning. There is also inadequate literature reporting predictive factors for dysphagia and health outcomes of patients with TBI and swallowing disorders for the South African context, which would provide management guidelines for Speech-Language Pathologists (SLPs) for patients with TBI and dysphagia. This study aims to begin to provide up-to-date information regarding the incidence of TBI and the prevalence of dysphagia in the population with TBI in Bloemfontein, South Africa. Predictive factors for dysphagia and health outcomes were also investigated in order to provide management guidelines for TBI-related dysphagia for SLPs. A prospective cohort study followed 77 participants aged 18 to 68 years (M = 33.1) with mild to severe traumatic brain injury, admitted to 2 state and 2 private hospitals in the Bloemfontein metropole, South Africa, to investigate the incidence of TBI and the prevalence of TBI-related dysphagia in the adult population in 2013. Participants were tracked from admission to hospital to discharge. Demographic and medical data was collected for each participant, including: gender, age, TBI aetiology, means of nutritional intake, respiratory status, length of hospital stay, and number of speech therapy sessions. Glasgow Coma Scale (GCS) scores at time of admission, swallowing evaluation, and discharge were noted as an indicator of TBI severity and each participant was assessed with the Mann Assessment of Swallowing Ability on admission and prior to discharge to assess the presence of dysphagia. The incidence of TBI for the Bloemfontein metropole was 353 per 100,000 people and was greater in the male than in the female population (11.83:1). The main mechanism for TBI in Bloemfontein was interpersonal violence (67.53%), followed by road traffic accidents (motor and pedestrian vehicle accidents; 23.38%). The prevalence rate for dysphagia was 32%. Twenty-eight percent of those who presented with dysphagia also aspirated. Severe TBI (GCS ≤ 8) was identified as a predictive factor for dysphagia. Participants with dysphagia had longer hospital stays (days; M = 22.04, SD = 17.67) than those with normal swallowing (M = 6.23, SD = 4.28), t(75) = 6.13, p < .001, and took significantly more days to achieve oral intake (M = 6.23, SD = 10.32) than those without dysphagia (M = .31, SD = 1.41), t(75) = 4.08, p < .001. Ventilation was associated with longer hospital stays, rs(25) = -.47, p = .02 and longer duration until achievement of oral intake, rs(22) = -.80, p < .001. Tracheotomised participants also had significantly longer hospital stays, rs(25) = -.67, p < .001, and took longer to achieve oral intake, rs(22) = -.52, p = .01. An increased period of time with a tracheostomy was also significantly associated with mortality, χ2(2, n = 11) = 6.52, p = .04. Participants with dysphagia (M = 3.84, SD = 5.44) required significantly more therapy sessions with an SLP than those without dysphagia (M = .15, SD = .64), t(75) = 4.85, p < .001, and those with low GCS scores were significantly less likely to achieve oral intake prior to discharge, rs(25) = -.45, p = .02, and had longer hospital stays than participants with mild head injuries, rs(25) = -.49, p = .01. All participants who received nutrition via nasogastric tubes returned to oral intake; however, individuals who had percutaneous endoscopic gastrostomies did not achieve oral intake prior to discharge. It is recommended that objective swallowing evaluations be conducted for patients admitted with severe TBIs, and patients with mild and moderate TBIs be screened to determine the presence of dysphagia. TBI prevention initiatives should be developed to reduce the incidence of TBI, specifically in the young adult male population.

Blast-related mild traumatic brain injury (mTBI) is a common injury among Operation Enduring Freedom/Operation Iraqi Freedom (OEF/OIF) veterans due to the frequent use of improvised explosive devices (IEDs). A significant minority of veterans with blast-related mTBI complain of postconcussion symptoms (PCS) and cognitive difficulties, even years after the injury. Studies have suggested that these behavioral sequelae are primarily linked to mental health disorders such as posttraumatic stress disorder (PTSD). However, mTBI is associated with neural changes and the impact of these changes on behavioral sequelae is unclear. As such, this dissertation had three goals. First, this dissertation assessed whether the severity of PCS in blast-exposed individuals is associated with the extent of mTBI-related neural injury. Results revealed that individuals with mTBI with loss of consciousness (LOC) had significantly more white matter abnormalities than no-TBI controls and that these white matter abnormalities were spatially variable across individuals. Importantly, the extent of white matter abnormality was associated with physical PCS severity and mediated the relationship between mTBI with LOC and physical PCS. Second, this dissertation examined whether these white matter abnormalities were also associated with overall cognitive impairment. In light of the observed variability in white matter injury, a measure of overall cognitive status that takes into account heterogeneity of cognitive impairment was used. Results showed that the extent of white matter abnormality was associated with cognitive status and mediated the relationship between mTBI with LOC and cognitive impairment. Third, this dissertation examined performance and brain function in the context of an experimental measure of cognitive control known to be sensitive to residual effects of mTBI. Results revealed that although behavioral performance was similar across groups, the mTBI group had enhanced functional connectivity between brain networks important for task performance, suggesting a potential compensatory mechanism in mTBI. Together, the findings of this dissertation suggest that mTBI is associated with structural and functional connectivity alterations years after the injury. Further, this dissertation suggests that whereas structural connectivity changes may have negative behavioral consequences, changes in functional connectivity may serve as a compensatory mechanism for successful performance.

People who suffer a traumatic brain injury (TBI) experience challenges in returning to work differently and at a rate that surpasses the return to work transition for people who experience other types of disabling injuries. In part, this challenge is a result of a lack of policy structure that promotes the successful return to work transition. The purpose of this ethnographic study was to explore the policy implications of the return to work transition for TBI survivors, address the gap in the literature, and identify key factors that contribute to the success of return-to-work programs in Washington State. A hybrid of Smith's institutional ethnography approach and Foucault's critique of bureaucratic institutions was used as the framework for this study. Data were gathered from 12 interviews and 2 focus groups with TBI survivors who had access to TBI support groups and employers connected to the TBI community. Data were inductively coded and categorized using a comparative analytical method. The study results indicate that an inclusive culture, collaborative communication, TBI-focused knowledge, integrated support, and survivor/employer motivation to interact are key factors in the successful return to work process. This study promotes positive social change by providing information for use in expanding TBI employment policy, TBI employment education, and accommodation practices. The study findings are intended to inform new policies to improve employment post-TBI outcomes for TBI survivors, employers, and their community.

abstract: Of the 2.87 million traumatic brain injuries (TBI) sustained yearly in the United States, 75% are diffuse injuries. A single TBI can have acute and chronic influences on the neuroendocrine system leading to hypothalamic-pituitary-adrenal axis (HPA) dysregulation and increased affective disorders. Preliminary data indicate TBI causes neuroinflammation in the hippocampus, likely due to axonal damage, and in the paraventricular nucleus of the hypothalamus (PVN), where no axonal damage is apparent. Mechanisms regulating neuroinflammation in the PVN are unknown. Furthermore, chronic stress causes HPA dysregulation and glucocorticoid receptor (GR)-mediated neuroinflammation in the PVN. The goal of this project was to evaluate neuroinflammation in the HPA axis and determine if GR levels change at 7 days post-injury (DPI). Adult male and female Sprague Dawley rats were subjected to midline fluid percussion injury. At 7 DPI, half of each brain was post-fixed for immunohistochemistry (IBA-1) and half biopsied for gene/protein analysis. IBA-1 staining was analyzed for microglia activation via skeleton analysis in the hypothalamus and hippocampus. Extracted RNA and protein were used to quantify mRNA expression and protein levels for GRs. Data indicate increased microglia cell number and decreased endpoints/cell and process length in the PVN of males, but not females. In the dentate gyrus, both males and females have an increased microglia cell number after TBI, but there is also an interaction between sex and injury in microglia presentation, where males exhibit a more robust effect than females. Both sexes have significant decreases of endpoints/cell and process length. In both regions, GR protein levels decreased for injured males, but in the hippocampus, GR levels increased for injured females. Data indicate that diffuse TBI causes alterations in microglia morphology and GR levels in the hypothalamus and hippocampus at 7 DPI, providing a potential mechanism for HPA axis dysregulation at a sub-acute time point. / Dissertation/Thesis / Masters Thesis Biology 2019

Bakgrund: Personer med traumatisk hjärnskada kan få långvariga kroniska besvär. Anhöriga är ofta involverade i deras vård och finns med under hela vårdförloppet. Anhöriga har också en viktig roll och ansvar för det vardagliga livet i hemmet. Syfte: Syftet var att beskriva anhörigas erfarenheter av att leva med en närstående med traumatisk hjärnskada. Metod: En allmän litteraturstudie genomfördes, där elva artiklar analyserades med hjälp av innehållsanalytiskt tillvägagångssätt. Resultat: Det framkom fyra kategorier ifrån resultatartiklarna: att ta ansvar och anta olika roller, att leva i en oviss och oförutsägbar situation, att få stöd och att finna en egen inre kraft. Det var en stor påfrestning för anhöriga att anta den vårdande rollen för att stödja den traumatiskt hjärnskadade. Ovissheten kring den traumatiskt hjärnskadades prognos tillsammans med bristen på information och kunskap, satte de anhöriga i stress. Behovet av stöd till anhöriga var multidimensionellt där det initiala stödet kom främst från sjukvårdspersonalen medan det senare i förloppet övergick till familjen och samhället. Anhöriga fick använda egna resurser och egen inre kraft för att hantera sin situation. Konklusion: För att underlätta livet för anhöriga och traumatiskt hjärnskadade, behöver vården ha bättre strategier och samhället ha bättre kunskap och förståelse för sjukdomen. / Background: Individuals with traumatic brain injury can sustain chronical lasting sequalae’s. Relatives are often involved in their care and present during the whole process. Relatives also have an important role and responsibility in the everyday life. Aim: The aim was to describe relatives’ experiences of living with a next of kin with traumatic brain injury. Method: A general literary study was performed, where eleven articles were analyzed, with content analytic approach. Result: Four categories emerged from the result articles: to take responsibility and adopt different roles, to live in an uncertain and unpredictable situation, to receive support and to find own inner strength. It was a big strain for relatives to take on the caring role of supporting the traumatic brain injured. The uncertainty of the prognose, along with the lack of information and knowledge, putted the relatives in distress. The need of support was multidimensional where the initial support came from healthcare personnel and then from family and community. Relatives had to use own resources and inner strength to manage their situation. Conclusion: To ease life for relatives and traumatic brain injured, health care needs to have better strategies and the community better knowledge and understanding for the disease.

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Indiana University-Purdue University Indianapolis (IUPUI) / Social support is a powerful therapeutic against fear and anxiety and is utilized in many psychotherapies. The concept that a familiar or friendly presence helps a person learn to overcome anxiety has been well-known for decades, yet, the basic neural mechanisms that regulate this psychosocial learning remain unknown. A first step towards elucidating these basic mechanisms is the development of a valid preclinical animal model. However, preclinical behavioral models exploring the use of a social presence in reducing anxiety have not been fully characterized. Therefore, it was our goal to identify a useful way in which to study the mechanisms of how a social presence can induce anxiolysis (the reduction of anxiety). We accomplished this goal by characterizing and validating a preclinical model, as well as demonstrating that the model was capable of measuring deficits in rats given a mild traumatic brain injury. To this end, we identified an existing, but uncharacterized model, the social interaction-habituation model, as an effective model of social familiarity-induced anxiolysis (SoFiA), which demonstrates socially enhanced safety learning, or psychosocial learning. We find that as social familiarity develops across time, anxiolysis develops. We identified that the use of a Bright Light Challenge is a useful anxiogenic stimulus to use during SI-habituation training. The anxiolysis acquired following SI-habituation testing is partner specific, and can be blocked by an inhibition of the medical prefrontal cortex, while it can be enhanced by D-cycloserine. We found that this model identified deficits in SoFiA acquisition in rodents exposed to a mild traumatic brain injury, which, in humans, has been linked to psychosocial deficits. This work is a step in creating ways in which we can study and better understand the regulatory processes of emotions mediated by social behavior.

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