Influence Of Traumatic Brain Injury Research Articles

Dissecting causal relationships between gut microbiome, immune cells, and brain injury: A Mendelian randomization study.

Increasing literature has affirmed that changes in the gut microbiome (GM) composition were linked to distinct brain injury (BI) through the gut-brain axis, but it is uncertain if such links reflect causality. Further, the immune cell changes mediating the impact of GM on BI are not completely understood. We made use of the summary statistics of 211 GM (MiBioGen consortium), 731 immune cells, and 2 different BIs (FinnGen consortium), namely traumatic BI (TBI) and focal BI (FBI), from the extensive genome-wide association studies to date. We executed bidirectional Mendelian randomization (MR) analyses to ascertain the causal relationships between the GM and BI, and 2-step MR to validate possible mediating immune cells. Additionally, thorough sensitivity analyses verified the heterogeneity, robustness, as well as horizontal pleiotropy of the results. Based on the results of inverse-variance weighted (IVW) and sensitivity analyses, in MR analyses, 5 specific GM taxa and 6 specific GM taxa were causally associated with FBI and TBI, respectively; 27 immunophenotypes and 39 immunophenotypes were causally associated with FBI and TBI, respectively. Remarkably, Anaerofilum, LachnospiraceaeNC2004group, RuminococcaceaeUCG004, CCR2 on myeloid dendritic cell (DC), CD123 on CD62L+ plasmacytoid DC, and CD123 on plasmacytoid DC were causally associated with TBI and FBI (all P < .040). However, our reverse MR did not indicate any influence of TBI and FBI on the specific GM. In mediation analysis, we found that the associations between Escherichia.Shigella and FBI were mediated by CD123 on CD62L + plasmacytoid DC in addition to CD123 on plasmacytoid DC, each accounting for 4.21% and 4.21%; the association between FamilyXIIIAD3011group and TBI was mediated by CCR2 on myeloid DC, with mediated proportions of 5.07%. No remarkable horizontal pleiotropy or heterogeneity of instrumental variables was detected. Our comprehensive MR analysis first provides insight into potential causal links between several specific GM taxa with FBI/TBI. Additionally, CD123 on plasmacytoid DC in conjunction with CCR2 on myeloid DC may function in gut microbiota-host crosstalk in FBI and TBI, correspondingly. Further studies are critical to unravel the underlying mechanisms of the links between GM and BI.

Unveiling the Impact: Exploring the Influence of Traumatic Brain Injury on Quality of Life and Life Satisfaction (P2-14.018)

Unveiling the Impact: Exploring the Influence of Traumatic Brain Injury on Quality of Life and Life Satisfaction (P2-14.018)

Influence of traumatic brain injury on ipsilateral and contralateral cortical perfusion in mice

Traumatic brain injury (TBI) is one of the most important causes of death in young adults. After brain injury cortical perfusion is impaired by cortical spreading depression, cerebral microvasospasm or microvascular thrombosis and contributes to secondary expansion of lesion into surrounding healthy brain tissue. The present study was designed to determine the regional cortical perfusion pattern after experimental TBI induced by controlled cortical impact (CCI) in male C57/BL6N mice. We performed a longitudinal time series analysis by Laser speckle contrast imaging (LSCI). Measurements were carried out before, immediately and 24 h after trauma. Immediately after CCI cortical perfusion in the lesion core dropped to 10 % of before injury (baseline; %BL) and to 21–24 %BL in the cortical area surrounding the core. Interestingly, cortical perfusion was also significantly reduced in the contralateral non-injured hemisphere (41–58 %BL) matching the corresponding brain region of the injured hemisphere. 24 h after CCI perfusion of the contralateral hemisphere returned to baseline level in the area corresponding to the lesion core, whereas the lateral area of the parietal cortex was hyperperfused (125 %BL). The lesion core region itself remained severely hypoperfused (18 to 26 %BL) during the observation period. TBI causes a maldistribution of both ipsi- and contralateral cerebral perfusion immediately after trauma, which persist for at least 24 h. Higher perfusion levels in the lesion core 24 h after trauma were associated with increased tissue damage, which supports the role of reperfusion injury for secondary brain damage after TBI.

The alteration of serum bile acid profile among traumatic brain injury patients: a small-scale prospective study.

Traumatic brain injury is one of the major causes of morbidity and mortality worldwide. With the development of bile acids as a potential treatment, to identify the influence of traumatic brain injury on bile acid metabolism shows growing importance. This present study did a preliminary exploration of the bile acid profile alteration among traumatic brain injury patients. In total, 14 patients and 7 healthy volunteers were enrolled. The bile acid profile of the blood samples were detected by an Ultra-performance Liquid Chromatography Mass Spectrometer/Mass Spectrometer system. It was found that 6 bile acids were statistically decreased in traumatic brain injury patients comparing with healthy volunteers: glycocholic acid (median level 44.4 ng/ml vs 98.7 ng/ml, p = 0.003), taurocholic acid (median level 10.9 ng/ml vs 19.5 ng/ml, p = 0.006), glycoursodeoxycholic acid (median level 17.4 ng/ml vs 71.4 ng/ml, p = 0.001), ursodeoxycholic acid (median level <1 ng/ml vs 32.4 ng/ml, p = 0.002), taurochenodeoxycholic acid (median level <1 ng/ml vs 53.6 ng/ml, p = 0.003) and glycochenodeoxycholic acid (GCDCA, median level 160 ng/ml vs 364 ng/ml, p<0.001). In conclusion, traumatic brain injury events are able to induce bile acid metabolism alteration in plasma and might cause reduction in glycocholic, taurocholic, glycoursodeoxycholic, ursodeoxycholic, taurochenodeoxycholic and glycochenodeoxycholic acid levels.

Influence of traumatic brain injury on extracellular tau elimination at the blood\u2013brain barrier

Repetitive head trauma has been associated with the accumulation of tau species in the brain. Our prior work showed brain vascular mural cells contribute to tau processing in the brain, and that these cells progressively degenerate following repetitive mild traumatic brain injury (r-mTBI). The current studies investigated the role of the cerebrovasculature in the elimination of extracellular tau from the brain, and the influence of r-mTBI on these processes. Following intracranial injection of biotin-labeled tau, the levels of exogenous labeled tau residing in the brain were elevated in a mouse model of r-mTBI at 12 months post-injury compared to r-sham mice, indicating reduced tau elimination from the brain following head trauma. This may be the result of decreased caveolin-1 mediated tau efflux at the blood–brain barrier (BBB), as the caveolin inhibitor, methyl-β-cyclodextrin, significantly reduced tau uptake in isolated cerebrovessels and significantly decreased the basolateral-to-apical transit of tau across an in vitro model of the BBB. Moreover, we found that the upstream regulator of endothelial caveolin-1, Mfsd2a, was elevated in r-mTBI cerebrovessels compared to r-sham, which coincided with a decreased expression of cerebrovascular caveolin-1 in the chronic phase following r-mTBI (> 3 months post-injury). Lastly, angiopoietin-1, a mural cell-derived protein governing endothelial Mfsd2a expression, was secreted from r-mTBI cerebrovessels to a greater extent than r-sham animals. Altogether, in the chronic phase post-injury, release of angiopoietin-1 from degenerating mural cells downregulates caveolin-1 expression in brain endothelia, resulting in decreased tau elimination across the BBB, which may describe the accumulation of tau species in the brain following head trauma.

A-99 Influence of TBI on Rate of Cognitive Decline in Clinically Normal Older Adults

Abstract Objective History of traumatic brain injury (TBI) is a potential risk factor for cognitive decline and neurodegenerative disease later in life, but findings have been inconsistent. We evaluate if past history of TBI affects rate of cognitive decline in clinically normal older adults. Method Participants were 190 cognitively normal (CDR &amp;lt; 0.5) older adults (age at baseline: M = 71.6, SD = 7.0) with positive history of TBI (TBI+; n = 83) or no history of TBI (TBI-; n = 107). A comprehensive neuropsychological battery of attention, memory, language, and executive functioning measures as well as functional questionnaires were administered longitudinally (number of visits: M = 3.4, SD = 1.3). Linear mixed effects models assessed the interaction between longitudinal health outcomes and TBI history. Results TBI+ showed a faster rate of decline in executive functioning (Stroop interference: p = 0.04), and a faster increase in functional impairment (Physical Activity Scale for the Elderly (PASE) total: p &amp;lt; 0.001; Unified Parkinson’s Disease Rating Scale (UPDRS) total: p = 0.002). Baseline performance on these tests did not distinguish TBI+ from TBI- (Stroop interference, p = 0.4; PASE, p = 0.5; and UPDRS, p = 0.1). TBI+ was not significantly different from TBI- on measures in other cognitive domains. Conclusions History of TBI was associated with faster rate of executive functioning decline and more rapid increase in objective and subjective functional impairment in cognitively normal older adults. Findings suggest that sustaining a TBI earlier in life could accelerate cognitive and functional changes even among clinically normal older adults.

Severity of military traumatic brain injury influences caregiver health-related quality of life.

To examine the influence of traumatic brain injury (TBI) severity on the health-related quality of life of caregivers providing care to service members/veterans (SMV) following a TBI. Research Method/Design: Thirty caregivers (90.0% female; 70.0% spouse; age: M = 39.5 years, SD = 10.7) of SMVs who sustained a mild, moderate, severe, or penetrating TBI were recruited from Walter Reed National Military Medical Center and via community outreach to participate in one of six focus groups. Caregivers were classified into 3 TBI severity/caregiver groups: (a) moderate/severe/penetrating TBI caregiver group (n = 11); (b) mild TBI caregiver group (n = 10); and (c) equivocal TBI caregiver group (n = 9). Thematic analysis using a constant comparative approach was conducted with qualitative analysis software to identify common themes across the 3 severity/caregiver groups. Eleven themes emerged: no time for self/needs last (83.3%), poor physical health (80.0%), increased stress/anxiety (76.7%), social isolation/loneliness (66.7%), lack of access to services (50.0%), impact on family life (46.7%), sleep issues (46.7%), finances/employment (36.7%), depression (30.0%), exhaustion (30.0%), and anger (16.7%). Exploratory pairwise comparisons revealed a higher proportion of the moderate/severe/penetrating TBI group endorsed 7 of the 11 themes (no time for self/needs last, increased stress/anxiety, impact on family life, sleep issues, finances/employment, exhaustion, anger, and increased stress/anxiety) compared with the other 2 groups. It is important that caregivers of SMVs receive long-term support in their caregiving and parenting roles. Further work is required to understand the challenges caregivers experience in accessing services they need and how to effectively meet their needs across the care continuum. (PsycINFO Database Record (c) 2020 APA, all rights reserved).

The influence of traumatic brain injury on the allocation of vertical spatial attention

ABSTRACTObjective: Research on impairments of spatial attention has primarily investigated hemispatial neglect in brain-lesioned patients, revealing decrements in the allocation of attention to right versus left egocentric or allocentric hemispace. Whereas head trauma might injure those parts of the brain that allocate vertical attention, little is known about the influence of trauma on the allocation of visuospatial attention in vertical space. Thus, the goal of this study was to learn if chronic moderate-to-severe traumatic brain injury (m/sTBI) alters the allocation of vertical visuospatial attention as assessed by the Attention Network Task (ANT). The ANT assesses the influence of Posner-type spatial cues and distractors using an Eriksen flanker task.Methods: 12 chronic m/sTBI patients and 12 demographically-matched neurologically-healthy controls (HCs) completed a version of the ANT wherein trials were coded for cue and target locations above and below central visual fixation. Trial-wise reaction times (RT) and accuracy were subjected to mixed-model ANOVAs and planned contrasts.Results: These data were subject to secondary analyses, which revealed that across groups, median RTs were significantly faster when targets occurred above than below the central visual fixation (p < .01); however, only HCs’ error rates differed as a function of target altitude. Unlike controls, m/sTBI survivors did not exhibit the anticipated upward error-rate attentional bias.Conclusions: As alteration of spatial attention can be a major cause of disability, present findings suggest that m/sTBI survivors exhibit this loss of normal upward attentional bias. Future studies are need to learn if these patients might benefit from treatment.

Long-Term Effects of Traumatic Brain Injury in a Mouse Model of Alzheimer's Disease.

Alzheimer’s disease (AD) is the leading cause of dementia worldwide, affecting over 10% of the elderly population. Epidemiological evidence indicates that traumatic brain injury (TBI) is an important risk factor for developing AD later in life. However, which injury-induced processes that contribute to the disease onset remains unclear. The aim with the present study was to identify cellular processes that could link TBI to AD development, by investigating the chronic impact of two different injury models, controlled cortical impact (CCI) and midline fluid percussion injury (mFPI). The trauma was induced in 3-month-old tg-ArcSwe mice, carrying the Arctic mutation along with the Swedish mutation, and the influence of TBI on AD progression was analyzed at 12- and 24-weeks post-injury. The long-term effect of the TBI on memory deficiency, amyloid-β (Aβ) pathology, neurodegeneration and inflammation was investigated by Morris water maze, PET imaging, immunohistochemistry, and biochemical analyses. Morris water maze analysis demonstrated that mice subjected to CCI or mFPI performed significantly worse than uninjured tg-ArcSwe mice, especially at the later time point. Moreover, the injured mice showed a late upregulation of reactive gliosis, which concurred with a more pronounced Aβ pathology, compared to uninjured AD mice. Our results suggest that the delayed glial activation following TBI may be an important link between the two diseases. However, further studies in both experimental models and human TBI patients will be required to fully elucidate the reasons why TBI increases the risk of neurodegeneration.

Postconcussive symptoms (PCS) following combat-related traumatic brain injury (TBI) in Veterans with posttraumatic stress disorder (PTSD): Influence of TBI, PTSD, and depression on symptoms measured by the Neurobehavioral Symptom Inventory (NSI)

Mild traumatic brain injury (mTBI) is commonly reported in recent combat Veterans. While the majority resolve, some Veterans develop postconcussive symptoms (PCS). Previous research suggests these symptoms are not specific to head injury and are often associated with psychiatric symptoms. The current study examines the relative contributions of posttraumatic stress, depressive symptoms, and TBI on postconcussive symptoms, and explores whether the relationship remains after controlling for symptom overlap. Two hundred eighteen combat Veterans from Operation Iraqi Freedom (OIF), Operation Enduring Freedom (OEF), and Operation New Dawn (OND) provided the data for this study as part of a baseline evaluation for inclusion into larger treatment study for posttraumatic stress disorder (PTSD). Participants completed the Brief Traumatic Brain Injury Screen (BTBIS), Neurobehavioral Symptom Inventory (NSI), PTSD Checklist-Stressor Version (PCL-S), Beck Depression Inventory-II (BDI-II). Significant differences in NSI total score between individuals with and without history of TBI were not found. A series of regression analyses demonstrated that Depression and PTSD were significant predictors of NSI score even after removal of NSI symptoms that overlap with PTSD or depression. TBI status was also a significant predictor of PCS in most models, but its relative contribution was much smaller than that of depression and PTSD. Within PTSD symptoms, hyperarousal cluster was a significant predictor of NSI scores. Findings demonstrate that depression and PTSD are related to PCS beyond similarities in construct. Further, within a primarily PTSD treatment-seeking population, these psychiatric symptoms appear to be a stronger contributor than TBI.

Trending Fibrinolytic Dysregulation: Fibrinolysis Shutdown in the Days After Injury Is Associated With Poor Outcome in Severely Injured Children.

To trend fibrinolysis after injury and determine the influence of traumatic brain injury (TBI) and massive transfusion on fibrinolysis status. Admission fibrinolytic derangement is common in injured children and adults, and is associated with poor outcome. No studies examine fibrinolysis days after injury. Prospective study of severely injured children at a level 1 pediatric trauma center. Rapid thromboelastography was obtained on admission and daily for up to 7 days. Standard definitions of hyperfibrinolysis (HF; LY30 ≥3), fibrinolysis shutdown (SD; LY30 ≤0.8), and normal (LY30 = 0.9-2.9) were applied. Antifibrinolytic use was documented. Outcomes were death, disability, and thromboembolic complications. Wilcoxon rank-sum and Fisher exact tests were performed. Exploratory subgroups included massively transfused and severe TBI patients. In all, 83 patients were analyzed with median (interquartile ranges) age 8 (4-12) and Injury Severity Score 22 (13-34), 73.5% blunt mechanism, 47% severe TBI, 20.5% massively transfused. Outcomes were 14.5% mortality, 43.7% disability, and 9.8% deep vein thrombosis. Remaining in or trending to SD was associated with death (P = 0.007), disability (P = 0.012), and deep vein thrombosis (P = 0.048). Median LY30 was lower on post-trauma day (PTD)1 to PTD4 in patients with poor compared with good outcome; median LY30 was lower on PTD1 to PTD3 in TBI patients compared with non-TBI patients. HF without associated shutdown was not related to poor outcome, but extreme HF (LY30 >30%, n = 3) was lethal. Also, 50% of massively transfused patients in hemorrhagic shock demonstrated SD physiology on admission. All with HF (fc31.2%) corrected after hemostatic resuscitation without tranexamic acid. Fibrinolysis shutdown is common postinjury and predicts poor outcomes. Severe TBI is associated with sustained shutdown. Empiric antifibrinolytics for children should be questioned; thromboelastography-directed selective use should be considered for documented HF.

The influence of traumatic brain injury on treatment outcomes of Concurrent Treatment for PTSD and Substance Use Disorders Using Prolonged Exposure (COPE) in veterans

BackgroundThe co-occurrence of posttraumatic stress disorder (PTSD), substance use disorders (SUD), and traumatic brain injury (TBI) in veterans of Operations Enduring/Iraqi Freedom and New Dawn has received much attention in the literature. Although hypotheses have been presented and disseminated that TBI history will negatively influence treatment response, little data exist to support these claims. The present study investigates the influence of TBI history on response to COPE (Concurrent Treatment of PTSD and SUD Using Prolonged Exposure), a 12-session, integrated psychotherapy designed to address co-occurring PTSD and SUD. MethodParticipants were 51 veterans with current PTSD and SUD enrolled in a clinical trial examining COPE. Assessments of PTSD symptoms, substance use, and depression were collected at baseline and each treatment session. A TBI measure was used to dichotomize veterans into groups with and without a history of TBI (ns=30 and 21, respectively). ResultsParticipants with and without TBI history demonstrated significant improvements in PTSD and depression symptoms during the course of treatment. However, participants with TBI history experienced less improvement relative to participants without TBI history. ConclusionsThe present findings suggest that, although patients with a TBI history respond to treatment, their response to treatment was less so than that observed in patients without a TBI history. As such, identification, symptom monitoring, and treatment practices may require alteration and further special consideration in individuals with PTSD, SUD and TBI.

Changes in Alcohol-Related Behavior Following an Incident of Traumatic Brain Injury

Pre-existing alcohol related complications are a common occurrence amongst individuals admitted for Traumatic Brain Injury (TBI) and is estimated to be about 44% to 66% in TBI patients. In fact, alcohol intoxication is a major cause of TBI. The contribution of alcohol abuse as a cause of TBI and its influence over the pathophysiology of TBI is well studied and well known. However, the influence of TBI on alcohol consumption is still in its preliminary stages. The underlying reasons for it may be the complex interaction between the pathological changes induced by TBI itself and changes in environmental factors following an episode of TBI. The resulting alteration in alcohol-related behaviors post-TBI can affect cognitive and neurological functions and thus can influence the overall recovery of the patient. Hence, understanding changes in alcohol behavior after TBI, with respect to the timing and causes responsible for the change, is important from the perspective of long-term outcome in these patients. In this review article, we discuss a number of studies to determine changes in alcohol drinking behavior following TBI and summarize the findings with respect to the timing of significant change in behavior, as well as the factors influencing this change. Overall it can provide an important piece of information regarding the preventive measures in a major subset of the population at risk of alcohol-use disorders and utilizing them at a time when the prevention can have a maximal impact.

Experimental Traumatic Brain Injury Induces Bone Loss in Rats.

Few studies have investigated the influence of traumatic brain injury (TBI) on bone homeostasis; however, pathophysiological mechanisms involved in TBI have potential to be detrimental to bone. The current study assessed the effect of experimental TBI in rats on the quantity and quality of two different weight-bearing bones, the femur and humerus. Rats were randomly assigned into either sham or lateral fluid percussion injury (FPI) groups. Open-field testing to assess locomotion was conducted at 1, 4, and 12 weeks post-injury, with the rats killed at 1 and 12 weeks post-injury. Bones were analyzed using peripheral quantitative computed tomography (pQCT), histomorphometric analysis, and three-point bending. pQCT analysis revealed that at 1 and 12 weeks post-injury, the distal metaphyseal region of femora from FPI rats had reduced cortical content (10% decrease at 1 week, 8% decrease at 12 weeks; p < 0.01) and cortical thickness (10% decrease at 1 week, 11% decrease at 12 weeks p < 0.001). There was also a 23% reduction in trabecular bone volume ratio at 1 week post-injury and a 27% reduction at 12 weeks post-injury in FPI rats compared to sham (p < 0.001). There were no differences in bone quantity and mechanical properties of the femoral midshaft between sham and TBI animals. There were no differences in locomotor outcomes, which suggested that post-TBI changes in bone were not attributed to immobility. Taken together, these findings indicate that this rat model of TBI was detrimental to bone and suggests a link between TBI and altered bone remodeling.

Chapter 14 - Systemic manifestations of traumatic brain injury

Traumatic brain injury (TBI) affects functioning of various organ systems in the absence of concomitant non-neurologic organ injury or systemic infection. The systemic manifestations of TBI can be mild or severe and can present in the acute phase or during the recovery phase. Non-neurologic organ dysfunction can manifest following mild TBI or severe TBI. The pathophysiology of systemic manifestations following TBI is multifactorial and involves an effect on the autonomic nervous system, involvement of the hypothalamic-pituitary axis, release of inflammatory mediators, and treatment modalities used for TBI. Endocrine dysfunction, electrolyte imbalance, and respiratory manifestations are common following TBI. The influence of TBI on systemic immune response, coagulation cascade, cardiovascular system, gastrointestinal system, and other systems is becoming more evident through animal studies and clinical trials. Systemic manifestations can independently act as risk factors for mortality and morbidity following TBI. Some conditions like neurogenic pulmonary edema and disseminated intravascular coagulation can adversely affect the outcome. Early recognition and treatment of systemic manifestations may improve the clinical outcome following TBI. Further studies are required especially in the field of neuroimmunology to establish the role of various biochemical cascades, not only in the pathophysiology of TBI but also in its systemic manifestations and outcome.

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Introduction: Multidrug resistance-associated protein 1 (MRP1) and p-glycoprotein (P-GP) are members of the ATP-binding cassette transporter family (ABCC1 and ABCB1, respectively). These key transporters efflux drugs and endogenous substrates out of the brain and may play an important role at the cell membrane level. The influence of traumatic brain injury (TBI) on MRP1 and P-GP expression is unknown. Hypothesis: Our objective was to qualitatively analyze MRP1 and P-GP expression in brain samples from patients acutely after severe TBI and compare them to samples from patients with chronic neurodegenerative disease (Alzheimer’s Disease [AD] or non-AD controls). Methods: Archived samples from our Brain Trauma and AD Research Centers were obtained under Institutional approval. Brain sections were processed for immunohistochemistry using antibodies against MRP1 (MRPr1, Enzo) or P-GP (JSB1, Abcam) using standard protocols. Cells were counterstained with hematoxylin and evaluated using light microscopy. Immunoreactivity (IR) was qualitatively scored based on intensity and # of IR+ cells using a 0-4+ scale in 3 cell types: endothelial cells (EC), neurons, and glia. Data for each cell type in each patient cohort are presented as median IR score. Results: In TBI patients (n=4) MRP1 IR was seen in EC (3+), neurons (2.5+), and glia (1.5+) while P-GP was rarely detected (median IR=0 for all cell types). In AD patients and non-AD controls (n=5-6) MRP1 IR was seen in EC (2+), neurons (2+), and glia (3+) while P-GP expression was seen in EC (1.5+), neurons (0.5+), and rarely glia (0). Conclusions: MRP1 but not P-GP was robustly detected after TBI in humans. Compared to AD and non-AD controls, MRP1 appears to be highly expressed in blood-brain barrier EC after TBI. MRP1 is also readily detected in neurons and glia after TBI, although greater expression was not seen in these two cell types. Our preliminary findings could have future implications for TBI patients receiving pharmacologic inhibitors and/or substrates of MRP1 and P-GP including agents currently in clinical use (e.g. opiates) or clinical trials (e.g. cyclosporine A) and could also have implications with regard to the brain’s biochemical milieu after TBI. Support: NS069247

Influence of traumatic brain injury on potassium and phosphorus homeostasis in critically ill multiple trauma patients

Objective The intent of this study was to ascertain whether multiple trauma patients with traumatic brain injury (TBI) had lower serum concentrations of potassium and phosphorus and required more aggressive supplementation than multiple trauma patients without TBI. Methods Ventilator-dependent adult patients without renal impairment who were admitted to the trauma intensive care unit or neurosurgical intensive care unit and who received enteral nutrition were evaluated for the first 14 d after hospital admission. Patients were grouped according to the presence or absence of TBI. Target serum concentrations for potassium and phosphorus were 4 mEq/L and 4 mg/dL, respectively. Electrolyte repletion therapy was given according to the nutritional support service guidelines. Results Fifty trauma patients (25 with and without TBI) were studied. Daily serum potassium concentrations were consistently lower for those with TBI ( P ≤ 0.001), whereas the mean net potassium intake was greater (1.3 ± 0.5 versus 0.7 ± 0.3 mEq · kg −1 · d −1, respectively, P ≤ 0.001). Serial serum phosphorus concentrations were similar between groups ( P = NS) except for a significantly lower serum phosphorus concentration for trauma patients with TBI on day 3 after hospital admission (2.5 ± 0.5 versus 2.9 ± 0.7 mg/dL, respectively, P ≤ 0.05). However, the mean net phosphorus intake was significantly greater for trauma patients with TBI (0.65 ± 0.25 versus 0.45 ± 0.17 mmol · kg −1 · d −1, P ≤ 0.001). Conclusion Potassium and phosphorus requirements are greater for multiple trauma patients with TBI compared with those without TBI.

Severe head injury promotes early caspase-dependent apoptosis in peripheral blood monocytes from multiply injured patients

Objective. To investigate the influence of traumatic brain injury (TBI) on immune function and viability of human peripheral monocytes in polytraumatized patients. Material and methods. This was a prospective, randomized, controlled clinical study conducted in a Level I trauma center. Multiply injured patients (n=42; mean age 42.4±15.5 years) with a mean Injury Severity Score (ISS) of 32.3±9.6 were compared to healthy controls (n=20; mean age 36.3±8.4 years). The methods used were clinical evaluation, scoring of injury severity (ISS, abbreviated injury scores), multiple organ dysfunction score, real-time reverse transcription polymerase chain reaction, Western blotting and fluorescent-activated cell sorting analyses of negatively isolated monocytes. The main outcome measures were overall clinical outcome, terminal deoxynucleotide transferase-mediated dUTP nick-end labeling (TUNEL) staining, expression of the Fas and tumor necrosis factor receptor I, expression of the mitochondrial proteins Bax and Bcl-2, ...

The influence of traumatic brain injury on acute stress disorder and post-traumatic stress disorder following motor vehicle accidents

This study compared the acute stress disorder and post traumatic stress disorder PTSD symptom profiles in motor vehicle accident survivors who sustained a mild traumatic brain injury MTBI or no TBI. Consecutive adult patients who sustained a MTBI n=79 and no TBI n=92 were assessed for acute stress disorder within 1 month of their trauma and reassessed for PTSD MTBI: n=63; non TBI; n=72 6 months post trauma. Comparable rates of acute stress disorder and PTSD were reported in MTBI and non TBI patients. Intrusive memories and fear and helplessness in response to the trauma were reported less frequently by MTBI than non TBI patients at the acute phase. Six months post trauma fewer MTBI patients than non TBI reported fear and helplessness in response to the trauma. These findings suggest that, whereas impaired consciousness at the time of a trauma may reduce the frequency of traumatic memories in the initial month post trauma, MTBI does not result in a different profile of longer term PTSD.

Money matters: a meta-analytic review of the effects of financial incentives on recovery after closed-head injury

The authors evaluated the impact of financial incentives on disability, symptoms, and objective findings after closed-head injury. Meta-analysis was used to review the literature. Seventeen reports, covering 18 study groups and a total of 2,353 subjects, contained data from which effect sizes could be calculated. Effect sizes were aggregated after weighting for group size. After discussion, there was 100% agreement between the authors on all calculations. A moderate overall effect size, 0.47, was found. The effect was particularly strong for mild head trauma. The data showed more abnormality and disability in patients with financial incentives despite less severe injuries. Clinical evaluation of patients after closed-head injury, particularly mild head trauma, must include consideration of the effect of financial incentives on symptoms and disability.