Substance P Mediates Reduced Pneumonia Rates After Traumatic Brain Injury
Yang, Sung; Stepien, David; Hanseman, Dennis; Robinson, Bryce; Goodman, Michael D.; Pritts, Timothy A.; Caldwell, Charles C.; Remick, Daniel G.; Lentsch, Alex B.
2014-01-01
Objectives Traumatic brain injury results in significant morbidity and mortality and is associated with infectious complications, particularly pneumonia. However, whether traumatic brain injury directly impacts the host response to pneumonia is unknown. The objective of this study was to determine the nature of the relationship between traumatic brain injury and the prevalence of pneumonia in trauma patients and investigate the mechanism of this relationship using a murine model of traumatic brain injury with pneumonia. Design Data from the National Trauma Data Bank and a murine model of traumatic brain injury with postinjury pneumonia. Setting Academic medical centers in Cincinnati, OH, and Boston, MA. Patients/Subjects Trauma patients in the National Trauma Data Bank with a hospital length of stay greater than 2 days, age of at least 18 years at admission, and a blunt mechanism of injury. Subjects were female ICR mice 8–10 weeks old. Interventions Administration of a substance P receptor antagonist in mice. Measurements and Main Results Pneumonia rates were measured in trauma patients before and after risk adjustment using propensity scoring. In addition, survival and pulmonary inflammation were measured in mice undergoing traumatic brain injury with or without pneumonia. After risk adjustment, we found that traumatic brain injury patients had significantly lower rates of pneumonia compared to blunt trauma patients without traumatic brain injury. A murine model of traumatic brain injury reproduced these clinical findings with mice subjected to traumatic brain injury demonstrating increased bacterial clearance and survival after induction of pneumonia. To determine the mechanisms responsible for this improvement, the substance P receptor was blocked in mice after traumatic brain injury. This treatment abrogated the traumatic brain injury–associated increases in bacterial clearance and survival. Conclusions The data demonstrate that patients with traumatic brain injury have lower rates of pneumonia compared to non–head-injured trauma patients and suggest that the mechanism of this effect occurs through traumatic brain injury–induced release of substance P, which improves innate immunity to decrease pneumonia. PMID:25014065
Substance P mediates reduced pneumonia rates after traumatic brain injury.
Yang, Sung; Stepien, David; Hanseman, Dennis; Robinson, Bryce; Goodman, Michael D; Pritts, Timothy A; Caldwell, Charles C; Remick, Daniel G; Lentsch, Alex B
2014-09-01
Traumatic brain injury results in significant morbidity and mortality and is associated with infectious complications, particularly pneumonia. However, whether traumatic brain injury directly impacts the host response to pneumonia is unknown. The objective of this study was to determine the nature of the relationship between traumatic brain injury and the prevalence of pneumonia in trauma patients and investigate the mechanism of this relationship using a murine model of traumatic brain injury with pneumonia. Data from the National Trauma Data Bank and a murine model of traumatic brain injury with postinjury pneumonia. Academic medical centers in Cincinnati, OH, and Boston, MA. Trauma patients in the National Trauma Data Bank with a hospital length of stay greater than 2 days, age of at least 18 years at admission, and a blunt mechanism of injury. Subjects were female ICR mice 8-10 weeks old. Administration of a substance P receptor antagonist in mice. Pneumonia rates were measured in trauma patients before and after risk adjustment using propensity scoring. In addition, survival and pulmonary inflammation were measured in mice undergoing traumatic brain injury with or without pneumonia. After risk adjustment, we found that traumatic brain injury patients had significantly lower rates of pneumonia compared to blunt trauma patients without traumatic brain injury. A murine model of traumatic brain injury reproduced these clinical findings with mice subjected to traumatic brain injury demonstrating increased bacterial clearance and survival after induction of pneumonia. To determine the mechanisms responsible for this improvement, the substance P receptor was blocked in mice after traumatic brain injury. This treatment abrogated the traumatic brain injury-associated increases in bacterial clearance and survival. The data demonstrate that patients with traumatic brain injury have lower rates of pneumonia compared to non-head-injured trauma patients and suggest that the mechanism of this effect occurs through traumatic brain injury-induced release of substance P, which improves innate immunity to decrease pneumonia.
Modeling Pediatric Brain Trauma: Piglet Model of Controlled Cortical Impact.
Pareja, Jennifer C Munoz; Keeley, Kristen; Duhaime, Ann-Christine; Dodge, Carter P
2016-01-01
The brain has different responses to traumatic injury as a function of its developmental stage. As a model of injury to the immature brain, the piglet shares numerous similarities in regards to morphology and neurodevelopmental sequence compared to humans. This chapter describes a piglet scaled focal contusion model of traumatic brain injury that accounts for the changes in mass and morphology of the brain as it matures, facilitating the study of age-dependent differences in response to a comparable mechanical trauma.
Opendak, Maya; Sullivan, Regina M.
2016-01-01
Background Trauma has neurobehavioral effects when experienced at any stage of development, but trauma experienced in early life has unique neurobehavioral outcomes related to later life psychiatric sequelae. Recent evidence has further highlighted the context of infant trauma as a critical variable in determining its immediate and enduring consequences. Trauma experienced from an attachment figure, such as occurs in cases of caregiver child maltreatment, is particularly detrimental. Methods Using data primarily from rodent models, we review the literature on the interaction between trauma and attachment in early life, which highlights the role of the caregiver’s presence in engagement of attachment brain circuitry and suppressing threat processing by the amygdala. We then consider how trauma with and without the caregiver produces long-term changes in emotionality and behavior, and suggest that these experiences initiate distinct pathways to pathology. Results Together these data suggest that infant trauma processing and its enduring effects are impacted by both the immaturity of brain areas for processing trauma and the unique functioning of the early-life brain, which is biased toward processing information within the attachment circuitry. Conclusion An understanding of developmental differences in trauma processing as well as the critical role of the caregiver in further altering early life brain processing of trauma is important for developing age-relevant treatment and interventions. Highlights of this article Trauma experienced in early life has been linked with life-long outcomes for mental health through a mechanism that remains unclear. Trauma experienced in the presence of a caregiver has unique consequences. The infant brain is predisposed toward processing information using attachment circuitry rather than threat circuitry. Data from rodent models suggest that repeated trauma in the presence of a caregiver prematurely engages brain areas important for threat, which may play a role in deleterious outcome. PMID:27837581
Hsu, Wei-Cherng; Yu, Chun-Hsien; Kung, Woon-Man; Huang, Kuo-Feng
2018-06-01
Surgical brain injury may result in irreversible neurological deficits. Our previous report showed that partial regeneration of a traumatic brain lesion is achieved by implantation of collagen glycosaminoglycan (CGM). Matrix metalloproteinases (MMPs) may play an important role in neurogenesis but there is currently a lack of studies displaying the relationship between the stimulation of MMPs and neurogenesis after collagen glycosaminoglycan implantation following surgical brain trauma. The present study was carried out to further examine the expression of MMP2 and MMP9 after implantation of collagen glycosaminoglycan (CGM) following surgical brain trauma. Using the animal model of surgically induced brain lesion, we implanted CGM into the surgical trauma. Rats were thus divided into three groups: (1) sham operation group: craniotomy only; (2) lesion (L) group: craniotomy + surgical trauma lesion; (3) lesion + CGM (L + CGM) group: CGM implanted following craniotomy and surgical trauma lesion. Cells positive for SOX2 (marker of proliferating neural progenitor cells) and matrix metalloproteinases (MMP2 and MMP9) in the lesion boundary zone were assayed and analyzed by immunofluorescence and ELISA commercial kits, respectively. Our results demonstrated that following implantation of CGM after surgical brain trauma, significant increases in MMP2 + /SOX2 + cells and MMP9 + /SOX2 + cells were seen within the lesion boundary zone in the L + CGM group. Tissue protein concentrations of MMP2 and MMP9 also increased after CGM scaffold implantation. These findings suggest that implantation of a CGM scaffold alone after surgical brain trauma can enhance the expression of MMP2 and MMP9 accompanied by neurogenesis.
Egawa, Junji; Schilling, Jan M; Cui, Weihua; Posadas, Edmund; Sawada, Atsushi; Alas, Basheer; Zemljic-Harpf, Alice E; Fannon-Pavlich, McKenzie J; Mandyam, Chitra D; Roth, David M; Patel, Hemal H; Patel, Piyush M; Head, Brian P
2017-08-01
Studies in vitro and in vivo demonstrate that membrane/lipid rafts and caveolin (Cav) organize progrowth receptors, and, when overexpressed specifically in neurons, Cav-1 augments neuronal signaling and growth and improves cognitive function in adult and aged mice; however, whether neuronal Cav-1 overexpression can preserve motor and cognitive function in the brain trauma setting is unknown. Here, we generated a neuron-targeted Cav-1-overexpressing transgenic (Tg) mouse [synapsin-driven Cav-1 (SynCav1 Tg)] and subjected it to a controlled cortical impact model of brain trauma and measured biochemical, anatomic, and behavioral changes. SynCav1 Tg mice exhibited increased hippocampal expression of Cav-1 and membrane/lipid raft localization of postsynaptic density protein 95, NMDA receptor, and tropomyosin receptor kinase B. When subjected to a controlled cortical impact, SynCav1 Tg mice demonstrated preserved hippocampus-dependent fear learning and memory, improved motor function recovery, and decreased brain lesion volume compared with wild-type controls. Neuron-targeted overexpression of Cav-1 in the adult brain prevents hippocampus-dependent learning and memory deficits, restores motor function after brain trauma, and decreases brain lesion size induced by trauma. Our findings demonstrate that neuron-targeted Cav-1 can be used as a novel therapeutic strategy to restore brain function and prevent trauma-associated maladaptive plasticity.-Egawa, J., Schilling, J. M., Cui, W., Posadas, E., Sawada, A., Alas, B., Zemljic-Harpf, A. E., Fannon-Pavlich, M. J., Mandyam, C. D., Roth, D. M., Patel, H. H., Patel, P. M., Head, B. P. Neuron-specific caveolin-1 overexpression improves motor function and preserves memory in mice subjected to brain trauma. © FASEB.
Targeting Epigenetic Mechanisms in Pain Due to Trauma and Traumatic Brain Injury (TBI)
2015-10-01
particularly likely to involve TBI, peripheral trauma or both. Disability due to pain and other causes is very high amongst such patients. We have no...effective approaches to reducing the likelihood of developing chronic pain after TBI or peripheral injuries, and the mechanisms supporting such pain...brain or peripheral trauma may support chronic pain. Our work to-date has established a rodent model of TBI in combination with injury to a limb as a
Cisler, Josh M.; Bush, Keith; James, G. Andrew; Smitherman, Sonet; Kilts, Clinton D.
2015-01-01
Posttraumatic Stress Disorder (PTSD) is characterized by intrusive recall of the traumatic memory. While numerous studies have investigated the neural processing mechanisms engaged during trauma memory recall in PTSD, these analyses have only focused on group-level contrasts that reveal little about the predictive validity of the identified brain regions. By contrast, a multivariate pattern analysis (MVPA) approach towards identifying the neural mechanisms engaged during trauma memory recall would entail testing whether a multivariate set of brain regions is reliably predictive of (i.e., discriminates) whether an individual is engaging in trauma or non-trauma memory recall. Here, we use a MVPA approach to test 1) whether trauma memory vs neutral memory recall can be predicted reliably using a multivariate set of brain regions among women with PTSD related to assaultive violence exposure (N=16), 2) the methodological parameters (e.g., spatial smoothing, number of memory recall repetitions, etc.) that optimize classification accuracy and reproducibility of the feature weight spatial maps, and 3) the correspondence between brain regions that discriminate trauma memory recall and the brain regions predicted by neurocircuitry models of PTSD. Cross-validation classification accuracy was significantly above chance for all methodological permutations tested; mean accuracy across participants was 76% for the methodological parameters selected as optimal for both efficiency and accuracy. Classification accuracy was significantly better for a voxel-wise approach relative to voxels within restricted regions-of-interest (ROIs); classification accuracy did not differ when using PTSD-related ROIs compared to randomly generated ROIs. ROI-based analyses suggested the reliable involvement of the left hippocampus in discriminating memory recall across participants and that the contribution of the left amygdala to the decision function was dependent upon PTSD symptom severity. These results have methodological implications for real-time fMRI neurofeedback of the trauma memory in PTSD and conceptual implications for neurocircuitry models of PTSD that attempt to explain core neural processing mechanisms mediating PTSD. PMID:26241958
Cisler, Josh M; Bush, Keith; James, G Andrew; Smitherman, Sonet; Kilts, Clinton D
2015-01-01
Posttraumatic Stress Disorder (PTSD) is characterized by intrusive recall of the traumatic memory. While numerous studies have investigated the neural processing mechanisms engaged during trauma memory recall in PTSD, these analyses have only focused on group-level contrasts that reveal little about the predictive validity of the identified brain regions. By contrast, a multivariate pattern analysis (MVPA) approach towards identifying the neural mechanisms engaged during trauma memory recall would entail testing whether a multivariate set of brain regions is reliably predictive of (i.e., discriminates) whether an individual is engaging in trauma or non-trauma memory recall. Here, we use a MVPA approach to test 1) whether trauma memory vs neutral memory recall can be predicted reliably using a multivariate set of brain regions among women with PTSD related to assaultive violence exposure (N=16), 2) the methodological parameters (e.g., spatial smoothing, number of memory recall repetitions, etc.) that optimize classification accuracy and reproducibility of the feature weight spatial maps, and 3) the correspondence between brain regions that discriminate trauma memory recall and the brain regions predicted by neurocircuitry models of PTSD. Cross-validation classification accuracy was significantly above chance for all methodological permutations tested; mean accuracy across participants was 76% for the methodological parameters selected as optimal for both efficiency and accuracy. Classification accuracy was significantly better for a voxel-wise approach relative to voxels within restricted regions-of-interest (ROIs); classification accuracy did not differ when using PTSD-related ROIs compared to randomly generated ROIs. ROI-based analyses suggested the reliable involvement of the left hippocampus in discriminating memory recall across participants and that the contribution of the left amygdala to the decision function was dependent upon PTSD symptom severity. These results have methodological implications for real-time fMRI neurofeedback of the trauma memory in PTSD and conceptual implications for neurocircuitry models of PTSD that attempt to explain core neural processing mechanisms mediating PTSD.
Paik, Ho Kyu; Oh, Chang-Hyun; Choi, Kang; Kim, Chul-Eung; Yoon, Seung Hwan
2011-01-01
Objective The purpose of this study is to confirm whether brain disease or brain trauma actually affect psychopathology in young male group in Korea. Methods The authors manually reviewed the result of Korean military multiphasic personal inventory (KMPI) in the examination of conscription in Korea from January 2008 to May 2010. There were total 237 young males in this review. Normal volunteers group (n=150) was composed of those who do not have history of brain disease or brain trauma. Brain disease group (n=33) was consisted of those with history of brain disease. Brain trauma group (n=54) was consisted of those with history of brain trauma. The results of KMPI in each group were compared. Results Abnormal results of KMPI were found in both brain disease and trauma groups. In the brain disease group, higher tendencies of faking bad response, anxiety, depression, somatization, personality disorder, schizophrenic and paranoid psychopathy was observed and compared to the normal volunteers group. In the brain trauma group, higher tendencies of faking-good, depression, somatization and personality disorder was observed and compared to the normal volunteers group. Conclusion Young male with history of brain disease or brain trauma may have higher tendencies to have abnormal results of multiphasic personal inventory test compared to young male without history of brain disease or brain trauma, suggesting that damaged brain may cause psychopathology in young male group in Korea. PMID:22053230
2011-01-01
Background Head trauma is one of the most important clinical issues that not only can be fatal and disabling, requiring long-term treatment and care, but also can cause heavy financial burden. Formation or distribution of free oxygen radicals should be decreased to enable fixing of poor neurological outcomes and to prevent neuronal damage secondary to ischemia after trauma. Coenzyme Q10 (CoQ10), a component of the mitochondrial electron transport chain, is a strong antioxidant that plays a role in membrane stabilization. In this study, the role of CoQ10 in the treatment of head trauma is researched by analyzing the histopathological and biochemical effects of CoQ10 administered after experimental traumatic brain injury in rats. A traumatic brain-injury model was created in all rats. Trauma was inflicted on rats by the free fall of an object of 450 g weight from a height of 70 cm on the frontoparietal midline onto a metal disc fixed between the coronal and the lambdoid sutures after a midline incision was carried out. Results In the biochemical tests, tissue malondialdehyde (MDA) levels were significantly higher in the traumatic brain-injury group compared to the sham group (p < 0.05). Administration of CoQ10 after trauma was shown to be protective because it significantly lowered the increased MDA levels (p < 0.05). Comparing the superoxide dismutase (SOD) levels of the four groups, trauma + CoQ10 group had SOD levels ranging between those of sham group and traumatic brain-injury group, and no statistically significant increase was detected. Histopathological results showed a statistically significant difference between the CoQ10 and the other trauma-subjected groups with reference to vascular congestion, neuronal loss, nuclear pyknosis, nuclear hyperchromasia, cytoplasmic eosinophilia, and axonal edema (p < 0.05). Conclusion Neuronal degenerative findings and the secondary brain damage and ischemia caused by oxidative stress are decreased by CoQ10 use in rats with traumatic brain injury. PMID:21801363
Stimulating neuroregeneration as a therapeutic drug approach for traumatic brain injury
Mueller, Bernhard K; Mueller, Reinhold; Schoemaker, Hans
2009-01-01
Traumatic brain injury, a silent epidemic of modern societies, is a largely neglected area in drug development and no drug is currently available for the treatment of patients suffering from brain trauma. Despite this grim situation, much progress has been made over the last two decades in closely related medical indications, such as spinal cord injury, giving rise to a more optimistic approach to drug development in brain trauma. Fundamental insights have been gained with animal models of central nervous system (CNS) trauma and spinal cord injury. Neuroregenerative drug candidates have been identified and two of these have progressed to clinical development for spinal cord injury patients. If successful, these drug candidates may be used to treat brain trauma patients. Significant progress has also been made in understanding the fundamental molecular mechanism underlying irreversible axonal growth arrest in the injured CNS of higher mammals. From these studies, we have learned that the axonal retraction bulb, previously regarded as a marker for failure of regenerative growth, is not static but dynamic and, therefore, amenable to pharmacotherapeutic approaches. With the development of modified magnetic resonance imaging methods, fibre tracts can be visualised in the living human brain and such imaging methods will soon be used to evaluate the neuroregenerative potential of drug candidates. These significant advances are expected to fundamentally change the often hopeless situation of brain trauma patients and will be the first step towards overcoming the silent epidemic of brain injury. PMID:19422372
Gianakis, Anastasia; McNett, Molly; Belle, Josie; Moran, Cristina; Grimm, Dawn
2015-01-01
Ventilator-associated pneumonia (VAP) rates remain highest among trauma and brain injured patients; yet, no research compares VAP risk factors between the 2 groups. This retrospective, case-controlled study identified risk factors for VAP among critically ill trauma patients with and without brain injury. Data were abstracted on trauma patients with (cases) and without (controls) brain injury. Data gathered on n = 157 subjects. Trauma patients with brain injury had more emergent and field intubations. Age was strongest predictor of VAP in cases, and ventilator days predicted VAP in controls. Trauma patients with brain injury may be at higher risk for VAP.
Brain Metabolic Changes in Rats following Acoustic Trauma
He, Jun; Zhu, Yejin; Aa, Jiye; Smith, Paul F.; De Ridder, Dirk; Wang, Guangji; Zheng, Yiwen
2017-01-01
Acoustic trauma is the most common cause of hearing loss and tinnitus in humans. However, the impact of acoustic trauma on system biology is not fully understood. It has been increasingly recognized that tinnitus caused by acoustic trauma is unlikely to be generated by a single pathological source, but rather a complex network of changes involving not only the auditory system but also systems related to memory, emotion and stress. One obvious and significant gap in tinnitus research is a lack of biomarkers that reflect the consequences of this interactive “tinnitus-causing” network. In this study, we made the first attempt to analyse brain metabolic changes in rats following acoustic trauma using metabolomics, as a pilot study prior to directly linking metabolic changes to tinnitus. Metabolites in 12 different brain regions collected from either sham or acoustic trauma animals were profiled using a gas chromatography mass spectrometry (GC/MS)-based metabolomics platform. After deconvolution of mass spectra and identification of the molecules, the metabolomic data were processed using multivariate statistical analysis. Principal component analysis showed that metabolic patterns varied among different brain regions; however, brain regions with similar functions had a similar metabolite composition. Acoustic trauma did not change the metabolite clusters in these regions. When analyzed within each brain region using the orthogonal projection to latent structures discriminant analysis sub-model, 17 molecules showed distinct separation between control and acoustic trauma groups in the auditory cortex, inferior colliculus, superior colliculus, vestibular nucleus complex (VNC), and cerebellum. Further metabolic pathway impact analysis and the enrichment overview with network analysis suggested the primary involvement of amino acid metabolism, including the alanine, aspartate and glutamate metabolic pathways, the arginine and proline metabolic pathways and the purine metabolic pathway. Our results provide the first metabolomics evidence that acoustic trauma can induce changes in multiple metabolic pathways. This pilot study also suggests that the metabolomic approach has the potential to identify acoustic trauma-specific metabolic shifts in future studies where metabolic changes are correlated with the animal's tinnitus status. PMID:28392756
The Impact of Childhood Trauma on Brain Development: A Literature Review and Supporting Handouts
ERIC Educational Resources Information Center
Kirouac, Samantha; McBride, Dawn Lorraine
2009-01-01
This project provides a comprehensive overview of the research literature on the brain and how trauma impacts brain development, structures, and functioning. A basic exploration of childhood trauma is outlined in this project, as it is essential in making associations and connections to brain development. Childhood trauma is processed in the…
Effects of lateral fluid percussion injury on cholinergic markers in the newborn piglet brain.
Donat, Cornelius K; Walter, Bernd; Kayser, Tanja; Deuther-Conrad, Winnie; Schliebs, Reinhard; Nieber, Karen; Bauer, Reinhard; Härtig, Wolfgang; Brust, Peter
2010-02-01
Traumatic brain injury is a leading cause of death and disability in children. Studies using adult animal models showed alterations of the central cholinergic neurotransmission as a result of trauma. However, there is a lack of knowledge about consequences of brain trauma on cholinergic function in the immature brain. It is hypothesized that trauma affects the relative acetylcholine esterase activity and causes a loss of cholinergic neurons in the immature brain. Severe fluid percussion trauma (FP-TBI, 3.8+/-0.3atm) was induced in 15 female newborn piglets, monitored for 6h and compared with 12 control animals. The hemispheres ipsilateral to FP-TBI obtained from seven piglets were used for acetylcholine esterase histochemistry on frozen sagittal slices, while regional cerebral blood flow and oxygen availability was determined in the remaining eight FP-TBI animals. Post-fixed slices were immunohistochemically labelled for choline acetyltransferase as well as for low-affinity neurotrophin receptor in order to characterize cholinergic neurons in the basal forebrain. Regional cerebral blood flow and brain oxygen availability were reduced during the first 2h after FP-TBI (P<0.05). In addition, acetylcholine esterase activity was significantly increased in the neocortex, basal forebrain, hypothalamus and medulla after trauma (P<0.05), whereas the number of choline acetyltransferase and low-affinity neurotrophin receptor positive cells in the basal forebrain were unaffected by the injury. Thus, traumatic brain injury evoked an increased relative activity of the acetylcholine esterase in the immature brain early after injury, without loss of cholinergic neurons in the basal forebrain. These changes may contribute to developmental impairments after immature traumatic brain injury. Copyright 2009 ISDN. Published by Elsevier Ltd. All rights reserved.
Psychoneuroimmunology of Early-Life Stress: The Hidden Wounds of Childhood Trauma?
Danese, Andrea; J Lewis, Stephanie
2017-01-01
The brain and the immune system are not fully formed at birth, but rather continue to mature in response to the postnatal environment. The two-way interaction between the brain and the immune system makes it possible for childhood psychosocial stressors to affect immune system development, which in turn can affect brain development and its long-term functioning. Drawing from experimental animal models and observational human studies, we propose that the psychoneuroimmunology of early-life stress can offer an innovative framework to understand and treat psychopathology linked to childhood trauma. Early-life stress predicts later inflammation, and there are striking analogies between the neurobiological correlates of early-life stress and of inflammation. Furthermore, there are overlapping trans-diagnostic patterns of association of childhood trauma and inflammation with clinical outcomes. These findings suggest new strategies to remediate the effect of childhood trauma before the onset of clinical symptoms, such as anti-inflammatory interventions and potentiation of adaptive immunity. Similar strategies might be used to ameliorate the unfavorable treatment response described in psychiatric patients with a history of childhood trauma. PMID:27629365
Osier, Nicole; Dixon, C. Edward
2017-01-01
Controlled cortical impact (CCI) is a commonly used and highly regarded model of brain trauma that uses a pneumatically or electromagnetically controlled piston to induce reproducible and well-controlled injury. The CCI model was originally used in ferrets and it has since been scaled for use in many other species. This chapter will describe the historical development of the CCI model, compare and contrast the pneumatic and electromagnetic models, and summarize key short- and long-term consequences of TBI that have been gleaned using this model. In accordance with the recent efforts to promote high-quality evidence through the reporting of common data elements (CDEs), relevant study details—that should be reported in CCI studies—will be noted. PMID:27604719
Osier, Nicole; Dixon, C Edward
2016-01-01
Controlled cortical impact (CCI) is a commonly used and highly regarded model of brain trauma that uses a pneumatically or electromagnetically controlled piston to induce reproducible and well-controlled injury. The CCI model was originally used in ferrets and it has since been scaled for use in many other species. This chapter will describe the historical development of the CCI model, compare and contrast the pneumatic and electromagnetic models, and summarize key short- and long-term consequences of TBI that have been gleaned using this model. In accordance with the recent efforts to promote high-quality evidence through the reporting of common data elements (CDEs), relevant study details-that should be reported in CCI studies-will be noted.
Cancel, A; Comte, M; Truillet, R; Boukezzi, S; Rousseau, P-F; Zendjidjian, X Y; Sage, T; Lazerges, P-E; Guedj, E; Khalfa, S; Azorin, J-M; Blin, O; Fakra, E
2015-10-01
Psychosocial trauma during childhood is associated with schizophrenia vulnerability. The pattern of grey matter decrease is similar to brain alterations seen in schizophrenia. Our objective was to explore the links between childhood trauma, brain morphology and schizophrenia symptoms. Twenty-one patients with schizophrenia stabilized with atypical antipsychotic monotherapy and 30 healthy control subjects completed the study. Anatomical MRI images were analysed using optimized voxel-based morphometry (VBM). Childhood trauma was assessed with the Childhood Trauma Questionnaire, and symptoms were rated on the Scale for the Assessment of Negative Symptoms (SANS) and Scale for the Assessment of Positive Symptoms (SAPS) (disorganization, positive and negative symptoms). In the schizophrenia group, we used structural equation modelling in a path analysis. Total grey matter volume was negatively associated with emotional neglect (EN) in patients with schizophrenia. Whole-brain VBM analyses of grey matter in the schizophrenia group revealed a specific inversed association between EN and the right dorsolateral prefrontal cortex (DLPFC). Path analyses identified a well-fitted model in which EN predicted grey matter density in DLPFC, which in turn predicted the disorganization score. Our findings suggest that EN during childhood could have an impact on psychopathology in schizophrenia, which would be mediated by developmental effects on brain regions such as the DLPFC. © 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
The protective effect of 2-mercaptoethane sulfonate (MESNA) against traumatic brain injury in rats.
Yilmaz, Erdal Resit; Kertmen, Hayri; Gürer, Bora; Kanat, Mehmet Ali; Arikok, Ata Türker; Ergüder, Berrin Imge; Hasturk, Askin Esen; Ergil, Julide; Sekerci, Zeki
2013-01-01
The agent, 2-mercaptoethane sulfonate (MESNA), is a synthetic small molecule, widely used as a systemic protective agent against chemotherapy toxicity, but is primarily used to reduce hemorrhagic cystitis induced by cyclophosphamide. Because MESNA has potential antioxidant and cytoprotective effects, so we hypothesized that MESNA may protect the brain against traumatic injury. Thirty-two rats were randomized into four groups of eight animals each; Group 1 (sham), Group 2 (trauma), Group 3 (150 mg/kg MESNA), Group 4 (30 mg/kg methylprednisolone). Only skin incision was performed in the sham group. In all the other groups, the traumatic brain injury model was created by an object weighing 450 g falling freely from a height of 70 cm through a copper tube on to the metal disc over the skull. The drugs were administered immediately after the injury. The animals were killed 24 h later. Brain tissues were extracted for analysis, where levels of tissue malondialdehyde, caspase-3, glutathione peroxidase, superoxide dismutase, nitric oxide, nitric oxide synthetase and xanthine oxidase were analyzed. Also, histopathological evaluation of the tissues was performed. After head trauma, tissue malondialdehyde levels increased; these levels were significantly decreased by MESNA administration. Caspase-3 levels were increased after trauma, but no effect of MESNA was determined in caspase-3 activity. Following trauma, both glutathione peroxidase and superoxide dismutase levels were decreased; MESNA increased the activity of both these antioxidant enzymes. Also, after trauma, nitric oxide, nitric oxide synthetase and xanthine oxidase levels were increased; administration of MESNA significantly decreased the levels of nitric oxide, nitric oxide synthetase and xanthine oxidase, promising an antioxidant activity. Histopathological analysis showed that MESNA protected the brain tissues well from injury. Although further studies considering different dose regimens and time intervals are required, MESNA was shown to be at least as effective as methylprednisolone in the traumatic brain injury model.
Berger, Rachel Pardes; Pak, Brian J; Kolesnikova, Mariya D; Fromkin, Janet; Saladino, Richard; Herman, Bruce E; Pierce, Mary Clyde; Englert, David; Smith, Paul T; Kochanek, Patrick M
2017-06-05
Abusive head trauma is the leading cause of death from physical abuse. Missing the diagnosis of abusive head trauma, particularly in its mild form, is common and contributes to increased morbidity and mortality. Serum biomarkers may have potential as quantitative point-of-care screening tools to alert physicians to the possibility of intracranial hemorrhage. To identify and validate a set of biomarkers that could be the basis of a multivariable model to identify intracranial hemorrhage in well-appearing infants using the Ziplex System. Binary logistic regression was used to develop a multivariable model incorporating 3 serum biomarkers (matrix metallopeptidase-9, neuron-specific enolase, and vascular cellular adhesion molecule-1) and 1 clinical variable (total hemoglobin). The model was then prospectively validated. Multiplex biomarker measurements were performed using Flow-Thru microarray technology on the Ziplex System, which has potential as a point-of-care system. The model was tested at 3 pediatric emergency departments in level I pediatric trauma centers (Children's Hospital of Pittsburgh of University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania; Primary Children's Hospital, Salt Lake City, Utah; and Lurie Children's Hospital, Chicago, Illinois) among well-appearing infants who presented for care owing to symptoms that placed them at increased risk of abusive head trauma. The study took place from November 2006 to April 2014 at Children's Hospital of Pittsburgh, June 2010 to August 2013 at Primary Children's Hospital, and January 2011 to August 2013 at Lurie Children's Hospital. A mathematical model that can predict acute intracranial hemorrhage in infants at increased risk of abusive head trauma. The multivariable model, Biomarkers for Infant Brain Injury Score, was applied prospectively to 599 patients. The mean (SD) age was 4.7 (3.1) months. Fifty-two percent were boys, 78% were white, and 8% were Hispanic. At a cutoff of 0.182, the model was 89.3% sensitive (95% CI, 87.7-90.4) and 48.0% specific (95% CI, 47.3-48.9) for acute intracranial hemorrhage. Positive and negative predictive values were 21.3% and 95.6%, respectively. The model was neither sensitive nor specific for atraumatic brain abnormalities, isolated skull fractures, or chronic intracranial hemorrhage. The Biomarkers for Infant Brain Injury Score, a multivariable model using 3 serum biomarker concentrations and serum hemoglobin, can identify infants with acute intracranial hemorrhage. Accurate and timely identification of intracranial hemorrhage in infants without a history of trauma in whom trauma may not be part of the differential diagnosis has the potential to decrease morbidity and mortality from abusive head trauma.
Luh, Clara; Gruss, Marco; Radyushkin, Konstantin; Hirnet, Tobias; Werner, Christian; Engelhard, Kristin; Franks, Nicholas P; Thal, Serge C; Dickinson, Robert
2015-01-01
Objectives To determine the neuroprotective efficacy of the inert gas xenon following traumatic brain injury, and to determine whether application of xenon has a clinically relevant therapeutic time window. Design Controlled animal study. Setting University research laboratory. Subjects Male C57BL/6N mice (n=196) Interventions 75% xenon, 50% xenon or 30% xenon, with 25% oxygen (balance nitrogen) treatment following mechanical brain lesion by controlled cortical impact. Measurements & Main Results Outcome following trauma was measured using: 1) functional neurological outcome score, 2) histological measurement of contusion volume, 3) analysis of locomotor function and gait. Our study shows that xenon-treatment improves outcome following traumatic brain injury. Neurological outcome scores were significantly (p<0.05) better in xenon-treated groups in the early phase (24 hours) and up to 4 days after injury. Contusion volume was significantly (p<0.05) reduced in the xenon-treated groups. Xenon treatment significantly (p<0.05) reduced contusion volume when xenon was given 15 minutes after injury or when treatment was delayed 1 hour or 3 hours after injury. Neurological outcome was significantly (p<0.05) improved when xenon treatment was given 15 minutes or 1 hour after injury. Improvements in locomotor function (p<0.05) were observed in the xenon-treated group, 1 month after trauma. Conclusions These results show for the first time that xenon improves neurological outcome and reduces contusion volume following traumatic brain injury in mice. In this model, xenon application has a therapeutic time window of up to at least 3 hours. These findings support the idea that xenon may be of benefit as a neuroprotective treatment in brain trauma patients. PMID:25188549
Campos-Pires, Rita; Armstrong, Scott P; Sebastiani, Anne; Luh, Clara; Gruss, Marco; Radyushkin, Konstantin; Hirnet, Tobias; Werner, Christian; Engelhard, Kristin; Franks, Nicholas P; Thal, Serge C; Dickinson, Robert
2015-01-01
To determine the neuroprotective efficacy of the inert gas xenon following traumatic brain injury and to determine whether application of xenon has a clinically relevant therapeutic time window. Controlled animal study. University research laboratory. Male C57BL/6N mice (n = 196). Seventy-five percent xenon, 50% xenon, or 30% xenon, with 25% oxygen (balance nitrogen) treatment following mechanical brain lesion by controlled cortical impact. Outcome following trauma was measured using 1) functional neurologic outcome score, 2) histological measurement of contusion volume, and 3) analysis of locomotor function and gait. Our study shows that xenon treatment improves outcome following traumatic brain injury. Neurologic outcome scores were significantly (p < 0.05) better in xenon-treated groups in the early phase (24 hr) and up to 4 days after injury. Contusion volume was significantly (p < 0.05) reduced in the xenon-treated groups. Xenon treatment significantly (p < 0.05) reduced contusion volume when xenon was given 15 minutes after injury or when treatment was delayed 1 or 3 hours after injury. Neurologic outcome was significantly (p < 0.05) improved when xenon treatment was given 15 minutes or 1 hour after injury. Improvements in locomotor function (p < 0.05) were observed in the xenon-treated group, 1 month after trauma. These results show for the first time that xenon improves neurologic outcome and reduces contusion volume following traumatic brain injury in mice. In this model, xenon application has a therapeutic time window of up to at least 3 hours. These findings support the idea that xenon may be of benefit as a neuroprotective treatment in patients with brain trauma.
Abookasis, David; Volkov, Boris; Shochat, Ariel; Kofman, Itamar
2016-04-01
Optical techniques have gained substantial interest over the past four decades for biomedical imaging due to their unique advantages, which may suggest their use as alternatives to conventional methodologies. Several optical techniques have been successfully adapted to clinical practice and biomedical research to monitor tissue structure and function in both humans and animal models. This paper reviews the analysis of the optical properties of brain tissue in the wavelength range between 500 and 1000 nm by three different diffuse optical reflectance methods: spatially modulated illumination, orthogonal diffuse light spectroscopy, and dual-wavelength laser speckle imaging, to monitor changes in brain tissue morphology, chromophore content, and metabolism following head injury. After induction of closed head injury upon anesthetized mice by weight-drop method, significant changes in hemoglobin oxygen saturation, blood flow, and metabolism were readily detectible by all three optical setups, up to 1 h post-trauma. Furthermore, the experimental results clearly demonstrate the feasibility and reliability of the three methodologies, and the differences between the system performances and capabilities are also discussed. The long-term goal of this line of study is to combine these optical systems to study brain pathophysiology in high spatiotemporal resolution using additional models of brain trauma. Such combined use of complementary algorithms should fill the gaps in each system's capabilities, toward the development of a noninvasive, quantitative tool to expand our knowledge of the principles underlying brain function following trauma, and to monitor the efficacy of therapeutic interventions in the clinic.
Abookasis, David; Volkov, Boris; Shochat, Ariel; Kofman, Itamar
2016-01-01
Abstract. Optical techniques have gained substantial interest over the past four decades for biomedical imaging due to their unique advantages, which may suggest their use as alternatives to conventional methodologies. Several optical techniques have been successfully adapted to clinical practice and biomedical research to monitor tissue structure and function in both humans and animal models. This paper reviews the analysis of the optical properties of brain tissue in the wavelength range between 500 and 1000 nm by three different diffuse optical reflectance methods: spatially modulated illumination, orthogonal diffuse light spectroscopy, and dual-wavelength laser speckle imaging, to monitor changes in brain tissue morphology, chromophore content, and metabolism following head injury. After induction of closed head injury upon anesthetized mice by weight-drop method, significant changes in hemoglobin oxygen saturation, blood flow, and metabolism were readily detectible by all three optical setups, up to 1 h post-trauma. Furthermore, the experimental results clearly demonstrate the feasibility and reliability of the three methodologies, and the differences between the system performances and capabilities are also discussed. The long-term goal of this line of study is to combine these optical systems to study brain pathophysiology in high spatiotemporal resolution using additional models of brain trauma. Such combined use of complementary algorithms should fill the gaps in each system’s capabilities, toward the development of a noninvasive, quantitative tool to expand our knowledge of the principles underlying brain function following trauma, and to monitor the efficacy of therapeutic interventions in the clinic. PMID:27175372
Rhinn, Hervé; Marchand-Leroux, Catherine; Croci, Nicole; Plotkine, Michel; Scherman, Daniel; Escriou, Virginie
2008-01-01
Background Traumatic brain injury models are widely studied, especially through gene expression, either to further understand implied biological mechanisms or to assess the efficiency of potential therapies. A large number of biological pathways are affected in brain trauma models, whose elucidation might greatly benefit from transcriptomic studies. However the suitability of reference genes needed for quantitative RT-PCR experiments is missing for these models. Results We have compared five potential reference genes as well as total cDNA level monitored using Oligreen reagent in order to determine the best normalizing factors for quantitative RT-PCR expression studies in the early phase (0–48 h post-trauma (PT)) of a murine model of diffuse brain injury. The levels of 18S rRNA, and of transcripts of β-actin, glyceraldehyde-3P-dehydrogenase (GAPDH), β-microtubulin and S100β were determined in the injured brain region of traumatized mice sacrificed at 30 min, 3 h, 6 h, 12 h, 24 h and 48 h post-trauma. The stability of the reference genes candidates and of total cDNA was evaluated by three different methods, leading to the following rankings as normalization factors, from the most suitable to the less: by using geNorm VBA applet, we obtained the following sequence: cDNA(Oligreen); GAPDH > 18S rRNA > S100β > β-microtubulin > β-actin; by using NormFinder Excel Spreadsheet, we obtained the following sequence: GAPDH > cDNA(Oligreen) > S100β > 18S rRNA > β-actin > β-microtubulin; by using a Confidence-Interval calculation, we obtained the following sequence: cDNA(Oligreen) > 18S rRNA; GAPDH > S100β > β-microtubulin > β-actin. Conclusion This work suggests that Oligreen cDNA measurements, 18S rRNA and GAPDH or a combination of them may be used to efficiently normalize qRT-PCR gene expression in mouse brain trauma injury, and that β-actin and β-microtubulin should be avoided. The potential of total cDNA as measured by Oligreen as a first-intention normalizing factor with a broad field of applications is highlighted. Pros and cons of the three methods of normalization factors selection are discussed. A generic time- and cost-effective procedure for normalization factor validation is proposed. PMID:18611280
Hanlon, Lauren A.; Huh, Jimmy W.
2016-01-01
Elevated microglial/macrophage-associated biomarkers in the cerebrospinal fluid of infant victims of abusive head trauma (AHT) suggest that these cells play a role in the pathophysiology of the injury. In a model of AHT in 11-day-old rats, 3 impacts (24 hours apart) resulted in spatial learning and memory deficits and increased brain microglial/macrophage reactivity, traumatic axonal injury, neuronal degeneration, and cortical and white-matter atrophy. The antibiotic minocycline has been effective in decreasing injury-induced microglial/macrophage activation while simultaneously attenuating cellular and functional deficits in models of neonatal hypoxic ischemia, but the potential for this compound to rescue deficits after impact-based trauma to the immature brain remains unexplored. Acute minocycline administration in this model of AHT decreased microglial/macrophage reactivity in the corpus callosum of brain-injured animals at 3 days postinjury, but this effect was lost by 7 days postinjury. Additionally, minocycline treatment had no effect on traumatic axonal injury, neurodegeneration, tissue atrophy, or spatial learning deficits. Interestingly, minocycline-treated animals demonstrated exacerbated injury-induced spatial memory deficits. These results contrast with previous findings in other models of brain injury and suggest that minocycline is ineffective in reducing microglial/macrophage activation and ameliorating injury-induced deficits following repetitive neonatal traumatic brain injury. PMID:26825312
Influence of oxygen therapy on glucose-lactate metabolism after diffuse brain injury.
Reinert, Michael; Schaller, Benoit; Widmer, Hans Rudolf; Seiler, Rolf; Bullock, Ross
2004-08-01
Severe traumatic brain injury (TBI) imposes a huge metabolic load on brain tissue, which can be summarized initially as a state of hypermetabolism and hyperglycolysis. In experiments O2 consumption has been shown to increase early after trauma, especially in the presence of high lactate levels and forced O2 availability. In recent clinical studies the effect of increasing O2 availability on brain metabolism has been analyzed. By their nature, however, clinical trauma models suffer from a heterogeneous injury distribution. The aim of this study was to analyze, in a standardized diffuse brain injury model, the effect of increasing the fraction of inspired O2 on brain glucose and lactate levels, and to compare this effect with the metabolism of the noninjured sham-operated brain. A diffuse severe TBI model developed by Foda and Maramarou, et al., in which a 420-g weight is dropped from a height of 2 m was used in this study. Forty-one male Wistar rats each weighing approximately 300 g were included. Anesthesized rats were monitored by placing a femoral arterial line for blood pressure and blood was drawn for a blood gas analysis. Two time periods were defined: Period A was defined as preinjury and Period B as postinjury. During Period B two levels of fraction of inspired oxygen (FiO2) were studied: air (FiO2 0.21) and oxygen (FiO2 1). Four groups were studied including sham-operated animals: air-air-sham (AAS); air-O2-sham (AOS); air-air-trauma (AAT); and air-O2-trauma (AOT). In six rats the effect of increasing the FiO2 on serum glucose and lactate was analyzed. During Period B lactate values in the brain determined using microdialysis were significantly lower (p < 0.05) in the AOT group than in the AAT group and glucose values in the brain determined using microdialysis were significantly higher (p < 0.04). No differences were demonstrated in the other groups. Increasing the FiO2 had no significant effect on the serum levels of glucose and lactate. Increasing the FiO2 influences dialysate glucose and lactate levels in injured brain tissue. Using an FiO2 of 1 influences brain metabolism in such a way that lactate is significantly reduced and glucose significantly increased. No changes in dialysate glucose and lactate values were found in the noninjured brain.
Khaksari, Mohammad; Mahmmodi, Reza; Shahrokhi, Nader; Shabani, Mohammad; Joukar, Siavash; Aqapour, Mobin
2013-01-01
Objective(s): Brain edema is one of the most serious causes of death within the first few days after trauma brain injury (TBI). In this study we have investigated the role of Shilajit on brain edema, blood-brain barrier (BBB) permeability, intracranial pressure (ICP) and neurologic outcomes following brain trauma. Materials and Methods: Diffuse traumatic brain trauma was induced in rats by drop of a 250 g weight from a 2 m high (Marmarou’s methods). Animals were randomly divided into 5 groups including sham, TBI, TBI-vehicle, TBI-Shi150 group and TBI-Shi250 group. Rats were undergone intraperitoneal injection of Shilajit and vehicle at 1, 24, 48 and 72 hr after trauma. Brain water content, BBB permeability, ICP and neurologic outcomes were finally measured. Results: Brain water and Evans blue dye contents showed significant decrease in Shilajit-treated groups compared to the TBI-vehicle and TBI groups. Intracranial pressure at 24, 48 and 72 hr after trauma had significant reduction in Shilajit-treated groups as compared to TBI-vehicle and TBI groups (P<0.001). The rate of neurologic outcomes improvement at 4, 24, 48 and 72 hr after trauma showed significant increase in Shilajit-treated groups in comparison to theTBI- vehicle and TBI groups (P <0.001). Conclusion: The present results indicated that Shilajit may cause in improvement of neurologic outcomes through decreasing brain edema, disrupting of BBB, and ICP after the TBI. PMID:23997917
Khaksari, Mohammad; Mahmmodi, Reza; Shahrokhi, Nader; Shabani, Mohammad; Joukar, Siavash; Aqapour, Mobin
2013-07-01
Brain edema is one of the most serious causes of death within the first few days after trauma brain injury (TBI). In this study we have investigated the role of Shilajit on brain edema, blood-brain barrier (BBB) permeability, intracranial pressure (ICP) and neurologic outcomes following brain trauma. Diffuse traumatic brain trauma was induced in rats by drop of a 250 g weight from a 2 m high (Marmarou's methods). Animals were randomly divided into 5 groups including sham, TBI, TBI-vehicle, TBI-Shi150 group and TBI-Shi250 group. Rats were undergone intraperitoneal injection of Shilajit and vehicle at 1, 24, 48 and 72 hr after trauma. Brain water content, BBB permeability, ICP and neurologic outcomes were finally measured. Brain water and Evans blue dye contents showed significant decrease in Shilajit-treated groups compared to the TBI-vehicle and TBI groups. Intracranial pressure at 24, 48 and 72 hr after trauma had significant reduction in Shilajit-treated groups as compared to TBI-vehicle and TBI groups (P<0.001). The rate of neurologic outcomes improvement at 4, 24, 48 and 72 hr after trauma showed significant increase in Shilajit-treated groups in comparison to theTBI- vehicle and TBI groups (P <0.001). The present results indicated that Shilajit may cause in improvement of neurologic outcomes through decreasing brain edema, disrupting of BBB, and ICP after the TBI.
Interpersonal violence in posttraumatic women: brain networks triggered by trauma-related pictures.
Neumeister, Paula; Feldker, Katharina; Heitmann, Carina Y; Helmich, Ruth; Gathmann, Bettina; Becker, Michael P I; Straube, Thomas
2017-04-01
Interpersonal violence (IPV) is one of the most frequent causes for the development of posttraumatic stress disorder (PTSD) in women. Trauma-related triggers have been proposed to evoke automatic emotional responses in PTSD. The present functional magnetic resonance study investigated the neural basis of trauma-related picture processing in women with IPV-PTSD (n = 18) relative to healthy controls (n = 18) using a newly standardized trauma-related picture set and a non-emotional vigilance task. We aimed to identify brain activation and connectivity evoked by trauma-related pictures, and associations with PTSD symptom severity. We found hyperactivation during trauma-related vs neutral picture processing in both subcortical [basolateral amygdala (BLA), thalamus, brainstem] and cortical [anterior cingulate cortex (ACC), medial prefrontal cortex (mPFC), insula, occipital cortex] regions in IPV-PTSD. In patients, brain activation in amygdala, ACC, insula, occipital cortex and brainstem correlated positively with symptom severity. Furthermore, connectivity analyses revealed hyperconnectivity between BLA and dorsal ACC/mPFC. Results show symptom severity-dependent brain activation and hyperconnectivity in response to trauma-related pictures in brain regions related to fear and visual processing in women suffering from IPV-PTSD. These brain mechanisms appear to be associated with immediate responses to trauma-related triggers presented in a non-emotional context in this PTSD subgroup. © The Author (2016). Published by Oxford University Press.
Comparative Effectiveness of Family Problem-Solving Therapy (F-PST) for Adolescent TBI
2018-01-25
Tbi; Intracranial Edema; Brain Edema; Craniocerebral Trauma; Head Injury; Brain Hemorrhage, Traumatic; Subdural Hematoma; Brain Concussion; Head Injuries, Closed; Epidural Hematoma; Cortical Contusion; Wounds and Injuries; Disorders of Environmental Origin; Trauma, Nervous System; Brain Injuries
Role of erythropoietin in the brain
Noguchi, Constance Tom; Asavaritikrai, Pundit; Teng, Ruifeng; Jia, Yi
2007-01-01
Multi-tissue erythropoietin receptor (EPO-R) expression provides for erythropoietin (EPO) activity beyond its known regulation of red blood cell production. This review highlights the role of EPO and EPO-R in brain development and neuroprotection. EPO-R brain expression includes neural progenitor cells (NPC), neurons, glial cells and endothelial cells. EPO is produced in brain in a hypoxia sensitive manner, stimulates NPC proliferation and differentiation, and neuron survival, and contributes to ischemic preconditioning. Mice lacking EPO or EPO-R exhibit increased neural cell apoptosis during development before embryonic death due to severe anemia. EPO administration provides neural protection in animal models of brain ischemia and trauma, reducing the extent of injury and damage. EPO stimulation of endothelial cells contributes to neuroprotection and is of particular importance since only low levels of EPO appear to cross the blood-brain barrier when administered at high dose intravenously. The therapeutic potential of EPO for brain ischemia/trauma and neurodegenerative diseases has shown promise in early clinical trial and awaits further validation. PMID:17482474
Clark, Ian A.; Mackay, Clare E.
2015-01-01
This hypothesis and theory paper presents a pragmatic framework to help bridge the clinical presentation and neuroscience of intrusive memories following psychological trauma. Intrusive memories are a hallmark symptom of post-traumatic stress disorder (PTSD). However, key questions, including those involving etiology, remain. In particular, we know little about the brain mechanisms involved in why only some moments of the trauma return as intrusive memories while others do not. We first present an overview of the patient experience of intrusive memories and the neuroimaging studies that have investigated intrusive memories in PTSD patients. Next, one mechanism of how to model intrusive memories in the laboratory, the trauma film paradigm, is examined. In particular, we focus on studies combining the trauma film paradigm with neuroimaging. Stemming from the clinical presentation and our current understanding of the processes involved in intrusive memories, we propose a framework in which an intrusive memory comprises five component parts; autobiographical (trauma) memory, involuntary recall, negative emotions, attention hijacking, and mental imagery. Each component part is considered in turn, both behaviorally and from a brain imaging perspective. A mapping of these five components onto our understanding of the brain is described. Unanswered questions that exist in our understanding of intrusive memories are considered using the proposed framework. Overall, we suggest that mental imagery is key to bridging the experience, memory, and intrusive recollection of the traumatic event. Further, we suggest that by considering the brain mechanisms involved in the component parts of an intrusive memory, in particular mental imagery, we may be able to aid the development of a firmer bridge between patients’ experiences of intrusive memories and the clinical neuroscience behind them. PMID:26257660
Childhood Trauma in Today's Urban Classroom: Moving beyond the Therapist's Office
ERIC Educational Resources Information Center
R. B.-Banks, Yvonne; Meyer, Joseph
2017-01-01
Childhood trauma leaves its marks on the brain (Sandi, 2013) with unseen scars as evident in brain research. Addressing childhood trauma in today's urban classrooms is no small feat. According to the 2011-12 National Survey of Children's Health, nearly 35 million children in the United States are living with emotional and psychological trauma.…
Kesinger, Matthew R; Juengst, Shannon B; Bertisch, Hillary; Niemeier, Janet P; Krellman, Jason W; Pugh, Mary Jo; Kumar, Raj G; Sperry, Jason L; Arenth, Patricia M; Fann, Jesse R; Wagner, Amy K
2016-08-01
To determine whether severity of head and extracranial injuries (ECI) is associated with suicidal ideation (SI) or suicide attempt (SA) after traumatic brain injury (TBI). Factors associated with SI and SA were assessed in this inception cohort study using data collected 1, 2, and 5 years post-TBI from the National Trauma Data Bank and Traumatic Brain Injury Model Systems (TBIMS) databases. Level I trauma centers, inpatient rehabilitation centers, and the community. Participants with TBI from 15 TBIMS Centers with linked National Trauma Data Bank trauma data (N=3575). Not applicable. SI was measured via the Patient Health Questionnaire 9 (question 9). SA in the last year was assessed via interview. ECI was measured by the Injury Severity Scale (nonhead) and categorized as none, mild, moderate, or severe. There were 293 (8.2%) participants who had SI without SA and 109 (3.0%) who had SA at least once in the first 5 years postinjury. Random effects logit modeling showed a higher likelihood of SI when ECI was severe (odds ratio=2.73; 95% confidence interval, 1.55-4.82; P=.001). Drug use at time of injury was also associated with SI (odds ratio=1.69; 95% confidence interval, 1.11-2.86; P=.015). Severity of ECI was not associated with SA. Severe ECI carried a nearly 3-fold increase in the odds of SI after TBI, but it was not related to SA. Head injury severity and less severe ECI were not associated with SI or SA. These findings warrant additional work to identify factors associated with severe ECI that make individuals more susceptible to SI after TBI. Copyright © 2016 American Congress of Rehabilitation Medicine. Published by Elsevier Inc. All rights reserved.
The Biology of Trauma: Implications for Treatment
ERIC Educational Resources Information Center
Solomon, Eldra P.; Heide, Kathleen M.
2005-01-01
During the past 20 years, the development of brain imaging techniques and new biochemical approaches has led to increased understanding of the biological effects of psychological trauma. New hypotheses have been generated about brain development and the roots of antisocial behavior. We now understand that psychological trauma disrupts homeostasis…
He-Ne ILLLI used for brain trauma: a clinical observation of 46 cases
NASA Astrophysics Data System (ADS)
Yang, Da-Ke; Ru, Zheng-Guo; Ge, Sheng-Li; Shuo, Wei-Lan
1998-11-01
With the background that ILLLI can lower the viscosity of blood, improve the microcirculation, we investigated and compared the therapeutic effect of conventional drug therapy and ILLLI combined drug therapy for brain trauma. We found that ILLLI combined drug therapy could effectively alleviate some symptoms such as headache, vertigo, nausea, vomiting, blurred vision, anorexia caused by brain trauma. the therapeutic effect of treated group was prior to control group.
Traumatic Brain Injury as a Cause of Behavior Disorders.
ERIC Educational Resources Information Center
Nordlund, Marcia R.
There is increasing evidence that many children and adolescents who display behavior disorders have sustained a traumatic brain injury. Traumatic brain injury can take the following forms: closed head trauma in which the brain usually suffers diffuse damage; open head injury which usually results in specific focal damage; or internal trauma (e.g.,…
Kohrt, Brandon A; Hruschka, Daniel J
2010-06-01
In the aftermath of a decade-long Maoist civil war in Nepal and the recent relocation of thousands of Bhutanese refugees from Nepal to Western countries, there has been rapid growth of mental health and psychosocial support programs, including posttraumatic stress disorder treatment, for Nepalis and ethnic Nepali Bhutanese. This medical anthropology study describes the process of identifying Nepali idioms of distress and local ethnopsychology and ethnophysiology models that promote effective communication about psychological trauma in a manner that minimizes stigma for service users. Psychological trauma is shown to be a multifaceted concept that has no single linguistic corollary in the Nepali study population. Respondents articulated different categories of psychological trauma idioms in relation to impact on the heart-mind, brain-mind, body, spirit, and social status, with differences in perceived types of traumatic events, symptom sets, emotion clusters and vulnerability. Trauma survivors felt blamed for experiencing negative events, which were seen as karma transmitting past life sins or family member sins into personal loss. Some families were reluctant to seek care for psychological trauma because of the stigma of revealing this bad karma. In addition, idioms related to brain-mind dysfunction contributed to stigma, while heart-mind distress was a socially acceptable reason for seeking treatment. Different categories of trauma idioms support the need for multidisciplinary treatment with multiple points of service entry.
Paquola, Casey; Bennett, Maxwell R; Lagopoulos, Jim
2016-10-01
Childhood trauma has been associated with long term effects on prefrontal-limbic grey matter. A literature search was conducted to identify structural magnetic resonance imaging studies of adults with a history of childhood trauma. We performed three meta-analyses. Hedges' g effect sizes were calculated for each study providing hippocampal or amygdala volumes of trauma and non-trauma groups. Seed based differential mapping was utilised to synthesise whole brain voxel based morphometry (VBM) studies. A total of 38 articles (17 hippocampus, 13 amygdala, 19 whole brain VBM) were included in the meta-analyses. Trauma cohorts exhibited smaller hippocampus and amygdala volumes bilaterally. The most robust findings of the whole brain VBM meta-analysis were reduced grey matter in the right dorsolateral prefrontal cortex and right hippocampus amongst adults with a history of childhood trauma. Subgroup analyses and meta-regressions showed results were moderated by age, gender, the cohort's psychiatric health and the study's definition of childhood trauma. We provide evidence of abnormal grey matter in prefrontal-limbic brain regions of adults with a history of childhood maltreatment. Copyright © 2016 Elsevier Ltd. All rights reserved.
S100B blood levels and childhood trauma in adolescent inpatients.
Falcone, Tatiana; Janigro, Damir; Lovell, Rachel; Simon, Barry; Brown, Charles A; Herrera, Mariela; Myint, Aye Mu; Anand, Amit
2015-03-01
Serum levels of the astrocytic protein S100B have been reported to indicate disruption of the blood-brain barrier. In this study, we investigated the relationship between S100B levels and childhood trauma in a child psychiatric inpatient unit. Levels of S100B were measured in a group of youth with mood disorders or psychosis with and without history of childhood trauma as well as in healthy controls. Study participants were 93 inpatient adolescents admitted with a diagnosis of psychosis (N = 67), or mood disorder (N = 26) and 22 healthy adolescents with no history of trauma or psychiatric illness. Childhood trauma was documented using the Life Events Checklist (LEC) and Adverse Child Experiences (ACE). In a multivariate regression model, suicidality scores and trauma were the only two variables which were independently related to serum S100B levels. Patients with greater levels of childhood trauma had significantly higher S100B levels even after controlling for intensity of suicidal ideation. Patients with psychotic diagnoses and mood disorders did not significantly differ in their levels of S100B. Patients exposed to childhood trauma were significantly more likely to have elevated levels of S100B (p < .001) than patients without trauma, and patients with trauma had significantly higher S100B levels (p < .001) when compared to the control group. LEC (p = 0.046), and BPRS-C suicidality scores (p = 0.001) significantly predicted S100B levels. Childhood trauma can potentially affect the integrity of the blood-brain barrier as indicated by associated increased S100B levels. Copyright © 2014 Elsevier Ltd. All rights reserved.
A Review of Neuroimaging Findings in Repetitive Brain Trauma
Koerte, Inga K.; Lin, Alexander P.; Willems, Anna; Muehlmann, Marc; Hufschmidt, Jakob; Coleman, Michael J.; Green, Isobel; Liao, Huijun; Tate, David F.; Wilde, Elisabeth A.; Pasternak, Ofer; Bouix, Sylvain; Rathi, Yogesh; Bigler, Erin D.; Stern, Robert A.; Shenton, Martha E.
2017-01-01
Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease confirmed at post-mortem. Those at highest risk are professional athletes who participate in contact sports and military personnel who are exposed to repetitive blast events. All neuropathologically-confirmed CTE cases, to date, have had a history of repetitive head impacts. This suggests that repetitive head impacts may be necessary for the initiation of the pathogenetic cascade that, in some cases, leads to CTE. Importantly, while all CTE appears to result from repetitive brain trauma, not all repetitive brain trauma results in CTE. Magnetic resonance imaging has great potential for understanding better the underlying mechanisms of repetitive brain trauma. In this review we provide an overview of advanced imaging techniques currently used to investigate brain anomalies. We also provide an overview of neuroimaging findings in those exposed to repetitive head impacts in the acute/subacute and chronic phase of injury and in more neurodegenerative phases of injury, as well as in military personnel exposed to repetitive head impacts. Finally, we discuss future directions for research that will likely lead to a better understanding of the underlying mechanisms separating those who recover from repetitive brain trauma versus those who go on to develop CTE. PMID:25904047
Quantifying Discretization Effects on Brain Trauma Simulations
2016-01-01
arbitrarily formed meshes can propagate error when resolving interactions among the skull , cerebrospinal fluid, and brain. We compared Lagrangian, pure...embedded methods from top to bottom. ......3 Fig. 2 Loading node-set for Eulerian rotational problem. The dark shaded area around the skull is the area to...and top inner edges of the skull . The example shown is a Lagrangian rotational model. The red and green materials represent the brain and skull
Bernick, Charles; Banks, Sarah J; Shin, Wanyong; Obuchowski, Nancy; Butler, Sam; Noback, Michael; Phillips, Michael; Lowe, Mark; Jones, Stephen; Modic, Michael
2015-01-01
Objectives Cumulative head trauma may alter brain structure and function. We explored the relationship between exposure variables, cognition and MRI brain structural measures in a cohort of professional combatants. Methods 224 fighters (131 mixed martial arts fighters and 93 boxers) participating in the Professional Fighters Brain Health Study, a longitudinal cohort study of licensed professional combatants, were recruited, as were 22 controls. Each participant underwent computerised cognitive testing and volumetric brain MRI. Fighting history including years of fighting and fights per year was obtained from self-report and published records. Statistical analyses of the baseline evaluations were applied cross-sectionally to determine the relationship between fight exposure variables and volumes of the hippocampus, amygdala, thalamus, caudate, putamen. Moreover, the relationship between exposure and brain volumes with cognitive function was assessed. Results Increasing exposure to repetitive head trauma measured by number of professional fights, years of fighting, or a Fight Exposure Score (FES) was associated with lower brain volumes, particularly the thalamus and caudate. In addition, speed of processing decreased with decreased thalamic volumes and with increasing fight exposure. Higher scores on a FES used to reflect exposure to repetitive head trauma were associated with greater likelihood of having cognitive impairment. Conclusions Greater exposure to repetitive head trauma is associated with lower brain volumes and lower processing speed in active professional fighters. PMID:25633832
Miller Ferguson, Nikki; Sarnaik, Ajit; Miles, Darryl; Shafi, Nadeem; Peters, Mark J; Truemper, Edward; Vavilala, Monica S; Bell, Michael J; Wisniewski, Stephen R; Luther, James F; Hartman, Adam L; Kochanek, Patrick M
2017-08-01
Small series have suggested that outcomes after abusive head trauma are less favorable than after other injury mechanisms. We sought to determine the impact of abusive head trauma on mortality and identify factors that differentiate children with abusive head trauma from those with traumatic brain injury from other mechanisms. First 200 subjects from the Approaches and Decisions in Acute Pediatric Traumatic Brain Injury Trial-a comparative effectiveness study using an observational, cohort study design. PICUs in tertiary children's hospitals in United States and abroad. Consecutive children (age < 18 yr) with severe traumatic brain injury (Glasgow Coma Scale ≤ 8; intracranial pressure monitoring). None. Demographics, injury-related scores, prehospital, and resuscitation events were analyzed. Children were dichotomized based on likelihood of abusive head trauma. A total of 190 children were included (n = 35 with abusive head trauma). Abusive head trauma subjects were younger (1.87 ± 0.32 vs 9.23 ± 0.39 yr; p < 0.001) and a greater proportion were female (54.3% vs 34.8%; p = 0.032). Abusive head trauma were more likely to 1) be transported from home (60.0% vs 33.5%; p < 0.001), 2) have apnea (34.3% vs 12.3%; p = 0.002), and 3) have seizures (28.6% vs 7.7%; p < 0.001) during prehospital care. Abusive head trauma had a higher prevalence of seizures during resuscitation (31.4 vs 9.7%; p = 0.002). After adjusting for covariates, there was no difference in mortality (abusive head trauma, 25.7% vs nonabusive head trauma, 18.7%; hazard ratio, 1.758; p = 0.60). A similar proportion died due to refractory intracranial hypertension in each group (abusive head trauma, 66.7% vs nonabusive head trauma, 69.0%). In this large, multicenter series, children with abusive head trauma had differences in prehospital and in-hospital secondary injuries which could have therapeutic implications. Unlike other traumatic brain injury populations in children, female predominance was seen in abusive head trauma in our cohort. Similar mortality rates and refractory intracranial pressure deaths suggest that children with severe abusive head trauma may benefit from therapies including invasive monitoring and adherence to evidence-based guidelines.
Hypersomnia Following Traumatic Brain Injury
Watson, Nathaniel F; Dikmen, Sureyya; Machamer, Joan; Doherty, Michael; Temkin, Nancy
2007-01-01
Study Objectives: To evaluate the prevalence and natural history of sleepiness following traumatic brain injury. Methods: This prospective cohort study used the Sickness Impact Profile to evaluate sleepiness in 514 consecutive subjects with traumatic brain injury (TBI), 132 non-cranial trauma controls, and 102 trauma-free controls 1 month and 1 year after injury. Results: Fifty-five percent of TBI subjects, 41% of non-cranial trauma controls, and 3% of trauma-free controls endorsed 1 or more sleepiness items 1 month following injury (p < .001). One year following injury, 27% of TBI subjects, 23% of non-cranial trauma controls, and 1% of trauma-free controls endorsed 1 or more sleepiness items (p < .001). Patients with TBI were sleepier than non-cranial trauma controls at 1 month (p < .02) but not 1 year after injury. Brain-injured subjects were divided into injury-severity groups based on time to follow commands (TFC). At 1 month, the non-cranial trauma controls were less sleepy than the 1- to 6-day (p < .05), 7- to 13-day (p < .01), and 14-day or longer (p < .01) TFC groups. In addition, the ≤ 24-hour group was less sleepy then the 7- to 13-day and 14-day or longer groups (each p < .05). At 1 year, the non-cranial trauma control group (p < .05) and the ≤ 24-hour TFC group (p < .01) were less sleepy than the 14-day or longer TFC group. Sleepiness improved in 84% to 100% of subjects in the TBI TFC groups, as compared with 78% of the non-cranial trauma control group (p < .01). Conclusions: Sleepiness is common following traumatic injury, particularly TBI, with more severe injuries resulting in greater sleepiness. Sleepiness improves in many patients, particularly those with TBI. However, about a quarter of TBI subjects and non-cranial trauma control subjects remained sleepy 1 year after injury. Citation: Watson NF; Dikmen S; Machamer J et al. Hypersomnia following traumatic brain injury. J Clin Sleep Med 2007;3(4):363-368. PMID:17694724
Majidi, Seyed Ali; Ayoubian, Ali; Mardani, Sheida; Hashemidehaghi, Zahra
2014-01-01
Head trauma is the main cause of disabilities and death among young people, and the side effects of head trauma pose some of the greatest medical challenges. Rapid diagnosis and the use of proper treatments can prevent more severe brain damage. The purpose of this research was to determine the quality of nursing services provided to brain trauma patients in hospitals in Guilan Province, Iran. The study was conducted as a descriptive, cross-sectional study in the emergency wards of selected hospitals in Guilan in 2012. The research population was comprised of all the brain trauma patients in these hospitals. We developed a two-section questionnaire, ascertained its validity, and determined that it had a reliability of 88% (Cronbach's alpha). Subsequently, we used the questionnaire for gathering data. The data were analyzed using SPSS statistical software, and descriptive analysis tests (frequency rate and average) and deductive analyses tests (chi-squared) also were used. The results showed that the quality of health services provided to brain-trauma patients in the emergency ward was at the moderate level of 58.8% of the cases and at a low level in 41.2% of the cases. Based on the results that showed that the services were of moderate quality, the staff members in the emergency ward were required to update their knowledge and use the required measures to minimize or prevent side effects in brain-trauma patients; clearly, mastery of such measures was a real need among the emergency ward's staff.
Lyoo, In Kyoon; Kim, Jieun E; Yoon, Sujung J; Hwang, Jaeuk; Bae, Sujin; Kim, Dajung J
2011-07-01
A multiwave longitudinal neuroimaging study in a cohort of direct survivors of a South Korean subway disaster, most of whom recovered from posttraumatic stress disorder 5 years after trauma, provided a unique opportunity to investigate the brain correlates of recovery from a severe psychological trauma. To investigate region-specific brain mobilization during successful recovery from posttraumatic stress disorder by assessing cortical thickness multiple times from early after trauma to recovery, and to examine whether a brain-derived neurotrophic factor gene polymorphism was associated with this brain mobilization. Five-year follow-up case-control study conducted from 2003-2007. Seoul National University and Hospital. Thirty psychologically traumatized disaster survivors and 36 age- and sex-matched control group members recruited from the disaster registry and local community, respectively, who contributed 156 high-resolution brain magnetic resonance images during 3 waves of assessments. Cerebral cortical thickness measured in high-resolution anatomic magnetic resonance images using a validated cortical thickness analysis tool and its prospective changes from early after trauma to recovery in trauma-exposed individuals and controls. Trauma-exposed individuals had greater dorsolateral prefrontal cortical (DLPFC) thickness 1.42 years after trauma (right DLPFC, 5.4%; left superior frontal cortex, 5.8%; and left inferior frontal cortex, 5.3% [all clusters, P ≤ .01]) relative to controls. Thicknesses gradually normalized over time during recovery. We found a positive linear trend, with trauma-exposed individuals with a valine/valine genotype having the greatest DLPFC cortical thickness, followed by those with a methionine genotype and controls (P < .001 for trend). Greater DLPFC thickness was associated with greater posttraumatic stress disorder symptom reductions and better recovery. The DLPFC region might play an important role in psychological recovery from a severely traumatic event in humans.
... in association with spinal cord injury, multiple sclerosis, cerebral palsy, stroke, brain or head trauma, amyotrophic lateral sclerosis, ... in association with spinal cord injury, multiple sclerosis, cerebral palsy, stroke, brain or head trauma, amyotrophic lateral sclerosis, ...
ERIC Educational Resources Information Center
Kleim, Jeffrey A.; Jones, Theresa A.
2008-01-01
Purpose: This paper reviews 10 principles of experience-dependent neural plasticity and considerations in applying them to the damaged brain. Method: Neuroscience research using a variety of models of learning, neurological disease, and trauma are reviewed from the perspective of basic neuroscientists but in a manner intended to be useful for the…
Lu, Shaojia; Gao, Weijia; Wei, Zhaoguo; Wang, Dandan; Hu, Shaohua; Huang, Manli; Xu, Yi; Li, Lingjiang
2017-06-01
Childhood trauma confers great risk for the development of multiple psychiatric disorders; however, the neural basis for this association is still unknown. The present resting-state functional magnetic resonance imaging study aimed to detect the effects of childhood trauma on brain function in a group of young healthy adults. In total, 24 healthy individuals with childhood trauma and 24 age- and sex-matched adults without childhood trauma were recruited. Each participant underwent resting-state functional magnetic resonance imaging scanning. Intra-regional brain activity was evaluated by regional homogeneity method and compared between groups. Areas with altered regional homogeneity were further selected as seeds in subsequent functional connectivity analysis. Statistical analyses were performed by setting current depression and anxiety as covariates. Adults with childhood trauma showed decreased regional homogeneity in bilateral superior temporal gyrus and insula, and the right inferior parietal lobule, as well as increased regional homogeneity in the right cerebellum and left middle temporal gyrus. Regional homogeneity values in the left middle temporal gyrus, right insula and right cerebellum were correlated with childhood trauma severity. In addition, individuals with childhood trauma also exhibited altered default mode network, cerebellum-default mode network and insula-default mode network connectivity when the left middle temporal gyrus, right cerebellum and right insula were selected as seed area, respectively. The present outcomes suggest that childhood trauma is associated with disturbed intrinsic brain function, especially the default mode network, in adults even without psychiatric diagnoses, which may mediate the relationship between childhood trauma and psychiatric disorders in later life.
Effect of skull flexural properties on brain response during dynamic head loading - biomed 2013.
Harrigan, T P; Roberts, J C; Ward, E E; Carneal, C M; Merkle, A C
2013-01-01
The skull-brain complex is typically modeled as an integrated structure, similar to a fluid-filled shell. Under dynamic loads, the interaction of the skull and the underlying brain, cerebrospinal fluid, and other tissue produces the pressure and strain histories that are the basis for many theories meant to describe the genesis of traumatic brain injury. In addition, local bone strains are of interest for predicting skull fracture in blunt trauma. However, the role of skull flexure in the intracranial pressure response to blunt trauma is complex. Since the relative time scales for pressure and flexural wave transmission across the skull are not easily separated, it is difficult to separate out the relative roles of the mechanical components in this system. This study uses a finite element model of the head, which is validated for pressure transmission to the brain, to assess the influence of skull table flexural stiffness on pressure in the brain and on strain within the skull. In a Human Head Finite Element Model, the skull component was modified by attaching shell elements to the inner and outer surfaces of the existing solid elements that modeled the skull. The shell elements were given the properties of bone, and the existing solid elements were decreased so that the overall stiffness along the surface of the skull was unchanged, but the skull table bending stiffness increased by a factor of 2.4. Blunt impact loads were applied to the frontal bone centrally, using LS-Dyna. The intracranial pressure predictions and the strain predictions in the skull were compared for models with and without surface shell elements, showing that the pressures in the mid-anterior and mid-posterior of the brain were very similar, but the strains in the skull under the loads and adjacent to the loads were decreased 15% with stiffer flexural properties. Pressure equilibration to nearly hydrostatic distributions occurred, indicating that the important frequency components for typical impact loading are lower than frequencies based on pressure wave propagation across the skull. This indicates that skull flexure has a local effect on intracranial pressures but that the integrated effect of a dome-like structure under load is a significant part of load transfer in the skull in blunt trauma.
Exposure to sub-concussive head injury in boxing and other sports.
Erlanger, David M
2015-01-01
Current characterizations of chronic traumatic brain injury (CTBI) in boxing, football and other sports are reviewed in the context of the history of research on sub-concussive brain trauma in athletes. The utility of exposure models for understanding CTBI in boxers is examined and concerns regarding the paucity of findings supportive of an exposure model for CTBI in football players are discussed. Recommendations for development of exposure models for sport-specific phenotypic characterizations of CTBI are presented.
... cord. This syndrome can be caused by stroke, multiple sclerosis, tumors, epilepsy, brain or spinal cord trauma, or ... cord. This syndrome can be caused by stroke, multiple sclerosis, tumors, epilepsy, brain or spinal cord trauma, or ...
What boxing tells us about repetitive head trauma and the brain.
Bernick, Charles; Banks, Sarah
2013-01-01
Boxing and other combat sports may serve as a human model to study the effects of repetitive head trauma on brain structure and function. The initial description of what is now known as chronic traumatic encephalopathy (CTE) was reported in boxers in 1928. In the ensuing years, studies examining boxers have described the clinical features of CTE, its relationship to degree of exposure to fighting, and an array of radiologic findings. The field has been hampered by issues related to study design, lack of longitudinal follow-up, and absence of agreed-upon clinical criteria for CTE. A recently launched prospective cohort study of professional fighters, the Professional Fighters Brain Health Study, attempts to overcome some of the problems in studying fighters. Here, we review the cross-sectional results from the first year of the project.
Hruschka, Daniel J.
2013-01-01
In the aftermath of a decade-long Maoist civil war in Nepal and the recent relocation of thousands of Bhutanese refugees from Nepal to Western countries, there has been rapid growth of mental health and psychosocial support programs, including posttraumatic stress disorder (PTSD) treatment, for Nepalis and ethnic Nepali Bhutanese. This medical anthropology study describes the process of identifying Nepali idioms of distress and local ethnopsychology and ethnophysiology models that promote effective communication about psychological trauma in a manner that minimizes stigma for service users. Psychological trauma is shown to be a multi-faceted concept that has no single linguistic corollary in the Nepali study population. Respondents articulated different categories of psychological trauma idioms in relation to impact upon the heart-mind, brain-mind, body, spirit, and social status, with differences in perceived types of traumatic events, symptom sets, emotion clusters, and vulnerability. Trauma survivors felt blamed for experiencing negative events, which were seen as karma transmitting past life sins or family member sins into personal loss. Some families were reluctant to seek care for psychological trauma because of the stigma of revealing this bad karma. In addition, idioms related to brain-mind dysfunction contributed to stigma while heart-mind distress was a socially acceptable reason for seeking treatment. Different categories of trauma idioms support the need for multidisciplinary treatment with multiple points of service entry. PMID:20309724
Operation Brain Trauma Therapy Extended Studies
2015-05-01
peaks in the TBI models. It is also possible that the use of a craniotomy in all 3 models results in an under- estimation of the potential benefit of...traditional strategies, namely, osmolar therapy (mannitol or hypertonic saline administration), CSF drainage , craniectomy, limitation of fluid administration
Differential Response of Neural Cells to Trauma-Induced Swelling In Vitro.
Jayakumar, A R; Taherian, M; Panickar, K S; Shamaladevi, N; Rodriguez, M E; Price, B G; Norenberg, M D
2018-02-01
Brain edema and the associated increase in intracranial pressure are major consequences of traumatic brain injury (TBI) that accounts for most early deaths after TBI. We recently showed that acute severe trauma to cultured astrocytes results in cell swelling. We further examined whether trauma induces cell swelling in neurons and microglia. We found that severe trauma also caused cell swelling in cultured neurons, whereas no swelling was observed in microglia. While severe trauma caused cell swelling in both astrocytes and neurons, mild trauma to astrocytes, neurons, and microglia failed to cell swelling. Since extracellular levels of glutamate are increased in brain post-TBI and microglia are known to release cytokine, and direct exposure of astrocytes to these molecules are known to stimulate cell swelling, we examined whether glutamate or cytokines have any additive effect on trauma-induced cell swelling. Exposure of cultured astrocytes to trauma caused cell swelling, and such swelling was potentiated by the exposure of traumatized astrocytes to glutamate and cytokines. Conditioned medium (CM) from traumatized astrocytes had no effect on neuronal swelling post-trauma, while CM from traumatized neurons and microglia potentiated the effect of trauma on astrocyte swelling. Further, trauma significantly increased the Na-K-Cl co-transporter (NKCC) activity in neurons, and that inhibition of NKCC activity diminished the trauma-induced neuronal swelling. Our results indicate that a differential sensitivity to trauma-induced cell swelling exists in neural cells and that neurons and microglia are likely to be involved in the potentiation of the astrocyte swelling post-trauma.
Fawzi, Mounir H; Kira, Ibrahim A; Fawzi, Mohab M; Mohamed, Hanan E; Fawzi, Maggie M
2013-01-01
We aimed to investigate the relation of trauma profile to schizophrenia psychopathology in a sample of Egyptian drug-naïve adolescent patients with first-episode schizophrenia. In addition, a hypothesized mediating effect of brain-derived neurotrophic factor (BDNF) in this relation was formally tested. We assessed 74 eligible outpatients using the Positive and Negative Syndrome Scale (PANSS) for measuring psychopathology. Trauma histories were recorded with the help of the Cumulative Trauma Measure. Serum BDNF levels were estimated by enzyme-linked immunosorbent assay. Total cumulative trauma, personal identity trauma, and survival trauma were found to be the significant predictors for schizophrenia psychopathology. BDNF fully mediated the associations between total cumulative trauma and overall schizophrenia psychopathology. BDNF also mediated the associations between some types of trauma and both PANSS-positive and PANSS-negative symptom factors. We concluded that total cumulative trauma and certain trauma types are linked with schizophrenia psychopathology. BDNF appears to mediate these links.
Fan, Hui-yu; Zhang, Qin-ting; Tang, Tao; Cai, Wei-xiong
2016-04-01
To explore the main performance of personality change in people with mild psychiatric impairments which due to the brain trauma caused by traffic accidents and its value in assessment of psychiatric impairment. The condition of personality change of patients with traumatic brain injury caused by traffic accident was evaluated by the Scale of Personality Change Post-traumatic Brain Injury (SPCPTBI). Furthermore, the correlation between the personality change and the degrees of traumatic brain injury and psychiatric impairment were explored. Results In 271 samples, 239 (88.2%) with personality changes. Among these 239 samples, 178 (65.7%), 46 (17.0%), 15 (5.5%) with mild, moderate and severe personality changes, respectively. The ratio based on the extent of personality changes to the degree of brain trauma was not significant (P > 0.05), but the total score difference between the groups was significant (P < 0.05). There was no statistical significance between the medium and high severity brain trauma groups. The higher degree of personality changes, the higher rank of mental disabilities. The total score difference of the scale of personality change among the different mild psychiatric impairment group was significant (P<0.05). The difference between other psychiatric impairment levels had statistical significance (P < 0.05) except level 7 and 8. The occurrence of personality change due to traumatic brain injury caused by traffic accident was high. Correlations exist between the personality change and the degree of psychiatric impairment. Personality change due to brain trauma caused by traffic accident can be assessed effectively by means of SPCPTBI, and the correlation between the total score and the extent of traumatic brain injury can be found.
Cost-effectiveness of the PECARN rules in children with minor head trauma.
Nishijima, Daniel K; Yang, Zhuo; Urbich, Michael; Holmes, James F; Zwienenberg-Lee, Marike; Melnikow, Joy; Kuppermann, Nathan
2015-01-01
To improve the efficiency and appropriateness of computed tomography (CT) use in children with minor head trauma, clinical prediction rules were derived and validated by the Pediatric Emergency Care Applied Research Network (PECARN). The objective of this study was to conduct a cost-effectiveness analysis comparing the PECARN traumatic brain injury prediction rules to usual care for selective CT use. We used decision analytic modeling to project the outcomes, costs, and cost-effectiveness of applying the PECARN rules compared with usual care in a hypothetical cohort of 1,000 children with minor blunt head trauma. Clinical management was directed by level of risk as specified by the presence or absence of variables in the PECARN traumatic brain injury prediction rules. Immediate costs of care (diagnostic testing, treatment [not including clinician time], and hospital stay) were derived on single-center data. Quality-adjusted life-year losses related to the sequelae of clinically important traumatic brain injuries and to radiation-induced cancers, number of CT scans, number of radiation-induced cancers, number of missed clinically important traumatic brain injury, and total costs were evaluated. Compared with the usual care strategy, the PECARN strategy was projected to miss slightly more children with clinically important traumatic brain injuries (0.26 versus 0.02 per 1,000 children) but used fewer cranial CT scans (274 versus 353), resulted in fewer radiation-induced cancers (0.34 versus 0.45), cost less ($904,940 versus $954,420), and had lower net quality-adjusted life-year loss (-4.64 versus -5.79). Because the PECARN strategy was more effective (less quality-adjusted life-year loss) and less costly, it dominated the usual care strategy. Results were robust under sensitivity analyses. Application of the PECARN traumatic brain injury prediction rules for children with minor head trauma would lead to beneficial outcomes and more cost-effective care. Copyright © 2014 American College of Emergency Physicians. Published by Elsevier Inc. All rights reserved.
Yin, Terry; Lindley, Timothy E.; Albert, Gregory W.; Ahmed, Raheel; Schmeiser, Peter B.; Grady, M. Sean; Howard, Matthew A.; Welsh, Michael J.
2013-01-01
Traumatic brain injury (TBI) is a common cause of morbidity and mortality in people of all ages. Following the acute mechanical insult, TBI evolves over the ensuing minutes and days. Understanding the secondary factors that contribute to TBI might suggest therapeutic strategies to reduce the long-term consequences of brain trauma. To assess secondary factors that contribute to TBI, we studied a lateral fluid percussion injury (FPI) model in mice. Following FPI, the brain cortex became acidic, consistent with data from humans following brain trauma. Administering HCO3 − after FPI prevented the acidosis and reduced the extent of neurodegeneration. Because acidosis can activate acid sensing ion channels (ASICs), we also studied ASIC1a−/− mice and found reduced neurodegeneration after FPI. Both HCO3 − administration and loss of ASIC1a also reduced functional deficits caused by FPI. These results suggest that FPI induces cerebral acidosis that activates ASIC channels and contributes to secondary injury in TBI. They also suggest a therapeutic strategy to attenuate the adverse consequences of TBI. PMID:23991103
1981-10-01
measure for Central Nervus System is the Glasgow Cons Score (GCS), a scale of brain and spinal cord injury (Langfitt [1978]), and is itself an additive...concerns directly relating to the injury itself were identified. These were: 1. Ventilation Severity 2 Circulation Severity 3. Central Nervous System ...interacting system within which these concerns represent interacting parts. Most trauma involves only one of these systems , but more than one may be
Ganoderma Lucidum Protects Rat Brain Tissue Against Trauma-Induced Oxidative Stress.
Özevren, Hüseyin; İrtegün, Sevgi; Deveci, Engin; Aşır, Fırat; Pektanç, Gülsüm; Deveci, Şenay
2017-10-01
Traumatic brain injury causes tissue damage, breakdown of cerebral blood flow and metabolic regulation. This study aims to investigate the protective influence of antioxidant Ganoderma lucidum ( G. lucidum ) polysaccharides (GLPs) on brain injury in brain-traumatized rats. Sprague-Dawley conducted a head-traumatized method on rats by dropping off 300 g weight from 1 m height. Groups were categorized as control, G. lucidum , trauma, trauma+ G. lucidum (20 mL/kg per day via gastric gavage). Brain tissues were dissected from anesthetized rats 7 days after injury. For biochemical analysis, malondialdehyde, glutathione and myeloperoxidase values were measured. In histopathological examination, neuronal damage in brain cortex and changes in blood brain barrier were observed. In the analysis of immunohistochemical and western blot, p38 mitogen-activated protein kinase, vascular endothelial growth factor and cluster of differentiation 68 expression levels were shown. These analyzes demonstrated the beneficial effects of GLPs on brain injury. We propose that GLPs treatment after brain injury could be an alternative treatment to decraseing inflammation and edema, preventing neuronal and glial cells degeneration if given in appropriate dosage and in particular time intervals.
Cao, Yuli; Risling, Mårten; Malm, Elisabeth; Sondén, Anders; Bolling, Magnus Frödin; Sköld, Mattias K
2016-01-01
The mechanisms involved in traumatic brain injury have yet to be fully characterized. One mechanism that, especially in high-energy trauma, could be of importance is cavitation. Cavitation can be described as a process of vaporization, bubble generation, and bubble implosion as a result of a decrease and subsequent increase in pressure. Cavitation as an injury mechanism is difficult to visualize and model due to its short duration and limited spatial distribution. One strategy to analyze the cellular response of cavitation is to employ suitable in vitro models. The flyer-plate model is an in vitro high-energy trauma model that includes cavitation as a trauma mechanism. A copper fragment is accelerated by means of a laser, hits the bottom of a cell culture well causing cavitation, and shock waves inside the well and cell medium. We have found the flyer-plate model to be efficient, reproducible, and easy to control. In this study, we have used the model to analyze the cellular response to microcavitation in SH-SY5Y neuroblastoma, Caco-2, and C6 glioma cell lines. Mitotic activity in neuroblastoma and glioma was investigated with BrdU staining, and cell numbers were calculated using automated time-lapse imaging. We found variations between cell types and between different zones surrounding the lesion with these methods. It was also shown that the injured cell cultures released S-100B in a dose-dependent manner. Using gene expression microarray, a number of gene families of potential interest were found to be strongly, but differently regulated in neuroblastoma and glioma at 24 h post trauma. The data from the gene expression arrays may be used to identify new candidates for biomarkers in cavitation trauma. We conclude that our model is useful for studies of trauma in vitro and that it could be applied in future treatment studies.
Physical Trauma as an Etiological Agent in Mental Retardation.
ERIC Educational Resources Information Center
Angle, Carol R., Ed.; Bering, Edgar A., Jr., Ed.
The conference on Physical Trauma as a Cause of Mental Retardation dealt with two major areas of etiological concern - postnatal and perinatal trauma. Following two introductory statements on the problem of and issues related to mental retardation (MR) after early trauma to the brain, five papers on the epidemiology of head trauma cover…
Gurevich, B; Artru, A A; Lam, A M; Mueller, A L; Merkind, V; Talmor, D; Katchko, L; Shapira, Y
1998-06-01
The authors sought to determine whether 3,3-bis (3-fluorophenyl) propylamine (NPS 846), a novel noncompetitive N-methyl-D-aspartate receptor antagonist, alters outcome after closed head trauma in rats. The experimental variables were: presence or absence of closed head trauma, treatment with NPS 846 or no treatment, and time at which the rats were killed (24 or 48 hours). The NPS 846 (1 mg/kg) was administered intraperitoneally at 1 and 3 hours after closed head trauma or sham operation. Outcome measures were the neurological severity score (NSS), ischemic tissue volume, hemorrhagic necrosis volume, and specific gravity, water content, and concentrations of calcium, sodium, potassium, and magnesium in brain tissue. The following closed head trauma-induced changes in the injured hemisphere (expressed as the mean +/- the standard deviation) were reversed by NPS 846: decreased specific gravity of 1.035 +/- 0.006 at 24 hours was increased to 1.042 +/- 0.004; the decreased potassium level of 0.583 +/- 0.231 mg/L at 48 hours and at 24 hours was increased to 2.442 +/- 0.860 mg/L; the increased water content of 84.7 +/- 2.6% at 24 hours was decreased to 79.8 +/- 2%; the increased calcium level of 0.592 +/- 0.210 mg/L at 24 hours was decreased to 0.048 +/- 0.029 mg/L; and the increased sodium level of 2.035 +/- 0.649 mg/L was decreased to 0.631 +/- 0.102 mg/L. Administration of NPS 846 also lowered the NSS (improved neurological status) at 48 hours (7 +/- 3) and caused no significant changes in ischemic tissue or hemorrhagic necrosis volumes in the injured hemisphere at 24 or 48 hours. In this model of closed head trauma, NPS 846 improved neurological outcome, delayed the onset of brain edema, and improved brain tissue ion homeostasis.
Brain trauma and autophagy: What flies and mice can teach us about conserved responses.
Ratliff, Eric P; Barekat, Ayeh; Lipinski, Marta M; Finley, Kim D
2016-11-01
Drosophila models have been successfully used to identify many genetic components that affect neurodegenerative disorders. Recently, there has been a growing interest in identifying innate and environmental factors that influence the individual outcomes following traumatic brain injury (TBI). This includes both severe TBI and more subtle, mild TBI (mTBI), which is common in people playing contact sports. Autophagy, as a clearance pathway, exerts protective effects in multiple neurological disease models. In a recent publication, we highlighted the development of a novel repetitive mTBI system using Drosophila, which recapitulates several phenotypes associated with trauma in mammalian models. In particular, flies subjected to mTBI exhibit an acute impairment of the macroautophagy/autophagy pathway that is restored 1 wk following traumatic injury exposure. These phenotypes closely resemble temporary autophagy defects observed in a mouse TBI model. Through these studies, we also identified methods to directly assess autophagic responses in the fly nervous system and laid the groundwork for future studies designed to identify genetic, epigenetic and environmental factors that have an impact on TBI outcomes.
Long-term consequences of repetitive brain trauma: chronic traumatic encephalopathy.
Stern, Robert A; Riley, David O; Daneshvar, Daniel H; Nowinski, Christopher J; Cantu, Robert C; McKee, Ann C
2011-10-01
Chronic traumatic encephalopathy (CTE) has been linked to participation in contact sports such as boxing and American football. CTE results in a progressive decline of memory and cognition, as well as depression, suicidal behavior, poor impulse control, aggressiveness, parkinsonism, and, eventually, dementia. In some individuals, it is associated with motor neuron disease, referred to as chronic traumatic encephalomyelopathy, which appears clinically similar to amyotrophic lateral sclerosis. Results of neuropathologic research has shown that CTE may be more common in former contact sports athletes than previously believed. It is believed that repetitive brain trauma, with or possibly without symptomatic concussion, is responsible for neurodegenerative changes highlighted by accumulations of hyperphosphorylated tau and TDP-43 proteins. Given the millions of youth, high school, collegiate, and professional athletes participating in contact sports that involve repetitive brain trauma, as well as military personnel exposed to repeated brain trauma from blast and other injuries in the military, CTE represents an important public health issue. Focused and intensive study of the risk factors and in vivo diagnosis of CTE will potentially allow for methods to prevent and treat these diseases. Research also will provide policy makers with the scientific knowledge to make appropriate guidelines regarding the prevention and treatment of brain trauma in all levels of athletic involvement as well as the military theater. Copyright © 2011 American Academy of Physical Medicine and Rehabilitation. Published by Elsevier Inc. All rights reserved.
Sommer, Jens Bak; Norup, Anne; Poulsen, Ingrid; Morgensen, Jesper
2013-09-01
To examine cognitive activity limitations and predictors of outcome 1 year post-trauma in patients admitted to sub-acute rehabilitation after severe traumatic brain injury. The study included 119 patients with severe traumatic brain injury admitted to centralized sub-acute rehabilitation in the Eastern part of Denmark during a 5-year period from 2005 to 2009. Level of consciousness was assessed consecutively during rehabilitation and at 1 year post-trauma. Severity of traumatic brain injury was classified according to duration of post-traumatic amnesia. The cognitive subscale of Functional Independence MeasureTM (Cog-FIM) was used to assess cognitive activity limitations. Multivariate logistic regression analyses were performed to identify predictors of an independent level of functioning. The majority of patients progressed to a post-confusional level of consciousness during the first year post-trauma. At follow-up 33-58% of patients had achieved functional independence within the cognitive domains on the Cog-FIM. Socio-economic status, duration of acute care and post-traumatic amnesia were significant predictors of outcome. Substantial recovery was documented among patients with severe traumatic brain injury during the first year post-trauma. The results of the current study suggest that absence of consciousness at discharge from acute care should not preclude patients from being referred to specialized sub-acute rehabilitation.
Neural Systems for Cognitive and Emotional Processing in Posttraumatic Stress Disorder
Brown, Vanessa M.; Morey, Rajendra A.
2012-01-01
Individuals with posttraumatic stress disorder (PTSD) show altered cognition when trauma-related material is present. PTSD may lead to enhanced processing of trauma-related material, or it may cause impaired processing of trauma-unrelated information. However, other forms of emotional information may also alter cognition in PTSD. In this review, we discuss the behavioral and neural effects of emotion processing on cognition in PTSD, with a focus on neuroimaging results. We propose a model of emotion-cognition interaction based on evidence of two network models of altered brain activation in PTSD. The first is a trauma-disrupted network made up of ventrolateral PFC, dorsal anterior cingulate cortex (ACC), hippocampus, insula, and dorsomedial PFC that are differentially modulated by trauma content relative to emotional trauma-unrelated information. The trauma-disrupted network forms a subnetwork of regions within a larger, widely recognized network organized into ventral and dorsal streams for processing emotional and cognitive information that converge in the medial PFC and cingulate cortex. Models of fear learning, while not a cognitive process in the conventional sense, provide important insights into the maintenance of the core symptom clusters of PTSD such as re-experiencing and hypervigilance. Fear processing takes place within the limbic corticostriatal loop composed of threat-alerting and threat-assessing components. Understanding the disruptions in these two networks, and their effect on individuals with PTSD, will lead to an improved knowledge of the etiopathogenesis of PTSD and potential targets for both psychotherapeutic and pharmacotherapeutic interventions. PMID:23162499
Fever in trauma patients: evaluation of risk factors, including traumatic brain injury.
Bengualid, Victoria; Talari, Goutham; Rubin, David; Albaeni, Aiham; Ciubotaru, Ronald L; Berger, Judith
2015-03-01
The role of fever in trauma patients remains unclear. Fever occurs as a response to release of cytokines and prostaglandins by white blood cells. Many factors, including trauma, can trigger release of these factors. To determine whether (1) fever in the first 48 hours is related to a favorable outcome in trauma patients and (2) fever is more common in patients with head trauma. Retrospective study of trauma patients admitted to the intensive care unit for at least 2 days. Data were analyzed by using multivariate analysis. Of 162 patients studied, 40% had fever during the first 48 hours. Febrile patients had higher mortality rates than did afebrile patients. When adjusted for severity of injuries, fever did not correlate with mortality. Neither the incidence of fever in the first 48 hours after admission to the intensive care unit nor the number of days febrile in the unit differed between patients with and patients without head trauma (traumatic brain injury). About 70% of febrile patients did not have a source found for their fever. Febrile patients without an identified source of infection had lower peak white blood cell counts, lower maximum body temperature, and higher minimum platelet counts than did febrile patients who had an infectious source identified. The most common infection was pneumonia. No relationship was found between the presence of fever during the first 48 hours and mortality. Patients with traumatic brain injury did not have a higher incidence of fever than did patients without traumatic brain injury. About 30% of febrile patients had an identifiable source of infection. Further studies are needed to understand the origin and role of fever in trauma patients. ©2015 American Association of Critical-Care Nurses.
Noain, Daniela; Büchele, Fabian; Schreglmann, Sebastian R; Valko, Philipp O; Gavrilov, Yuri V; Morawska, Marta M; Imbach, Lukas L; Baumann, Christian R
2018-01-01
Although sleep-wake disturbances are prevalent and well described after traumatic brain injury, their pathophysiology remains unclear, most likely because human traumatic brain injury is a highly heterogeneous entity that makes the systematic study of sleep-wake disturbances in relation to trauma-induced histological changes a challenging task. Despite increasing interest, specific and effective treatment strategies for post-traumatic sleep-wake disturbances are still missing. With the present work, therefore, we aimed at studying acute and chronic sleep-wake disturbances by electrophysiological means, and at assessing their histological correlates after closed diffuse traumatic brain injury in rats with the ultimate goal of generating a model of post-traumatic sleep-wake disturbances and associated histopathological findings that accurately represents the human condition. We assessed sleep-wake behavior by means of standard electrophysiological recordings before and 1, 7, and 28 days after sham or traumatic brain injury procedures. Sleep-wake findings were then correlated to immunohistochemically labeled and stereologically quantified neuronal arousal systems. Compared with control animals, we found that closed diffuse traumatic brain injury caused increased sleep need one month after trauma, and sleep was more consolidated. As histological correlate, we found a reduced number of histamine immunoreactive cells in the tuberomammillary nucleus, potentially related to increased neuroinflammation. Monoaminergic and hypocretinergic neurotransmitter systems in the hypothalamus and rostral brainstem were not affected, however. These results suggest that our rat traumatic brain injury model reflects human post-traumatic sleep-wake disturbances and associated histopathological findings very accurately, thus providing a study platform for novel treatment strategies for affected patients.
Quidé, Y; O'Reilly, N; Watkeys, O J; Carr, V J; Green, M J
2018-07-01
Childhood trauma is a risk factor for psychosis. Deficits in response inhibition are common to psychosis and trauma-exposed populations, and associated brain functions may be affected by trauma exposure in psychotic disorders. We aimed to identify the influence of trauma-exposure on brain activation and functional connectivity during a response inhibition task. We used functional magnetic resonance imaging to examine brain function within regions-of-interest [left and right inferior frontal gyrus (IFG), right dorsolateral prefrontal cortex, right supplementary motor area, right inferior parietal lobule and dorsal anterior cingulate cortex], during the performance of a Go/No-Go Flanker task, in 112 clinical cases with psychotic disorders and 53 healthy controls (HCs). Among the participants, 71 clinical cases and 21 HCs reported significant levels of childhood trauma exposure, while 41 clinical cases and 32 HCs did not. In the absence of effects on response inhibition performance, childhood trauma exposure was associated with increased activation in the left IFG, and increased connectivity between the left IFG seed region and the cerebellum and calcarine sulcus, in both cases and healthy individuals. There was no main effect of psychosis, and no trauma-by-psychosis interaction for any other region-of-interest. Within the clinical sample, the effects of trauma-exposure on the left IFG activation were mediated by symptom severity. Trauma-related increases in activation of the left IFG were not associated with performance differences, or dependent on clinical diagnostic status; increased IFG functionality may represent a compensatory (overactivation) mechanism required to exert adequate inhibitory control of the motor response.
Tse, Kwong Ming; Tan, Long Bin; Lee, Shu Jin; Lim, Siak Piang; Lee, Heow Pueh
2015-06-01
In spite of anatomic proximity of the facial skeleton and cranium, there is lack of information in the literature regarding the relationship between facial and brain injuries. This study aims to correlate brain injuries with facial injuries using finite element method (FEM). Nine common impact scenarios of facial injuries are simulated with their individual stress wave propagation paths in the facial skeleton and the intracranial brain. Fractures of cranio-facial bones and intracranial injuries are evaluated based on the tolerance limits of the biomechanical parameters. General trend of maximum intracranial biomechanical parameters found in nasal bone and zygomaticomaxillary impacts indicates that severity of brain injury is highly associated with the proximity of location of impact to the brain. It is hypothesized that the midface is capable of absorbing considerable energy and protecting the brain from impact. The nasal cartilages dissipate the impact energy in the form of large scale deformation and fracture, with the vomer-ethmoid diverging stress to the "crumpling zone" of air-filled sphenoid and ethmoidal sinuses; in its most natural manner, the face protects the brain. This numerical study hopes to provide surgeons some insight in what possible brain injuries to be expected in various scenarios of facial trauma and to help in better diagnosis of unsuspected brain injury, thereby resulting in decreasing the morbidity and mortality associated with facial trauma. Copyright © 2015 Elsevier Ltd. All rights reserved.
Karstens, Aimee J; Ajilore, Olusola; Rubin, Leah H; Yang, Shaolin; Zhang, Aifeng; Leow, Alex; Kumar, Anand; Lamar, Melissa
2017-11-01
Trauma and depression are associated with brain structural alterations; their combined effects on these outcomes are unclear. We previously reported a negative effect of trauma, independent of depression, on verbal learning and memory; less is known about underlying structural associates. We investigated separate and interactive associations of trauma and depression on brain structure. Adults aged 30-89 (N = 203) evaluated for depression (D+) and trauma history (T+) using structured clinical interviews were divided into 53 D+T+, 42 D+T-, 50 D-T+, and 58 D-T-. Multivariable linear regressions examined the separate and interactive associations of depression and trauma with prefrontal and temporal lobe cortical thickness composites and hippocampal volumes adjusting for age, sex, predicted verbal IQ, comorbid anxiety, and vascular risk. Significant results informed analyses of tract-based structural connectomic measures of efficiency and centrality. Trauma, independent of depression, was associated with greater left prefrontal cortex (PFC) thickness, in particular the medial orbitofrontal cortex and pars orbitalis. A trauma × depression interaction was observed for the right PFC in age-stratified analyses: Older D + T+ had reduced PFC thickness compared with older D - T+ individuals. Regardless of age, trauma was associated with more left medial orbitofrontal cortex efficiency and less pars orbitalis centrality. In the T+ group, left pars orbitalis cortical thickness and centrality negatively correlated with verbal learning. Trauma, independent of depression, associated with altered PFC characteristics, morphologically and in terms of structural network communication and influence. Additionally, findings suggest that there may be a combined effect of trauma and depression in older adults. Copyright © 2017 John Wiley & Sons, Ltd. Copyright © 2017 John Wiley & Sons, Ltd.
Wang, Guanghuan; Yu, Xiaojun; Wang, Dian; Xu, Xiaohu; Chen, Guang; Jiang, Xuewu
2015-01-01
Background Severe trauma can cause secondary multiple organ dysfunction syndrome (MODS) and death. Oxidative stress and/or excitatory neurotoxicity are considered as the final common pathway in nerve cell injuries. Zinc is the cofactor of the redox enzyme, and the effect of the excitatory neurotoxicity is related to N-methyl-D-aspartic acid receptor (NMDAR). Material/Methods We investigated the levels of zinc and brainstem NMDAR in a rabbit model of severe trauma. Zinc and serum biochemical profiles were determined. Immunohistochemistry was used to detect brainstem N-methyl-D-aspartic acid receptor 1 (NR1), N-methyl-D-aspartic acid receptor 2A (NR2A), and N-methyl-D-aspartic acid receptor 2B (NR2B) expression. Results Brain and brainstem Zn levels increased at 12 h, but serum Zn decreased dramatically after the trauma. NR1 in the brainstem dorsal regions increased at 6 h after injury and then decreased. NR2A in the dorsal regions decreased to a plateau at 12 h after trauma. The levels of NR2B were lowest in the death group in the brainstem. Serum zinc was positively correlated with NR2A and 2B and negatively correlated with zinc in the brain. Correlations were also found between the brainstem NR2A and that of the dorsal brainstem, as well as between brainstem NR2A and changes in NR2B. There was a negative correlation between zinc and NR2A. Conclusions Severe trauma led to an acute reduction of zinc enhancing oxidative stress and the changes of NMDAR causing the neurotoxicity of the nerve cells. This may be a mechanism for the occurrence of MODS or death after trauma. PMID:26335029
Professional fighters brain health study: rationale and methods.
Bernick, Charles; Banks, Sarah; Phillips, Michael; Lowe, Mark; Shin, Wanyong; Obuchowski, Nancy; Jones, Stephen; Modic, Michael
2013-07-15
Repetitive head trauma is a risk factor for Alzheimer's disease and is the primary cause of chronic traumatic encephalopathy. However, little is known about the natural history of, and risk factors for, chronic traumatic encephalopathy or about means of early detection and intervention. The Professional Fighters Brain Health Study is a longitudinal study of active professional fighters (boxers and mixed martial artists), retired professional fighters, and controls matched for age and level of education. The main objective of the Professional Fighters Brain Health Study is to determine the relationships between measures of head trauma exposure and other potential modifiers and changes in brain imaging and neurological and behavioral function over time. The study is designed to extend over 5 years, and we anticipate enrollment of more than 400 boxers and mixed martial artists. Participants will undergo annual evaluations that include 3-tesla magnetic resonance imaging scanning, computerized cognitive assessments, speech analysis, surveys of mood and impulsivity, and blood sampling for genotyping and exploratory biomarker studies. Statistical models will be developed and validated to predict early and progressive changes in brain structure and function. A composite fight exposure index, developed as a summary measure of cumulative traumatic exposure, shows promise as a predictor of brain volumes and cognitive function.
Glymphatic system disruption as a mediator of brain trauma and chronic traumatic encephalopathy.
Sullan, Molly J; Asken, Breton M; Jaffee, Michael S; DeKosky, Steven T; Bauer, Russell M
2018-01-01
Traumatic brain injury (TBI) is an increasingly important issue among veterans, athletes and the general public. Difficulties with sleep onset and maintenance are among the most commonly reported symptoms following injury, and sleep debt is associated with increased accumulation of beta amyloid (Aβ) and phosphorylated tau (p-tau) in the interstitial space. Recent research into the glymphatic system, a lymphatic-like metabolic clearance mechanism in the central nervous system (CNS) which relies on cerebrospinal fluid (CSF), interstitial fluid (ISF), and astrocytic processes, shows that clearance is potentiated during sleep. This system is damaged in the acute phase following mTBI, in part due to re-localization of aquaporin-4 channels away from astrocytic end feet, resulting in reduced potential for waste removal. Long-term consequences of chronic dysfunction within this system in the context of repetitive brain trauma and insomnia have not been established, but potentially provide one link in the explanatory chain connecting repetitive TBI with later neurodegeneration. Current research has shown p-tau deposition in perivascular spaces and along interstitial pathways in chronic traumatic encephalopathy (CTE), pathways related to glymphatic flow; these are the main channels by which metabolic waste is cleared. This review addresses possible links between mTBI-related damage to glymphatic functioning and physiological changes found in CTE, and proposes a model for the mediating role of sleep disruption in increasing the risk for developing CTE-related pathology and subsequent clinical symptoms following repetitive brain trauma. Copyright © 2017 Elsevier Ltd. All rights reserved.
Thalamic inflammation after brain trauma is associated with thalamo-cortical white matter damage.
Scott, Gregory; Hellyer, Peter J; Ramlackhansingh, Anil F; Brooks, David J; Matthews, Paul M; Sharp, David J
2015-12-01
Traumatic brain injury can trigger chronic neuroinflammation, which may predispose to neurodegeneration. Animal models and human pathological studies demonstrate persistent inflammation in the thalamus associated with axonal injury, but this relationship has never been shown in vivo. Using [(11)C]-PK11195 positron emission tomography, a marker of microglial activation, we previously demonstrated thalamic inflammation up to 17 years after traumatic brain injury. Here, we use diffusion MRI to estimate axonal injury and show that thalamic inflammation is correlated with thalamo-cortical tract damage. These findings support a link between axonal damage and persistent inflammation after brain injury.
Lactate storm marks cerebral metabolism following brain trauma.
Lama, Sanju; Auer, Roland N; Tyson, Randy; Gallagher, Clare N; Tomanek, Boguslaw; Sutherland, Garnette R
2014-07-18
Brain metabolism is thought to be maintained by neuronal-glial metabolic coupling. Glia take up glutamate from the synaptic cleft for conversion into glutamine, triggering glial glycolysis and lactate production. This lactate is shuttled into neurons and further metabolized. The origin and role of lactate in severe traumatic brain injury (TBI) remains controversial. Using a modified weight drop model of severe TBI and magnetic resonance (MR) spectroscopy with infusion of (13)C-labeled glucose, lactate, and acetate, the present study investigated the possibility that neuronal-glial metabolism is uncoupled following severe TBI. Histopathology of the model showed severe brain injury with subarachnoid and hemorrhage together with glial cell activation and positive staining for Tau at 90 min post-trauma. High resolution MR spectroscopy of brain metabolites revealed significant labeling of lactate at C-3 and C-2 irrespective of the infused substrates. Increased (13)C-labeled lactate in all study groups in the absence of ischemia implied activated astrocytic glycolysis and production of lactate with failure of neuronal uptake (i.e. a loss of glial sensing for glutamate). The early increase in extracellular lactate in severe TBI with the injured neurons rendered unable to pick it up probably contributes to a rapid progression toward irreversible injury and pan-necrosis. Hence, a method to detect and scavenge the excess extracellular lactate on site or early following severe TBI may be a potential primary therapeutic measure. © 2014 by The American Society for Biochemistry and Molecular Biology, Inc.
Golub, Y; Canneva, F; Funke, R; Frey, S; Distler, J; von Hörsten, S; Freitag, C M; Kratz, O; Moll, G H; Solati, J
2016-11-01
Maternal posttraumatic stress disorder (PTSD) following trauma exposure during pregnancy is associated with an increased risk of affective disorders in children. To investigate the mechanisms by which prenatal trauma and/or maternal PTSD affect brain development and behavior we established a mouse model of prenatal traumatic (PT) experience based on the application of an electric foot shock to C57Bl/6N female mice on the gestational day 12 during their pregnancy. The model is based on a previously validated animal model of PTSD. We found high anxiety levels and poor maternal care along with reduced serum prolactin and increased corticosterone levels in dams following maternal trauma (MT). PT-pups were born smaller and stayed smaller throughout their life. We show increased time and frequency of ultrasonic calls in PT-pups when separated from the mothers on the postnatal day (PND) 9. Cross-fostering experiments reveal lower anxiety levels in PT pups raised by healthy mothers as compared to trauma-naive pups raised by MT-dams. Importantly, the combination of prenatal trauma and being raised by a traumatized mother leads to: (1) the highest corticosterone levels in pups, (2) longest USV-call time and (3) highest anxiety levels in comparison to other experimental groups. Our data indicates a distinct change in maternal care following MT which is possibly associated with trauma-induced decrease in prolactin levels. Furthermore, we show that maternal behavior is crucial for the development of the offspring anxiety and specific aspects in maternal care overwrite to a significant extend the effects of in utero and postnatal environment. © 2016 Wiley Periodicals, Inc. Develop Neurobiol 76: 1254-1265, 2016. © 2016 Wiley Periodicals, Inc.
Operation Brain Trauma Therapy
2016-12-01
either clinical trials in TBI if shown to be highly effective across OBTT, or tested in a precision medicine TBI phenotype (such as contusion) based...clinical trial if shown to be potently effective in one of the models in OBTT (i.e., a model that mimicked a specific clinical TBI phenotype). In... effective drug seen thus far in primary screening albeit with benefit highly model dependent, largely restricted to the CCI model. This suggests
Jochems, D; Leenen, L P H; Hietbrink, F; Houwert, R M; van Wessem, K J P
2018-05-23
Central nervous system (CNS) related injuries and exsanguination have been the most common causes of death in trauma for decades. Despite improvements in haemorrhage control in recent years exsanguination is still a major cause of death. We conducted a prospective database study to investigate the current incidence of haemorrhage related mortality. A prospective database study of all trauma patients admitted to an urban major trauma centre between January 2007 and December 2016 was conducted. All in-hospital trauma deaths were included. Cause of death was reviewed by a panel of trauma surgeons. Patients who were dead on arrival were excluded. Trends in demographics and outcome were analysed per year. Further, 2 time periods (2007-2012 and 2013-2016) were selected representing periods before and after implementation of haemostatic resuscitation and damage control procedures in our hospital to analyse cause of death into detail. 11,553 trauma patients were admitted, 596 patients (5.2%) died. Mean age of deceased patients was 61 years and 61% were male. Mechanism of injury (MOI) was blunt in 98% of cases. Mean ISS was 28 with head injury the most predominant injury (mean AIS head 3.4). There was no statistically significant difference in sex and MOI over time. Even though deceased patients were older in 2016 compared to 2007 (67 vs. 46 years, p < 0.001), mortality was lower in later years (p = 0.02). CNS related injury was the main cause of death in the whole decade; 58% of patients died of CNS in 2007-2012 compared to 76% of patients in 2013-2016 (p = 0.001). In 2007-2012 9% died of exsanguination compared to 3% in 2013-2016 (p = 0.001). In this cohort in a major trauma centre death by exsanguination has decreased to 3% of trauma deaths. The proportion of traumatic brain injury has increased over time and has become the most common cause of death in blunt trauma. Besides on-going prevention of brain injury future studies should focus on treatment strategies preventing secondary damage of the brain once the injury has occurred. Copyright © 2018 Elsevier Ltd. All rights reserved.
Gutierrez, E; Huang, Y; Haglid, K; Bao, F; Hansson, H A; Hamberger, A; Viano, D
2001-03-01
Rapid head rotation is a major cause of brain damage in automobile crashes and falls. This report details a new model for rotational acceleration about the center of mass of the rabbit head. This allows the study of brain injury without translational acceleration of the head. Impact from a pneumatic cylinder was transferred to the skull surface to cause a half-sine peak acceleration of 2.1 x 10(5) rad/s2 and 0.96-ms pulse duration. Extensive subarachnoid hemorrhages and small focal bleedings were observed in the brain tissue. A pronounced reactive astrogliosis was found 8-14 days after trauma, both as networks around the focal hemorrhages and more diffusely in several brain regions. Astrocytosis was prominent in the gray matter of the cerebral cortex, layers II-V, and in the granule cell layer and around the axons of the pyramidal neurons in the hippocampus. The nuclei of cranial nerves, such as the hypoglossal and facial nerves, also showed intense astrocytosis. The new model allows study of brain injuries from head rotation in the absence of translational influences.
Head trauma in the cat: 2. assessment and management of traumatic brain injury.
Garosi, Laurent; Adamantos, Sophie
2011-11-01
Feline trauma patients are commonly seen in general practice and frequently have sustained some degree of brain injury. Cats with traumatic brain injuries may have a variety of clinical signs, ranging from minor neurological deficits to life-threatening neurological impairment. Appropriate management depends on prompt and accurate patient assessment, and an understanding of the pathophysiology of brain injury. The most important consideration in managing these patients is maintenance of cerebral perfusion and oxygenation. For cats with severe head injury requiring decompressive surgery, early intervention is critical. There is a limited clinical evidence base to support the treatment of traumatic brain injury in cats, despite its relative frequency in general practice. Appropriate therapy is, therefore, controversial in veterinary medicine and mostly based on experimental studies or human head trauma studies. This review, which sets out to describe the specific approach to diagnosis and management of traumatic brain injury in cats, draws on the current evidence, as far as it exists, as well as the authors' clinical experience. Copyright © 2011 ISFM and AAFP. Published by Elsevier Ltd. All rights reserved.
Management and outcome of mechanically ventilated neurologic patients.
Pelosi, Paolo; Ferguson, Niall D; Frutos-Vivar, Fernando; Anzueto, Antonio; Putensen, Christian; Raymondos, Konstantinos; Apezteguia, Carlos; Desmery, Pablo; Hurtado, Javier; Abroug, Fekri; Elizalde, José; Tomicic, Vinko; Cakar, Nahit; Gonzalez, Marco; Arabi, Yaseen; Moreno, Rui; Esteban, Andres
2011-06-01
To describe and compare characteristics, ventilatory practices, and associated outcomes among mechanically ventilated patients with different types of brain injury and between neurologic and nonneurologic patients. Secondary analysis of a prospective, observational, and multicenter study on mechanical ventilation. Three hundred forty-nine intensive care units from 23 countries. We included 552 mechanically ventilated neurologic patients (362 patients with stroke and 190 patients with brain trauma). For comparison we used a control group of 4,030 mixed patients who were ventilated for nonneurologic reasons. None. We collected demographics, ventilatory settings, organ failures, and complications arising during ventilation and outcomes. Multivariate logistic regression analysis was performed with intensive care unit mortality as the dependent variable. At admission, a Glasgow Coma Scale score ≤8 was observed in 68% of the stroke, 77% of the brain trauma, and 29% of the nonneurologic patients. Modes of ventilation and use of a lung-protective strategy within the first week of mechanical ventilation were similar between groups. In comparison with nonneurologic patients, patients with neurologic disease developed fewer complications over the course of mechanical ventilation with the exception of a higher rate of ventilator-associated pneumonia in the brain trauma cohort. Neurologic patients showed higher rates of tracheotomy and longer duration of mechanical ventilation. Mortality in the intensive care unit was significantly (p < .001) higher in patients with stroke (45%) than in brain trauma (29%) and nonneurologic disease (30%). Factors associated with mortality were: stroke (in comparison to brain trauma), Glasgow Coma Scale score on day 1, and severity at admission in the intensive care unit. In our study, one of every five mechanically ventilated patients received this therapy as a result of a neurologic disease. This cohort of patients showed a higher mortality rate than nonneurologic patients despite a lower incidence of extracerebral organ dysfunction.
Chronic traumatic encephalopathy.
Omalu, Bennet
2014-01-01
Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative syndrome, which is caused by single, episodic, or repetitive blunt force impacts to the head and transfer of acceleration-deceleration forces to the brain. CTE presents clinically as a composite syndrome of mood disorders and behavioral and cognitive impairment, with or without sensorimotor impairment. Symptoms of CTE may begin with persistent symptoms of acute traumatic brain injury (TBI) following a documented episode of brain trauma or after a latent period that may range from days to weeks to months and years, up to 40 years following a documented episode of brain trauma or cessation of repetitive TBI. Posttraumatic encephalopathy is distinct from CTE, can be comorbid with CTE, and is a clinicopathologic syndrome induced by focal and/or diffuse, gross and/or microscopic destruction of brain tissue following brain trauma. The brain of a CTE sufferer may appear grossly unremarkable, but shows microscopic evidence of primary and secondary proteinopathies. The primary proteinopathy of CTE is tauopathy, while secondary proteinopathies may include, but are not limited to, amyloidopathy and TDP proteinopathy. Reported prevalence rates of CTE in cohorts exposed to TBI ranges from 3 to 80% across age groups. © 2014 S. Karger AG, Basel.
Major trauma: the unseen financial burden to trauma centres, a descriptive multicentre analysis.
Curtis, Kate; Lam, Mary; Mitchell, Rebecca; Dickson, Cara; McDonnell, Karon
2014-02-01
This research examines the existing funding model for in-hospital trauma patient episodes in New South Wales (NSW), Australia and identifies factors that cause above-average treatment costs. Accurate information on the treatment costs of injury is needed to guide health-funding strategy and prevent inadvertent underfunding of specialist trauma centres, which treat a high trauma casemix. Admitted trauma patient data provided by 12 trauma centres were linked with financial data for 2008-09. Actual costs incurred by each hospital were compared with state-wide Australian Refined Diagnostic Related Groups (AR-DRG) average costs. Patient episodes where actual cost was higher than AR-DRG cost allocation were examined. There were 16693 patients at a total cost of AU$178.7million. The total costs incurred by trauma centres were $14.7million above the NSW peer-group average cost estimates. There were 10 AR-DRG where the total cost variance was greater than $500000. The AR-DRG with the largest proportion of patients were the upper limb injury categories, many of whom had multiple body regions injured and/or a traumatic brain injury (P<0.001). AR-DRG classifications do not adequately describe the trauma patient episode and are not commensurate with the expense of trauma treatment. A revision of AR-DRG used for trauma is needed. WHAT IS KNOWN ABOUT THIS TOPIC? Severely injured trauma patients often have multiple injuries, in more than one body region and the determination of appropriate AR-DRG can be difficult. Pilot research suggests that the AR-DRG do not accurately represent the care that is required for these patients. WHAT DOES THIS PAPER ADD? This is the first multicentre analysis of treatment costs and coding variance for major trauma in Australia. This research identifies the limitations of the current AR-DRGS and those that are particularly problematic. The value of linking trauma registry and financial data within each trauma centre is demonstrated. WHAT ARE THE IMPLICATIONS FOR PRACTITIONERS? Further work should be conducted between trauma services, clinical coding and finance departments to improve the accuracy of clinical coding, review funding models and ensure that AR-DRG allocation is commensurate with the expense of trauma treatment.
Gene-environment interaction of ApoE genotype and combat exposure on PTSD.
Lyons, Michael J; Genderson, Margo; Grant, Michael D; Logue, Mark; Zink, Tyler; McKenzie, Ruth; Franz, Carol E; Panizzon, Matthew; Lohr, James B; Jerskey, Beth; Kremen, William S
2013-10-01
Factors determining who develops PTSD following trauma are not well understood. The €4 allele of the apolipoprotein E (apoE) gene is associated with dementia and unfavorable outcome following brain insult. PTSD is also associated with dementia. Given evidence that psychological trauma adversely affects the brain, we hypothesized that the apoE genotype moderates effects of psychological trauma on PTSD pathogenesis. To investigate the moderation of the relationship between PTSD symptoms and combat exposure, we used 172 participants with combat trauma sustained during the Vietnam War. PTSD symptoms were the dependent variable and number of combat experiences, apoE genotype, and the combat experiences × apoE genotype interaction were predictors. We also examined the outcome of a diagnosis of PTSD (n = 39) versus no PTSD diagnosis (n = 131). The combat × apoE genotype interaction was significant for both PTSD symptoms (P = .014) and PTSD diagnosis (P = .009). ApoE genotype moderates the relationship between combat exposure and PTSD symptoms. Although the pathophysiology of PTSD is not well understood, the €4 allele is related to reduced resilience of the brain to insult. Our results are consistent with the €4 allele influencing the effects of psychological trauma on the brain, thereby affecting the risk of PTSD. © 2013 Wiley Periodicals, Inc.
Magnetic Resonance, Functional (fMRI) -- Brain
... thought, speech, movement and sensation, which is called brain mapping. help assess the effects of stroke, trauma, or degenerative disease (such as Alzheimer's) on brain function. monitor the growth and function of brain ...
Ojo, Joseph O.; Greenberg, M. Banks; Leary, Paige; Mouzon, Benoit; Bachmeier, Corbin; Mullan, Michael; Diamond, David M.; Crawford, Fiona
2014-01-01
Co-morbid mild traumatic brain injury (mTBI) and post-traumatic stress disorder (PTSD) has become the signature disorder for returning combat veterans. The clinical heterogeneity and overlapping symptomatology of mTBI and PTSD underscore the need to develop a preclinical model that will enable the characterization of unique and overlapping features and allow discrimination between both disorders. This study details the development and implementation of a novel experimental paradigm for PTSD and combined PTSD-mTBI. The PTSD paradigm involved exposure to a danger-related predator odor under repeated restraint over a 21 day period and a physical trauma (inescapable footshock). We administered this paradigm alone, or in combination with a previously established mTBI model. We report outcomes of behavioral, pathological and biochemical profiles at an acute timepoint. PTSD animals demonstrated recall of traumatic memories, anxiety and an impaired social behavior. In both mTBI and combination groups there was a pattern of disinhibitory like behavior. mTBI abrogated both contextual fear and impairments in social behavior seen in PTSD animals. No major impairment in spatial memory was observed in any group. Examination of neuroendocrine and neuroimmune responses in plasma revealed a trend toward increase in corticosterone in PTSD and combination groups, and an apparent increase in Th1 and Th17 proinflammatory cytokine(s) in the PTSD only and mTBI only groups respectively. In the brain there were no gross neuropathological changes in any groups. We observed that mTBI on a background of repeated trauma exposure resulted in an augmentation of axonal injury and inflammatory markers, neurofilament L and ICAM-1 respectively. Our observations thus far suggest that this novel stress-trauma-related paradigm may be a useful model for investigating further the overlapping and distinct spatio-temporal and behavioral/biochemical relationship between mTBI and PTSD experienced by combat veterans. PMID:25002839
Retroclival collections associated with abusive head trauma in children.
Silvera, V Michelle; Danehy, Amy R; Newton, Alice W; Stamoulis, Catherine; Carducci, Chiara; Grant, P Ellen; Wilson, Celeste R; Kleinman, Paul K
2014-12-01
Retroclival collections are rare lesions reported almost exclusively in children and strongly associated with trauma. We examine the incidence and imaging characteristics of retroclival collections in young children with abusive head trauma. We conducted a database search to identify children with abusive head trauma ≤ 3 years of age with brain imaging performed between 2007 and 2013. Clinical data and brain images of 65 children were analyzed. Retroclival collections were identified in 21 of 65 (32%) children. Ten (48%) were subdural, 3 (14%) epidural, 2 (10%) both, and 6 (28%) indeterminate. Only 8 of 21 retroclival collections were identifiable on CT and most were low or intermediate in attenuation. Eighteen of 21 retroclival collections were identifiable on MRI: 3 followed cerebral spinal fluid in signal intensity and 15 were bloody/proteinaceous. Additionally, 2 retroclival collections demonstrated a fluid-fluid level and 2 enhanced in the 5 children who received contrast material. Sagittal T1-weighted images, sagittal fluid-sensitive sequences, and axial FLAIR (fluid-attenuated inversion recovery) images showed the retroclival collections best. Retroclival collections were significantly correlated with supratentorial and posterior fossa subdural hematomas and were not statistically correlated with skull fracture or parenchymal brain injury. Retroclival collections, previously considered rare lesions strongly associated with accidental injury, were commonly identified in this cohort of children with abusive head trauma, suggesting that retroclival collections are an important component of the imaging spectrum in abusive head trauma. Retroclival collections were better demonstrated on MRI than CT, were commonly identified in conjunction with intracranial subdural hematomas, and were not significantly correlated with the severity of brain injury or with skull fractures.
Leute, P J F; Moos, R N M; Osterhoff, G; Volbracht, J; Simmen, H-P; Ciritsis, B D
2015-06-01
Alcohol abuse has been associated with aggressive behavior and interpersonal violence. Aim of the study was to investigate the role of alcohol consumption in a population of young adults with mild traumatic brain injuries and the attendant epidemiological circumstances of the trauma. All cases of mild traumatic brain injury among young adults under 30 with an injury severity score <16 who were treated as inpatients between 2009 and 2012 at our trauma center were analyzed with regard to the influence of alcohol consumption by multiple regression analysis. 793 patients, 560 men, and 233 women were included. The age median was 23 (range 14-30). Alcohol consumption was present in 302 cases. Most common trauma mechanism was interpersonal violence followed by simple falls on even ground. Alcohol consumption was present more often in men, unemployed men, patients who had interpersonal violence as a trauma mechanism, and in patients who were admitted to the hospital at weekends or during night time. It also increased the odds ratio to suffer concomitant injuries, open wounds, or fractures independently from the trauma mechanism. Length of hospital stay or incapacity to work did not increase with alcohol consumption. Among young adults men and unemployed men have a higher statistical probability to have consumed alcohol prior to suffering mild traumatic brain injury. The most common trauma mechanism in this age group is interpersonal violence and occurs more often in patients who have consumed alcohol. Alcohol consumption and interpersonal violence increase the odds ratio for concomitant injuries, open wounds, and fractures independently from another.
Opendak, Maya; Gould, Elizabeth; Sullivan, Regina
2017-01-01
Animals, including humans, require a highly coordinated and flexible system of social behavior and threat evaluation. However, trauma can disrupt this system, with the amygdala implicated as a mediator of these impairments in behavior. Recent evidence has further highlighted the context of infant trauma as a critical variable in determining its immediate and enduring consequences, with trauma experienced from an attachment figure, such as occurs in cases of caregiver-child maltreatment, as particularly detrimental. This review focuses on the unique role of caregiver presence during early-life trauma in programming deficits in social behavior and threat processing. Using data primarily from rodent models, we describe the interaction between trauma and attachment during a sensitive period in early life, which highlights the role of the caregiver’s presence in engagement of attachment brain circuitry and suppressing threat processing by the amygdala. These data suggest that trauma experienced directly from an abusive caregiver and trauma experienced in the presence of caregiver cues produce similar neurobehavioral deficits, which are unique from those resulting from trauma alone. We go on to integrate this information into social experience throughout the lifespan, including consequences for complex scenarios, such as dominance hierarchy formation and maintenance. PMID:28254197
Lasting retinal injury in a mouse model of blast-induced trauma
USDA-ARS?s Scientific Manuscript database
Traumatic brain injury (TBI) due to blast exposure is currently the most prevalent of war injuries. While secondary ocular blast injuries due to flying debris are more common, primary ocular blast exposure has been reported among survivors of explosions, but with limited understanding of the resulti...
Feasibility Study of Pharmacological Treatment to Reduce Morbidity and Mortality after Brain Injury.
1987-05-01
preliminary study of human stroke patients with hemiparesis showed an acceleration of recovery cumpared to placebo controls (15). The most frequent...cause of permanent disability is cerebral trauma (61) and a model of cortical cotusion producing hemiparesis in rats has been developed (21). The purpose
In-Vitro Approaches for Studying Blast-Induced Traumatic Brain Injury
Chen, Yung Chia; Smith, Douglas H.
2009-01-01
Abstract Traumatic brain injury caused by explosive or blast events is currently divided into four phases: primary, secondary, tertiary, and quaternary blast injury. These phases of blast-induced traumatic brain injury (bTBI) are biomechanically distinct, and can be modeled in both in-vivo and in-vitro systems. The purpose of this review is to consider the mechanical phases of bTBI, how these phases are reproduced with in-vitro models, and to review findings from these models to assess how each phase of bTBI can be examined in more detail. Highlighted are some important gaps in the literature that may be addressed in the future to better identify the exact contributing mechanisms for bTBI. These in-vitro models, viewed in combination with in-vivo models and clinical studies, can be used to assess both the mechanisms and possible treatments for this type of trauma. PMID:19397424
Rebooting the Brain: Using Early Childhood Education to Heal Trauma from Abuse and Neglect
ERIC Educational Resources Information Center
McLintock, Ben
2011-01-01
Abused and neglected children live in a world that usually includes some sort of violence, chaos, and tremendous physical and mental stress. This toxic environment wreaks havoc on a child's developing brain. This article discusses how to use early childhood education to heal trauma from abuse and neglect. It shares the story of two children, Bryce…
Targeting Microglia to Prevent Post-Traumatic Epilepsy
2012-07-01
long-term effects of nigral lipopolysaccharide administration on dopaminergic dysfunction and glial cell activation. Eur J Neurosci 22 :317-330...attenuating damaging effects of hyperexcitability in the brain induced by inflammation resulting from glial cell immune responses to trauma. We are...damaging effects of hyperexcitability in the brain induced by inflammation resulting from glial cell immune responses to trauma. We are exploring two
Effects of psychological and biomechanical trauma on brain and behavior
McAllister, Thomas W.; Stein, Murray B.
2011-01-01
The current conflicts in Iraq and Afghanistan have resulted in a large cohort of military personnel exposed to combat-related psychological trauma as well as biomechanical trauma, including proximity to blast events. Historically, the long-term effects of both types of trauma have been viewed as having different neural substrates, with some controversy over the proper attribution of such symptoms evident after each of the major conflicts of the last century. Recently, great effort has been directed toward distinguishing which neuropsychiatric sequelae are due to which type of trauma. Of interest, however, is that the chronic effects of exposure to either process are associated with a significant overlap in clinical symptoms. Furthermore, similar brain regions are vulnerable to the effects of either psychological or biomechanical trauma, raising the possibility that shared mechanisms may underlie the clinically observed overlap in symptom profile. This paper reviews the literature on the neural substrate of biomechanical and psychological injury and discusses the implications for evaluation and treatment of the neuropsychiatric sequelae of these processes. PMID:20955325
The Gut Microbiome and Mental Health: Implications for Anxiety- and Trauma-Related Disorders.
Malan-Muller, Stefanie; Valles-Colomer, Mireia; Raes, Jeroen; Lowry, Christopher A; Seedat, Soraya; Hemmings, Sian M J
2018-02-01
Biological psychiatry research has long focused on the brain in elucidating the neurobiological mechanisms of anxiety- and trauma-related disorders. This review challenges this assumption and suggests that the gut microbiome and its interactome also deserve attention to understand brain disorders and develop innovative treatments and diagnostics in the 21st century. The recent, in-depth characterization of the human microbiome spurred a paradigm shift in human health and disease. Animal models strongly suggest a role for the gut microbiome in anxiety- and trauma-related disorders. The microbiota-gut-brain (MGB) axis sits at the epicenter of this new approach to mental health. The microbiome plays an important role in the programming of the hypothalamic-pituitary-adrenal (HPA) axis early in life, and stress reactivity over the life span. In this review, we highlight emerging findings of microbiome research in psychiatric disorders, focusing on anxiety- and trauma-related disorders specifically, and discuss the gut microbiome as a potential therapeutic target. 16S rRNA sequencing has enabled researchers to investigate and compare microbial composition between individuals. The functional microbiome can be studied using methods involving metagenomics, metatranscriptomics, metaproteomics, and metabolomics, as discussed in the present review. Other factors that shape the gut microbiome should be considered to obtain a holistic view of the factors at play in the complex interactome linked to the MGB. In all, we underscore the importance of microbiome science, and gut microbiota in particular, as emerging critical players in mental illness and maintenance of mental health. This new frontier of biological psychiatry and postgenomic medicine should be embraced by the mental health community as it plays an ever-increasing transformative role in integrative and holistic health research in the next decade.
Popkirov, Stoyan; Carson, Alan J; Stone, Jon
2018-04-14
A history of head injury is common in patients with psychogenic nonepileptic seizures (PNES). This association has so far been interpreted as either spurious or psychologically mediated. Biased recall and misattribution could foster illness beliefs about brain damage that promote symptom production. Furthermore, the emotional impact of head injury could induce long-term changes in stress responsivity. Lastly, maladaptive cognitive-behavioural processes involving symptom modelling and aversive conditioning, known to play a role in functional neurological disorders, could contribute to the development of PNES after head trauma. Lesional effects of head injury, on the other hand, remain unexplored in the context of PNES. However, even mild traumatic brain injury without structural MRI abnormalities on routine imaging can lead to disruptions of network connectivity that correlate with short-term cognitive impairments and psychiatric symptoms. Since alterations in global functional connectivity have been demonstrated in PNES patients using imaging and electroencephalography, we hypothesize that, in some patients, TBI and the associated disruption of long-range association fibres could contribute to the individual propensity for dissociative experiences in general and PNES in particular. This possibility is explored in the context of new cognitive-behavioural models of PNES pathogenesis, and the concept of a "dissociogenic" brain lesion is introduced. Copyright © 2018 British Epilepsy Association. Published by Elsevier Ltd. All rights reserved.
Hu, Yi; Wu, Yue; Tian, Kunlun; Lan, Dan; Chen, Xiangyun; Xue, Mingying; Liu, Liangming; Li, Tao
2015-05-01
Traumatic brain injury (TBI) is often associated with uncontrolled hemorrhagic shock (UHS), which contributes significantly to the mortality of severe trauma. Studies have demonstrated that permissive hypotension resuscitation improves the survival for uncontrolled hemorrhage. What the ideal target mean arterial pressure (MAP) is for TBI with UHS remains unclear. With the rat model of TBI in combination with UHS, we investigated the effects of a series of target resuscitation pressures (MAP from 50-90 mm Hg) on animal survival, brain perfusion, and organ function before hemorrhage controlled. Rats in 50-, 60-, and 70-mm Hg target MAP groups had less blood loss and less fluid requirement, a better vital organ including mitochondrial function and better cerebral blood flow, and animal survival (8, 6, and 7 of 10, respectively) than 80- and 90-mm Hg groups. The 70-mm Hg group had a better cerebral blood flow and cerebral mitochondrial function than in 50- and 60-mm Hg groups. In contrast, 80- and 90-mm Hg groups resulted in an excessive hemodilution, a decreased blood flow, an increased brain water content, and more severe cerebral edema. A 50-mm Hg target MAP is not suitable for the resuscitation of TBI combined with UHS. A 70 mm Hg of MAP is the ideal target resuscitation pressure for this trauma, which can keep sufficient perfusion to the brain and keep good organ function including cerebral mitochondrial function. Copyright © 2015 Elsevier Inc. All rights reserved.
Baerg, Joanne; Thirumoorthi, Arul; Hazboun, Rajaie; Vannix, Rosemary; Krafft, Paul; Zouros, Alexander
2017-11-01
The aim of the study was to compare the cervical spine (c-spine) pattern of injury and outcomes in children below 3 y with a head injury from confirmed inflicted versus accidental trauma. After Institutional Review Board approval, data were prospectively collected between July 2011 and January 2016. Inclusion criteria were age below 3 y, a loss of consciousness, and any one of the following initial head computed tomography (CT) findings (subdural hematoma, intraventricular, intraparenchymal, subarachnoid hemorrhage, or cerebral edema). A protocol of brain and neck magnetic resonance imaging and magnetic resonance angiography was instituted. Brain and neck imaging results, clinical variables, and outcomes were recorded. Data were compared by t-test for continuous and Fisher exact test for categorical variables. 73 children were identified, 52 (71%) with inflicted and 21 (29%) with accidental trauma. The median age was 11 mo; (range: 1-35 mo). Ten (14%) had c-spine injuries, 7/52 (13%) inflicted, and 3/21 (14%) accidental. The mechanism was shaking for all inflicted and motor vehicle accident or pedestrian struck for accidental c-spine injuries. The inflicted group were significantly younger (P = 0.03), had higher Injury Severity Scores (P = 0.02), subdural hematomas (P = 0.03), fractures (P = 0.03), retinal hemorrhages (P = 0.02), brain infarcts (P = 0.01), and required cardiopulmonary resuscitation (P = 0.01). Seven with inflicted trauma died from brain injury (9.5%), one had atlanto-occipital dissociation. Six mortalities (86%) had no c-spine injury. Six with inflicted c-spine injuries survived with neurologic impairment, whereas three with accidental survived without disability, including one atlanto-occipital dissociation. Compared to accidental trauma, young children with inflicted c-spine injuries have more multisystem trauma, long-term disability from brain injury, and an injury pattern consistent with shaking. Copyright © 2017 Elsevier Inc. All rights reserved.
Clinical review: Statins and trauma - a systematic review
2013-01-01
Statins, in addition to their lipid-lowering properties, have anti-inflammatory actions. The aim of this review is to evaluate the effect of pre-injury statin use, and statin treatment following injury. MEDLINE, EMBASE, and CENTRAL databases were searched to January 2012 for randomised and observational studies of statins in trauma patients in general, and in patients who have suffered traumatic brain injury, burns, and fractures. Of 985 identified citations, 7 (4 observational studies and 3 randomised controlled trials (RCTs)) met the inclusion criteria. Two studies (both observational) were concerned with trauma patients in general, two with patients who had suffered traumatic brain injury (one observational, one RCT), two with burns patients (one observational, one RCT), and one with fracture healing (RCT). Two of the RCTs relied on surrogate outcome measures. The observational studies were deemed to be at high risk of confounding, and the RCTs at high risk of bias. Three of the observational studies suggested improvements in a number of clinical outcomes in patients taking statins prior to injury (mortality, infection, and septic shock in burns patients; mortality in trauma patients in general; mortality in brain injured patients) whereas one, also of trauma patients in general, showed no difference in mortality or infection, and an increased risk of multi-organ failure. Two of three RCTs on statin treatment in burns patients and brain injured patients showed improvements in E-selectin levels and cognitive function. The third, of patients with radial fractures, showed no acceleration in fracture union. In conclusion, there is some evidence that pre-injury statin use and post-injury statin treatment may have a beneficial effect in patients who have suffered general trauma, traumatic brain injury, and burns. However, these studies are at high risk of confounding and bias, and should be regarded as 'hypothesisgenerating'. A well-designed RCT is required to determine the therapeutic efficacy in improving outcomes in this patient population. PMID:23751018
Types of traumatic brain injury and regional cerebral blood flow assessed by 99mTc-HMPAO SPECT.
Yamakami, I; Yamaura, A; Isobe, K
1993-01-01
To investigate the relationship between focal and diffuse traumatic brain injury (TBI) and regional cerebral blood flow (rCBF), rCBF changes in the first 24 hours post-trauma were studied in 12 severe head trauma patients using single photon emission computed tomography (SPECT) with 99mtechnetium-hexamethyl propyleneamine oxime. Patients were classified as focal or diffuse TBI based on x-ray computed tomographic (X-CT) findings and neurological signs. In six patients with focal damage, SPECT demonstrated 1) perfusion defect (focal severe ischemia) in the brain region larger than the brain contusion by X-CT, 2) hypoperfusion (focal CBF reduction) in the brain region without abnormality by X-CT, and 3) localized hyperperfusion (focal CBF increase) in the surgically decompressed brain after decompressive craniectomy. Focal damage may be associated with a heterogeneous CBF change by causing various focal CBF derangements. In six patients with diffuse damage, SPECT revealed hypoperfusion in only one patient. Diffuse damage may be associated with a homogeneous CBF change by rarely causing focal CBF derangements. The type of TBI, focal or diffuse, determines the type of CBF change, heterogeneous or homogeneous, in the acute severe head trauma patient.
Bader, Mary Kay; Stutzman, Sonja E; Palmer, Sylvain; Nwagwu, Chiedozie I; Goodman, Gary; Whittaker, Margie; Olson, Daiwai M
2014-12-01
The Brain Trauma Foundation has developed treatment guidelines for the care of patients with acute traumatic brain injury. However, a method to provide broad acceptance and application of these guidelines has not been published. To describe methods for the development, funding, and continued educational efforts of the Adam Williams Initiative; the experiences from the first 10 years may serve as a template for hospitals and nurses that seek to engage in long-term quality improvement collaborations with foundations and/or industry. In 2004, the nonprofit Adam Williams Initiative was established with the goal of providing education and resources that would encourage hospitals across the United States to incorporate the Brain Trauma Foundation's guidelines into practice. Between 2004 and 2014, 37 hospitals have been funded by the Adam Williams Initiative and have had staff members participate in an immersion experience at Mission Hospital (Mission Viejo, California) during which team members received both didactic and hands-on education in the care of traumatic brain injury. Carefully cultivated relationships and relentless teamwork have contributed to successful implementation of the Brain Trauma Foundation's guidelines in US hospitals. ©2014 American Association of Critical-Care Nurses.
Hensler, T; Sauerland, S; Riess, P; Hess, S; Helling, H J; Andermahr, J; Bouillon, B; Neugebauer, E A
2000-10-01
Besides interleukin (IL)-10, accumulating evidence from in vitro studies has indicated a strong antiinflammatory capacity for IL-13. A prospective clinical study was undertaken to assess the influence of additional brain injury on systemic IL-10 and IL-13 levels as markers for the antiinflammatory state in trauma patients. The course of IL-10 and IL-13 plasma levels from 32 patients with an isolated severe head trauma (SHT), 50 patients with multiple injuries and additional SHT and 39 patients with multiple injuries without SHT was detected using ELISA-technique. Blood samples from 37 healthy blood donors were analysed for control. IL-10 levels were significantly elevated in all 3 injury groups within 3 h after trauma. The lowest initial release was detected in patients with an isolated SHT (Injury severity score; ISS: 18.1 +/- 5.6). No difference could be demonstrated for the IL-10 levels from multiple injured patients with (ISS: 35.3 +/- 9.6) or without additional SHT (ISS: 25.5 +/- 11.7), though there were relevant differences in the ISS. In contrast, the IL-13 plasma levels were not elevated systemically after trauma. IL-10 but not IL-13 is a detectable antiinflammatory marker in trauma patients with or without brain injury and to a minor degree in patients with an isolated SHT.
Grüßer, Linda; Blaumeiser-Debarry, Rosmarie; Krings, Matthias; Kremer, Benedikt; Höllig, Anke; Rossaint, Rolf; Coburn, Mark
2017-01-01
Despite years of research, treatment of traumatic brain injury (TBI) remains challenging. Considerable data exists that some volatile anesthetics might be neuroprotective. However, several studies have also revealed a rather neurotoxic profile of anesthetics. In this study, we investigated the effects of argon 50%, desflurane 6% and their combination in an in vitro TBI model with incubation times similar to narcotic time slots in a daily clinical routine. Organotypic hippocampal brain slices of 5- to 7-day-old mice were cultivated for 14 days before TBI was performed. Slices were eventually incubated for 2 hours in an atmosphere containing no anesthetic gas, argon 50% or desflurane 6% or both. Trauma intensity was evaluated via fluorescent imagery. Our results show that neither argon 50% nor desflurane 6% nor their combination could significantly reduce the trauma intensity in comparison to the standard atmosphere. However, in comparison to desflurane 6%, argon 50% displayed a rather neuroprotective profile within the first 2 hours after a focal mechanical trauma ( P = 0.015). A 2-hour incubation in an atmosphere containing both gases, argon 50% and desflurane 6%, did not result in significant effects in comparison to the argon 50% group or the desflurane 6% group. Our findings demonstrate that within a 2-hour incubation time neither argon nor desflurane could affect propidium iodide-detectable cell death in an in vitro TBI model in comparison to the standard atmosphere, although cell death was less with argon 50% than with desflurane 6%. The results show that within this short time period processes concerning the development of secondary injury are already taking place and may be manipulated by argon.
Acute respiratory distress syndrome in blunt trauma: identification of independent risk factors.
Miller, Preston R; Croce, Martin A; Kilgo, Patrick D; Scott, John; Fabian, Timothy C
2002-10-01
Acute respiratory distress syndrome (ARDS) is a major contributor to morbidity and mortality in trauma patients. Although many injuries and conditions are believed to be associated with ARDS independent risk factors in trauma patients and their relative importance in development of the syndrome are undefined. The aim of this project is to identify independent risk factors for the development of ARDS in blunt trauma patients and to examine the contributions of each factor to ARDS development. Patients with ARDS were identified from the registry of a Level I trauma center over a 4.5-year period. Records were reviewed for demographics, injury characteristics, transfusion requirements, and hospital course. Variables examined included age >65 years, Injury Severity Score (ISS) >25, hypotension on admission (systolic blood pressure <90), significant metabolic acidosis (base deficit <-5.0), severe brain injury as shown by a Glasgow Coma Scale score (GCS) <8 on admission, 24-hour transfusion requirement >10 units packed red blood cells, pulmonary contusion (PC), femur fracture, and major infection (pneumonia, empyema, or intra-abdominal abscess). Both univariate and stepwise logistic regression were used to identify independent risk factors, and receiver operating characteristic curve (ROC) analysis was used to determine the relative contribution of each risk factor. A total of 4397 patients having sustained blunt trauma were admitted to the intensive care unit and survived >24 hours between October 1995 and May 2000. Of these patients 200 (4.5%) developed ARDS. All studied variables were significantly associated with ARDS in univariate analyses. Stepwise logistic regression, however, demonstrated age >65 years, ISS >25, hypotension on admission, 24-hour transfusion requirement >10 units, and pulmonary contusion as independent risk factors, whereas admission metabolic acidosis, femur fracture, infection, and severe brain injury were not. Using a model based on the logistic regression equation derived yields better than 80 per cent discrimination in ARDS patients. The risk factors providing the greatest contribution to ARDS development were ISS >25 (ROC area 0.72) and PC (ROC area 0.68) followed by large transfusion requirement (ROC area 0.56), admission hypotension (ROC area 0.57), and age >65 (ROC area 0.54). Independent risk factors for ARDS in blunt trauma include ISS >25, PC, age >65 years, hypotension on admission, and 24-hour transfusion requirement >10 units but not admission metabolic acidosis, femur fracture, infection, or severe brain injury. Assessment of these variables allows accurate estimate of risk in the majority of cases, and the most potent contributors to the predictive value of the model are ISS >25 and PC. Improvement in understanding of which patients are actually at risk may allow for advances in treatment as well as prevention in the future.
Grassin-Delyle, S; Theusinger, O M; Albrecht, R; Mueller, S; Spahn, D R; Urien, S; Stein, P
2018-06-01
Tranexamic acid is used both pre-hospital and in-hospital as an antifibrinolytic drug to treat or prevent hyperfibrinolysis in trauma patients; dosing, however, remains empirical. We aimed to measure plasma levels of tranexamic acid in patients receiving pre-hospital anti-hyperfibrinolytic therapy and to build a population pharmacokinetic model to propose an optimised dosing regimen. Seventy-three trauma patients were enrolled and each received tranexamic acid 1 g intravenously pre-hospital. A blood sample was drawn after arrival in the emergency department, and we measured the plasma tranexamic acid concentration using liquid chromatography-mass spectrometry, and modelled the data using non-linear mixed effect modelling. Tranexamic acid was administered at a median (IQR [range]) time of 43 (30-55 [5-135]) min after trauma. Plasma tranexamic acid levels were determined on arrival at hospital, 57 (43-70 [20-148]) min after pre-hospital administration of the drug. The measured concentration was 28.7 (21.5-38.5 [8.7-89.0]) μg.ml -1 . Our subjects had sustained severe trauma; injury severity score 20 (16-29 [5-75]), including penetrating injury in 2.8% and isolated traumatic brain injury in 19.7%. The pharmacokinetics were ascribed a two-compartment open model with body-weight as the main covariate. As tranexamic acid concentrations may fall below therapeutic levels during initial hospital treatment, we propose additional dosing schemes to maintain a specific target blood concentration for as long as required. This is the first study to investigate plasma level and pharmacokinetics of tranexamic acid after pre-hospital administration in trauma patients. Our proposed dosing regimen could be used in subsequent clinical trials to better study efficacy and tolerance profiles with controlled blood concentrations. © 2018 The Association of Anaesthetists of Great Britain and Ireland.
Inflicted Skeletal Trauma: The Relationship of Perpetrators to Their Victims
ERIC Educational Resources Information Center
Starling, Suzanne P.; Sirotnak, Andrew P.; Heisler, Kurt W.; Barnes-Eley, Myra L.
2007-01-01
Objective: Although inflicted skeletal trauma is a very common presentation of child abuse, little is known about the perpetrators of inflicted skeletal injuries. Studies exist describing perpetrators of inflicted traumatic brain injury, but no study has examined characteristics of perpetrators of inflicted skeletal trauma. Methods: All cases of…
Brain Injury Association of America
... Only) 1-800-444-6443 Welcome to the Brain Injury Association of America (BIAA) Brain injury is not an event or an outcome. ... misunderstood, under-funded neurological disease. People who sustain brain injuries must have timely access to expert trauma ...
The Role of Perfluorocarbons in Mitigating Traumatic Brain Injury
2014-05-01
the lesion. The effect of closed head trauma upon Glycolysis , as measured by the 2-Deoxyglucose method, is well known, and the findings in this...model accord quite closely with human TBI. However, the effect of Penetrating TBI upon glycolysis has never been studied, in any animal model, nor in...tested was seen upon VO2 in the PBBI model (Fig.17-18) However, significant improvements in glycolysis could be observed, especially with Perftec
Ates, Tuncay; Gezercan, Yurdal; Menekse, Guner; Turkoz, Yusuf; Parlakpinar, Hakan; Okten, Ali Ihsan; Akyuva, Yener; Onal, Selami Cagatay
2017-01-01
To evaluate the effects of cerebroventricular administration of hyperoncotic/hyperosmotic agents on edematous brain tissue in rats with experimental head trauma. The study included 54 female Sprague-Dawley rats with weights ranging between 200 and 250 g. Six experimental groups were examined with each group containing 9 rats. All rats were exposed to head trauma, and treatment groups were administered 2 µl of one of the drugs (albumin, mannitol, hypertonic sodium chloride (NaCl), glycerin and dextran) 6, 12 and 24 hours after the trauma via the cerebroventricular route and using a stereotactic device. Rats were sacrificed 48 hours after the trauma, and brain tissues were extracted without damage. Biochemical analyses including reduced glutathione (GSH), nitric oxide (NO), malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), and interleukin 1 beta (IL-1β) were performed on the injured left hemisphere. Compared with the control group, the albumin, mannitol, 3% NaCl and glycerin treatment groups revealed dramatic increases in GSH levels (p < 0.001). Levels of MDA, which is the end-product of brain edema and lipid peroxidation, failed to show a statistically significant decrease, but there was a decreasing trend observed in the inter-group comparisons. NO levels were also decreased in the 3% NaCl treatment group. An analysis of TNF-α and IL-1β, two proinflammatory cytokines associated with the trauma, revealed that IL-1β decreased significantly in all treatment groups (p=0.001), whereas no significant difference was detected in TNF-α levels. Cerebroventricular administration of hyperoncotic/hyperosmotic agents provides substantial effects on the treatment of brain edema.
Brain Trauma Foundation Guideline Compliance: Results of a Multidisciplinary, International Survey.
Hirschi, Ryan; Rommel, Casey; Letsinger, Joshua; Nirula, Raminder; Hawryluk, Gregory W J
2018-05-09
Brain Trauma Foundation (BTF) guidelines reflect evidence-based best practices in management of traumatic brain injury. The aim of this study was to examine self-reported physician compliance and predictors of compliance related to BTF guidelines. We conducted an international, multidisciplinary survey examining self-reported adherence to BTF guidelines and multiple factors potentially affecting adherence. We also surveyed intracranial pressure monitoring practices. Of 154 physician respondents, 15.9% reported their institutions "always" follow BTF guidelines and 72.2% reported that they follow them "most of the time." Personal volume of traumatic brain injury cases and years in practice were not significantly related to adherence. Reported adherence varied significantly in association with respondent's institutional trauma level (P = 0.0010): 17.3% of practitioners at level I, 13.0% at level II, and 0% at level III trauma centers reported "always" following guidelines. Reported adherence to guidelines also varied significantly in association with provider specialty (P = 0.015) and institutional volume of severe traumatic brain injury cases (P = 0.008). Regarding intracranial pressure monitoring practices, 52% of respondents used external ventricular drains, 21% used intraparenchymal monitors, and 27% had no preference (P < 0.001). Of respondents not routinely using external ventricular drains, 36% claimed to "always" follow guidelines. There was no apparent association between type of intracranial pressure monitoring used and reported guideline adherence. Few respondents reported their institutions "always" follow BTF guidelines. General surgeons and providers at high-volume level I trauma centers were more likely to comply with guidelines. Differences in survey responses based on provider and institutional characteristics may help target educational efforts. Copyright © 2018 Elsevier Inc. All rights reserved.
Harris, Katie; Armstrong, Scott P; Campos-Pires, Rita; Kiru, Louise; Franks, Nicholas P; Dickinson, Robert
2013-11-01
Xenon, the inert anesthetic gas, is neuroprotective in models of brain injury. The authors investigate the neuroprotective mechanisms of the inert gases such as xenon, argon, krypton, neon, and helium in an in vitro model of traumatic brain injury. The authors use an in vitro model using mouse organotypic hippocampal brain slices, subjected to a focal mechanical trauma, with injury quantified by propidium iodide fluorescence. Patch clamp electrophysiology is used to investigate the effect of the inert gases on N-methyl-D-aspartate receptors and TREK-1 channels, two molecular targets likely to play a role in neuroprotection. Xenon (50%) and, to a lesser extent, argon (50%) are neuroprotective against traumatic injury when applied after injury (xenon 43±1% protection at 72 h after injury [N=104]; argon 30±6% protection [N=44]; mean±SEM). Helium, neon, and krypton are devoid of neuroprotective effect. Xenon (50%) prevents development of secondary injury up to 48 h after trauma. Argon (50%) attenuates secondary injury, but is less effective than xenon (xenon 50±5% reduction in secondary injury at 72 h after injury [N=104]; argon 34±8% reduction [N=44]; mean±SEM). Glycine reverses the neuroprotective effect of xenon, but not argon, consistent with competitive inhibition at the N-methyl-D-aspartate receptor glycine site mediating xenon neuroprotection against traumatic brain injury. Xenon inhibits N-methyl-D-aspartate receptors and activates TREK-1 channels, whereas argon, krypton, neon, and helium have no effect on these ion channels. Xenon neuroprotection against traumatic brain injury can be reversed by increasing the glycine concentration, consistent with inhibition at the N-methyl-D-aspartate receptor glycine site playing a significant role in xenon neuroprotection. Argon and xenon do not act via the same mechanism.
In vivo functional photoacoustic tomography of traumatic brain injury in rats
NASA Astrophysics Data System (ADS)
Oh, Jung-Taek; Song, Kwang-Hyung; Li, Meng-Lin; Stoica, George; Wang, Lihong V.
2006-02-01
In this study, we demonstrate the potential of photoacoustic tomography for the study of traumatic brain injury (TBI) in rats in vivo. Based on spectroscopic photoacoustic tomography that can detect the absorption rates of oxy- and deoxy-hemoglobins, the blood oxygen saturation and total blood volume in TBI rat brains were visualized. Reproducible cerebral trauma was induced using a fluid percussion TBI device. The time courses of the hemodynamic response following the trauma initiation were imaged with multi-wavelength photoacoustic tomography with bandwidth-limited spatial resolution through the intact skin and skull. In the pilot set of experiments, trauma induced hematomas and blood oxygen saturation level changes were detected, a finding consistent with the known physiological responses to TBI. This new imaging method will be useful for future studies on TBI-related metabolic activities and the effects of therapeutic agents.
... id=258&terms=cpr. Accessed Oct. 8, 2014. Traumatic brain injury. The Merck Manual Professional Edition. http://www.merckmanuals.com/professional/injuries_poisoning/traumatic_brain_injury_tbi/traumatic_brain_injury.html. Accessed Oct. 8, ...
Effects of HIV and childhood trauma on brain morphometry and neurocognitive function.
Spies, Georgina; Ahmed-Leitao, Fatima; Fennema-Notestine, Christine; Cherner, Mariana; Seedat, Soraya
2016-04-01
A wide spectrum of neurocognitive deficits characterises HIV infection in adults. HIV infection is additionally associated with morphological brain abnormalities affecting neural substrates that subserve neurocognitive function. Early life stress (ELS) also has a direct influence on brain morphology. However, the combined impact of ELS and HIV on brain structure and neurocognitive function has not been examined in an all-female sample with advanced HIV disease. The present study examined the effects of HIV and childhood trauma on brain morphometry and neurocognitive function. Structural data were acquired using a 3T Magnetom MRI scanner, and a battery of neurocognitive tests was administered to 124 women: HIV-positive with ELS (n = 32), HIV-positive without ELS (n = 30), HIV-negative with ELS (n = 31) and HIV-negative without ELS (n = 31). Results revealed significant group volumetric differences for right anterior cingulate cortex (ACC), bilateral hippocampi, corpus callosum, left and right caudate and left and right putamen. Mean regional volumes were lowest in HIV-positive women with ELS compared to all other groups. Although causality cannot be inferred, findings also suggest that alterations in the left frontal lobe, right ACC, left hippocampus, corpus callosum, left and right amygdala and left caudate may be associated with poorer neurocognitive performance in the domains of processing speed, attention/working memory, abstraction/executive functions, motor skills, learning and language/fluency with these effects more pronounced in women living with both HIV and childhood trauma. This study highlights the potential contributory role of childhood trauma to brain alterations and neurocognitive decline in HIV-infected individuals.
Trimmel, H; Herzer, G; Schöchl, H; Voelckel, W G
2017-09-01
Traumatic brain injury (TBI) and hemorrhagic shock due to uncontrolled bleeding are the major causes of death after severe trauma. Mortality rates are threefold higher in patients suffering from multiple injuries and additionally TBI. Factors known to impair outcome after TBI, namely hypotension, hypoxia, hypercapnia, acidosis, coagulopathy and hypothermia are aggravated by the extent and severity of extracerebral injuries. The mainstays of TBI intensive care may be, at least temporarily, contradictory to the trauma care concept for multiple trauma patients. In particular, achieving normotension in uncontrolled bleeding situations, maintenance of normocapnia in traumatic lung injury and thromboembolic prophylaxis are prone to discussion. Due to an ongoing uncertainty about the definition of normotensive blood pressure values, a cerebral perfusion pressure-guided cardiovascular management is of key importance. In contrast, there is no doubt that early goal directed coagulation management improves outcome in patients with TBI and multiple trauma. The timing of subsequent surgical interventions must be based on the development of TBI pathology; therefore, intensive care of multiple trauma patients with TBI requires an ongoing and close cooperation between intensivists and trauma surgeons in order to individualize patient care.
Gülşen, İsmail; Ak, Hakan; Karadaş, Sevdegül; Demır, İsmail; Bulut, Mehmet Deniz; Yaycioğlu, Soner
2014-01-01
Objective. To investigate the indications to receive brain computed tomography (CT) scan and to define the pathological findings in children younger than three years of age with minor head trauma in emergency departments. Methods. In this study, hospital case notes of 1350 children attending the emergency department of Bitlis State Hospital between January 2011 and June 2013 were retrospectively reviewed. 508 children under 3 years of age with minor head trauma were included in this study. We also asked 37 physicians about the indications for requiring CT in these children. Results. This study included 508 children, 233 (45,9%) of whom were female and 275 were male. In 476 (93,7%) children, the brain CT was completely normal. 89,2% of physicians asked in the emergency department during that time interval reported that they requested CT scan to protect themselves against malpractice litigation. Conclusion. In infants and children with minor head trauma, most CT scans were unnecessary and the fear of malpractice litigation of physicians was the most common reason for requesting a CT. PMID:24724031
Trauma-Sensitive Schools: An Evidence-Based Approach
ERIC Educational Resources Information Center
Plumb, Jacqui L.; Bush, Kelly A.; Kersevich, Sonia E.
2016-01-01
Adverse childhood experiences (ACEs) are a common and pervasive problem. There is a positive correlation between ACEs and difficulties across the lifespan. Unlike healthy forms of stress, ACEs have a detrimental impact on the developing brain. There are three types of trauma: acute, chronic, and complex. Most ACEs are considered complex trauma,…
Curing "moral disability": brain trauma and self-control in Victorian science and fiction.
Schillace, Brandy L
2013-12-01
While, historically, the disabled body has appeared in literature as "monstrous," burgeoning psychological theories of the Victorian period predicated an unusual shift. In a culture of sexual anxiety and fears of devolution and moral decay, the physically disabled and "weak" are portrayed as strangely free from moral corruption. Unlike the cultural link between deviance and disability witnessed in the medical literature and eugenic approach to generation, authors of narrative fiction-particularly Charles Dickens, but Wilkie Collins, Charlotte Yonge, and others as well-portray disabled characters as "purified," and trauma itself as potentially sanitizing. This present paper argues that such constructions were made possible by developments in the treatment of insanity. "Curing 'Moral Disability': Brain Trauma and Self-Control in Victorian Fiction," examines the concept of trauma-as-cure. Throughout the Victorian period, case studies on brain trauma appeared in widely circulated journals like the Lancet, concurrently with burgeoning theories about psychological disturbance and "moral insanity." While not widely practiced until the early twentieth century, attempts at surgical "cures" aroused curiosity and speculation-the traumatic event that could free sufferers from deviance. This work provides a unique perspective on representations of disability as cure in the nineteenth century as a means of giving voice to the marginalized, disabled, and disempowered.
Underbody Blast Models of TBI Caused by Hyper-Acceleration and Secondary Head Impact
2014-02-01
Cleveland RO, Tanzi RE, Stanton PK, McKee AC. (2012) Chronic traumatic encephalopathy in blast-exposed military veterans and a blast neurotrauma mouse model...exposure, remove brains, and process for electron microscopic analysis of cyto- and axonal ultrastructure and for histochemical evidence of acute ...of Trauma and Acute Care Surgery (see Appendix). These observations include increased axonopathy (silver staining) in the cerebellum and astrocyte
Bolster, F; Ali, Z; Daly, B
2017-12-01
To document the detection of underlying low-attenuation spinal cord or brain stem injuries in the presence of the "pseudo-CT myelogram sign" (PCMS) on post-mortem computed tomography (PMCT). The PCMS was identified on PMCT in 20 decedents (11 male, nine female; age 3-83 years, mean age 35.3 years) following fatal blunt trauma at a single forensic centre. Osseous and ligamentous craniocervical region injuries and brain stem or spinal cord trauma detectable on PMCT were recorded. PMCT findings were compared to conventional autopsy in all cases. PMCT-detected transection of the brain stem or high cervical cord in nine of 10 cases compared to autopsy (90% sensitivity). PMCT was 92.86% sensitive in detection of atlanto-occipital joint injuries (n=14), and 100% sensitive for atlanto-axial joint (n=8) injuries. PMCT detected more cervical spine and skull base fractures (n=22, and n=10, respectively) compared to autopsy (n=13, and n=5, respectively). The PCMS is a novel description of a diagnostic finding, which if present in fatal craniocervical region trauma, is very sensitive for underlying spinal cord and brain stem injuries not ordinarily visible on PMCT. Its presence may also predict major osseous and/or ligamentous injuries in this region when anatomical displacement is not evident on PMCT. Copyright © 2017 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved.
High risk of hypogonadism after traumatic brain injury: clinical implications.
Agha, Amar; Thompson, Christopher J
2005-01-01
Several recent studies have convincingly documented a close association between traumatic brain injury (TBI) and pituitary dysfunction. Post-traumatic hypogonadism is very common in the acute post-TBI phase, though most cases recover within six to twelve months following trauma. The functional significance of early hypogonadism, which may reflect adaptation to acute illness, is not known. Hypogonadism persists, however, in 10-17% of long-term survivors. Sex steroid deficiency has implications beyond psychosexual function and fertility for survivors of TBI. Muscle weakness may impair functional recovery from trauma and osteoporosis may be exacerbated by immobility secondary to trauma. Identification and appropriate and timely management of post-traumatic hypogonadism is important in order to optimise patient recovery from head trauma, improve quality of life and avoid the long-term adverse consequences of untreated sex steroid deficiency.
Effects of subconcussive head trauma on the default mode network of the brain.
Johnson, Brian; Neuberger, Thomas; Gay, Michael; Hallett, Mark; Slobounov, Semyon
2014-12-01
Although they are less severe than a full blown concussive episodes, subconcussive impacts happen much more frequently and current research has suggested this form of head trauma may have an accumulative effect and lead to neurological impairment later in life. To investigate the acute effects that subconcussive head trauma may have on the default mode network of the brain resting-state, functional magnetic resonance was performed. Twenty-four current collegiate rugby players were recruited and all subjects underwent initial scanning 24 h prior to a scheduled full contact game to provide a baseline. Follow-up scanning of the rugby players occurred within 24 h following that game to assess acute effects from subconcussive head trauma. Differences between pre-game and post-game scans showed both increased connectivity from the left supramarginal gyrus to bilateral orbitofrontal cortex and decreased connectivity from the retrosplenial cortex and dorsal posterior cingulate cortex. To assess whether or not a history of previous concussion may lead to a differential response following subconcussive impacts, subjects were further divided into two subgroups based upon history of previous concussion. Individuals with a prior history of concussion exhibited only decreased functional connectivity following exposure to subconcussive head trauma, while those with no history showed increased connectivity. Even acute exposure to subconcussive head trauma demonstrates the ability to alter functional connectivity and there is possible evidence of a differential response in the brain for those with and without a history of concussion.
Jeong, Hee-Won; Choi, Seung-Won; Youm, Jin-Young; Lim, Jeong-Wook; Kwon, Hyon-Jo; Song, Shi-Hun
2017-11-01
Among pediatric injury, brain injury is a leading cause of death and disability. To improve outcomes, many developed countries built neurotrauma databank (NTDB) system but there was not established nationwide coverage NTDB until 2009 and there have been few studies on pediatric traumatic head injury (THI) patients in Korea. Therefore, we analyzed epidemiology and outcome from the big data of pediatric THI. We collected data on pediatric patients from 23 university hospitals including 9 regional trauma centers from 2010 to 2014 and analyzed their clinical factors (sex, age, initial Glasgow coma scale, cause and mechanism of head injury, presence of surgery). Among all the 2617 THI patients, total number of pediatric patients was 256. The average age of the subjects was 9.07 (standard deviation±6.3) years old. The male-to female ratio was 1.87 to 1 and male dominance increases with age. The most common cause for trauma were falls and traffic accidents. Age ( p =0.007), surgery ( p <0.001), mechanism of trauma ( p =0.016), subdural hemorrhage (SDH) ( p <0.001), diffuse axonal injury (DAI) ( p <0.001) were statistically significant associated with severe brain injury. Falls were the most common cause of trauma, and age, surgery, mechanism of trauma, SDH, DAI increased with injury severity. There is a critical need for effective fall and traffic accidents prevention strategies for children, and we should give attention to these predicting factors for more effective care.
Öğrenci, Ahmet; Koban, Orkun; Ekşi, Murat; Yaman, Onur; Dalbayrak, Sedat
2017-01-01
AIM: This study aimed to make a retrospective analysis of pediatric patients with head traumas that were admitted to one hospital setting and to make an analysis of the patients for whom follow-up CT scans were obtained. METHODS: Pediatric head trauma cases were retrospectively retrieved from the hospital’s electronic database. Patients’ charts, CT scans and surgical notes were evaluated by one of the authors. Repeat CT scans for operated patients were excluded from the total number of repeat CT scans. RESULTS: One thousand one hundred and thirty-eight pediatric patients were admitted to the clinic due to head traumas. Brain CT scan was requested in 863 patients (76%) in the cohort. Follow-up brain CT scans were obtained in 102 patients. Additional abnormal finding requiring surgical intervention was observed in only one patient (isolated 4th ventricle hematoma) on the control CTs (1% of repeat CT scans), who developed obstructive hydrocephalus. None of the patients with no more than 1 cm epidural hematoma in its widest dimension and repeat CT scans obtained 1.5 hours after the trauma necessitated surgery. CONCLUSION: Follow-up CT scans changed clinical approach in only one patient in the present series. When ordering CT scan in the follow-up of pediatric traumas, benefits and harms should be weighted based upon time interval from trauma onset to initial CT scan and underlying pathology. PMID:29104682
Acute costs and predictors of higher treatment costs of trauma in New South Wales, Australia.
Curtis, Kate; Lam, Mary; Mitchell, Rebecca; Black, Deborah; Taylor, Colman; Dickson, Cara; Jan, Stephen; Palmer, Cameron S; Langcake, Mary; Myburgh, John
2014-01-01
Accurate economic data are fundamental for improving current funding models and ultimately in promoting the efficient delivery of services. The financial burden of a high trauma casemix to designated trauma centres in Australia has not been previously determined, and there is some evidence that the episode funding model used in Australia results in the underfunding of trauma. To describe the costs of acute trauma admissions in trauma centres, identify predictors of higher treatment costs and cost variance in New South Wales (NSW), Australia. Data linkage of admitted trauma patient and financial data provided by 12 Level 1 NSW trauma centres for the 08/09 financial year was performed. Demographic, injury details and injury scores were obtained from trauma registries. Individual patient general ledger costs (actual trauma patient costs), Australian Refined Diagnostic Related Groups (AR-DRG) and state-wide average costs (which form the basis of funding) were obtained. The actual costs incurred by the hospital were then compared with the state-wide AR-DRG average costs. Multivariable multiple linear regression was used for identifying predictors of costs. There were 17,522 patients, the average per patient cost was $10,603 and the median was $4628 (interquartile range: $2179-10,148). The actual costs incurred by trauma centres were on average $134 per bed day above AR-DRG costs-determined costs. Falls, road trauma and violence were the highest causes of total cost. Motor cyclists and pedestrians had higher median costs than motor vehicle occupants. As a result of greater numbers, patients with minor injury had comparable total costs with those generated by patients with severe injury. However the median cost of severely injured patients was nearly four times greater. The count of body regions injured, sex, length of stay, serious traumatic brain injury and admission to the Intensive Care Unit were significantly associated with increased costs (p<0.001). This multicentre trauma costing study demonstrated the feasibility of trauma registry and financial data linkage. Discrepancies between the observed costs of care in these 12 trauma centres and the NSW average AR-DRG costs suggest that trauma care is currently underfunded in NSW. Crown Copyright © 2012. Published by Elsevier Ltd. All rights reserved.
Systemic progesterone for modulating electrocautery-induced secondary brain injury.
Un, Ka Chun; Wang, Yue Chun; Wu, Wutian; Leung, Gilberto Ka Kit
2013-09-01
Bipolar electrocautery is an effective and commonly used haemostatic technique but it may also cause iatrogenic brain trauma due to thermal injury and secondary inflammatory reactions. Progesterone has anti-inflammatory and neuroprotective actions in traumatic brain injury. However, its potential use in preventing iatrogenic brain trauma has not been explored. We conducted a pilot animal study to investigate the effect of systemic progesterone on brain cellular responses to electrocautery-induced injury. Adult male Sprague-Dawley rats received standardized bipolar electrocautery (40 W for 2 seconds) over the right cerebral cortex. The treatment group received progesterone intraperitoneally 2 hours prior to surgery; the control group received the drug vehicle only. Immunohistochemical studies showed that progesterone could significantly reduce astrocytic hypertrophy on postoperative day 1, 3 and 7, as well as macrophage infiltration on day 3. The number of astrocytes, however, was unaffected. Our findings suggest that progesterone should be further explored as a neuroprotective agent against electrocautery-induced or other forms of iatrogenic trauma during routine neurosurgical procedures. Future studies may focus on different dosing regimens, neuronal survival, functional outcome, and to compare progesterone with other agents such as dexamethasone. Copyright © 2013 Elsevier Ltd. All rights reserved.
ERIC Educational Resources Information Center
Yorke, Jan
2010-01-01
Emotional stress and trauma impacts the neurobiology of children. They are especially vulnerable given the developmental plasticity of the brain. The neural synaptic circular processes between the anterior cingulated cortex, prefrontal cortex, amygdala and the hypothalamus are altered. Trauma results in the release of the peptide glucocortisoid,…
Long Term Effects of Soft Splints on Stroke Patients and Patients With Disorders of Consciousness
2017-06-01
Brain Injuries; Disorder of Consciousness; Stroke; Spasticity as Sequela of Stroke; Contracture; Hypertonic Disorder; Central Nervous System Diseases; Pathologic Processes; Craniocerebral Trauma; Trauma, Nervous System; Neurocognitive Disorders
Isolated brain stem edema in a pediatric patient with head trauma: a case report.
Basarslan, K; Basarslan, F; Karakus, A; Yilmaz, C
2015-01-01
Brain stem is the most vital part of our body and is a transitional region of the brain that connects the cerebrum with the spinal cord. Though, being small in size, it is full of indispensible functions such as the breathing, heart beat. Injury to the brain stem has similar effects as a brain injury, but it is more fatal. Use of the Glasgow Coma Score as a prognostic indicator of outcome in patients with head injuries is widely accepted in clinical practice. Traumatic brain stem edema in children is rare, but is associated with poor outcome. The question is that whether it is being aware of computerized tomography appearance of the posterior fossa when initial evaluating pediatric patients with head trauma at emergency clinics. Normal and edematous brain stem without an additional pathology are slightly different and not distinguished easily. On the other hand, brain stem edema should be promptly identified and appropriately treated in a short time.
Acute pathophysiological processes after ischaemic and traumatic brain injury.
Kunz, Alexander; Dirnagl, Ulrich; Mergenthaler, Philipp
2010-12-01
Ischaemic stroke and brain trauma are among the leading causes of mortality and long-term disability in the western world. Enormous endeavours have been made to elucidate the complex pathophysiology of ischaemic and traumatic brain injury with the intention of developing new therapeutic strategies for patients suffering from these devastating diseases. This article reviews the current knowledge on cascades that are activated after ischaemic and traumatic brain injury and that lead to progression of tissue damage. Main attention will be on pathophysiological events initiated after ischaemic stroke including excitotoxicity, oxidative/nitrosative stress, peri-infarct depolarizations, apoptosis and inflammation. Additionally, specific pathophysiological aspects after traumatic brain injury will be discussed along with their similarities and differences to ischaemic brain injury. This article provides prerequisites for understanding the therapeutic strategies for stroke and trauma patients which are addressed in other articles of this issue. Copyright © 2010 Elsevier Ltd. All rights reserved.
The role of autophagy in acute brain injury: A state of flux?
Wolf, Michael S; Bayır, Hülya; Kochanek, Patrick M; Clark, Robert S B
2018-04-26
It is established that increased autophagy is readily detectable after various types of acute brain injury, including trauma, focal and global cerebral ischemia. What remains controversial, however, is whether this heightened detection of autophagy in brain represents a homeostatic or pathologic process, or an epiphenomenon. The ultimate role of autophagy after acute brain injury likely depends upon: 1) the degree of brain injury and the overall autophagic burden; 2) the capacity of individual cell types to ramp up autophagic flux; 3) the local redox state and signaling of parallel cell death pathways; 4) the capacity to eliminate damage associated molecular patterns and toxic proteins and metabolites both intra- and extracellularly; and 5) the timing of the pro- or anti-autophagic intervention. In this review, we attempt to reconcile conflicting studies that support both a beneficial and detrimental role for autophagy in models of acute brain injury. Copyright © 2018 Elsevier Inc. All rights reserved.
Coqueugniot, Hélène; Dutour, Olivier; Arensburg, Baruch; Duday, Henri; Vandermeersch, Bernard; Tillier, Anne-marie
2014-01-01
The Qafzeh site (Lower Galilee, Israel) has yielded the largest Levantine hominin collection from Middle Palaeolithic layers which were dated to circa 90–100 kyrs BP or to marine isotope stage 5b–c. Within the hominin sample, Qafzeh 11, circa 12–13 yrs old at death, presents a skull lesion previously attributed to a healed trauma. Three dimensional imaging methods allowed us to better explore this lesion which appeared as being a frontal bone depressed fracture, associated with brain damage. Furthermore the endocranial volume, smaller than expected for dental age, supports the hypothesis of a growth delay due to traumatic brain injury. This trauma did not affect the typical human brain morphology pattern of the right frontal and left occipital petalia. It is highly probable that this young individual suffered from personality and neurological troubles directly related to focal cerebral damage. Interestingly this young individual benefited of a unique funerary practice among the south-western Asian burials dated to Middle Palaeolithic. PMID:25054798
Marusak, Hilary A; Etkin, Amit; Thomason, Moriah E
2015-01-01
Childhood trauma exposure is a potent risk factor for psychopathology. Emerging research suggests that aberrant saliency processing underlies the link between early trauma exposure and later cognitive and socioemotional deficits that are hallmark of several psychiatric disorders. Here, we examine brain and behavioral responses during a face categorization conflict task, and relate these to intrinsic connectivity of the salience network (SN). The results demonstrate a unique pattern of SN dysfunction in youth exposed to trauma (n = 14) relative to comparison youth (n = 19) matched on age, sex, IQ, and sociodemographic risk. We find that trauma-exposed youth are more susceptible to conflict interference and this correlates with higher fronto-insular responses during conflict. Resting-state functional connectivity data collected in the same participants reveal increased connectivity of the insula to SN seed regions that is associated with diminished reward sensitivity, a critical risk/resilience trait following stress. In addition to altered intrinsic connectivity of the SN, we observed altered connectivity between the SN and default mode network (DMN) in trauma-exposed youth. These data uncover network-level disruptions in brain organization following one of the strongest predictors of illness, early life trauma, and demonstrate the relevance of observed neural effects for behavior and specific symptom dimensions. SN dysfunction may serve as a diathesis that contributes to illness and negative outcomes following childhood trauma.
Long-Term Effects of Acute Stress on the Prefrontal-Limbic System in the Healthy Adult
Wei, Dongtao; Du, Xue; Zhang, Qinglin; Liu, Guangyuan; Qiu, Jiang
2017-01-01
Most people are exposed to at least one traumatic event during the course of their lives, but large numbers of people do not develop posttraumatic stress disorders. Although previous studies have shown that repeated and chronic stress change the brain’s structure and function, few studies have focused on the long-term effects of acute stressful exposure in a nonclinical sample, especially the morphology and functional connectivity changes in brain regions implicated in emotional reactivity and emotion regulation. Forty-one months after the 5/12 Wenchuan earthquake, we investigated the effects of trauma exposure on the structure and functional connectivity of the brains of trauma-exposed healthy individuals compared with healthy controls matched for age, sex, and education. We then used machine-learning algorithms with the brain structural features to distinguish between the two groups at an individual level. In the trauma-exposed healthy individuals, our results showed greater gray matter density in prefrontal-limbic brain systems, including the dorsal anterior cingulate cortex, medial prefrontal cortex, amygdala and hippocampus, than in the controls. Further analysis showed stronger amygdala-hippocampus functional connectivity in the trauma-exposed healthy compared to the controls. Our findings revealed that survival of traumatic experiences, without developing PTSD, was associated with greater gray matter density in the prefrontal-limbic systems related to emotional regulation. PMID:28045980
Graef, F.; Seemann, R.; Garbe, A.; Schmidt-Bleek, K.; Schaser, K-D.; Keller, J.; Duda, G.; Tsitsilonis, S.
2017-01-01
Patients with traumatic brain injury (TBI) and long-bone fractures can show increased callus formation. This effect has already been reproduced in wild-type (wt) mice. However, the mechanisms remain poorly understood. Leptin is significantly increased following TBI, while its role in bone healing remains unclear. The aim of this study was to evaluate fracture healing in leptin-deficient ob/ob mice and to measure any possible impact of TBI on callus formation. 138 female, 12 weeks old, ob/ob mice were divided into four groups: Control, fracture, TBI and combined trauma. Osteotomies were stabilized with an external fixator; TBI was induced with Controlled Cortical Impact Injury. Callus bridging was weekly evaluated with in vivo micro-CT. Biomechanical testing was performed ex vivo. Micro-CT showed high non-union rates after three and four weeks in the fracture and combined trauma group. No differences were observed in callus volume, density and biomechanical properties at any time point. This study shows that bony bridging is impaired in the present leptin-deficient trauma model. Furthermore, the phenomenon of increased callus formation after TBI could not be reproduced in ob/ob mice, as in wt mice. Our findings suggest that the increased callus formation after TBI may be dependent on leptin signaling. PMID:28574414
de Guise, E; LeBlanc, J; Feyz, M; Lamoureux, J; Greffou, S
2017-01-01
The goal of this study was to identify factors that would predict short-term neuropsychological outcome in patients with traumatic brain injury (TBI) hospitalized in an acute rehabilitation setting. Data was collected in the context of an acute early rehabilitation setting of a trauma centre. A brief neuropsychological assessment was carried out for 348 patients within a month following their trauma. Length of post-traumatic amnesia (PTA) was the best predictor of behavioural, memory and executive function variables within a month post TBI. The odds of being agitated, labile, irritable and disinhibited at one month post trauma were almost six times higher for those with PTA that lasted more than 7 days compared to those with a PTA of less than 24 hours. Also, the odds of having a higher mental manipulation score (less significant executive function impairment) were almost two times lower for those with frontal lesions, and three to six times lower for those with PTA of more than 24 hours. In addition, TBI severity, education and age were considered good predictors of some aspects of neuropsychological outcome. This model may help clinicians and administrators recognize the probable post-traumatic deficits as quickly as possible and to plan interventions as well as post-acute discharge orientation accordingly and early on.
Shucard, Janet Louise; Cox, Jennifer; Shucard, David William; Fetter, Holly; Chung, Charles; Ramasamy, Deepa; Violanti, John
2012-10-30
Traumatic experiences and subsequent symptoms of posttraumatic stress disorder (PTSD) have been shown to affect brain structure and function. Although police officers are routinely exposed to traumatic events, the neurobehavioral effects of trauma in this population have rarely been studied. In this study, police officers with exposure to trauma-related stressors underwent structural magnetic resonance imaging (MRI). They also provided valence and arousal ratings of neutral and negative (trauma-related) picture stimuli. Relationships were examined among PTSD symptom scores (avoidance, reexperiencing, and hyperarousal), picture ratings, structural MRI measures, and number of trauma exposures. We hypothesized that greater PTSD symptomatology would be related to higher valence and arousal ratings of trauma-related stimuli and to decreased volume of limbic and Basal ganglia structures. Results revealed that officers with higher reexperiencing scores tended to have higher arousal ratings of negative pictures and reduced amygdala, thalamus, and globus pallidus volumes. There was a trend toward higher reexperiencing and reduced hippocampal volume. The frequency of traumatic exposures was also related to MRI measures of atrophy and to increased PTSD symptomatology. These findings suggest that chronic reexperiencing of traumatic events may result in volumetric reductions in brain structures associated with autonomic arousal and the acquisition of conditioned fear. Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.
Modelling Cerebral Blood Flow and Temperature Using a Vascular Porous Model
NASA Astrophysics Data System (ADS)
Blowers, Stephen; Thrippleton, Michael; Marshall, Ian; Harris, Bridget; Andrews, Peter; Valluri, Prashant
2016-11-01
Macro-modelling of cerebral blood flow can assist in determining the impact of temperature intervention to reduce permanent tissue damage during instances of brain trauma. Here we present a 3D two phase fluid-porous model for simulating blood flow through the capillary region linked to intersecting 1D arterial and venous vessel trees. This combined vasculature porous (VaPor) model simulates both flow and energy balances, including heat from metabolism, using a vasculature extracted from MRI data which are expanded upon using a tree generation algorithm. Validation of temperature balance has been achieved using rodent brain data. Direct flow validation is not as straight forward due to the method used in determining regional cerebral blood flow (rCBF). In-vivo measurements are achieved using a tracer, which disagree with direct measurements of simulated flow. However, by modelling a virtual tracer, rCBF values are obtained that agree with those found in literature. Temperature profiles generated with the VaPor model show a reduction in core brain temperature after cooling the scalp not seen previously in other models.
Sashindranath, Maithili; Sales, Eunice; Daglas, Maria; Freeman, Roxann; Samson, Andre L.; Cops, Elisa J.; Beckham, Simone; Galle, Adam; McLean, Catriona; Morganti-Kossmann, Cristina; Rosenfeld, Jeffrey V.; Madani, Rime; Vassalli, Jean-Dominique; Su, Enming J.; Lawrence, Daniel A.
2012-01-01
The neurovascular unit provides a dynamic interface between the circulation and central nervous system. Disruption of neurovascular integrity occurs in numerous brain pathologies including neurotrauma and ischaemic stroke. Tissue plasminogen activator is a serine protease that converts plasminogen to plasmin, a protease that dissolves blood clots. Besides its role in fibrinolysis, tissue plasminogen activator is abundantly expressed in the brain where it mediates extracellular proteolysis. However, proteolytically active tissue plasminogen activator also promotes neurovascular disruption after ischaemic stroke; the molecular mechanisms of this process are still unclear. Tissue plasminogen activator is naturally inhibited by serine protease inhibitors (serpins): plasminogen activator inhibitor-1, neuroserpin or protease nexin-1 that results in the formation of serpin:protease complexes. Proteases and serpin:protease complexes are cleared through high-affinity binding to low-density lipoprotein receptors, but their binding to these receptors can also transmit extracellular signals across the plasma membrane. The matrix metalloproteinases are the second major proteolytic system in the mammalian brain, and like tissue plasminogen activators are pivotal to neurological function but can also degrade structures of the neurovascular unit after injury. Herein, we show that tissue plasminogen activator potentiates neurovascular damage in a dose-dependent manner in a mouse model of neurotrauma. Surprisingly, inhibition of activity following administration of plasminogen activator inhibitor-1 significantly increased cerebrovascular permeability. This led to our finding that formation of complexes between tissue plasminogen activator and plasminogen activator inhibitor-1 in the brain parenchyma facilitates post-traumatic cerebrovascular damage. We demonstrate that following trauma, the complex binds to low-density lipoprotein receptors, triggering the induction of matrix metalloproteinase-3. Accordingly, pharmacological inhibition of matrix metalloproteinase-3 attenuates neurovascular permeability and improves neurological function in injured mice. Our results are clinically relevant, because concentrations of tissue plasminogen activator: plasminogen activator inhibitor-1 complex and matrix metalloproteinase-3 are significantly elevated in cerebrospinal fluid of trauma patients and correlate with neurological outcome. In a separate study, we found that matrix metalloproteinase-3 and albumin, a marker of cerebrovascular damage, were significantly increased in brain tissue of patients with neurotrauma. Perturbation of neurovascular homeostasis causing oedema, inflammation and cell death is an important cause of acute and long-term neurological dysfunction after trauma. A role for the tissue plasminogen activator–matrix metalloproteinase axis in promoting neurovascular disruption after neurotrauma has not been described thus far. Targeting tissue plasminogen activator: plasminogen activator inhibitor-1 complex signalling or downstream matrix metalloproteinase-3 induction may provide viable therapeutic strategies to reduce cerebrovascular permeability after neurotrauma. PMID:22822039
ERIC Educational Resources Information Center
Goodwin-Glick, Kelly L.
2017-01-01
Childhood trauma is prevalent and has a profound impact on student learning, behaviors, social-emotional well-being (Perfect et al., 2016), physical health, relationships (Tishelman et al., 2010), and brain architecture (Perry, 2001). Trauma-informed care professional development (PD) within the school setting is a relatively new notion for school…
Barriers to compliance with evidence-based care in trauma.
Rayan, Nadine; Barnes, Sunni; Fleming, Neil; Kudyakov, Rustam; Ballard, David; Gentilello, Larry M; Shafi, Shahid
2012-03-01
We have preciously demonstrated that trauma patients receive less than two-thirds of the care recommended by evidence-based medicine. The purpose of this study was to identify patients least likely to receive optimal care. Records of a random sample of 774 patients admitted to a Level I trauma center (2006-2008) with moderate to severe injuries (Abbreviated Injury Scale score ≥3) were reviewed for compliance with 25 trauma-specific processes of care (T-POC) endorsed by Advanced Trauma Life Support, Eastern Association for the Surgery of Trauma, the Brain Trauma Foundation, Surgical Care Improvement Project, and the Glue Grant Consortium based on evidence or consensus. These encompassed all aspects of trauma care, including initial evaluation, resuscitation, operative care, critical care, rehabilitation, and injury prevention. Multivariate logistic regression was used to identify patients likely to receive recommended care. Study patients were eligible for a total of 2,603 T-POC, of which only 1,515 (58%) were provided to the patient. Compliance was highest for T-POC involving resuscitation (83%) and was lowest for neurosurgical interventions (17%). Increasing severity of head injuries was associated with lower compliance, while intensive care unit stay was associated with higher compliance. There was no relationship between compliance and patient demographics, socioeconomic status, overall injury severity, or daily volume of trauma admissions. Little over half of recommended care was delivered to trauma patients with moderate to severe injuries. Patients with increasing severity of traumatic brain injuries were least likely to receive optimal care. However, differences among patient subgroups are small in relation to the overall gap between observed and recommended care. II.
Neural correlates of childhood trauma with executive function in young healthy adults.
Lu, Shaojia; Pan, Fen; Gao, Weijia; Wei, Zhaoguo; Wang, Dandan; Hu, Shaohua; Huang, Manli; Xu, Yi; Li, Lingjiang
2017-10-03
The aim of this study was to investigate the relationship among childhood trauma, executive impairments, and altered resting-state brain function in young healthy adults. Twenty four subjects with childhood trauma and 24 age- and gender-matched subjects without childhood trauma were recruited. Executive function was assessed by a series of validated test procedures. Localized brain activity was evaluated by fractional amplitude of low frequency fluctuation (fALFF) method and compared between two groups. Areas with altered fALFF were further selected as seeds in subsequent functional connectivity analysis. Correlations of fALFF and connectivity values with severity of childhood trauma and executive dysfunction were analyzed as well. Subjects with childhood trauma exhibited impaired executive function as assessed by Wisconsin Card Sorting Test and Stroop Color Word Test. Traumatic individuals also showed increased fALFF in the right precuneus and decreased fALFF in the right superior temporal gyrus. Significant correlations of specific childhood trauma severity with executive dysfunction and fALFF value in the right precuneus were found in the whole sample. In addition, individuals with childhood trauma also exhibited diminished precuneus-based connectivity in default mode network with left ventromedial prefrontal cortex, left orbitofrontal cortex, and right cerebellum. Decreased default mode network connectivity was also associated with childhood trauma severity and executive dysfunction. The present findings suggest that childhood trauma is associated with executive deficits and aberrant default mode network functions even in healthy adults. Moreover, this study demonstrates that executive dysfunction is related to disrupted default mode network connectivity.
Kim, Jae Hwan; Lee, Yong Woo; Park, Kyung Ah; Lee, Won Taek; Lee, Jong Eun
2010-01-01
Brain edema is frequently shown after cerebral ischemia. It is an expansion of brain volume because of increasing water content in brain. It causes to increase mortality after stroke. Agmatine, formed by the decarboxylation of -arginine by arginine decarboxylase, has been shown to be neuroprotective in trauma and ischemia models. The purpose of this study was to investigate the effect of agmatine for brain edema in ischemic brain damage and to evaluate the expression of aquaporins (AQPs). Results showed that agmatine significantly reduced brain swelling volume 22 h after 2 h middle cerebral artery occlusion in mice. Water content in brain tissue was clearly decreased 24 h after ischemic injury by agmatine treatment. Blood–brain barrier (BBB) disruption was diminished with agmatine than without. The expressions of AQPs-1 and -9 were well correlated with brain edema as water channels, were significantly decreased by agmatine treatment. It can thus be suggested that agmatine could attenuate brain edema by limitting BBB disruption and blocking the accumulation of brain water content through lessening the expression of AQP-1 after cerebral ischemia. PMID:20029450
Neigh, G N; Ritschel, L A; Kilpela, L S; Harrell, C S; Bourke, C H
2013-09-26
The genetic, biological, and environmental backgrounds of an organism fundamentally influence the balance between risk and resilience to stress. Sex, age, and environment transact with responses to trauma in ways that can mitigate or exacerbate the likelihood that post-traumatic stress disorder will develop. Translational approaches to modeling affective disorders in animals will ultimately provide novel treatments and a better understanding of the neurobiological underpinnings behind these debilitating disorders. The extant literature on trauma/stress has focused predominately on limbic and cortical structures that innervate the hypothalamic-pituitary-adrenal axis and influence glucocorticoid-mediated negative feedback. It is through these neuroendocrine pathways that a self-perpetuating fear memory can propagate the long-term effects of early life trauma. Recent work incorporating translational approaches has provided novel pathways that can be influenced by early life stress, such as the glucocorticoid receptor chaperones, including FKBP51. Animal models of stress have differing effects on behavior and endocrine pathways; however, complete models replicating clinical characteristics of risk and resilience have not been rigorously studied. This review discusses a four-factor model that considers the importance of studying both risk and resilience in understanding the developmental response to trauma/stress. Consideration of the multifactorial nature of clinical populations in the design of preclinical models and the application of preclinical findings to clinical treatment approaches comprise the core of translational reciprocity, which is discussed in the context of the four-factor model. Copyright © 2012 IBRO. Published by Elsevier Ltd. All rights reserved.
Hausdörfer, J; Heller, W; Junger, H; Oldenkott, P; Stunkat, R
1976-10-01
The response of the 2,3-diphosphoglycerate (DPG) levels in the blood and brain tissue to a craniocerebral trauma of varying severity was studied in anaesthetized rats. A trauma producing cerebral contusion was followed within two hours by a highly significant rise in DPG concentration in the blood as compared with the control animals or only mildly traumatized rats. The DPG levels in the brain tissue showed no significant differences. Similar changes in DPG concentration were observed in the blood of patients with craniocerebral injuries. The DPG-mediated increased release of oxygen to the tissues represents a compensatory mechanism and is pathognomic for craniocerebral trauma. Patients undergoing surgery with extracorporeal circulation lack this mechanism for counteracting hypoxaemia; already during thoracotomy the DPG concentration in the blood fell significantly and did not reach its original level until 72 hours after the operation. In stored, ACD stabilized, blood the DPG concentration gradually decreases. Estimations carried out over 28 days showed a continuous statistically significant loss of DPG. After 24 hours the DPG levels in stored blood had already dropped to the lower limits of normal - a fact that has to be taken into account in massive blood transfusions.
Martin, GT
2016-01-01
In the 20th century, the complications of head injuries were controlled but not eliminated. The wars of the 21st century turned attention to blast, the instant of impact and the primary injury of concussion. Computer calculations have established that in the first 5 milliseconds after the impact, four independent injuries on the brain are inflicted: 1) impact and its shockwave, 2) deceleration, 3) rotation and 4) skull deformity with vibration (or resonance). The recovery, pathology and symptoms after acute brain trauma have always been something of a puzzle. The variability of these four modes of injury, along with a variable reserve of neurones, explains some of this problem. PMID:26688392
Baltazar, Gerard Anthony; Pate, Amy J; Panigrahi, Benita; Sharp, Audrey; Smith, Michael; Chendrasekhar, Akella
2015-01-01
Prevention of secondary brain injury is a key component of acute management of patients with severe traumatic brain injury (TBI). Haemoglobin concentration may have an impact on optimization of cerebral oxygenation. Patients with TBI may best be served by an organized trauma service. The objective is to determine if haemoglobin concentration or dedicated trauma admission has an impact on outcomes after severe TBI. This study retrospectively analysed consecutive patients with severe TBI admitted to a level-I trauma centre over 3 years. Patients <16 years-old and with length of stay (LOS) <24 hours were excluded. Data were collected on demographics; injury severity; LOS; admission service; survival to discharge; and haemoglobin levels from hospital days 1-7. Data were also collected on number of transfusions of packed red blood cells. The sample was stratified based on admission service and survival to discharge. Of 147 patients (age = 54.1 ± 3.7 years), overall mortality rate was 15.4% (n = 23). Overall, non-survivors had lower daily and 7-day mean haemoglobin levels (10.7 ± 0.9 vs. 12.9 ± 0.4 g dL(-1), p < 0.001). Non-surgical admissions had lower haemoglobin levels and a higher mortality rate (28.9% vs. 12.2%, p < 0.001) compared to dedicated trauma admissions. Among patients with severe TBI, higher haemoglobin levels and maintenance as a dedicated trauma admission are associated with higher survival to discharge.
Shors, Tracey J; Tobόn, Krishna; DiFeo, Gina; Durham, Demetrius M; Chang, Han Yan M
2016-01-25
Sexual aggression can disrupt processes related to learning as females emerge from puberty into young adulthood. To model these experiences in laboratory studies, we developed SCAR, which stands for Sexual Conspecific Aggressive Response. During puberty, a rodent female is paired daily for 30-min with a sexually-experienced adult male. During the SCAR experience, the male tracks the anogenital region of the female as she escapes from pins. Concentrations of the stress hormone corticosterone were significantly elevated during and after the experience. Moreover, females that were exposed to the adult male throughout puberty did not perform well during training with an associative learning task nor did they learn well to express maternal behaviors during maternal sensitization. Most females that were exposed to the adult male did not learn to care for offspring over the course of 17 days. Finally, females that did not express maternal behaviors retained fewer newly-generated cells in their hippocampus whereas those that did express maternal behaviors retained more cells, most of which would differentiate into neurons within weeks. Together these data support SCAR as a useful laboratory model for studying the potential consequences of sexual aggression and trauma for the female brain during puberty and young adulthood.
CSF-Biomarkers in Olympic Boxing: Diagnosis and Effects of Repetitive Head Trauma
Neselius, Sanna; Brisby, Helena; Theodorsson, Annette; Blennow, Kaj; Zetterberg, Henrik; Marcusson, Jan
2012-01-01
Background Sports-related head trauma is common but still there is no established laboratory test used in the diagnostics of minimal or mild traumatic brain injuries. Further the effects of recurrent head trauma on brain injury markers are unknown. The purpose of this study was to investigate the relationship between Olympic (amateur) boxing and cerebrospinal fluid (CSF) brain injury biomarkers. Methods The study was designed as a prospective cohort study. Thirty Olympic boxers with a minimum of 45 bouts and 25 non-boxing matched controls were included in the study. CSF samples were collected by lumbar puncture 1–6 days after a bout and after a rest period for at least 14 days. The controls were tested once. Biomarkers for acute and chronic brain injury were analysed. Results NFL (mean ± SD, 532±553 vs 135±51 ng/L p = 0.001), GFAP (496±238 vs 247±147 ng/L p<0.001), T-tau (58±26 vs 49±21 ng/L p<0.025) and S-100B (0.76±0.29 vs 0.60±0.23 ng/L p = 0.03) concentrations were significantly increased after boxing compared to controls. NFL (402±434 ng/L p = 0.004) and GFAP (369±113 ng/L p = 0.001) concentrations remained elevated after the rest period. Conclusion Increased CSF levels of T-tau, NFL, GFAP, and S-100B in >80% of the boxers demonstrate that both the acute and the cumulative effect of head trauma in Olympic boxing may induce CSF biomarker changes that suggest minor central nervous injuries. The lack of normalization of NFL and GFAP after the rest period in a subgroup of boxers may indicate ongoing degeneration. The recurrent head trauma in boxing may be associated with increased risk of chronic traumatic brain injury. PMID:22496755
CSF-biomarkers in Olympic boxing: diagnosis and effects of repetitive head trauma.
Neselius, Sanna; Brisby, Helena; Theodorsson, Annette; Blennow, Kaj; Zetterberg, Henrik; Marcusson, Jan
2012-01-01
Sports-related head trauma is common but still there is no established laboratory test used in the diagnostics of minimal or mild traumatic brain injuries. Further the effects of recurrent head trauma on brain injury markers are unknown. The purpose of this study was to investigate the relationship between Olympic (amateur) boxing and cerebrospinal fluid (CSF) brain injury biomarkers. The study was designed as a prospective cohort study. Thirty Olympic boxers with a minimum of 45 bouts and 25 non-boxing matched controls were included in the study. CSF samples were collected by lumbar puncture 1-6 days after a bout and after a rest period for at least 14 days. The controls were tested once. Biomarkers for acute and chronic brain injury were analysed. NFL (mean ± SD, 532±553 vs 135±51 ng/L p = 0.001), GFAP (496±238 vs 247±147 ng/L p<0.001), T-tau (58±26 vs 49±21 ng/L p<0.025) and S-100B (0.76±0.29 vs 0.60±0.23 ng/L p = 0.03) concentrations were significantly increased after boxing compared to controls. NFL (402±434 ng/L p = 0.004) and GFAP (369±113 ng/L p = 0.001) concentrations remained elevated after the rest period. Increased CSF levels of T-tau, NFL, GFAP, and S-100B in >80% of the boxers demonstrate that both the acute and the cumulative effect of head trauma in Olympic boxing may induce CSF biomarker changes that suggest minor central nervous injuries. The lack of normalization of NFL and GFAP after the rest period in a subgroup of boxers may indicate ongoing degeneration. The recurrent head trauma in boxing may be associated with increased risk of chronic traumatic brain injury.
[First aid system for trauma: development and status].
Chen, D K; Lin, W C; Zhang, P; Kuang, S J; Huang, W; Wang, T B
2017-04-18
With the great progress of the economy, the level of industrialization has been increasing year by year, which leads to an increase in accidental trauma accidents. Chinese annual death of trauma is already more than 400 000, which makes trauma the fifth most common cause of death, following malignant tumor, heart, brain and respiratory diseases. Trauma is the leading cause of the death of young adults. At the same time, trauma has become a serious social problem in peace time. Trauma throws great treats on human health and life. As an important part in the medical and social security system, the emergency of trauma system occupies a very important position in the emergency medical service system. In European countries as well as the United States and also many other developed countries, trauma service system had a long history, and progressed to an advanced stage. However, Chinese trauma service system started late and is still developing. It has not turned into a complete and standardized system yet. This review summarizes the histories and current situations of the development of traumatic first aid system separately in European countries, the United States and our country. Special attentions are paid to the effects of the pre- and in-hospital emergency care. We also further try to explore the Chinese trauma emergency model that adapts to the situations of China and characteristics of different regions of China. Our review also introduces the trauma service system that suits the situations of China proposed by Professor Jiang Baoguo's team in details, taking Chinese conditions into account, they conducted a thematic study and made an expert consensus on pre-hospital emergency treatment of severe trauma, providing a basic routine and guidance of severe trauma treatment for those pre-hospital emergency physicians. They also advised to establish independent trauma disciplines and trauma specialist training systems, and to build the regional trauma care system as well as the standards for graded treatment, thus establishing a multiple disciplinary team (MDT) of severe trauma. In this way, we can reduce the mortality and disability risks of severe trauma, improve the quality of patients' life, and save more lives.
Katayama, Y; Kawamata, T
2003-01-01
The early massive edema caused by severe cerebral contusion results in progressive intracranial pressure (ICP) elevation and clinical deterioration within 24-72 hours post-trauma. Surgical excision of the necrotic brain tissue represents the only therapy, which can provide satisfactory control of the elevated ICP and clinical deterioration. In order to elucidate the mechanisms underlying the early massive edema, we have carried out a series of detailed clinical studies. Diffusion magnetic resonance (MR) imaging and apparent diffusion co-efficient (ADC) mapping suggest that cells in the central area of contusion undergo shrinkage, disintegration and homogenization, whereas cellular swelling is predominant in the peripheral area during the period of 24-72 hours post-trauma. The ADC values in the central and peripheral areas are maximally dissociated during this period. A large amount of edema fluid accumulates within the necrotic brain tissue of the central area beginning at approximately 24 hours post-trauma. We have found that fluid-blood interface formation within the central area does not represent an uncommon finding in various neuroimaging examinations of cerebral contusions, indicating layering of red blood cells within the necrotic brain tissue accumulating voluminous edema fluid. Intravenous slow infusion of gadolinium-DTPA and delayed MR imaging revealed that the central area of contusion can be enhanced at 24-48 hours post-trauma. implying that water supply from the blood vessels is not completely interrupted. Necrotic brain tissue sampled from the central area of contusion during surgery demonstrates a very high osmolality. It appears that the capacitance for edema fluid accumulation increases in the central area, whereas cellular swelling in the peripheral area elevates the resistance for edema fluid propagation. Combination of these circumstances may facilitate edema fluid accumulation in the central area. We also suggest that the dissociation of ADC values and high osmolality within the necrotic brain tissue may generate an osmotic potential across the central and peripheral areas and contribute to the early massive edema caused by cerebral contusion.
Effect of gamma-hydroxybutyric acid on tissue Na+,K- ATPase levels after experimental head trauma.
Yosunkaya, A; Ustün, M E; Bariskaner, H; Tavlan, A; Gürbilek, M
2004-05-01
A failure of the Na(+),K(+)-ATPase activity (which is essential for ion flux across the cell membranes) occurs in many pathological conditions and may lead to cell dysfunction or even cell death. By altering the concentration of specific opioid peptides, gamma-hydroxybutyric acid (GHB) may change ion flux across cell membranes and produce the 'channel arrest' which we assumed will inhibit the failure of Na+,K(+)-ATPase activity and therefore lead to energy conservation and cell protection. Therefore we planned this study to see the effects of GHB at two different doses on Na(+),K(+)-ATPase activity in an experimental head trauma model. Forty New Zealand rabbits were divided equally into four groups: group I was the sham-operated group, group II (untreated group), group III received head trauma and intravenous (i.v.) 500 mg/kg GHB and group IV received head trauma and i.v. 50 mg/kg GHB. Head trauma was delivered by performing a craniectomy over the right hemisphere and dropping a weight of 10 g from a height of 80 cm. The non-traumatized (left) side was named as 'a' and the traumatized (right) side as 'b'. One hour after the trauma in groups II and III and craniotomy in group I, brain cortices were resected from both sides and in group I only from the right side was the tissue Na-K-ATPase activity determined. The mean +/- SD of Na(+),K(+)-ATPase levels of each group are as follows: group I - 5.97 +/- 0.55; group IIa - 3.90 +/- 1.08; group IIb - 3.58 +/- 0.90; group IIIa - 5.53 +/- 0.60; group IIIb - 5.33 +/- 0.88; group IVa - 5.05 +/- 0.72; group IVb - 4.93 +/- 0.67. The Na(+),K(+)-ATPase levels of group IIa, IIb, IVa and IVb were significantly different from group S (P < 0.05). There were also significant differences between group IIa and groups IIIa and IVa; group IIb and groups IIIb and IVb (P < 0.05). We conclude that GHB is effective in suppressing the decrease in Na(+),K(+)-ATPase levels in brain tissue at two different dose schedules after head trauma.
Interhemispheric Information Transfer: A New Diagnostic Method for Mild Traumatic Brain Injury
2011-10-01
brain tumors, meningitis, cerebral palsy, encephalitis, brain abscesses , vascular malformations, cerebrovascular disease, Alzheimer’s disease...disease including head trauma with loss of consciousness 2) Having a contraindication to MRI such as pregnancy, breast feeding, surgical clips
Hashemi, Behrooz; Amanat, Mahnaz; Baratloo, Alireza; Forouzanfar, Mohammad Mehdi; Rahmati, Farhad; Motamedi, Maryam; Safari, Saeed
2016-11-01
To date, many prognostic models have been proposed to predict the outcome of patients with traumatic brain injuries. External validation of these models in different populations is of great importance for their generalization. The present study was designed, aiming to determine the value of CRASH prognostic model in prediction of 14-day mortality (14-DM) and 6-month unfavorable outcome (6-MUO) of patients with traumatic brain injury. In the present prospective diagnostic test study, calibration and discrimination of CRASH model were evaluated in head trauma patients referred to the emergency department. Variables required for calculating CRASH expected risks (ER), and observed 14-DM and 6-MUO were gathered. Then ER of 14-DM and 6-MUO were calculated. The patients were followed for 6 months and their 14-DM and 6-MUO were recorded. Finally, the correlation of CRASH ER and the observed outcome of the patients was evaluated. The data were analyzed using STATA version 11.0. In this study, 323 patients with the mean age of 34.0 ± 19.4 years were evaluated (87.3% male). Calibration of the basic and CT models in prediction of 14-day and 6-month outcome were in the desirable range (P < 0.05). Area under the curve in the basic model for prediction of 14-DM and 6-MUO were 0.92 (95% CI: 0.89-0.96) and 0.92 (95% CI: 0.90-0.95), respectively. In addition, area under the curve in the CT model for prediction of 14-DM and 6-MUO were 0.93 (95% CI: 0.91-0.97) and 0.93 (95% CI: 0.91-0.96), respectively. There was no significant difference between the discriminations of the two models in prediction of 14-DM (p = 0.11) and 6-MUO (p = 0.1). The results of the present study showed that CRASH prediction model has proper discrimination and calibration in predicting 14-DM and 6-MUO of head trauma patients. Since there was no difference between the values of the basic and CT models, using the basic model is recommended to simplify the risk calculations.
Federal Register 2010, 2011, 2012, 2013, 2014
2013-03-25
... structural brain lesion). (1) If a mariner is determined to be low-risk for seizure recurrence, does not... penetrating head injury; (b) Intracerebral hemorrhage of any etiology, including stroke and trauma; (c) Brain... hemorrhage; (f) Post-operative brain surgery with significant brain hemorrhage; or (g) Brain tumor. (4) Under...
Sen, Arko; Gurdziel, Katherine; Liu, Jenney; Qu, Wen; Nuga, Oluwademi O; Burl, Rayanne B; Hüttemann, Maik; Pique-Regi, Roger; Ruden, Douglas M
2017-01-01
Traumatic brain injury (TBI) can cause persistent pathological alteration of neurons. This may lead to cognitive dysfunction, depression and increased susceptibility to life threatening diseases, such as epilepsy and Alzheimer's disease. To investigate the underlying genetic and molecular basis of TBI, we subjected w 1118 Drosophila melanogaster to mild closed head trauma and found that mitochondrial activity is reduced in the brains of these flies 24 h after inflicting trauma. To determine the transcriptomic changes after mild TBI, we collected fly heads 24 h after inflicting trauma, and performed RNA-seq analyses. Classification of alternative splicing changes showed selective retention (RI) of long introns (>81 bps), with a mean size of ~3,000 nucleotides. Some of the genes containing RI showed a significant reduction in transcript abundance and are involved in mitochondrial metabolism such as Isocitrate dehydrogenase (Idh), which makes α-KG, a co-factor needed for both DNA and histone demethylase enzymes. The long introns are enriched in CA-rich motifs known to bind to Smooth (Sm), a heterogeneous nuclear ribonucleoprotein L (hnRNP-L) class of splicing factor, which has been shown to interact with the H3K36 histone methyltransferase, SET2, and to be involved in intron retention in human cells. H3K36me3 is a histone mark that demarcates exons in genes by interacting with the mRNA splicing machinery. Mutating sm ( sm 4 /Df) resulted in loss of both basal and induced levels of RI in many of the same long-intron containing genes. Reducing the levels of Kdm4A, the H3K36me3 histone demethylase, also resulted in loss of basal levels of RI in many of the same long-intron containing genes. Chromatin immunoprecipitation followed by deep sequencing (ChIP-seq) for H3K36me3 revealed increased levels of this histone modification in retained introns post-trauma at CA-rich motifs. Based on these results, we propose a model in which TBI temporarily decreases mitochondrial activity in the brain 24 h after inflicting trauma, which decreases α-KG levels, and increases H3K36me3 levels and intron retention of long introns by decreasing Kdm4A activity. The consequent reduction in mature mRNA levels in metabolism genes, such as Idh, further reduces α-KG levels in a negative feedback loop. We further propose that decreasing metabolism after TBI in such a manner is a protective mechanism that gives the brain time to repair cellular damage induced by TBI.
Functional MR imaging assessment of a non-responsive brain injured patient.
Moritz, C H; Rowley, H A; Haughton, V M; Swartz, K R; Jones, J; Badie, B
2001-10-01
Functional magnetic resonance imaging (fMRI) was requested to assist in the evaluation of a comatose 38-year-old woman who had sustained multiple cerebral contusions from a motor vehicle accident. Previous electrophysiologic studies suggested absence of thalamocortical processing in response to median nerve stimulation. Whole-brain fMRI was performed utilizing visual, somatosensory, and auditory stimulation paradigms. Results demonstrated intact task-correlated sensory and cognitive blood oxygen level dependent (BOLD) hemodynamic response to stimuli. Electrodiagnostic studies were repeated and evoked potentials indicated supratentorial recovery in the cerebrum. At 3-months post trauma the patient had recovered many cognitive & sensorimotor functions, accurately reflecting the prognostic fMRI evaluation. These results indicate that fMRI examinations may provide a useful evaluation for brain function in non-responsive brain trauma patients.
Risk of traumatic brain injuries in children younger than 24 months with isolated scalp hematomas.
Dayan, Peter S; Holmes, James F; Schutzman, Sara; Schunk, Jeffrey; Lichenstein, Richard; Foerster, Lillian A; Hoyle, John; Atabaki, Shireen; Miskin, Michelle; Wisner, David; Zuspan, SallyJo; Kuppermann, Nathan
2014-08-01
We aimed to determine the association between scalp hematoma characteristics and traumatic brain injuries in young children with blunt head trauma who have no other symptoms or signs suggestive of traumatic brain injuries (defined as "isolated scalp hematomas"). This was a secondary analysis of children younger than 24 months with minor blunt head trauma from a prospective cohort study in 25 Pediatric Emergency Care Applied Research Network emergency departments. Treating clinicians completed a structured data form. For children with isolated scalp hematomas, we determined the prevalence of and association between scalp hematoma characteristics and (1) clinically important traumatic brain injury (death, neurosurgery for traumatic brain injury, intubation >24 hours for traumatic brain injury, or positive computed tomography (CT) scan in association with hospitalization ≥2 nights for traumatic brain injury); and (2) traumatic brain injury on CT. Of 10,659 patients younger than 24 months were enrolled, 2,998 of 10,463 (28.7%) with complete data had isolated scalp hematomas. Clinically important traumatic brain injuries occurred in 12 patients (0.4%; 95% confidence interval [CI] 0.2% to 0.7%); none underwent neurosurgery (95% CI 0% to 0.1%). Of 570 patients (19.0%) for whom CTs were obtained, 50 (8.8%; 95% CI 6.6% to 11.4%) had traumatic brain injuries on CT. Younger age, non-frontal scalp hematoma location, increased scalp hematoma size, and severe injury mechanism were independently associated with traumatic brain injury on CT. In patients younger than 24 months with isolated scalp hematomas, a minority received CTs. Despite the occasional presence of traumatic brain injuries on CT, the prevalence of clinically important traumatic brain injuries was very low, with no patient requiring neurosurgery. Clinicians should use patient age, scalp hematoma location and size, and injury mechanism to help determine which otherwise asymptomatic children should undergo neuroimaging after minor head trauma. Copyright © 2014 American College of Emergency Physicians. Published by Mosby, Inc. All rights reserved.
Lee, Royce J; Fanning, Jennifer R; Coccaro, Emil F
2016-05-01
Childhood trauma is a risk factor for personality disorder. We have previously shown that childhood trauma is associated with increased central corticotrophin-releasing hormone concentration in adults with personality disorder. In the brain, the release of corticotrophin-releasing hormone can be stimulated by noradrenergic neuronal activity, raising the possibility that childhood trauma may affect the hypothalamic-pituitary adrenal (HPA) axis by altering brain noradrenergic function. In this study, we sought to test the hypothesis that childhood trauma is associated with blunted growth hormone response to the α-2 adrenergic autoreceptor agonist clonidine. All subjects provided written informed consent. Twenty personality disordered and twenty healthy controls (without personality disorder or Axis I psychopathology) underwent challenge with clonidine, while plasma Growth Hormone (GH) concentration was monitored by intravenous catheter. On a different study session, subjects completed the Childhood Trauma Questionnaire and underwent diagnostic interviews. Contrary to our a priori hypothesis, childhood trauma was associated with enhanced GH response to clonidine. This positive relationship was present in the group of 40 subjects and in the subgroup 20 personality disordered subjects, but was not detected in the healthy control subjects when analyzed separately. The presence of personality disorder was unrelated to the magnitude of GH response. Childhood trauma is positively correlated with GH response to clonidine challenge in adults with personality disorder. Enhanced rather that blunted GH response differentiates childhood trauma from previously identified negative predictors of GH response, such as anxiety or mood disorder. Copyright © 2016 Elsevier Ltd. All rights reserved.
Jayakumar, A R; Bak, L K; Rama Rao, K V; Waagepetersen, H S; Schousboe, A; Norenberg, M D
2016-02-01
Traumatic brain injury (TBI) is a devastating neurological disorder that usually presents in acute and chronic forms. Brain edema and associated increased intracranial pressure in the early phase following TBI are major consequences of acute trauma. On the other hand, neuronal injury, leading to neurobehavioral and cognitive impairments, that usually develop months to years after single or repetitive episodes of head trauma, are major consequences of chronic TBI. The molecular mechanisms responsible for TBI-induced injury, however, are unclear. Recent studies have suggested that early mitochondrial dysfunction and subsequent energy failure play a role in the pathogenesis of TBI. We therefore examined whether oxidative metabolism of (13)C-labeled glucose, lactate or glutamine is altered early following in vitro mechanical percussion-induced trauma (5 atm) to neurons (4-24 h), and whether such events contribute to the development of neuronal injury. Cell viability was assayed using the release of the cytoplasmic enzyme lactate dehydrogenase (LDH), together with fluorescence-based cell staining (calcein and ethidium homodimer-1 for live and dead cells, respectively). Trauma had no effect on the LDH release in neurons from 1 to 18 h. However, a significant increase in LDH release was detected at 24 h after trauma. Similar findings were identified when traumatized neurons were stained with fluorescent markers. Additionally (13)C-labeling of glutamate showed a small, but statistically significant decrease at 14 h after trauma. However, trauma had no effect on the cycling ratio of the TCA cycle at any time-period examined. These findings indicate that trauma does not cause a disturbance in oxidative metabolism of any of the substrates used for neurons. Accordingly, such metabolic disturbance does not appear to contribute to the neuronal death in the early stages following trauma.
Chronic Subdural Hematoma in the Aged, Trauma or Degeneration?
Lee, Kyeong-Seok
2016-01-01
Chronic subdural hematomas (CSHs) are generally regarded to be a traumatic lesion. It was regarded as a stroke in 17th century, an inflammatory disease in 19th century. From 20th century, it became a traumatic lesion. CSH frequently occur after a trauma, however, it cannot occur when there is no enough subdural space even after a severe head injury. CSH may occur without trauma, when there is sufficient subdural space. The author tried to investigate trends in the causation of CSH. By a review of literature, the author suggested a different view on the causation of CSH. CSH usually originated from either a subdural hygroma or an acute subdural hematoma. Development of CSH starts from the separation of the dural border cell (DBC) layer, which induces proliferation of DBCs with production of neomembrane. Capillaries will follow along the neomembrane. Hemorrhage would occur into the subdural fluid either by tearing of bridge veins or repeated microhemorrhage from the neomembrane. That is the mechanism of hematoma enlargement. Trauma or bleeding tendency may precipitate development of CSH, however, it cannot lead CSH, if there is no sufficient subdural space. The key determinant for development of CSH is a sufficient subdural space, in other words, brain atrophy. The most common and universal cause of brain atrophy is the aging. Modifying Virchow's description, CSH is sometimes traumatic, but most often caused by degeneration of the brain. Now, it is reasonable that degeneration of brain might play pivotal role in development of CSH in the aged persons.
Use of the emotional Stroop to assess psychological trauma following traumatic brain injury.
Coates, Richard C
2008-04-01
A modified Stroop task was used to investigate the hypothesis that implicit memory may be a possible mechanism for the development of acute stress disorder (ASD) in patients who have suffered a closed head injury. Three groups of hospital patients were compared within 1 month post-trauma: road traffic accident (RTA) patients with a brain injury (n = 15), RTA patients without a brain injury (n = 13) and a control group of orthopaedic and plastics patients (n = 15). Participants named colours of five types of words: RTA-related words, words related to hospitalization, obsessive-compulsive disorder (OCD) words, positive words and neutral words. Participants were also administered the Acute Stress Disorder Interview and the State-Trait Anxiety Inventory. Both RTA patients with and without a brain injury demonstrated significant interference on words related to an RTA. Significant interference was unexpectedly observed for OCD words in RTA patients. Control patients did not display significant interference effects. Findings suggested that patients, both with and without explicit recall for an RTA, responded similarly on a task involving implicit memory for trauma. Possible implications for ASD and Post-traumatic Stress Disorder are discussed.
Patel, Jayshil J; Rosenthal, Martin D; Miller, Keith R; Martindale, Robert G
2016-08-01
The purpose of this review is to describe established and emerging mechanisms of gut injury and dysfunction in trauma, describe emerging strategies to improve gut dysfunction, detail the effect of trauma on the gut microbiome, and describe the gut-brain connection in traumatic brain injury. Newer data suggest intraluminal contents, pancreatic enzymes, and hepatobiliary factors disrupt the intestinal mucosal layer. These mechanisms serve to perpetuate the inflammatory response leading to multiple organ dysfunction syndrome (MODS). To date, therapies to mitigate acute gut dysfunction have included enteral nutrition and immunonutrition; emerging therapies aimed to intestinal mucosal layer disruption, however, include protease inhibitors such as tranexamic acid, parenteral nutrition-supplemented bombesin, and hypothermia. Clinical trials to demonstrate benefit in humans are needed before widespread applications can be recommended. Despite resuscitation, gut dysfunction promotes distant organ injury. In addition, postresuscitation nosocomial and iatrogenic 'hits' exaggerate the immune response, contributing to MODS. This was a provocative concept, suggesting infectious and noninfectious causes of inflammation may trigger, heighten, and perpetuate an inflammatory response culminating in MODS and death. Emerging evidence suggests posttraumatic injury mechanisms, such as intestinal mucosal disruption and shifting of the gut microbiome to a pathobiome. In addition, traumatic brain injury activates the gut-brain axis and increases intestinal permeability.
Childhood trauma, midbrain activation and psychotic symptoms in borderline personality disorder
Nicol, K; Pope, M; Romaniuk, L; Hall, J
2015-01-01
Childhood trauma is believed to contribute to the development of borderline personality disorder (BPD), however the mechanism by which childhood trauma increases risk for specific symptoms of the disorder is not well understood. Here, we explore the relationship between childhood trauma, brain activation in response to emotional stimuli and psychotic symptoms in BPD. Twenty individuals with a diagnosis of BPD and 16 healthy controls were recruited to undergo a functional MRI scan, during which they viewed images of faces expressing the emotion of fear. Participants also completed the childhood trauma questionnaire (CTQ) and a structured clinical interview. Between-group differences in brain activation to fearful faces were limited to decreased activation in the BPD group in the right cuneus. However, within the BPD group, there was a significant positive correlation between physical abuse scores on the CTQ and BOLD signal in the midbrain, pulvinar and medial frontal gyrus to fearful (versus neutral) faces. In addition there was a significant correlation between midbrain activation and reported psychotic symptoms in the BPD group (P<0.05). These results show that physical abuse in childhood is, in individuals with BPD, associated with significantly increased activation of a network of brain regions including the midbrain in response to emotional stimuli. Sustained differences in the response of the midbrain to emotional stimuli in individuals with BPD who suffered childhood physical abuse may underlie the vulnerability of these patients to developing psychotic symptoms. PMID:25942040
Del Castillo-Calcáneo, Juan D; Bravo-Angel, Ulises; Mendez-Olan, Raúl; Rodriguez-Valencia, Francisco; Valdés-García, Javier; García-González, Ulises; Broc-Haro, Guy G
2016-01-01
Traumatic Brain Injury (TBI) is a major cause of death and disability in our society, we present the first case report of non-missile penetrating (NMP) cranial trauma with a machete in Mexico, and our objective by presenting this case is to prove the usefulness of recently proposed algorithms in the treatment of NMP PRESENTATION OF CASE: We present the case of a 47 year old woman who received a machete hit to the right side of her head during an assault., she arrived fully conscious to the emergency department (ED), computed tomography was performed and based on the findings of this study and in accordance to recently proposed algorithms for managing NMP cranial trauma a craniotomy was performed, at follow-up the patient presented wtih minor neurological disability in the form of left hemiparesis. Non-missile penetrating (NMP) lesions are defined as having an impact velocity of less than 100m/s, causing injury by laceration and maceration, An algorithm for treating NMP cranial trauma has been recently published in the Journal World Neurosurgery by De Holanda et al., in this case we followed the algorithm in order to provide best care available for our patient with good results. The use of current algorithms for managing NMP cranial trauma has proved to be very useful when applied on this particular case. GCS on admission is an important prognostic factor in NMP cranial trauma. Copyright © 2016 The Author(s). Published by Elsevier Ltd.. All rights reserved.
... involves the brain Liver failure Thyroid conditions that cause low thyroid hormone levels or very high thyroid hormone levels Brain disorders or injury, such as: Dementia or Alzheimer disease Head trauma Seizure Stroke Infections that affect ...
Schulz, Chris; Woerner, Ulrich; Luelsdorf, Peter
2008-04-01
The primary treatment of penetrating missile injuries of the brain includes debridement of the scalp, fractured skull, and necrotic brain parenchyma. It is acceptable to remove all bony and metallic fragments that are accessible without additional trauma to nondamaged brain regions. Therefore, bone chips and bullets are often initially retained in the brain and are supposedly responsible for delayed cerebral infections and posttraumatic seizures. We successfully operated on 3 patients electively to remove bony and metallic fragments secondarily after penetrating brain trauma. We used an electromagnetic neuronavigation system for preoperative planning and chose a less invasive approach for the exact intraoperative localization of the fragments. All fragments were extracted without any problems. No patients had any additional neurologic deficits, and no signs of cerebral infections or seizures occurred between 4 and 8 weeks after the operative revision. We recommend the implementation of neuronavigation techniques into the surgical strategy for secondary removal of retained missile fragments.
Cook, Rebecca S; Gillespie, Gordon L; Kronk, Rebecca; Daugherty, Margot C; Moody, Suzanne M; Allen, Lesley J; Shebesta, Kaaren B; Falcone, Richard A
2013-04-01
Nurses are key providers in the care of children with mild traumatic brain injury (mTBI). New treatment recommendations emphasize symptom assessment and brain rest guidelines to optimize recovery. This study compared pediatric trauma core nurses' knowledge, degree of confidence, and perceived change in practice following mTBI education. Twenty-eight trauma core nurses were invited to participate in this voluntary quasiexperimental, one-group pretest-posttest study. Multiple choice questions were developed to assess knowledge, and self-report Likert scale statements were used to evaluate confidence and change in practice. Baseline data of 25 trauma core nurses were assessed and then reassessed 1 month postintervention. Paired samples analysis showed significant improvement in knowledge (mean pretest: 33.6% vs. mean posttest score: 79.2%; 95% CI [35.6, 55.6]; t = 9.368; p < .001). All but two test questions yielded a significant increase in the number of participants with correct responses. Preintervention confidence was low (0-32% per question) and significantly increased postintervention (26%-84% per question). Despite increased administration of the symptom assessment and identification of interventions for symptom resolution posteducation (χ(2)6.125, p = .001), these scores remained low. Findings demonstrate that educational intervention effectively increased trauma core nurses' knowledge and confidence in applying content into practice. Postintervention scores did not uniformly increase, and not all trauma core nurses consistently transferred content into practice. Further research is recommended to evaluate which teaching method and curriculum content are most effective to educate trauma core nurses and registered nurses caring for patients with mTBI and to identify barriers to incorporating this knowledge in practice.
Boutin, Amélie; Moore, Lynne; Green, Robert S; Zarychanski, Ryan; Erdogan, Mete; Lauzier, François; English, Shane; Fergusson, Dean A; Butler, Michael; McIntyre, Lauralyn; Chassé, Michaël; Lessard Bonaventure, Paule; Léger, Caroline; Desjardins, Philippe; Griesdale, Donald; Lacroix, Jacques; Turgeon, Alexis F
2018-06-01
We aimed to evaluate the association between transfusion practices and clinical outcomes in patients with traumatic brain injury. We conducted a retrospective cohort study of adult patients with moderate or severe traumatic brain injury admitted to the intensive care unit (ICU) of a level I trauma center between 2009 and 2013. The associations between hemoglobin (Hb) level, red blood cell (RBC) transfusion and clinical outcomes were estimated using robust Poisson models and proportional hazard models with time-dependent variables, adjusted for confounders. We included 215 patients. Sixty-six patients (30.7%) were transfused during ICU stay. The median pre-transfusion Hb among transfused patients was 81g/L (IQR 67-100), while median nadir Hb among non-transfused patients was 110g/L (IQR 93-123). Poor outcomes were significantly more frequent in patients who were transfused (mortality risk ratio [RR]: 2.15 [95% CI 1.37-3.38] and hazard ratio: 3.06 [95% CI 1.57-5.97]; neurological complications RR: 3.40 [95% CI 1.35-8.56]; trauma complications RR: 1.65 [95% CI 1.31-2.08]; ICU length of stay geometric mean ratio: 1.42 [95% CI 1.06-1.92]). During ICU stay, transfused patients tended to have lower Hb levels and worse outcomes than patients who did not receive RBCs, after adjustment for confounders. Copyright © 2017 Elsevier Inc. All rights reserved.
The Impact of the Brain-Derived Neurotrophic Factor Gene on Trauma and Spatial Processing.
Miller, Jessica K; McDougall, Siné; Thomas, Sarah; Wiener, Jan
2017-11-27
The influence of genes and the environment on the development of Post-Traumatic Stress Disorder (PTSD) continues to motivate neuropsychological research, with one consistent focus being the Brain-Derived Neurotrophic Factor (BDNF) gene, given its impact on the integrity of the hippocampal memory system. Research into human navigation also considers the BDNF gene in relation to hippocampal dependent spatial processing. This speculative paper brings together trauma and spatial processing for the first time and presents exploratory research into their interactions with BDNF. We propose that quantifying the impact of BDNF on trauma and spatial processing is critical and may well explain individual differences in clinical trauma treatment outcomes and in navigation performance. Research has already shown that the BDNF gene influences PTSD severity and prevalence as well as navigation behaviour. However, more data are required to demonstrate the precise hippocampal dependent processing mechanisms behind these influences in different populations and environmental conditions. This paper provides insight from recent studies and calls for further research into the relationship between allocentric processing, trauma processing and BDNF. We argue that research into these neural mechanisms could transform PTSD clinical practice and professional support for individuals in trauma-exposing occupations such as emergency response, law enforcement and the military.
Pathogenesis of Brain Edema and Investigation into Anti-Edema Drugs
Michinaga, Shotaro; Koyama, Yutaka
2015-01-01
Brain edema is a potentially fatal pathological state that occurs after brain injuries such as stroke and head trauma. In the edematous brain, excess accumulation of extracellular fluid results in elevation of intracranial pressure, leading to impaired nerve function. Despite the seriousness of brain edema, only symptomatic treatments to remove edema fluid are currently available. Thus, the development of novel anti-edema drugs is required. The pathogenesis of brain edema is classified as vasogenic or cytotoxic edema. Vasogenic edema is defined as extracellular accumulation of fluid resulting from disruption of the blood-brain barrier (BBB) and extravasations of serum proteins, while cytotoxic edema is characterized by cell swelling caused by intracellular accumulation of fluid. Various experimental animal models are often used to investigate mechanisms underlying brain edema. Many soluble factors and functional molecules have been confirmed to induce BBB disruption or cell swelling and drugs targeted to these factors are expected to have anti-edema effects. In this review, we discuss the mechanisms and involvement of factors that induce brain edema formation, and the possibility of anti-edema drugs targeting them. PMID:25941935
Bauman, Richard A; Ling, Geoffrey; Tong, Lawrence; Januszkiewicz, Adolph; Agoston, Dennis; Delanerolle, Nihal; Kim, Young; Ritzel, Dave; Bell, Randy; Ecklund, James; Armonda, Rocco; Bandak, Faris; Parks, Steven
2009-06-01
Explosive blast has been extensively used as a tactical weapon in Operation Iraqi Freedom (OIF) and more recently in Operation Enduring Freedom(OEF). The polytraumatic nature of blast injuries is evidence of their effectiveness,and brain injury is a frequent and debilitating form of this trauma. In-theater clinical observations of brain-injured casualties have shown that edema, intracranial hemorrhage, and vasospasm are the most salient pathophysiological characteristics of blast injury to the brain. Unfortunately, little is known about exactly how an explosion produces these sequelae as well as others that are less well documented. Consequently, the principal objective of the current report is to present a swine model of explosive blast injury to the brain. This model was developed during Phase I of the DARPA (Defense Advanced Research Projects Agency) PREVENT (Preventing Violent Explosive Neurotrauma) blast research program. A second objective is to present data that illustrate the capabilities of this model to study the proximal biomechanical causes and the resulting pathophysiological, biochemical,neuropathological, and neurological consequences of explosive blast injury to the swine brain. In the concluding section of this article, the advantages and limitations of the model are considered, explosive and air-overpressure models are compared, and the physical properties of an explosion are identified that potentially contributed to the in-theater closed head injuries resulting from explosions of improvised explosive devices (IEDs).
Jouzdani, Saeid Rezaei; Ebrahimi, Ali; Rezaee, Maryam; Shishegar, Mehdi; Tavallaii, Abbas; Kaka, Gholamreza
2014-11-01
The primary goal of this study was to evaluate the incidence and characteristics of posttraumatic headache attributed to mild brain injury in military personnel in Iran within a prospective and observational study design. A prospective observational descriptive study was conducted with a cohort of military personnel under military education during a 6-month period at the Military Education Center in Isfahan, Iran. 322 military personnel under education were selected randomly and were given a 13-item mild brain injury questionnaire accompanied with affective disorders and headache questionnaires and were reevaluated after a 3-month interval. A total of 30 (9.3 %) of the 322 military personnel met criteria for a mild brain injury. Among them, 18 personnel (60 %) reported having headaches during the 3-month reevaluation. PTHs defined as headaches beginning within 1 week after a head trauma were present in 5.6 % of military personnel under study during 6 months. In total, 67 % of posttraumatic headaches (PTH) were classified as migrainous or possible migrainous features. Patients with affective disorders such as posttraumatic stress disorder and depression were at a higher risk for developing PTH following mild brain injury (p < 0.05). PTH did not relate to demographic factors such as age or type of trauma. Posttraumatic headache attributed to mild brain injury is a common disorder in military personnel. Migrainous features are predominant among them in comparison with the general population. PTH is not related to a type of trauma, but has association with affective disorders.
DARPA challenge: developing new technologies for brain and spinal injuries
NASA Astrophysics Data System (ADS)
Macedonia, Christian; Zamisch, Monica; Judy, Jack; Ling, Geoffrey
2012-06-01
The repair of traumatic injuries to the central nervous system remains among the most challenging and exciting frontiers in medicine. In both traumatic brain injury and spinal cord injuries, the ultimate goals are to minimize damage and foster recovery. Numerous DARPA initiatives are in progress to meet these goals. The PREventing Violent Explosive Neurologic Trauma program focuses on the characterization of non-penetrating brain injuries resulting from explosive blast, devising predictive models and test platforms, and creating strategies for mitigation and treatment. To this end, animal models of blast induced brain injury are being established, including swine and non-human primates. Assessment of brain injury in blast injured humans will provide invaluable information on brain injury associated motor and cognitive dysfunctions. The Blast Gauge effort provided a device to measure warfighter's blast exposures which will contribute to diagnosing the level of brain injury. The program Cavitation as a Damage Mechanism for Traumatic Brain Injury from Explosive Blast developed mathematical models that predict stresses, strains, and cavitation induced from blast exposures, and is devising mitigation technologies to eliminate injuries resulting from cavitation. The Revolutionizing Prosthetics program is developing an avant-garde prosthetic arm that responds to direct neural control and provides sensory feedback through electrical stimulation. The Reliable Neural-Interface Technology effort will devise technologies to optimally extract information from the nervous system to control next generation prosthetic devices with high fidelity. The emerging knowledge and technologies arising from these DARPA programs will significantly improve the treatment of brain and spinal cord injured patients.
Huijben, Jilske A; van der Jagt, Mathieu; Cnossen, Maryse C; Kruip, Marieke J H A; Haitsma, Iain K; Stocchetti, Nino; Maas, Andrew I R; Menon, David K; Ercole, Ari; Maegele, Marc; Stanworth, Simon J; Citerio, Giuseppe; Polinder, Suzanne; Steyerberg, Ewout W; Lingsma, Hester F
2017-11-21
Our aim was to describe current approaches and to quantify variability between European intensive care units (ICUs) in patients with traumatic brain injury (TBI). Therefore, we conducted a provider profiling survey as part of the Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI) study. The ICU Questionnaire was sent to 68 centers from 20 countries across Europe and Israel. For this study, we used ICU questions focused on 1) hemoglobin target level (Hb-TL), 2) coagulation management, and 3) deep venous thromboembolism (DVT) prophylaxis. Seventy-eight participants, mostly intensivists and neurosurgeons of 66 centers, completed the ICU questionnaire. For ICU-patients, half of the centers (N = 34; 52%) had a defined Hb-TL in their protocol. For patients with TBI, 26 centers (41%) indicated an Hb-TL between 70 and 90 g/L and 38 centers (59%) above 90 g/L. To treat trauma-related hemostatic abnormalities, the use of fresh frozen plasma (N = 48; 73%) or platelets (N = 34; 52%) was most often reported, followed by the supplementation of vitamin K (N = 26; 39%). Most centers reported using DVT prophylaxis with anticoagulants frequently or always (N = 62; 94%). In the absence of hemorrhagic brain lesions, 14 centers (21%) delayed DVT prophylaxis until 72 h after trauma. If hemorrhagic brain lesions were present, the number of centers delaying DVT prophylaxis for 72 h increased to 29 (46%). Overall, a lack of consensus exists between European ICUs on blood transfusion and coagulation management. The results provide a baseline for the CENTER-TBI study, and the large between-center variation indicates multiple opportunities for comparative effectiveness research.
Morey, R A; Dunsmoor, J E; Haswell, C C; Brown, V M; Vora, A; Weiner, J; Stjepanovic, D; Wagner, H R; Brancu, Mira; Marx, Christine E; Naylor, Jennifer C; Van Voorhees, Elizabeth; Taber, Katherine H; Beckham, Jean C; Calhoun, Patrick S; Fairbank, John A; Szabo, Steven T; LaBar, K S
2015-01-01
Fear conditioning is an established model for investigating posttraumatic stress disorder (PTSD). However, symptom triggers may vaguely resemble the initial traumatic event, differing on a variety of sensory and affective dimensions. We extended the fear-conditioning model to assess generalization of conditioned fear on fear processing neurocircuitry in PTSD. Military veterans (n=67) consisting of PTSD (n=32) and trauma-exposed comparison (n=35) groups underwent functional magnetic resonance imaging during fear conditioning to a low fear-expressing face while a neutral face was explicitly unreinforced. Stimuli that varied along a neutral-to-fearful continuum were presented before conditioning to assess baseline responses, and after conditioning to assess experience-dependent changes in neural activity. Compared with trauma-exposed controls, PTSD patients exhibited greater post-study memory distortion of the fear-conditioned stimulus toward the stimulus expressing the highest fear intensity. PTSD patients exhibited biased neural activation toward high-intensity stimuli in fusiform gyrus (P<0.02), insula (P<0.001), primary visual cortex (P<0.05), locus coeruleus (P<0.04), thalamus (P<0.01), and at the trend level in inferior frontal gyrus (P=0.07). All regions except fusiform were moderated by childhood trauma. Amygdala–calcarine (P=0.01) and amygdala–thalamus (P=0.06) functional connectivity selectively increased in PTSD patients for high-intensity stimuli after conditioning. In contrast, amygdala–ventromedial prefrontal cortex (P=0.04) connectivity selectively increased in trauma-exposed controls compared with PTSD patients for low-intensity stimuli after conditioning, representing safety learning. In summary, fear generalization in PTSD is biased toward stimuli with higher emotional intensity than the original conditioned-fear stimulus. Functional brain differences provide a putative neurobiological model for fear generalization whereby PTSD symptoms are triggered by threat cues that merely resemble the index trauma. PMID:26670285
Wofford, Kathryn L; Harris, James P; Browne, Kevin D; Brown, Daniel P; Grovola, Michael R; Mietus, Constance J; Wolf, John A; Duda, John E; Putt, Mary E; Spiller, Kara L; Cullen, D Kacy
2017-04-01
Despite increasing appreciation of the critical role that neuroinflammatory pathways play in brain injury and neurodegeneration, little is known about acute microglial reactivity following diffuse traumatic brain injury (TBI) - the most common clinical presentation that includes all concussions. Therefore, we investigated acute microglial reactivity using a porcine model of closed-head rotational velocity/acceleration-induced TBI that closely mimics the biomechanical etiology of inertial TBI in humans. We observed rapid microglial reactivity within 15min of both mild and severe TBI. Strikingly, microglial activation was restrained to regions proximal to individual injured neurons - as denoted by trauma-induced plasma membrane disruption - which served as epicenters of acute reactivity. Single-cell quantitative analysis showed that in areas free of traumatically permeabilized neurons, microglial density and morphology were similar between sham or following mild or severe TBI. However, microglia density increased and morphology shifted to become more reactive in proximity to injured neurons. Microglial reactivity around injured neurons was exacerbated following repetitive TBI, suggesting further amplification of acute neuroinflammatory responses. These results indicate that neuronal trauma rapidly activates microglia in a highly localized manner, and suggest that activated microglia may rapidly influence neuronal stability and/or pathophysiology after diffuse TBI. Copyright © 2017 Elsevier Inc. All rights reserved.
The consequence of spatial visual processing dysfunction caused by traumatic brain injury (TBI).
Padula, William V; Capo-Aponte, Jose E; Padula, William V; Singman, Eric L; Jenness, Jonathan
2017-01-01
A bi-modal visual processing model is supported by research to affect dysfunction following a traumatic brain injury (TBI). TBI causes dysfunction of visual processing affecting binocularity, spatial orientation, posture and balance. Research demonstrates that prescription of prisms influence the plasticity between spatial visual processing and motor-sensory systems improving visual processing and reducing symptoms following a TBI. The rationale demonstrates that visual processing underlies the functional aspects of binocularity, balance and posture. The bi-modal visual process maintains plasticity for efficiency. Compromise causes Post Trauma Vision Syndrome (PTVS) and Visual Midline Shift Syndrome (VMSS). Rehabilitation through use of lenses, prisms and sectoral occlusion has inter-professional implications in rehabilitation affecting the plasticity of the bi-modal visual process, thereby improving binocularity, spatial orientation, posture and balance Main outcomes: This review provides an opportunity to create a new perspective of the consequences of TBI on visual processing and the symptoms that are often caused by trauma. It also serves to provide a perspective of visual processing dysfunction that has potential for developing new approaches of rehabilitation. Understanding vision as a bi-modal process facilitates a new perspective of visual processing and the potentials for rehabilitation following a concussion, brain injury or other neurological events.
Neuroprotective properties of epoetin alfa.
Cerami, Anthony; Brines, Michael; Ghezzi, Pietro; Cerami, Carla; Itri, Loretta M
2002-01-01
Erythropoietin and its receptor function as primary mediators of the normal physiological response to hypoxia. Erythropoietin is recognized for its central role in erythropoiesis, but studies in which recombinant human erythropoietin (epoetin alfa) is injected directly into ischaemic rodent brain show that erythropoietin also mediates neuroprotection. Abundant expression of the erythropoietin receptor has been observed at brain capillaries, which could provide a route for circulating erythropoietin to enter the brain. In confirmation of this hypothesis, systemic administration of epoetin alfa before or up to 6 h after focal brain ischaemia reduced injury by 50-75%. Epoetin alfa also limited the extent of concussive brain injury, the immune damage in experimental autoimmune encephalomyelitis and excitotoxicity induced by kainate. Thus, systemically administered epoetin alfa in animal models has neuroprotective effects, demonstrating its potential use after brain injury, trauma and multiple sclerosis. It is evident that erythropoietin has biological activities in addition to increasing red cell mass. Given the excellent safety profile of epoetin alfa, clinical trials evaluating systemically administered epoetin alfa as a general neuroprotective treatment are warranted.
ERIC Educational Resources Information Center
Barr, Donald A.
2018-01-01
Many kindergarten teachers have encountered children who enter school lacking the ability to control their behavior, but they may not understand the social and biological processes behind these children's disruptive behavior. The author reviews research into early childhood brain development to explain how trauma and chronic stress can make it…
Syed Hassan, Syed Tajuddin; Jamaludin, Husna; Abd Raman, Rosna; Mohd Riji, Haliza; Wan Fei, Khaw
2013-01-01
Context As with care giving and rehabilitation in chronic illnesses, the concern with traumatic brain injury (TBI), particularly with diffuse axonal injury (DAI), is that the caregivers are so overwhelmingly involved in caring and rehabilitation of the victim that in the process they become traumatized themselves. This review intends to shed light on the hidden and silent trauma sustained by the caregivers of severe brain injury survivors. Motor vehicle accident (MVA) is the highest contributor of TBI or DAI. The essence of trauma is the infliction of pain and suffering and having to bear the pain (i.e. by the TBI survivor) and the burden of having to take care and manage and rehabilitate the TBI survivor (i.e. by the TBI caregiver). Moreover many caregivers are not trained for their care giving task, thus compounding the stress of care giving and rehabilitating patients. Most research on TBI including DAI, focus on the survivors and not on the caregivers. TBI injury and its effects and impacts remain the core question of most studies, which are largely based on the quantitative approach. Evidence Acquisition Qualitative research can better assess human sufferings such as in the case of DAI trauma. While quantitative research can measure many psychometric parameters to assess some aspects of trauma conditions, qualitative research is able to fully reveal the meaning, ramification and experience of TBI trauma. Both care giving and rehabilitation are overwhelmingly demanding; hence , they may complicate the caregivers’ stress. However, some positive outcomes also exist. Results Caregivers involved in caring and rehabilitation of TBI victims may become mentally traumatized. Posttraumatic recovery of the TBI survivor can enhance the entire family’s closeness and bonding as well as improve the mental status of the caregiver. Conclusions A long-term longitudinal study encompassing integrated research is needed to fully understand the traumatic experiences of caregivers. Unless research on TBI or DAI trauma is given its proper attention, the burden of trauma and injury on societies will continue to exacerbate globally. PMID:24350153
Cattane, Nadia; Rossi, Roberta; Lanfredi, Mariangela; Cattaneo, Annamaria
2017-06-15
According to several studies, the onset of the Borderline Personality Disorder (BPD) depends on the combination between genetic and environmental factors (GxE), in particular between biological vulnerabilities and the exposure to traumatic experiences during childhood. We have searched for studies reporting possible alterations in several biological processes and brain morphological features in relation to childhood trauma experiences and to BPD. We have also looked for epigenetic mechanisms as they could be mediators of the effects of childhood trauma in BPD vulnerability. We prove the role of alterations in Hypothalamic-Pituitary-Adrenal (HPA) axis, in neurotrasmission, in the endogenous opioid system and in neuroplasticity in the childhood trauma-associated vulnerability to develop BPD; we also confirm the presence of morphological changes in several BPD brain areas and in particular in those involved in stress response. Not so many studies are available on epigenetic changes in BPD patients, although these mechanisms are widely investigated in relation to stress-related disorders. A better comprehension of the biological and epigenetic mechanisms, affected by childhood trauma and altered in BPD patients, could allow to identify "at high risk" subjects and to prevent or minimize the development of the disease later in life.
Surviving Traumatic Brain Injury: A Study of Post Acute Rehabilitation Services.
ERIC Educational Resources Information Center
Schuyler, Suellen
The problems facing a rehabilitation counselor in successfully working with survivors of brain trauma are myriad. This review examined evaluation techniques, rehabilitation therapies, and existing services that have proven effective with traumatic brain injury (TBI) clients. There is a gap in rehabilitation services that results in the TBI…
Federal Register 2010, 2011, 2012, 2013, 2014
2011-11-28
... Brain Injury: Prevention, Diagnosis, Treatment and Recovery for the Iraq and Afghanistan Cohort Notice... Clinical Practice of Psychological Health and Traumatic Brain Injury: Prevention, Diagnosis, Treatment and... clinical practices for psychological health and traumatic brain injury (TBI) health concerns for returning...
Lytton, William W.
2009-01-01
Preface Epilepsy is a complex set of disorders that can involve many areas of cortex as well as underlying deep brain systems. The myriad manifestations of seizures, as varied as déjà vu and olfactory hallucination, can thereby give researchers insights into regional functions and relations. Epilepsy is also complex genetically and pathophysiologically, involving microscopic (ion channels, synaptic proteins), macroscopic (brain trauma and rewiring) and intermediate changes in a complex interplay of causality. It has long been recognized that computer modeling will be required to disentangle causality, to better understand seizure spread and to understand and eventually predict treatment efficacy. Over the past few years, substantial progress has been made modeling epilepsy at levels ranging from the molecular to the socioeconomic. We review these efforts and connect them to the medical goals of understanding and treating this disorder. PMID:18594562
Walshe, Criona M; Cooper, James D; Kossmann, Thomas; Hayes, Ivan; Iles, Linda
2007-06-01
A 19-year-old woman with multiple fractures and mild brain injury developed severe cerebral fat embolism syndrome after "damage control" orthopaedic surgery. Acetazolamide therapy to manage ocular trauma, in association with hyperchloraemia, caused a profound metabolic acidosis with appropriate compensatory hypocapnia. During ventilator weaning, unexpected brainstem coning followed increased sedation and brief normalisation of arterial carbon dioxide concentration. Autopsy found severe cerebral fat embolism and brain oedema. In patients with multiple trauma, cerebral fat embolism syndrome is difficult to diagnose, and may be more common after delayed fixation of long-bone fractures. Acetazolamide should be used with caution, as sudden restoration of normocapnia during compensated metabolic acidosis in patients with raised intracranial pressure may precipitate coning.
NASA Astrophysics Data System (ADS)
Standvoss, K.; Crijns, T.; Goerke, L.; Janssen, D.; Kern, S.; van Niedek, T.; van Vugt, J.; Alfonso Burgos, N.; Gerritse, E. J.; Mol, J.; van de Vooren, D.; Ghafoorian, M.; van den Heuvel, T. L. A.; Manniesing, R.
2018-02-01
The number and location of cerebral microbleeds (CMBs) in patients with traumatic brain injury (TBI) is important to determine the severity of trauma and may hold prognostic value for patient outcome. However, manual assessment is subjective and time-consuming due to the resemblance of CMBs to blood vessels, the possible presence of imaging artifacts, and the typical heterogeneity of trauma imaging data. In this work, we present a computer aided detection system based on 3D convolutional neural networks for detecting CMBs in 3D susceptibility weighted images. Network architectures with varying depth were evaluated. Data augmentation techniques were employed to improve the networks' generalization ability and selective sampling was implemented to handle class imbalance. The predictions of the models were clustered using a connected component analysis. The system was trained on ten annotated scans and evaluated on an independent test set of eight scans. Despite this limited data set, the system reached a sensitivity of 0.87 at 16.75 false positives per scan (2.5 false positives per CMB), outperforming related work on CMB detection in TBI patients.
Effects of LPS-induced immune activation prior to trauma exposure on PTSD-like symptoms in mice.
Deslauriers, Jessica; van Wijngaarde, Myrthe; Geyer, Mark A; Powell, Susan; Risbrough, Victoria B
2017-04-14
The prevalence of posttraumatic stress disorder (PTSD) is high in the armed services, with a rate up to 20%. Multiple studies have associated markers of inflammatory signaling prior to trauma with increased risk of PTSD, suggesting a potential role of the immune system in the development of this psychiatric disorder. One question that arises is if "priming" the immune system before acute trauma alters the stress response and increases enduring effects of trauma. We investigated the time course of inflammatory response to predator stress, a robust stressor that induces enduring PTSD-like behaviors, and the modulation of these effects via prior immune activation with the bacterial endotoxin, lipopolysaccharide (LPS), a Toll-like receptor 4 (TLR4) agonist. Mice exposed to predator stress exhibited decreased pro-/anti-inflammatory balance in the brain 6h after stress, suggesting that predator exposure acutely suppressed the immune system by increasing anti-inflammatory cytokines levels. Acute immune activation with LPS before a single predator stress did not alter the enduring avoidance behavior in stressed mice. Our findings suggest that acute inflammation, at least via TLR4 activation, is not sufficient to increase susceptibility for PTSD-like behaviors in this model. Future studies will examine if chronic inflammation is required to induce similar immune changes to those observed in PTSD patients in this model. Published by Elsevier B.V.
Chronic Subdural Hematoma in the Aged, Trauma or Degeneration?
2016-01-01
Chronic subdural hematomas (CSHs) are generally regarded to be a traumatic lesion. It was regarded as a stroke in 17th century, an inflammatory disease in 19th century. From 20th century, it became a traumatic lesion. CSH frequently occur after a trauma, however, it cannot occur when there is no enough subdural space even after a severe head injury. CSH may occur without trauma, when there is sufficient subdural space. The author tried to investigate trends in the causation of CSH. By a review of literature, the author suggested a different view on the causation of CSH. CSH usually originated from either a subdural hygroma or an acute subdural hematoma. Development of CSH starts from the separation of the dural border cell (DBC) layer, which induces proliferation of DBCs with production of neomembrane. Capillaries will follow along the neomembrane. Hemorrhage would occur into the subdural fluid either by tearing of bridge veins or repeated microhemorrhage from the neomembrane. That is the mechanism of hematoma enlargement. Trauma or bleeding tendency may precipitate development of CSH, however, it cannot lead CSH, if there is no sufficient subdural space. The key determinant for development of CSH is a sufficient subdural space, in other words, brain atrophy. The most common and universal cause of brain atrophy is the aging. Modifying Virchow's description, CSH is sometimes traumatic, but most often caused by degeneration of the brain. Now, it is reasonable that degeneration of brain might play pivotal role in development of CSH in the aged persons. PMID:26885279
Novel Model of Frontal Impact Closed Head Injury in the Rat
Kilbourne, Michael; Kuehn, Reed; Tosun, Cigdem; Caridi, John; Keledjian, Kaspar; Bochicchio, Grant; Scalea, Thomas; Gerzanich, Volodymyr
2009-01-01
Abstract Frontal impact, closed head trauma is a frequent cause of traumatic brain injury (TBI) in motor vehicle and sports accidents. Diffuse axonal injury (DAI) is common in humans and experimental animals, and results from shearing forces that develop within the anisotropic brain. Because the specific anisotropic properties of the brain are axis-dependent, the anatomical site where force is applied as well as the resultant acceleration, be it linear, rotational, or some combination, are important determinants of the resulting pattern of brain injury. Available rodent models of closed head injury do not reproduce the frontal impact commonly encountered in humans. Here we describe a new rat model of closed head injury that is a modification of the impact-acceleration model of Marmarou. In our model (the Maryland model), the impact force is applied to the anterior part of the cranium and produces TBI by causing anterior-posterior plus sagittal rotational acceleration of the brain inside the intact cranium. Skull fractures, prolonged apnea, and mortality were absent. The animals exhibited petechial hemorrhages, DAI marked by a bead-like pattern of β-amyloid precursor protein (β-APP) in damaged axons, and widespread upregulation of β-APP in neurons, with regions affected including the orbitofrontal cortex (coup), corpus callosum, caudate, putamen, thalamus, cerebellum, and brainstem. Activated caspase-3 was prominent in hippocampal neurons and Purkinje cells at the grey-white matter junction of the cerebellum. Neurobehavioral dysfunction, manifesting as reduced spontaneous exploration, lasted more than 1 week. We conclude that the Maryland model produces diffuse injuries that may be relevant to human brain injury. PMID:19929375
[Mild traumatic brain injury and postconcussive syndrome: a re-emergent questioning].
Auxéméry, Y
2012-09-01
Blast injuries are psychologically and physically devastating. Notably, primary blast injury occurs as a direct effect of changes in atmospheric pressure caused by a blast wave. The combat-related traumatic brain injuries (TBI) resulting from exposure to explosions is highly prevalent among military personnel who have served in current wars. Traumatic brain injury is a common cause of neurological damage and disability among civilians and servicemen. Most patients with TBI suffer a mild traumatic brain injury with transient loss of consciousness. A controversial issue in the field of head injury is the outcome of concussion. Most individuals with such injuries are not admitted to emergency units and receive a variable degree of medical attention. Nevertheless, cranial traumas vary in their mechanisms (blast, fall, road accident, bullet-induced craniocerebral injury) and in their gravity (from minor to severe). The majority of subjects suffering concussion have been exposed to explosion or blast injuries, which have caused minor cranial trauma. Although some authors refuse to accept the reality of post-concussion syndrome (PCS) and confuse it with masked depression, somatic illnesses or post-traumatic stress, we have raised the question again of its existence, without denying the intricate links with other psychiatric or neurological disorders. Although the mortality rate is negligible, the traumatic sequel after mild traumatic brain injury is clear. A difference in initial somatic severity is noted between the serious somatic consequences of a severe cranial trauma compared with the apparently benign consequences of a minor cranial trauma. However, the long-term consequences of the two types of impacts are far from negligible: PCS is a source of morbidity. The prognosis for minor cranial traumas is benign at vital level but a number of patients will develop long-term complaints, which contrast with the negativity of the clinical examination and complementary explorations. The origin of these symptoms questions their organic and psychological aetiologies, which are potentially associated or intricately linked. After a cerebral concussion patients report a cluster of symptoms referred to as postconcussive. Post-concussion syndrome lies within the confines of somatic symptoms (headaches, dizziness, and fatigue), cognitive symptoms (memory and concentration problems) and affective symptoms (irritability, emotional lability, depression, anxiety, trouble sleeping). The nosographical entity of post-concussion syndrome is still in the process of elaboration following the input of new research intended to determine a cluster of specific symptoms. The persistent post-concussion syndrome is believed to be due to the psychological effects of the injury, biological factors, or a combination of both. Considered in isolation, the symptoms of post-concussion syndrome are non-specific and come together with other diagnostic frameworks such as characterised depressive episodes and post-traumatic stress. Post-concussion syndrome is not specific to concussion but can be present in subjects without any previous cranial trauma. Blast trauma can thus be understood as experiencing a shockwave on the brain and as a psycho-traumatic event. The major methodological problem of the studies is the quantification of the functional symptoms present in different nosographical frameworks, which are often co-morbid. Post-traumatic stress disorder is one of several psychiatric disorders that may increase suffering and disability among people with mild traumatic brain injury; in addition mood disorders also seem to be frequent psychiatric complications among these patients. Psychotic disorders after TBI have been associated with several brain regions. The establishment of a causative relationship between TBI and psychiatric disorders is interesting in terms of our understanding of these possible sequelae of TBI. The grey substance of the grey nuclei of the base can also be altered by a scissoring mechanism of the perforating arteries. A cortical contusion through impression of the cortex on the contours of the cranium is frequent. The most common type of injury is traumatic axonal injury. Cerebral lesions that are secondary to TBI associate cell deaths through the mechanisms of apoptosis and necrosis concerning the nerve and glial cells. The scientific objective is to discover an anatomoclinical correlation between the symptoms of post-concussion syndrome and objectifiable brain damage. The predictive value of serum concentrations of the specific serum markers S-100B and neurone specific enolase has been established. Cerebral imaging will allow the mechanisms concerned in cranial trauma to be better understood and thus may allow these mechanisms to be linked with co-morbid post-traumatic psychiatric disorders such as depression. The pyschopathological approach provides supplementary enlightenment where neuroimaging studies struggle to establish precise anatomoclinical correlations between neurotraumatic lesions, state of post-traumatic stress, and PCS. Moving away from a purely scientific view to focus on subjectivity, PCS can establish itself in subjects with no history of head trauma thus showing purely psychic suffering. Is the former name of "subjective post-head injury syndrome" no longer pertinent since the neurobiological affections can be objectified? Yet, the latter does not necessarily explain the somatic symptoms. Beyond any opposition of a psychic or somatic causality, it shows the complexity of this interaction. Admittedly, looking for a neuropathological affection is particularly cardinal to propose an aetiological model and objectify the lesions, which should be documented using a forensic approach. However, within the context of treatment, this theoretical division of the brain and the mind becomes less operative: the psychotherapeutic support will on the contrary back the indivisibility of the subject, he/she, who faced the "clatter". Copyright © 2011 L’Encéphale, Paris. Published by Elsevier Masson SAS. All rights reserved.
ERIC Educational Resources Information Center
Craig, Susan E.
2016-01-01
According to the National Center for Mental Health Promotion and Youth Violence Prevention, about one quarter of children in the United States will witness or experience a traumatic event before the age of four. In this article, Susan E. Craig explains how these early trauma histories prime a child's brain to expect certain experiences,…
The Abusive Environment and the Child's Adaptation.
ERIC Educational Resources Information Center
Martin, Harold P.
The biologic and developmental problems of abused children are usually thought of etiologically in relation to the physical trauma which has been suffered. Indeed, physical trauma can cause death, brain damage, developmental delays and deviations in personality development. The environment in which the abused child grows and develops is a most…
Charry, Jose D; Tejada, Jorman H; Pinzon, Miguel A; Tejada, Wilson A; Ochoa, Juan D; Falla, Manuel; Tovar, Jesus H; Cuellar-Bahamón, Ana M; Solano, Juan P
2017-05-01
Traumatic brain injury (TBI) is of public health interest and produces significant mortality and disability in Colombia. Calculators and prognostic models have been developed to establish neurologic outcomes. We tested prognostic models (the Marshall computed tomography [CT] score, International Mission for Prognosis and Analysis of Clinical Trials in Traumatic Brain Injury (IMPACT), and Corticosteroid Randomization After Significant Head Injury) for 14-day mortality, 6-month mortality, and 6-month outcome in patients with TBI at a university hospital in Colombia. A 127-patient cohort with TBI was treated in a regional trauma center in Colombia over 2 years and bivariate and multivariate analyses were used. Discriminatory power of the models, their accuracy, and precision was assessed by both logistic regression and area under the receiver operating characteristic curve (AUC). Shapiro-Wilk, χ 2 , and Wilcoxon test were used to compare real outcomes in the cohort against predicted outcomes. The group's median age was 33 years, and 84.25% were male. The injury severity score median was 25, and median Glasgow Coma Scale motor score was 3. Six-month mortality was 29.13%. Six-month unfavorable outcome was 37%. Mortality prediction by Marshall CT score was 52.8%, P = 0.104 (AUC 0.585; 95% confidence interval [CI] 0 0.489-0.681), the mortality prediction by CRASH prognosis calculator was 59.9%, P < 0.001 (AUC 0.706; 95% CI 0.590-0.821), and the unfavorable outcome prediction by IMPACT was 77%, P < 0.048 (AUC 0.670; 95% CI 0.575-0.763). In a university hospital in Colombia, the Marshall CT score, IMPACT, and Corticosteroid Randomization After Significant Head Injury models overestimated the adverse neurologic outcome in patients with severe head trauma. Copyright © 2017 Elsevier Inc. All rights reserved.
Dobrachinski, Fernando; da Rosa Gerbatin, Rogério; Sartori, Gláubia; Ferreira Marques, Naiani; Zemolin, Ana Paula; Almeida Silva, Luiz Fernando; Franco, Jeferson Luis; Freire Royes, Luiz Fernando; Rechia Fighera, Michele; Antunes Soares, Félix Alexandre
2017-04-01
Traumatic brain injury (TBI) is a highly complex multi-factorial disorder. Experimental trauma involves primary and secondary injury cascades that underlie delayed neuronal dysfunction and death. Mitochondrial dysfunction and glutamatergic excitotoxicity are the hallmark mechanisms of damage. Accordingly, a successful pharmacological intervention requires a multi-faceted approach. Guanosine (GUO) is known for its neuromodulator effects in various models of brain pathology, specifically those that involve the glutamatergic system. The aim of the study was to investigate the GUO effects against mitochondrial damage in hippocampus and cortex of rats subjected to TBI, as well as the relationship of this effect with the glutamatergic system. Adult male Wistar rats were subjected to a unilateral moderate fluid percussion brain injury (FPI) and treated 15 min later with GUO (7.5 mg/kg) or vehicle (saline 0.9%). Analyses were performed in hippocampus and cortex 3 h post-trauma and revealed significant mitochondrial dysfunction, characterized by a disrupted membrane potential, unbalanced redox system, decreased mitochondrial viability, and complex I inhibition. Further, disruption of Ca 2+ homeostasis and increased mitochondrial swelling was also noted. Our results showed that mitochondrial dysfunction contributed to decreased glutamate uptake and levels of glial glutamate transporters (glutamate transporter 1 and glutamate aspartate transporter), which leads to excitotoxicity. GUO treatment ameliorated mitochondrial damage and glutamatergic dyshomeostasis. Thus, GUO might provide a new efficacious strategy for the treatment acute physiological alterations secondary to TBI.
Alali, Aziz S; McCredie, Victoria A; Mainprize, Todd G; Gomez, David; Nathens, Avery B
2017-10-01
Outcome after severe traumatic brain injury (TBI) differs substantially between hospitals. Explaining this variation begins with understanding the differences in structures and processes of care, particularly at intensive care units (ICUs) where acute TBI care takes place. We invited trauma medical directors (TMDs) from 187 centers participating in the American College of Surgeons Trauma Quality Improvement Program (ACS TQIP) to complete a survey. The survey domains included ICU model, type, availability of specialized units, staff, training programs, standard protocols and order sets, approach to withdrawal of life support, and perceived level of neurosurgeons' engagement in the ICU management of TBI. One hundred forty-two TMDs (76%) completed the survey. Severe TBI patients are admitted to dedicated neurocritical care units in 52 hospitals (37%), trauma ICUs in 44 hospitals (31%), general ICUs in 34 hospitals (24%), and surgical ICUs in 11 hospitals (8%). Fifty-seven percent are closed units. Board-certified intensivists directed 89% of ICUs, whereas 17% were led by neurointensivists. Sixty percent of ICU directors were general surgeons. Thirty-nine percent of hospitals had critical care fellowships and 11% had neurocritical care fellowships. Fifty-nine percent of ICUs had standard order sets and 61% had standard protocols specific for TBI, with the most common protocol relating to intracranial pressure management (53%). Only 43% of TMDs were satisfied with the current level of neurosurgeons' engagement in the ICU management of TBI; 46% believed that neurosurgeons should be more engaged; 11% believed they should be less engaged. In the largest survey of North American ICUs caring for TBI patients, there is substantial variation in the current approaches to ICU care for TBI, highlighting multiple opportunities for comparative effectiveness research.
Chen, Chiung M.; Yi, Hsiao-Ye; Yoon, Young-Hee; Dong, Chuanhui
2012-01-01
Objective: Premised on biological evidence from animal research, recent clinical studies have, for the most part, concluded that elevated blood alcohol concentration levels are independently associated with higher survival or decreased mortality in patients with moderate to severe traumatic brain injury (TBI). This study aims to provide some counterevidence to this claim and to further future investigations. Method: Incident data were drawn from the largest U.S. trauma registry, the National Trauma Data Bank, for emergency department admission years 2002–2006. TBI was identified according to the National Trauma Data Bank’s definition using International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM), codes. To eliminate confounding, the exact matching method was used to match alcohol-positive with alcohol-negative incidents on sex, age, race/ethnicity, and facility. Logistic regression compared in-hospital mortality between 44,043 alcohol-positive and 59,817 matched alcohol-negative TBI incidents, with and without causes and intents of TBI and Injury Severity Score as covariates. A sensitivity analysis was performed within a subsample of isolated moderate to severe TBI incidents. Results: Alcohol use at the time of injury was found to be significantly associated with an increased risk for TBI. Including varied causes and intents of TBI and Injury Severity Score as potential confounders in the regression model explained away the statistical significance of the seemingly protective effect of alcohol against TBI mortality for all TBIs and for isolated moderate to severe TBIs. Conclusions: The null finding shows that the purported reduction in TBI mortality attributed to positive blood alcohol likely is attributable to residual confounding. Accordingly, the risk of TBI associated with alcohol use should not be overlooked. PMID:22630791
Chen, Chiung M; Yi, Hsiao-Ye; Yoon, Young-Hee; Dong, Chuanhui
2012-07-01
Premised on biological evidence from animal research, recent clinical studies have, for the most part, concluded that elevated blood alcohol concentration levels are independently associated with higher survival or decreased mortality in patients with moderate to severe traumatic brain injury (TBI). This study aims to provide some counterevidence to this claim and to further future investigations. Incident data were drawn from the largest U.S. trauma registry, the National Trauma Data Bank, for emergency department admission years 2002-2006. TBI was identified according to the National Trauma Data Bank's definition using International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM), codes. To eliminate confounding, the exact matching method was used to match alcohol-positive with alcohol-negative incidents on sex, age, race/ethnicity, and facility. Logistic regression compared in-hospital mortality between 44,043 alcohol-positive and 59,817 matched alcohol-negative TBI incidents, with and without causes and intents of TBI and Injury Severity Score as covariates. A sensitivity analysis was performed within a subsample of isolated moderate to severe TBI incidents. Alcohol use at the time of injury was found to be significantly associated with an increased risk for TBI. Including varied causes and intents of TBI and Injury Severity Score as potential confounders in the regression model explained away the statistical significance of the seemingly protective effect of alcohol against TBI mortality for all TBIs and for isolated moderate to severe TBIs. The null finding shows that the purported reduction in TBI mortality attributed to positive blood alcohol likely is attributable to residual confounding. Accordingly, the risk of TBI associated with alcohol use should not be overlooked.
Mind, brain and body. Healing trauma: the way forward.
Wilkinson, Margaret
2017-09-01
The paper explores an interdisciplinary whole person approach to healing from trauma that conserves our rich inheritance from Jung but also takes on board insights from research in the areas of attachment, trauma and the neurobiology of emotion. It is now over 20 years since insights from neurobiology began to be used to inform clinical practice. The paper reviews key insights which have emerged, along with the ways they enable therapists to help mind, brain and body to heal and the ways in which they clarify why, in clinical practice, we do what we do. Traditionally the emphasis has been on words, interpretations, and meaning-making. Currently there is greater appreciation of the affective, relational, embodied aspects of therapeutic work and the way in which these relate to traumatic early interactive experience that is held outside of human awareness. The ways in which knowledge of particular systems of connectivity inform understanding of the whole mind-brain-body relationship are examined. The way forward for clinical practice to become more focused in order to help clients to heal in mind and body is reviewed. © 2017, The Society of Analytical Psychology.
Jeng, Toh Charng; Haspani, Mohd Saffari Mohd; Adnan, Johari Siregar; Naing, Nyi Nyi
2008-01-01
A repeat Computer Tomographic (CT) brain after 24–48 hours from the 1st scanning is usually practiced in most hospitals in South East Asia where intracranial pressure monitoring (ICP) is routinely not done. This interval for repeat CT would be shortened if there was a deterioration in Glasgow Coma Scale (GCS). Most of the time the prognosis of any intervention may be too late especially in hospitals with high patient-to-doctor ratio causing high mortality and morbidity. The purpose of this study was to determine the important predictors for early detection of Delayed Traumatic Intracranial Haemorrhage (DTICH) and Progressive Traumatic Brain Injury (PTBI) before deterioration of GCS occurred, as well as the most ideal timing of repeated CT brain for patients admitted in Malaysian hospitals. A total of 81 patients were included in this study over a period of six months. The CT scan brain was studied by comparing the first and second CT brain to diagnose the presence of DTICH/PTBI. The predictors tested were categorised into patient factors, CT brain findings and laboratory investigations. The mean age was 33.1 ± 15.7 years with a male preponderance of 6.36:1. Among them, 81.5% were patients from road traffic accidents with Glasgow Coma Scale ranging from 4 – 15 (median of 12) upon admission. The mean time interval delay between trauma and first CT brain was 179.8 ± 121.3 minutes for the PTBI group. The DTICH group, 9.9% of the patients were found to have new intracranial clots. Significant predictors detected were different referral hospitals (p=0.02), total GCS status (p=0.026), motor component of GCS (p=0.043), haemoglobin level (p<0.001), platelet count (p=0.011) and time interval between trauma and first CT brain (p=0.022). In the PTBI group, 42.0% of the patients were found to have new changes (new clot occurrence, old clot expansion and oedema) in the repeat CT brain. Univariate statistical analysis revealed that age (p=0.03), race (p=0.035), types of admission (p=0.024), GCS status (p=0.02), pupillary changes (p=0.014), number of intracranial lesion (p=0.004), haemoglobin level (p=0.038), prothrombin time (p=0.016) as the best predictors of early detection of changes. Multiple logistics regression analysis indicated that age, severity, GCS status (motor component) and GCS during admission were significantly associated with second CT scan with changes. This study showed that 9.9% of the total patients seen in the period of study had DTICH and 42% had PTBI. In the early period after traumatic head injury, the initial CT brain did not reveal the full extent of haemorrhagic injury and associated cerebral oedema. Different referral hospitals of different trauma level, GCS status, motor component of the GCS, haemoglobin level, platelet count and time interval between trauma and the first CT brain were the significant predictors for DTICH. Whereas the key determinants of PTBI were age, race, types of admission, GCS status, pupillary changes, number of intracranial bleed, haemoglobin level, prothrombin time and of course time interval between trauma and first CT brain. Any patients who had traumatic head injury in hospitals with no protocol of repeat CT scan or intracranial pressure monitoring especially in developing countries are advised to have to repeat CT brain at the appropriate quickest time . PMID:22589639
Zhou, R; Liu, B; Lin, K; Wang, R; Qin, Z; Liao, R; Qiu, Y
2015-07-01
Extracorporeal membrane oxygenation (ECMO) may offer life-saving treatment in severe pulmonary contusion or acute respiratory distress syndrome when conventional treatments have failed. However, because of the bleeding risk of systemic anticoagulation, ECMO should be performed only as a last resort in multiple trauma victims. Here, we report ECMO as a bridge for right main bronchus reconstruction and recovery of traumatic wet lung in a 31-year-old male multi-trauma patient with right main bronchial disruption, bilateral pulmonary contusion, cerebral contusion and long bone fracture. The patient was discharged without any obvious complication. ECMO support in a traumatic brain injured patient with severe hypoxemia caused by lung contusion and/or tracheal bronchus disruption is not an absolute contraindication. © The Author(s) 2014.
Domen, Patrick; Michielse, Stijn; Peeters, Sanne; Viechtbauer, Wolfgang; van Os, Jim; Marcelis, Machteld
2018-05-29
Decreased white matter (WM) integrity in patients with psychotic disorder has been a consistent finding in diffusion tensor imaging (DTI) studies. However, the contribution of environmental risk factors to these WM alterations is rarely investigated. The current study examines whether individuals with (increased risk for) psychotic disorder will show increased WM integrity change over time with increasing levels of childhood trauma and cannabis exposure. DTI scans were obtained from 85 patients with a psychotic disorder, 93 non-psychotic siblings and 80 healthy controls, of which 60% were rescanned 3 years later. In a whole-brain voxel-based analysis, associations between change in fractional anisotropy (ΔFA) and environmental exposures as well as interactions between group and environmental exposure in the model of FA and ΔFA were investigated. Analyses were adjusted for a priori hypothesized confounding variables: age, sex, and level of education. At baseline, no significant associations were found between FA and both environmental risk factors. At follow-up as well as over a 3-year interval, significant interactions between group and, respectively, cannabis exposure and childhood trauma exposure in the model of FA and ΔFA were found. Patients showed more FA decrease over time compared with both controls and siblings when exposed to higher levels of cannabis or childhood trauma. Higher levels of cannabis or childhood trauma may compromise connectivity over the course of the illness in patients, but not in individuals at low or higher than average genetic risk for psychotic disorder, suggesting interactions between the environment and illness-related factors.
Şahin, Sevim; Türkdoğan, Dilşad; Hacıfazlıoğlu, Nilüfer Eldeş; Yalçın, Emek Uyur; Eksen, Zehra Yılmaz; Ekinci, Gazanfer
2017-05-01
Global aphasia without hemiparesis is a rare condition often associated with embolic stroke. Posttraumatic causes have not been reported, in the literature, to our knowledge. We report a 15-year old boy with transient global aphasia without hemiparesis due to blunt head trauma. In our case, clinical findings occurred 1week later following head trauma. Emergence of the symptoms after a period of the first mechanical head trauma, draws attention to the importance of secondary process in traumatic brain injury. Copyright © 2016 Elsevier Ltd. All rights reserved.
... mistakenly attacks part of the nervous system) Side effects of some medicines Severe head trauma and other brain injuries Subarachnoid hemorrhage (a form of brain bleeding) Use of illegal stimulant drugs such as cocaine and amphetamines Symptoms Symptoms can include any of ...
Targeting Epigenetic Mechanisms in Pain due to Trauma and Traumatic Brain Injury(TBI)
2016-10-01
particularly likely to involve TBI, peripheral trauma or both. Disability due to pain and other causes is very high amongst such patients. We have no...Chemokine, Disability , Analgesia, Spinal Cord 16. SECURITY CLASSIFICATION OF: 17. LIMITATION OF ABSTRACT UU 18. NUMBER OF PAGES 15 19a. NAME OF...are particularly likely to involve TBI, peripheral trauma or both. Disability due to pain and other causes is very high amongst such patients. We have
Murrough, James W; Czermak, Christoph; Henry, Shannan; Nabulsi, Nabeel; Gallezot, Jean-Dominique; Gueorguieva, Ralitza; Planeta-Wilson, Beata; Krystal, John H; Neumaier, John F; Huang, Yiyun; Ding, Yu-Shin; Carson, Richard E; Neumeister, Alexander
2011-09-01
Serotonergic dysfunction is implicated in the pathogenesis of posttraumatic stress disorder (PTSD), and recent animal models suggest that disturbances in serotonin type 1B receptor function, in particular, may contribute to chronic anxiety. However, the specific role of the serotonin type 1B receptor has not been studied in patients with PTSD. To investigate in vivo serotonin type 1B receptor expression in individuals with PTSD, trauma-exposed control participants without PTSD (TC), and healthy (non-trauma-exposed) control participants (HC) using positron emission tomography and the recently developed serotonin type 1B receptor selective radiotracer [(11)C]P943. Cross-sectional positron emission tomography study under resting conditions. Academic and Veterans Affairs medical centers. Ninety-six individuals in 3 study groups: PTSD (n = 49), TC (n = 20), and HC (n = 27). Main Outcome Measure Regional [(11)C]P943 binding potential (BP(ND)) values in an a priori-defined limbic corticostriatal circuit investigated using multivariate analysis of variance and multiple regression analysis. A history of severe trauma exposure in the PTSD and TC groups was associated with marked reductions in [(11)C]P943 BP(ND) in the caudate, the amygdala, and the anterior cingulate cortex. Participant age at first trauma exposure was strongly associated with low [(11)C]P943 BP(ND). Developmentally earlier trauma exposure also was associated with greater PTSD symptom severity and major depression comorbidity. These data suggest an enduring effect of trauma history on brain function and the phenotype of PTSD. The association of early age at first trauma and more pronounced neurobiological and behavioral alterations in PTSD suggests a developmental component in the cause of PTSD.
Development of a skull/brain model for military wound ballistics studies.
Carr, Debra; Lindstrom, Anne-Christine; Jareborg, Andreas; Champion, Stephen; Waddell, Neil; Miller, David; Teagle, Michael; Horsfall, Ian; Kieser, Jules
2015-05-01
Reports on penetrating ballistic head injuries in the literature are dominated by case studies of suicides; the penetrating ammunition usually being .22 rimfire or shotgun. The dominating cause of injuries in modern warfare is fragmentation and hence, this is the primary threat that military helmets protect the brain from. When helmets are perforated, this is usually by bullets. In combat, 20% of penetrating injuries occur to the head and its wounding accounts for 50% of combat deaths. A number of head simulants are described in the academic literature, in ballistic test methods for helmets (including measurement of behind helmet blunt trauma, BHBT) and in the 'open' and 'closed' government literature of several nations. The majority of these models are not anatomically correct and are not assessed with high-velocity rifle ammunition. In this article, an anatomically correct 'skull' (manufactured from polyurethane) and 'brain' (manufactured from 10%, by mass, gelatine) model for use in military wound ballistic studies is described. Filling the cranium completely with gelatine resulted in a similar 'skull' fracture pattern as an anatomically correct 'brain' combined with a representation of cerebrospinal fluid. In particular, posterior cranial fossa and occipital fractures and brain ejection were observed. This pattern of injury compared favourably to reported case studies of actual incidents in the literature.
Neumeister, Alexander; Normandin, Marc D.; Pietrzak, Robert H.; Piomelli, Daniele; Zheng, Ming-Qiang; Gujarro-Anton, Ana; Potenza, Marc N.; Bailey, Christopher R.; Lin, Shu-fei; Najafzadeh, Soheila; Ropchan, Jim; Henry, Shannan; Corsi-Travali, Stefani; Carson, Richard E.; Huang, Yiyun
2013-01-01
Endocannabinoids and their attending cannabinoid type 1 receptor (CB1) have been implicated in animal models of posttraumatic stress disorder (PTSD). However, their specific role has not been studied in people with PTSD. Herein, we present an in vivo imaging study using positron emission tomography (PET) and the CB1-selective radioligand [11C]OMAR in individuals with PTSD, and healthy controls with lifetime histories of trauma (trauma controls [TC]) and those without such histories (healthy controls [HC]). Untreated individuals with PTSD (N=25) with non-combat trauma histories, and TC (N=12) and HC (N=23) participated in a magnetic resonance (MR) imaging scan and a resting PET scan with the CB1 receptor antagonist radiotracer [11C]OMAR, which measures volume of distribution (VT) linearly related to CB1 receptor availability. Peripheral levels of anandamide, 2-arachidonoylglycerol (2-AG), oleoylethanolamide (OEA), palmitoylethanolamide (PEA), and cortisol were also assessed. In the PTSD group, relative to the HC and TC groups, we found elevated brain-wide [11C]OMAR VT values (F(2,53)=7.96, p=.001; 19.5% and 14.5% higher, respectively) which were most pronounced in women (F(1,53)=5.52, p=.023). Anandamide concentrations were reduced in the PTSD relative to the TC (53.1% lower) and HC (58.2% lower) groups. Cortisol levels were lower in the PTSD and TC groups relative to the HC group. Three biomarkers examined collectively—OMAR VT, anandamide, and cortisol—correctly classified nearly 85% of PTSD cases. These results suggest that abnormal CB1 receptor-mediated anandamide signaling is implicated in the etiology of PTSD, and provide a promising neurobiological model to develop novel, evidence-based pharmacotherapies for this disorder. PMID:23670490
A web ontology for brain trauma patient computer-assisted rehabilitation.
Zikos, Dimitrios; Galatas, George; Metsis, Vangelis; Makedon, Fillia
2013-01-01
In this paper we describe CABROnto, which is a web ontology for the semantic representation of the computer assisted brain trauma rehabilitation. This is a novel and emerging domain, since it employs the use of robotic devices, adaptation software and machine learning to facilitate interactive and adaptive rehabilitation care. We used Protégé 4.2 and Protégé-Owl schema editor. The primary goal of this ontology is to enable the reuse of the domain knowledge. CABROnto has nine main classes, more than 50 subclasses, existential and cardinality restrictions. The ontology can be found online at Bioportal.
[Progress on neuropsychology and event-related potentials in patients with brain trauma].
Dong, Ri-xia; Cai, Wei-xiong; Tang, Tao; Huang, Fu-yin
2010-02-01
With the development of information technology, as one of the research frontiers in neurophysiology, event-related potentials (ERP) is concerned increasingly by international scholars, which provides a feasible and objective method for exploring cognitive function. There are many advances in neuropsychology due to new assessment tool for the last years. The basic theories in the field of ERP and neuropsychology were reviewed in this article. The research and development in evaluating cognitive function of patients with syndrome after brain trauma were focused in this review, and the perspectives for the future research of ERP was also explored.
Samadani, Uzma; Ritlop, Robert; Reyes, Marleen; Nehrbass, Elena; Li, Meng; Lamm, Elizabeth; Schneider, Julia; Shimunov, David; Sava, Maria; Kolecki, Radek; Burris, Paige; Altomare, Lindsey; Mehmood, Talha; Smith, Theodore; Huang, Jason H; McStay, Christopher; Todd, S Rob; Qian, Meng; Kondziolka, Douglas; Wall, Stephen; Huang, Paul
2015-04-15
Disconjugate eye movements have been associated with traumatic brain injury since ancient times. Ocular motility dysfunction may be present in up to 90% of patients with concussion or blast injury. We developed an algorithm for eye tracking in which the Cartesian coordinates of the right and left pupils are tracked over 200 sec and compared to each other as a subject watches a short film clip moving inside an aperture on a computer screen. We prospectively eye tracked 64 normal healthy noninjured control subjects and compared findings to 75 trauma subjects with either a positive head computed tomography (CT) scan (n=13), negative head CT (n=39), or nonhead injury (n=23) to determine whether eye tracking would reveal the disconjugate gaze associated with both structural brain injury and concussion. Tracking metrics were then correlated to the clinical concussion measure Sport Concussion Assessment Tool 3 (SCAT3) in trauma patients. Five out of five measures of horizontal disconjugacy were increased in positive and negative head CT patients relative to noninjured control subjects. Only one of five vertical disconjugacy measures was significantly increased in brain-injured patients relative to controls. Linear regression analysis of all 75 trauma patients demonstrated that three metrics for horizontal disconjugacy negatively correlated with SCAT3 symptom severity score and positively correlated with total Standardized Assessment of Concussion score. Abnormal eye-tracking metrics improved over time toward baseline in brain-injured subjects observed in follow-up. Eye tracking may help quantify the severity of ocular motility disruption associated with concussion and structural brain injury.
Ardley, Nicholas D; Lau, Ken K; Buchan, Kevin
2013-12-01
Cervical spine injuries occur in 4-8 % of adults with head trauma. Dual acquisition technique has been traditionally used for the CT scanning of brain and cervical spine. The purpose of this study was to determine the efficacy of radiation dose reduction by using a single acquisition technique that incorporated both anatomical regions with a dedicated neck detection algorithm. Thirty trauma patients for brain and cervical spine CT were included and were scanned with the single acquisition technique. The radiation doses from the single CT acquisition technique with the neck detection algorithm, which allowed appropriate independent dose administration relevant to brain and cervical spine regions, were recorded. Comparison was made both to the doses calculated from the simulation of the traditional dual acquisitions with matching parameters, and to the doses of retrospective dual acquisition legacy technique with the same sample size. The mean simulated dose for the traditional dual acquisition technique was 3.99 mSv, comparable to the average dose of 4.2 mSv from 30 previous patients who had CT of brain and cervical spine as dual acquisitions. The mean dose from the single acquisition technique was 3.35 mSv, resulting in a 16 % overall dose reduction. The images from the single acquisition technique were of excellent diagnostic quality. The new single acquisition CT technique incorporating the neck detection algorithm for brain and cervical spine significantly reduces the overall radiation dose by eliminating the unavoidable overlapping range between 2 anatomical regions which occurs with the traditional dual acquisition technique.
Ritlop, Robert; Reyes, Marleen; Nehrbass, Elena; Li, Meng; Lamm, Elizabeth; Schneider, Julia; Shimunov, David; Sava, Maria; Kolecki, Radek; Burris, Paige; Altomare, Lindsey; Mehmood, Talha; Smith, Theodore; Huang, Jason H.; McStay, Christopher; Todd, S. Rob; Qian, Meng; Kondziolka, Douglas; Wall, Stephen; Huang, Paul
2015-01-01
Abstract Disconjugate eye movements have been associated with traumatic brain injury since ancient times. Ocular motility dysfunction may be present in up to 90% of patients with concussion or blast injury. We developed an algorithm for eye tracking in which the Cartesian coordinates of the right and left pupils are tracked over 200 sec and compared to each other as a subject watches a short film clip moving inside an aperture on a computer screen. We prospectively eye tracked 64 normal healthy noninjured control subjects and compared findings to 75 trauma subjects with either a positive head computed tomography (CT) scan (n=13), negative head CT (n=39), or nonhead injury (n=23) to determine whether eye tracking would reveal the disconjugate gaze associated with both structural brain injury and concussion. Tracking metrics were then correlated to the clinical concussion measure Sport Concussion Assessment Tool 3 (SCAT3) in trauma patients. Five out of five measures of horizontal disconjugacy were increased in positive and negative head CT patients relative to noninjured control subjects. Only one of five vertical disconjugacy measures was significantly increased in brain-injured patients relative to controls. Linear regression analysis of all 75 trauma patients demonstrated that three metrics for horizontal disconjugacy negatively correlated with SCAT3 symptom severity score and positively correlated with total Standardized Assessment of Concussion score. Abnormal eye-tracking metrics improved over time toward baseline in brain-injured subjects observed in follow-up. Eye tracking may help quantify the severity of ocular motility disruption associated with concussion and structural brain injury. PMID:25582436
Hashemi, Behrooz; Amanat, Mahnaz; Baratloo, Alireza; Forouzanfar, Mohammad Mehdi; Rahmati, Farhad; Motamedi, Maryam; Safari, Saeed
2016-01-01
Introduction: To date, many prognostic models have been proposed to predict the outcome of patients with traumatic brain injuries. External validation of these models in different populations is of great importance for their generalization. The present study was designed, aiming to determine the value of CRASH prognostic model in prediction of 14-day mortality (14-DM) and 6-month unfavorable outcome (6-MUO) of patients with traumatic brain injury. Methods: In the present prospective diagnostic test study, calibration and discrimination of CRASH model were evaluated in head trauma patients referred to the emergency department. Variables required for calculating CRASH expected risks (ER), and observed 14-DM and 6-MUO were gathered. Then ER of 14-DM and 6-MUO were calculated. The patients were followed for 6 months and their 14-DM and 6-MUO were recorded. Finally, the correlation of CRASH ER and the observed outcome of the patients was evaluated. The data were analyzed using STATA version 11.0. Results: In this study, 323 patients with the mean age of 34.0 ± 19.4 years were evaluated (87.3% male). Calibration of the basic and CT models in prediction of 14-day and 6-month outcome were in the desirable range (P < 0.05). Area under the curve in the basic model for prediction of 14-DM and 6-MUO were 0.92 (95% CI: 0.89-0.96) and 0.92 (95% CI: 0.90-0.95), respectively. In addition, area under the curve in the CT model for prediction of 14-DM and 6-MUO were 0.93 (95% CI: 0.91-0.97) and 0.93 (95% CI: 0.91-0.96), respectively. There was no significant difference between the discriminations of the two models in prediction of 14-DM (p = 0.11) and 6-MUO (p = 0.1). Conclusion: The results of the present study showed that CRASH prediction model has proper discrimination and calibration in predicting 14-DM and 6-MUO of head trauma patients. Since there was no difference between the values of the basic and CT models, using the basic model is recommended to simplify the risk calculations. PMID:27800540
DOE Office of Scientific and Technical Information (OSTI.GOV)
Carranza, C; Lipnharski, I; Quails, N
Purpose: This retrospective study analyzes the exposure history of emergency department (ED) patients undergoing head and cervical spine trauma computed tomography (CT) studies. This study investigated dose levels received by trauma patients and addressed any potential concerns regarding radiation dose issues. Methods: Under proper IRB approval, a cohort of 300 trauma cases of head and cervical spine trauma CT scans received in the ED was studied. The radiological image viewing software of the hospital was used to view patient images and image data. The following parameters were extracted: the imaging history of patients, the reported dose metrics from the scannermore » including the volumetric CT Dose Index (CTDIvol) and Dose Length Product (DLP). A postmortem subject was scanned using the same scan techniques utilized in a standard clinical head and cervical spine trauma CT protocol with 120 kVp and 280 mAs. The CTDIvol was recorded for the subject and the organ doses were measured using optically stimulated luminescent (OSL) dosimeters. Typical organ doses to the brain, thyroid, lens, salivary glands, and skin, based on the cadaver studies, were then calculated and reported for the cohort. Results: The CTDIvol reported by the CT scanner was 25.5 mGy for the postmortem subject. The average CTDIvol from the patient cohort was 34.1 mGy. From these metrics, typical average organ doses in mGy were found to be: Brain (44.57), Thyroid (33.40), Lens (82.45), Salivary Glands (61.29), Skin (47.50). The imaging history of the cohort showed that on average trauma patients received 26.1 scans over a lifetime. Conclusion: The average number of scans received on average by trauma ED patients shows that radiation doses in trauma patients may be a concern. Available dose tracking software would be helpful to track doses in trauma ED patients, highlighting the importance of minimizing unnecessary scans and keeping doses ALARA.« less
Brain Injury Alters Volatile Metabolome
Cohen, Akiva S.; Gordon, Amy R.; Opiekun, Maryanne; Martin, Talia; Elkind, Jaclynn; Lundström, Johan N.; Beauchamp, Gary K.
2016-01-01
Chemical signals arising from body secretions and excretions communicate information about health status as have been reported in a range of animal models of disease. A potential common pathway for diseases to alter chemical signals is via activation of immune function—which is known to be intimately involved in modulation of chemical signals in several species. Based on our prior findings that both immunization and inflammation alter volatile body odors, we hypothesized that injury accompanied by inflammation might correspondingly modify the volatile metabolome to create a signature endophenotype. In particular, we investigated alteration of the volatile metabolome as a result of traumatic brain injury. Here, we demonstrate that mice could be trained in a behavioral assay to discriminate mouse models subjected to lateral fluid percussion injury from appropriate surgical sham controls on the basis of volatile urinary metabolites. Chemical analyses of the urine samples similarly demonstrated that brain injury altered urine volatile profiles. Behavioral and chemical analyses further indicated that alteration of the volatile metabolome induced by brain injury and alteration resulting from lipopolysaccharide-associated inflammation were not synonymous. Monitoring of alterations in the volatile metabolome may be a useful tool for rapid brain trauma diagnosis and for monitoring recovery. PMID:26926034
Xenon Protects against Blast-Induced Traumatic Brain Injury in an In Vitro Model.
Campos-Pires, Rita; Koziakova, Mariia; Yonis, Amina; Pau, Ashni; Macdonald, Warren; Harris, Katie; Edge, Christopher J; Franks, Nicholas P; Mahoney, Peter F; Dickinson, Robert
2018-04-15
The aim of this study was to evaluate the neuroprotective efficacy of the inert gas xenon as a treatment for patients with blast-induced traumatic brain injury in an in vitro laboratory model. We developed a novel blast traumatic brain injury model using C57BL/6N mouse organotypic hippocampal brain-slice cultures exposed to a single shockwave, with the resulting injury quantified using propidium iodide fluorescence. A shock tube blast generator was used to simulate open field explosive blast shockwaves, modeled by the Friedlander waveform. Exposure to blast shockwave resulted in significant (p < 0.01) injury that increased with peak-overpressure and impulse of the shockwave, and which exhibited a secondary injury development up to 72 h after trauma. Blast-induced propidium iodide fluorescence overlapped with cleaved caspase-3 immunofluorescence, indicating that shock-wave-induced cell death involves apoptosis. Xenon (50% atm) applied 1 h after blast exposure reduced injury 24 h (p < 0.01), 48 h (p < 0.05), and 72 h (p < 0.001) later, compared with untreated control injury. Xenon-treated injured slices were not significantly different from uninjured sham slices at 24 h and 72 h. We demonstrate for the first time that xenon treatment after blast traumatic brain injury reduces initial injury and prevents subsequent injury development in vitro. Our findings support the idea that xenon may be a potential first-line treatment for those with blast-induced traumatic brain injury.
The burden of traumatic brain injury among adolescent and young adult workers in Washington State.
Graves, Janessa M; Sears, Jeanne M; Vavilala, Monica S; Rivara, Frederick P
2013-06-01
This study describes injury characteristics and costs of work-related traumatic brain injury (WRTBI) among 16-24 year olds in Washington State between 1998 and 2008. WRTBIs were identified in the Washington Trauma Registry (WTR) and linked to workers' compensation (WC) claims data. Medical and time-loss compensation costs were compared between workers with isolated TBI and TBI with other trauma. Of 273 WRTBI cases identified, most (61.5%) were TBI with other trauma. One-third of WRTBI did not link to a WC claim. Medical costs averaged $88,307 (median $16,426) for isolated TBI cases, compared to $73,669 (median $41,167) for TBI with other trauma. Results highlight the financial impact of WRTBI among young workers. Multiple data sources provided a more comprehensive picture than a single data source alone. This linked-data approach holds great potential for future traumatic occupational injury research. TBI among young workers not only involves long-term health and psychological impacts, but is costly as well. Copyright © 2013 National Safety Council and Elsevier Ltd. All rights reserved.
[Hypothermia for intracranial hypertension].
Bruder, N; Velly, L; Codaccioni, J-L
2009-04-01
There is a large body of experimental evidence showing benefits of deliberate mild hypothermia (33-35 degrees C) on the injured brain as well as an improvement of neurological outcome after cardiac arrest in humans. However, the clinical evidence of any benefit of hypothermia following stroke, brain trauma and neonatal asphyxia is still lacking. Controversial results have been published in patients with brain trauma or neonatal asphyxia. Hypothermia can reduce the elevation of intracranial pressure, through mechanisms not completely understood. Hypothermia-induced hypocapnia should have a role on the reduction of intracranial pressure. The temperature target is unknown but no additional benefit was found below 34 degrees C. The duration of deliberate hypothermia for the treatment of elevated intracranial pressure might be at least 48 hours, and the subsequent rewarming period must be very slow to prevent adverse effects.
Butler, O; Adolf, J; Gleich, T; Willmund, G; Zimmermann, P; Lindenberger, U; Gallinat, J; Kühn, S
2017-02-14
Research investigating the effects of trauma exposure on brain structure and function in adults has mainly focused on post-traumatic stress disorder (PTSD), whereas trauma-exposed individuals without a clinical diagnoses often serve as controls. However, this assumes a dichotomy between clinical and subclinical populations that may not be supported at the neural level. In the current study we investigate whether the effects of repeated or long-term stress exposure on brain structure in a subclinical sample are similar to previous PTSD neuroimaging findings. We assessed 27 combat trauma-exposed individuals by means of whole-brain voxel-based morphometry on 3 T magnetic resonance imaging scans and identified a negative association between duration of military deployment and gray matter volumes in ventromedial prefrontal cortex (vmPFC) and dorsal anterior cingulate cortex (ACC). We also found a negative relationship between deployment-related gray matter volumes and psychological symptoms, but not between military deployment and psychological symptoms. To our knowledge, this is the first whole-brain analysis showing that longer military deployment is associated with smaller regional brain volumes in combat-exposed individuals without PTSD. Notably, the observed gray matter associations resemble those previously identified in PTSD populations, and concern regions involved in emotional regulation and fear extinction. These findings question the current dichotomy between clinical and subclinical populations in PTSD neuroimaging research. Instead, neural correlates of both stress exposure and PTSD symptomatology may be more meaningfully investigated at a continuous level.
Butler, O; Adolf, J; Gleich, T; Willmund, G; Zimmermann, P; Lindenberger, U; Gallinat, J; Kühn, S
2017-01-01
Research investigating the effects of trauma exposure on brain structure and function in adults has mainly focused on post-traumatic stress disorder (PTSD), whereas trauma-exposed individuals without a clinical diagnoses often serve as controls. However, this assumes a dichotomy between clinical and subclinical populations that may not be supported at the neural level. In the current study we investigate whether the effects of repeated or long-term stress exposure on brain structure in a subclinical sample are similar to previous PTSD neuroimaging findings. We assessed 27 combat trauma-exposed individuals by means of whole-brain voxel-based morphometry on 3 T magnetic resonance imaging scans and identified a negative association between duration of military deployment and gray matter volumes in ventromedial prefrontal cortex (vmPFC) and dorsal anterior cingulate cortex (ACC). We also found a negative relationship between deployment-related gray matter volumes and psychological symptoms, but not between military deployment and psychological symptoms. To our knowledge, this is the first whole-brain analysis showing that longer military deployment is associated with smaller regional brain volumes in combat-exposed individuals without PTSD. Notably, the observed gray matter associations resemble those previously identified in PTSD populations, and concern regions involved in emotional regulation and fear extinction. These findings question the current dichotomy between clinical and subclinical populations in PTSD neuroimaging research. Instead, neural correlates of both stress exposure and PTSD symptomatology may be more meaningfully investigated at a continuous level. PMID:28195568
2015-01-01
therapy CDC Centers for Disease Control and Prevention CESD Center for Epidemiologic Studies Depression Scale CGI-BP Clinical Global Impressions Scale for...dimensions GDS Geriatric Depression Scale HEDIS Healthcare Effectiveness Data and Information Set HOS Health Outcomes Survey HRQOL health-related quality of...TBI traumatic brain injury TF-CBT Trauma-Focused Cognitive–Behavioral Therapy TSC-40 Trauma Symptom Checklist—40 TSI Trauma Symptom Inventory VA U.S
Majercik, Sarah; Bledsoe, Joseph; Ryser, David; Hopkins, Ramona O; Fair, Joseph E; Brock Frost, R; MacDonald, Joel; Barrett, Ryan; Horn, Susan; Pisani, David; Bigler, Erin D; Gardner, Scott; Stevens, Mark; Larson, Michael J
2017-01-01
Day-of-injury (DOI) brain lesion volumes in traumatic brain injury (TBI) patients are rarely used to predict long-term outcomes in the acute setting. The purpose of this study was to investigate the relationship between acute brain injury lesion volume and rehabilitation outcomes in patients with TBI at a level one trauma center. Patients with TBI who were admitted to our rehabilitation unit after the acute care trauma service from February 2009-July 2011 were eligible for the study. Demographic data and outcome variables including cognitive and motor Functional Independence Measure (FIM) scores, length of stay (LOS) in the rehabilitation unit, and ability to return to home were obtained. The DOI quantitative injury lesion volumes and degree of midline shift were obtained from DOI brain computed tomography scans. A multiple stepwise regression model including 13 independent variables was created. This model was used to predict postrehabilitation outcomes, including FIM scores and ability to return to home. A p value less than 0.05 was considered significant. Ninety-six patients were enrolled in the study. Mean age was 43 ± 21 years, admission Glasgow Coma Score was 8.4 ± 4.8, Injury Severity Score was 24.7 ± 9.9, and head Abbreviated Injury Scale score was 3.73 ± 0.97. Acute hospital LOS was 12.3 ± 8.9 days, and rehabilitation LOS was 15.9 ± 9.3 days. Day-of-injury TBI lesion volumes were inversely associated with cognitive FIM scores at rehabilitation admission (p = 0.004) and discharge (p = 0.004) and inversely associated with ability to be discharged to home after rehabilitation (p = 0.006). In a cohort of patients with moderate to severe TBI requiring a rehabilitation unit stay after the acute care hospital stay, DOI brain injury lesion volumes are associated with worse cognitive FIM scores at the time of rehabilitation admission and discharge. Smaller-injury volumes were associated with eventual discharge to home. Volumetric neuroimaging in the acute injury phase may improve surgeons' ultimate outcome predictions in TBI patients. Prognostic/epidemiologic study, level V.
Majercik, Sarah; Bledsoe, Joseph; Ryser, David; Hopkins, Ramona O.; Fair, Joseph E.; Frost, R. Brock; MacDonald, Joel; Barrett, Ryan; Horn, Susan; Pisani, David; Bigler, Erin D.; Gardner, Scott; Stevens, Mark; Larson, Michael J.
2016-01-01
Introduction Day-of-injury (DOI) brain lesion volumes in traumatic brain injury (TBI) patients are rarely used to predict long-term outcomes in the acute setting. The purpose of this study was to investigate the relationship between acute brain injury lesion volume and rehabilitation outcomes in patients with TBI at a Level One Trauma Center. Methods Patients with TBI who were admitted to our rehabilitation unit after the acute care trauma service from February 2009-July 2011 were eligible for the study. Demographic data and outcome variables including cognitive and motor FIM scores, length of stay (LOS) in the rehabilitation unit, and ability to return to home were obtained. DOI quantitative injury lesion volumes and degree of midline shift were obtained from day-of-injury (DOI) brain computed tomography (CT) scans. A multiple step-wise regression model including 13 independent variables was created. This model was used to predict post-rehabilitation outcomes, including FIM scores and ability to return to home. P<0.05 was considered significant. Results 96 patients were enrolled in the study. Mean age was 43±21 years, admission Glasgow Coma Score 8.4±4.8, Injury Severity Score 24.7±9.9, and head Abbreviated Injury Scale score 3.73±0.97. Acute hospital length of stay (LOS) was 12.3±8.9 days and rehabilitation LOS was 15.9±9.3 days. Day-of-injury TBI lesion volumes were inversely associated with cognitive FIM scores at rehabilitation admission (p=0.004) and discharge (p=0.004) and inversely associated with ability to be discharged to home after rehabilitation (p=0.006). Conclusion In a cohort of patients with moderate to severe TBI requiring a rehabilitation unit stay after the acute care hospital stay, DOI brain injury lesion volumes are associated with worse cognitive FIM scores at the time of rehabilitation admission and discharge. Smaller injury volumes were associated with eventual discharge to home. Volumetric neuroimaging in the acute injury phase may improve surgeons’ ultimate outcome predictions in TBI patients. Level of Evidence/Study Type Level V, case series, Prognostic/Epidemiological PMID:27805992
Chang, Ronald; Folkerson, Lindley E; Sloan, Duncan; Tomasek, Jeffrey S; Kitagawa, Ryan S; Choi, H Alex; Wade, Charles E; Holcomb, John B
2017-02-01
Plasma-based resuscitation improves outcomes in trauma patients with hemorrhagic shock, while large-animal and limited clinical data suggest that it also improves outcomes and is neuroprotective in the setting of combined hemorrhage and traumatic brain injury. However, the choice of initial resuscitation fluid, including the role of plasma, is unclear for patients after isolated traumatic brain injury. We reviewed adult trauma patients admitted from January 2011 to July 2015 with isolated traumatic brain injury. "Early plasma" was defined as transfusion of plasma within 4 hours. Purposeful multiple logistic regression modeling was performed to analyze the relationship of early plasma and inhospital survival. After testing for interaction, subgroup analysis was performed based on the pattern of brain injury on initial head computed tomography: epidural hematoma, intraparenchymal contusion, subarachnoid hemorrhage, subdural hematoma, or multifocal intracranial hemorrhage. Of the 633 isolated traumatic brain injury patients included, 178 (28%) who received early plasma were injured more severely coagulopathic, hypoperfused, and hypotensive on admission. Survival was similar in the early plasma versus no early plasma groups (78% vs 84%, P = .08). After adjustment for covariates, early plasma was not associated with improved survival (odds ratio 1.18, 95% confidence interval 0.71-1.96). On subgroup analysis, multifocal intracranial hemorrhage was the largest subgroup with 242 patients. Of these, 61 (25%) received plasma within 4 hours. Within-group logistic regression analysis with adjustment for covariates found that early plasma was associated with improved survival (odds ratio 3.34, 95% confidence interval 1.20-9.35). Although early plasma transfusion was not associated with improved in-hospital survival for all isolated traumatic brain injury patients, early plasma was associated with increased in-hospital survival in those with multifocal intracranial hemorrhage. Copyright © 2016 Elsevier Inc. All rights reserved.
Brain stimulation in posttraumatic stress disorder
Novakovic, Vladan; Sher, Leo; Lapidus, Kyle A.B.; Mindes, Janet; A.Golier, Julia; Yehuda, Rachel
2011-01-01
Posttraumatic stress disorder (PTSD) is a complex, heterogeneous disorder that develops following trauma and often includes perceptual, cognitive, affective, physiological, and psychological features. PTSD is characterized by hyperarousal, intrusive thoughts, exaggerated startle response, flashbacks, nightmares, sleep disturbances, emotional numbness, and persistent avoidance of trauma-associated stimuli. The efficacy of available treatments for PTSD may result in part from relief of associated depressive and anxiety-related symptoms in addition to treatment of core symptoms that derive from reexperiencing, numbing, and hyperarousal. Diverse, heterogeneous mechanisms of action and the ability to act broadly or very locally may enable brain stimulation devices to address PTSD core symptoms in more targeted ways. To achieve this goal, specific theoretical bases derived from novel, well-designed research protocols will be necessary. Brain stimulation devices include both long-used and new electrical and magnetic devices. Electroconvulsive therapy (ECT) and Cranial electrotherapy stimulation (CES) have both been in use for decades; transcranial magnetic stimulation (TMS), magnetic seizure therapy (MST), deep brain stimulation (DBS), transcranial Direct Current Stimulation (tDCS), and vagus nerve stimulation (VNS) have been developed recently, over approximately the past twenty years. The efficacy of brain stimulation has been demonstrated as a treatment for psychiatric and neurological disorders such as anxiety (CES), depression (ECT, CES, rTMS, VNS, DBS), obsessive-compulsive disorder (OCD) (DBS), essential tremor, dystonia (DBS), epilepsy (DBS, VNS), Parkinson Disease (DBS), pain (CES), and insomnia (CES). To date, limited data on brain stimulation for PTSD offer only modest guidance. ECT has shown some efficacy in reducing comorbid depression in PTSD patients but has not been demonstrated to improve most core PTSD symptoms. CES and VNS have shown some efficacy in reducing anxiety, findings that may suggest possible utility in relieving PTSD-associated anxiety. Treatment of animal models of PTSD with DBS suggests potential human benefit. Additional research and novel treatment options for PTSD are urgently needed. The potential usefulness of brain stimulation in treating PTSD deserves further exploration. PMID:22893803
Harmsen, Annelieke Maria Karien; Giannakopoulos, Georgios; Franschman, Gaby; Christiaans, Herman; Bloemers, Frank
2017-04-01
Prehospital communication with Emergency Medical Services (EMS) is carried out in hectic situations. Proper communication among all medical personal is required to enhance collaboration, to provide the best care and enable shared situational awareness. The objective of this article was to give insight into current Dutch prehospital emergency care communication among all EMS and evaluate the usage of a new physician staffed helicopter EMS (P-HEMS) cancellation model. Trauma-related P-HEMS dispatches between November 1, 2014 and May 31, 2015 for the Lifeliner 1 were included; a random sample of 100 dispatches was generated. Tape recordings on all verbal prehospital communication between the dispatch center, EMS, and P-HEMS were transcribed and analyzed. Qualitative content analysis was performed, using open coding to code key messages. Ninety-two tape recordings were analyzed. The most frequent reason for P-HEMS dispatch was suspicion of brain injury (24%). The cancellation model was followed in 66%, overruled in 9%, and not applicable in 25%. The main reason for not adhering to the model was hemodynamic stability. In 5% of P-HEMS dispatches, a complete ABCD (airway, breathing, circulation, disability) methodology was used for handover, in 9% a complete Situation-Background-Assessment-Recommendation technique, in 2% a complete Mechanism-Injuries-Signs-Treatment method was used. The other handovers were incomplete. Prehospital handover between EMS on-scene and P-HEMS often entails insufficient information. The cancellation model for P-HEMS is frequently used and promotes adequate information transfer. To increase joined decision-making, more patient and situational information needs to be handed over. Standardization of prehospital trauma handovers will facilitate this and improve trauma patient's outcome. Copyright © 2016 Elsevier Inc. All rights reserved.
Characterization of Psychological and Biological Factors in an Animal Model of Warrior Stress
2013-07-26
blast/stress (257; 259), and presentation of effects of blast/stress on central monoamine activity ( 22 ). In each of these cases, the dependent...secreted by the pituitary gland. Prolactin is known to physiologically increase the stimulatory effect of ACTH-induced corticosterone secretion in...the stress field. J. Human Stress: 22 -36 165. McAllister TW, Stein MB. 2010. Effects of psychological and biomechanical trauma on brain and behavior
Severe Blunt Hepatic Trauma in Polytrauma Patient - Management and Outcome.
Doklestić, Krstina; Djukić, Vladimir; Ivančević, Nenad; Gregorić, Pavle; Lončar, Zlatibor; Stefanović, Branislava; Jovanović, Dušan; Karamarković, Aleksandar
2015-01-01
Despite the fact that treatment of liver injuries has dramatically evolved, severe liver traumas in polytraumatic patients still have a significant morbidity and mortality. The purpose of this study was to determine the options for surgical management of severe liver trauma as well as the outcome. In this retrospective study 70 polytraumatic patients with severe (American Association for the Surgery of Trauma [AAST] grade III-V) blunt liver injuries were operated on at the Clinic for Emergency Surgery. Mean age of patients was 48.26±16.80 years; 82.8% of patients were male. Road traffic accident was the leading cause of trauma, seen in 63 patients (90.0%). Primary repair was performed in 36 patients (51.4%), while damage control with perihepatic packing was done in 34 (48.6%). Complications related to the liver occurred in 14 patients (20.0%). Liver related mortality was 17.1%. Non-survivors had a significantly higher AAST grade (p=0.0001), higher aspartate aminotransferase level (p=0.01), lower hemoglobin level (p=0.0001), associated brain injury (p=0.0001), perioperative complications (p=0.001) and higher transfusion score (p=0.0001). The most common cause of mortality in the "early period" was uncontrolled bleeding, in the "late period" mortality was caused by sepsis and acute respiratory distress syndrome. Patients with high-grade liver trauma who present with hemorrhagic shock and associated severe injury should be managed operatively. Mortality from liver trauma is high for patients with higher AAST grade of injury, associated brain injury and massive transfusion score.
Yulug, Burak; Kilic, Ertugrul; Altunay, Serdar; Ersavas, Cenk; Orhan, Cemal; Dalay, Arman; Sahin, Nurhan; Tuzcu, Mehmet; Juturu, Vijaya; Sahin, Kazim
2018-04-30
Cinnamon cinnamon polyphenol extract is a traditional spice commonly used in different areas of the world for treatment of different disease conditions which are associated with inflammation and oxidative stress. Despite many preclinical studies showing the anti-oxidative, anti-inflammatory effects of CN, the underlying mechanisms in signaling pathways via which cinnamon protects the brain after brain trauma remained largely unknown. However, there is still no preclinical study delineating the possible molecular mechanism of neuroprotective effects cinnamon polyphenol extractin TBI.The primary aim of the current study was to test the hypothesis that cinnamon polyphenol extract administration would improve the histopathological outcomes and exert neuroprotective activity through its antioxidative and anti-inflammatory properties following TBI. To investigate the effects of cinnamon, we induced brain injury using a cold trauma model in mice that were treated with cinnamon polyphenol extract (10 mg/kg BW) or vehicle via intraperitoneal administration just after TBI. Mice were divided into two groups: TBI+vehicle group and TBI + cinnamon polyphenol extract group. Brain samples were collected 24 h later for analysis. We have shown that cinnamon polyphenol extract effectively reduced infarct and edema formation which were associated with significant alterations in inflammatory and oxidative parameters, including NF-κB, IL-1, IL-6, GFAP, NCAM and Nfr2 expressions. Our results identify an important neuroprotective role of cinnamon polyphenol extract in TBI which is mediated by its capability to suppress the inflammation and oxidative injury. Further, specially designed experimental studies to understand the molecular cross-talk between signaling pathways would provide valuable evidence for the therapeutic role of cinnamon in TBI and other TBI related conditions. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.
Computer modelling of epilepsy.
Lytton, William W
2008-08-01
Epilepsy is a complex set of disorders that can involve many areas of the cortex, as well as underlying deep-brain systems. The myriad manifestations of seizures, which can be as varied as déjà vu and olfactory hallucination, can therefore give researchers insights into regional functions and relations. Epilepsy is also complex genetically and pathophysiologically: it involves microscopic (on the scale of ion channels and synaptic proteins), macroscopic (on the scale of brain trauma and rewiring) and intermediate changes in a complex interplay of causality. It has long been recognized that computer modelling will be required to disentangle causality, to better understand seizure spread and to understand and eventually predict treatment efficacy. Over the past few years, substantial progress has been made in modelling epilepsy at levels ranging from the molecular to the socioeconomic. We review these efforts and connect them to the medical goals of understanding and treating the disorder.
Suzuki, Hideo; Luby, Joan L; Botteron, Kelly N; Dietrich, Rachel; McAvoy, Mark P; Barch, Deanna M
2014-07-01
Previous studies have examined the relationships between structural brain characteristics and early life stress in adults. However, there is limited evidence for functional brain variation associated with early life stress in children. We hypothesized that early life stress and trauma would be associated with increased functional brain activation response to negative emotional faces in children with and without a history of depression. Psychiatric diagnosis and life events in children (starting at age 3-5 years) were assessed in a longitudinal study. A follow-up magnetic resonance imaging (MRI) study acquired data (N = 115 at ages 7-12, 51% girls) on functional brain response to fearful, sad, and happy faces relative to neutral faces. We used a region-of-interest mask within cortico-limbic areas and conducted regression analyses and repeated-measures analysis of covariance. Greater activation responses to fearful, sad, and happy faces in the amygdala and its neighboring regions were found in children with greater life stress. Moreover, an association between life stress and left hippocampal and globus pallidus activity depended on children's diagnostic status. Finally, all children with greater life trauma showed greater bilateral amygdala and cingulate activity specific to sad faces but not the other emotional faces, although right amygdala activity was moderated by psychiatric status. These findings suggest that limbic hyperactivity may be a biomarker of early life stress and trauma in children and may have implications in the risk trajectory for depression and other stress-related disorders. However, this pattern varied based on emotion type and history of psychopathology. Copyright © 2014 American Academy of Child and Adolescent Psychiatry. Published by Elsevier Inc. All rights reserved.
Childhood trauma exposure and toxic stress: what the PNP needs to know.
Hornor, Gail
2015-01-01
Trauma exposure in childhood is a major public health problem that can result in lifelong mental and physical health consequences. Pediatric nurse practitioners must improve their skills in the identification of trauma exposure in children and their interventions with these children. This continuing education article will describe childhood trauma exposure (adverse childhood experiences) and toxic stress and their effects on the developing brain and body. Adverse childhood experiences include a unique set of trauma exposures. The adverse childhood experiences or trauma discussed in this continuing education offering will include childhood exposure to emotional abuse, physical abuse, sexual abuse, emotional neglect, physical neglect, domestic violence, household substance abuse, household mental illness, parental separation or divorce, and a criminal household member. Thorough and efficient methods of screening for trauma exposure will be discussed. Appropriate intervention after identification of trauma exposure will be explored. Copyright © 2015 National Association of Pediatric Nurse Practitioners. Published by Elsevier Inc. All rights reserved.
Lisieski, Michael J.; Eagle, Andrew L.; Conti, Alana C.; Liberzon, Israel; Perrine, Shane A.
2018-01-01
Post-traumatic stress disorder (PTSD) is a common, costly, and often debilitating psychiatric condition. However, the biological mechanisms underlying this disease are still largely unknown or poorly understood. Considerable evidence indicates that PTSD results from dysfunction in highly-conserved brain systems involved in stress, anxiety, fear, and reward. Pre-clinical models of traumatic stress exposure are critical in defining the neurobiological mechanisms of PTSD, which will ultimately aid in the development of new treatments for PTSD. Single prolonged stress (SPS) is a pre-clinical model that displays behavioral, molecular, and physiological alterations that recapitulate many of the same alterations observed in PTSD, illustrating its validity and giving it utility as a model for investigating post-traumatic adaptations and pre-trauma risk and protective factors. In this manuscript, we review the present state of research using the SPS model, with the goals of (1) describing the utility of the SPS model as a tool for investigating post-trauma adaptations, (2) relating findings using the SPS model to findings in patients with PTSD, and (3) indicating research gaps and strategies to address them in order to improve our understanding of the pathophysiology of PTSD. PMID:29867615
Sánchez, Álvaro I; Krafty, Robert T; Weiss, Harold B; Rubiano, Andrés M; Peitzman, Andrew B; Puyana, Juan Carlos
2011-01-01
Objective To determine trends for in-hospital survival and functional outcomes at acute care hospital discharge for severe adult traumatic brain injury (SATBI) patients in Pennsylvania, during 1998–2007. Methods Secondary analysis of the Pennsylvania trauma outcome study database. Main Outcome Measures Survival and functional status scores of five domains (feeding, locomotion, expression, transfer mobility, and social interaction) fitted into logistic regression models adjusted for age, sex, race, co-morbidities, injury mechanism, extra-cranial injuries, severity scores, hospital stay, trauma center, and hospital level. Sensitivity analyses for functional outcomes were performed. Results There were 26,234 SATBI patients. Annual numbers of SATBI increased from 1,757 to 3,808 during 1998–2007. Falls accounted for 47.7% of all SATBI. Survival increased significantly from 72.5% to 82.7% (OR 1.10, 95%CI 1.08–1.11, P<0.001). In sensitivity analyses, trends of complete independence in functional outcomes increased significantly for expression (OR 1.01, 95%CI 1.00–1.02, P=0.011) and social interaction (OR 1.01, 95%CI 1.00–1.03, P=0.002). There were no significant variations over time for feeding, locomotion, and transfer mobility. Conclusions Trends for SATBI served by Pennsylvania’s established trauma system showed increases in rates but substantial reductions in mortality and significant improvements in functional outcomes at discharge for expression and social interaction. PMID:21386713
Courtney, Amy; Courtney, Michael
2015-01-01
Primary blast-induced traumatic brain injury (bTBI) is a prevalent battlefield injury in recent conflicts, yet biomechanical mechanisms of bTBI remain unclear. Elucidating specific biomechanical mechanisms is essential to developing animal models for testing candidate therapies and for improving protective equipment. Three hypothetical mechanisms of primary bTBI have received the most attention. Because translational and rotational head accelerations are primary contributors to TBI from non-penetrating blunt force head trauma, the acceleration hypothesis suggests that blast-induced head accelerations may cause bTBI. The hypothesis of direct cranial transmission suggests that a pressure transient traverses the skull into the brain and directly injures brain tissue. The thoracic hypothesis of bTBI suggests that some combination of a pressure transient reaching the brain via the thorax and a vagally mediated reflex result in bTBI. These three mechanisms may not be mutually exclusive, and quantifying exposure thresholds (for blasts of a given duration) is essential for determining which mechanisms may be contributing for a level of blast exposure. Progress has been hindered by experimental designs, which do not effectively expose animal models to a single mechanism and by over-reliance on poorly validated computational models. The path forward should be predictive validation of computational models by quantitative confirmation with blast experiments in animal models, human cadavers, and biofidelic human surrogates over a range of relevant blast magnitudes and durations coupled with experimental designs, which isolate a single injury mechanism. PMID:26539158
Brain injury tolerance limit based on computation of axonal strain.
Sahoo, Debasis; Deck, Caroline; Willinger, Rémy
2016-07-01
Traumatic brain injury (TBI) is the leading cause of death and permanent impairment over the last decades. In both the severe and mild TBIs, diffuse axonal injury (DAI) is the most common pathology and leads to axonal degeneration. Computation of axonal strain by using finite element head model in numerical simulation can enlighten the DAI mechanism and help to establish advanced head injury criteria. The main objective of this study is to develop a brain injury criterion based on computation of axonal strain. To achieve the objective a state-of-the-art finite element head model with enhanced brain and skull material laws, was used for numerical computation of real world head trauma. The implementation of new medical imaging data such as, fractional anisotropy and axonal fiber orientation from Diffusion Tensor Imaging (DTI) of 12 healthy patients into the finite element brain model was performed to improve the brain constitutive material law with more efficient heterogeneous anisotropic visco hyper-elastic material law. The brain behavior has been validated in terms of brain deformation against Hardy et al. (2001), Hardy et al. (2007), and in terms of brain pressure against Nahum et al. (1977) and Trosseille et al. (1992) experiments. Verification of model stability has been conducted as well. Further, 109 well-documented TBI cases were simulated and axonal strain computed to derive brain injury tolerance curve. Based on an in-depth statistical analysis of different intra-cerebral parameters (brain axonal strain rate, axonal strain, first principal strain, Von Mises strain, first principal stress, Von Mises stress, CSDM (0.10), CSDM (0.15) and CSDM (0.25)), it was shown that axonal strain was the most appropriate candidate parameter to predict DAI. The proposed brain injury tolerance limit for a 50% risk of DAI has been established at 14.65% of axonal strain. This study provides a key step for a realistic novel injury metric for DAI. Copyright © 2016 Elsevier Ltd. All rights reserved.
Severity scores in trauma patients admitted to ICU. Physiological and anatomic models.
Serviá, L; Badia, M; Montserrat, N; Trujillano, J
2018-02-02
The goals of this project were to compare both the anatomic and physiologic severity scores in trauma patients admitted to intensive care unit (ICU), and to elaborate mixed statistical models to improve the precision of the scores. A prospective study of cohorts. The combined medical/surgical ICU in a secondary university hospital. Seven hundred and eighty trauma patients admitted to ICU older than 16 years of age. Anatomic models (ISS and NISS) were compared and combined with physiological models (T-RTS, APACHE II [APII], and MPM II). The probability of death was calculated following the TRISS method. The discrimination was assessed using ROC curves (ABC [CI 95%]), and the calibration using the Hosmer-Lemeshoẃs H test. The mixed models were elaborated with the tree classification method type Chi Square Automatic Interaction Detection. A 14% global mortality was recorded. The physiological models presented the best discrimination values (APII of 0.87 [0.84-0.90]). All models were affected by bad calibration (P<.01). The best mixed model resulted from the combination of APII and ISS (0.88 [0.83-0.90]). This model was able to differentiate between a 7.5% mortality for elderly patients with pathological antecedents and a 25% mortality in patients presenting traumatic brain injury, from a pool of patients with APII values ranging from 10 to 17 and an ISS threshold of 22. The physiological models perform better than the anatomical models in traumatic patients admitted to the ICU. Patients with low scores in the physiological models require an anatomic analysis of the injuries to determine their severity. Copyright © 2017 Elsevier España, S.L.U. y SEMICYUC. All rights reserved.
Neuroprotection against Surgically-Induced Brain Injury
Jadhav, Vikram; Solaroglu, Ihsan; Obenaus, Andre; Zhang, John H.
2007-01-01
Background Neurosurgical procedures are carried out routinely in health institutions across the world. A key issue to be considered during neurosurgical interventions is that there is always an element of inevitable brain injury that results from the procedure itself due to the unique nature of the nervous system. Brain tissue at the periphery of the operative site is at risk of injury by various means including incisions and direct trauma, electrocautery, hemorrhage, and retractor stretch. Methods/Results In the present review we will elaborate upon this surgically-induced brain injury and also present a novel animal model to study it. Additionally, we will summarize preliminary results obtained by pretreatment with PP1, a src tyrosine kinase inhibitor reported to have neuroprotective properties in in-vivo experimental studies. Any form of pretreatment to limit the damage to the susceptible functional brain tissue during neurosurgical procedures may have a significant impact on the patient recovery. Conclusion This brief review is intended to raise the question of ‘neuroprotection against surgically-induced brain injury’ in the neurosurgical scientific community and stimulate discussions. PMID:17210286
Predictors of Outcome following Acquired Brain Injury in Children
ERIC Educational Resources Information Center
Johnson, Abigail R.; DeMatt, Ellen; Salorio, Cynthia F.
2009-01-01
Acquired brain injury (ABI) in children and adolescents can result from multiple causes, including trauma, central nervous system infections, noninfectious disorders (epilepsy, hypoxia/ischemia, genetic/metabolic disorders), tumors, and vascular abnormalities. Prediction of outcomes is important, to target interventions, allocate resources,…
Trauma Spectrum Disorders: Emerging Perspectives on the Impact on Military and Veteran Families
ERIC Educational Resources Information Center
O'Donnell, Lolita; Begg, Lisa; Lipson, Linda; Elvander, Erika
2011-01-01
This article summarizes the findings from the Second Annual Trauma Spectrum Disorders Conference, which was held in December 2009 and was sponsored by the Defense Centers of Excellence for Psychological Health and Traumatic Brain Injury in conjunction with the Department of Veterans Affairs and the National Institutes of Health. The conference…
The changing nature of death on the trauma service.
Kahl, Jessica E; Calvo, Richard Y; Sise, Michael J; Sise, C Beth; Thorndike, Jonathan F; Shackford, Steven R
2013-08-01
Recent innovations in care have improved survival following injury. Coincidentally, the population of elderly injured patients with preexisting comorbidities has increased. We hypothesized that this increase in elderly injured patients may have combined with recent care innovations to alter the causes of death after trauma. We reviewed demographics, injury characteristics, and cause of death of in-hospital deaths of patients admitted to our Level I trauma service from 2000 through 2011. Cause of death was classified as acute hemorrhagic shock; severe traumatic brain injury or high spinal cord injury; complications of preexisting medical condition only (PM); survivable trauma combined with complications of preexisting medical condition (TCoM); multiple-organ failure, sepsis, or adult respiratory distress syndrome (MOF/S/ARDS), or trauma not otherwise categorized (e.g., asphyxiation). Major trauma care advances implemented on our service during the period were identified, and trends in the causes of death were analyzed. Of the 27,276 admissions, 819 (3%) eligible nonsurvivors were identified for the cause-of-death analyses. Causes of death were severe traumatic brain injury or high spinal cord injury at 44%, acute hemorrhagic shock at 28%, PM at 11%, TCoM at 10%, MOF/S/ARDS at 2%, and trauma not otherwise categorized at 5%. Mean age at death increased across the study interval (range, 47-57 years), while mean Injury Severity Score (ISS) decreased (range, 28-35). There was a significant increase in deaths because of TCoM (3.3-20.9%) and PM (6.7-16.4%), while deaths caused by MOF/S/ARDS decreased from 5% to 0% by 2007. Compared with year 2000, the annual adjusted mortality rate decreased consistently starting in 2009, after the 2002 to 2007 adoption of four major trauma practice guidelines. Mortality caused by preexisting medical conditions has increased, while markedly fewer deaths resulted from the complications of injury. Future improvements in outcomes will require improvement in the management of elderly trauma patients with comorbid conditions.
Bachi, Keren; Parvaz, Muhammad A; Moeller, Scott J; Gan, Gabriela; Zilverstand, Anna; Goldstein, Rita Z; Alia-Klein, Nelly
2018-01-01
Background : Childhood trauma affects neurodevelopment and promotes vulnerability to impaired constraint, depression, and addiction. Reduced gray matter concentration (GMC) in the mesocorticolimbic regions implicated in reward processing and cognitive control may be an underlying substrate, as documented separately in addiction and for childhood trauma. The purpose of this study was to understand the contribution of childhood maltreatment to GMC effects in individuals with cocaine use disorder. Methods : Individuals with cocaine use disorder were partitioned into groups of low vs. high childhood trauma based on median split of the total score of the Childhood Trauma Questionnaire (CTQ; CUD-L, N = 23; CUD-H, N = 24) and compared with age, race, and gender matched healthy controls with low trauma ( N = 29). GMC was obtained using voxel-based morphometry applied to T1-weighted MRI scans. Drug use, depression and constraint were assessed with standardized instruments. Results : Whole-brain group comparisons showed reduced GMC in the right lateral orbitofrontal cortex (OFC) in CUD-H as compared with controls (cluster-level p FWE-corr < 0.001) and CUD-L (cluster-level p FWE-corr = 0.035); there were no significant differences between CUD-L and controls. A hierarchical regression analysis across both CUD groups revealed that childhood trauma, but not demographics and drug use, and beyond constraint and depression, accounted for 37.7% of the variance in the GMC in the right lateral OFC ( p < 0.001). Conclusions : Beyond other contributing factors, childhood trauma predicted GMC reductions in the OFC in individuals with cocaine use disorder. These findings underscore a link between premorbid environmental stress and morphological integrity of a brain region central for behaviors underlying drug addiction. These results further highlight the importance of accounting for childhood trauma, potentially as a factor predisposing to addiction, when examining and interpreting neural alterations in cocaine addicted individuals.
Bachi, Keren; Parvaz, Muhammad A.; Moeller, Scott J.; Gan, Gabriela; Zilverstand, Anna; Goldstein, Rita Z.; Alia-Klein, Nelly
2018-01-01
Background: Childhood trauma affects neurodevelopment and promotes vulnerability to impaired constraint, depression, and addiction. Reduced gray matter concentration (GMC) in the mesocorticolimbic regions implicated in reward processing and cognitive control may be an underlying substrate, as documented separately in addiction and for childhood trauma. The purpose of this study was to understand the contribution of childhood maltreatment to GMC effects in individuals with cocaine use disorder. Methods: Individuals with cocaine use disorder were partitioned into groups of low vs. high childhood trauma based on median split of the total score of the Childhood Trauma Questionnaire (CTQ; CUD-L, N = 23; CUD-H, N = 24) and compared with age, race, and gender matched healthy controls with low trauma (N = 29). GMC was obtained using voxel-based morphometry applied to T1-weighted MRI scans. Drug use, depression and constraint were assessed with standardized instruments. Results: Whole-brain group comparisons showed reduced GMC in the right lateral orbitofrontal cortex (OFC) in CUD-H as compared with controls (cluster-level pFWE-corr < 0.001) and CUD-L (cluster-level pFWE-corr = 0.035); there were no significant differences between CUD-L and controls. A hierarchical regression analysis across both CUD groups revealed that childhood trauma, but not demographics and drug use, and beyond constraint and depression, accounted for 37.7% of the variance in the GMC in the right lateral OFC (p < 0.001). Conclusions: Beyond other contributing factors, childhood trauma predicted GMC reductions in the OFC in individuals with cocaine use disorder. These findings underscore a link between premorbid environmental stress and morphological integrity of a brain region central for behaviors underlying drug addiction. These results further highlight the importance of accounting for childhood trauma, potentially as a factor predisposing to addiction, when examining and interpreting neural alterations in cocaine addicted individuals. PMID:29497369
Samanamalee, Samitha; Sigera, Ponsuge Chathurani; De Silva, Ambepitiyawaduge Pubudu; Thilakasiri, Kaushila; Rashan, Aasiyah; Wadanambi, Saman; Jayasinghe, Kosala Saroj Amarasiri; Dondorp, Arjen M; Haniffa, Rashan
2018-01-08
This study evaluates post-ICU outcomes of patients admitted with moderate and severe Traumatic Brain Injury (TBI) in a tertiary neurocritical care unit in an low middle income country and the performance of trauma scores: A Severity Characterization of Trauma, Trauma and Injury Severity Score, Injury Severity Score and Revised Trauma Score in this setting. Adult patients directly admitted to the neurosurgical intensive care units of the National Hospital of Sri Lanka between 21st July 2014 and 1st October 2014 with moderate or severe TBI were recruited. A telephone administered questionnaire based on the Glasgow Outcome Scale Extended (GOSE) was used to assess functional outcome of patients at 3 and 6 months after injury. The economic impact of the injury was assessed before injury, and at 3 and 6 months after injury. One hundred and one patients were included in the study. Survival at ICU discharge, 3 and 6 months after injury was 68.3%, 49.5% and 45.5% respectively. Of the survivors at 3 months after injury, 43 (86%) were living at home. Only 19 (38%) patients had a good recovery (as defined by GOSE 7 and 8). Three months and six months after injury, respectively 25 (50%) and 14 (30.4%) patients had become "economically dependent". Selected trauma scores had poor discriminatory ability in predicting mortality. This observational study of patients sustaining moderate or severe TBI in Sri Lanka (a LMIC) reveals only 46% of patients were alive at 6 months after ICU discharge and only 20% overall attained a good (GOSE 7 or 8) recovery. The social and economic consequences of TBI were long lasting in this setting. Injury Severity Score, Revised Trauma Score, A Severity Characterization of Trauma and Trauma and Injury Severity Score, all performed poorly in predicting mortality in this setting and illustrate the need for setting adapted tools.
Gavrilovski, M; El-Zanfaly, M; Lyon, R M
2018-04-20
Major trauma can result in both life-threatening haemorrhage and traumatic brain injury (TBI). The pre-hospital management of these conditions, particularly in relation to the cardiovascular system, is very different. TBI can result in cardiovascular instability but the exact incidence remains poorly described. This study explores the incidence of cardiovascular instability in patients undergoing pre-hospital anaesthesia for suspected TBI. Retrospective case series of all pre-hospital trauma patients attended by Kent, Surrey & Sussex Air Ambulance Trust (United Kingdom) trauma team during the period 1 January 2015-31 December 2016. Patients were included if they showed clinical signs of TBI, underwent pre-hospital anaesthesia and hospital computed tomography scanning subsequently confirmed an isolated TBI. Out of 121 patients with confirmed isolated TBI, 68 were cardiovascularly stable throughout the pre-anaesthesia phase, whilst 53 (44%) showed signs of instability (HR > 100bpm and/or SBP < 100 mmHg pre-anaesthesia). Hypotension (SBP < 100) with or without tachycardia was present in 14 (12%) patients. 10 (8%) patients with isolated TBI received pre-hospital blood product transfusion. Increased awareness that traumatic brain injury can cause significant derangement to heart rate and blood pressure, even in the absence of major haemorrhage, would allow the pre-hospital clinician to treat cardiovascular instability with the most appropriate means, such as crystalloid and vasopressors, to limit secondary brain injury. Copyright © 2018. Published by Elsevier Ltd.
Cerebroprotective effect of combined treatment with pyrazidol and bemitil in craniocerebral trauma.
Zarubina, I V; Kuritsyna, N A; Shabanov, P D
2004-07-01
Monotherapy of consequences of craniocerebral trauma with pyrazidol (1 mg/kg) produced an anxiolytic effect in animals highly resistant to hypoxia and activating effect on low resistant animals. Treatment with bemitil in a dose of 25 mg/kg produced a cerebroprotective effect and normalized individual behavioral characteristics, parameters of energy metabolism, and state of the antioxidant system in the brain of highly and low resistant rats. The effect of bemitil was most pronounced in highly resistant animals. During combined treatment, pyrazidol and bemitil had an additive effect in animals of both groups. They normalized behavioral reactions and prevented the development of metabolic disturbances in the brain.
Hicks, R R; Baldwin, S A; Scheff, S W
1997-01-01
Disruption of the blood-brain barrier (BBB) and neuronal cytoskeletal damage were evaluated in two commonly used rat models of traumatic brain injury. Adult rats received a lateral cortical impact (CI) or lateral fluid percussion (FP) injury of mild or moderate severity or a sham procedure. Six hours after trauma, the brains were removed and analyzed with immunocytochemical techniques for alterations in the serum protein, IgG, and the cytoskeletal protein, microtubule-associated protein 2 (MAP2). Both models induced profound alterations in these proteins in the ipsilateral cortex and hippocampus compared to sham-injured controls. Following an injury of moderate severity, the CI injury resulted in greater IgG extravasation in the cortex and hippocampus than the FP injury. Conversely, after a mild injury, IgG extravasation in the hippocampus was greater for FP than CI. All of the animals in the CI group and most of the FP group showed a loss of MAP2 in the hippocampus. The specific subregions within the cortex and hippocampus that were affected by the injury varied between models, despite having identical impact sites. These data demonstrate that there are both similarities and differences between a CI and FP injury on vascular and neuronal cystoskeletal integrity, which should be considered when utilizing these animal models to study selected features of human head injury.
Developing a Family-Centered Care Model for Critical Care After Pediatric Traumatic Brain Injury.
Moore, Megan; Robinson, Gabrielle; Mink, Richard; Hudson, Kimberly; Dotolo, Danae; Gooding, Tracy; Ramirez, Alma; Zatzick, Douglas; Giordano, Jessica; Crawley, Deborah; Vavilala, Monica S
2015-10-01
This study examined the family experience of critical care after pediatric traumatic brain injury in order to develop a model of specific factors associated with family-centered care. Qualitative methods with semi-structured interviews were used. Two level 1 trauma centers. Fifteen mothers of children who had an acute hospital stay after traumatic brain injury within the last 5 years were interviewed about their experience of critical care and discharge planning. Participants who were primarily English, Spanish, or Cantonese speaking were included. None. Content analysis was used to code the transcribed interviews and develop the family-centered care model. Three major themes emerged: 1) thorough, timely, compassionate communication, 2) capacity building for families, providers, and facilities, and 3) coordination of care transitions. Participants reported valuing detailed, frequent communication that set realistic expectations and prepared them for decision making and outcomes. Areas for capacity building included strategies to increase provider cultural humility, parent participation in care, and institutional flexibility. Coordinated care transitions, including continuity of information and maintenance of partnerships with families and care teams, were highlighted. Participants who were not primarily English speaking reported particular difficulty with communication, cultural understanding, and coordinated transitions. This study presents a family-centered traumatic brain injury care model based on family perspectives. In addition to communication and coordination strategies, the model offers methods to address cultural and structural barriers to meeting the needs of non-English-speaking families. Given the stress experienced by families of children with traumatic brain injury, careful consideration of the model themes identified here may assist in improving overall quality of care to families of hospitalized children with traumatic brain injury.
Computed tomography and clinical outcome in patients with severe traumatic brain injury.
Stenberg, Maud; Koskinen, Lars-Owe D; Jonasson, Per; Levi, Richard; Stålnacke, Britt-Marie
2017-01-01
To study: (i) acute computed tomography (CT) characteristics and clinical outcome; (ii) clinical course and (iii) Corticosteroid Randomisation after Significant Head Injury acute calculator protocol (CRASH) model and clinical outcome in patients with severe traumatic brain injury (sTBI). Initial CT (CT i ) and CT 24 hours post-trauma (CT 24 ) were evaluated according to Marshall and Rotterdam classifications. Rancho Los Amigos Cognitive Scale-Revised (RLAS-R) and Glasgow Outcome Scale Extended (GOSE) were assessed at three months and one year post-trauma. The prognostic value of the CRASH model was evaluated. Thirty-seven patients were included. Marshall CT i and CT 24 were significantly correlated with RLAS-R at three months. Rotterdam CT 24 was significantly correlated with GOSE at three months. RLAS-R and the GOSE improved significantly from three months to one year. CRASH predicted unfavourable outcome at six months for 81% of patients with bad outcome and for 85% of patients with favourable outcome according to GOSE at one year. Neither CT nor CRASH yielded clinically useful predictions of outcome at one year post-injury. The study showed encouragingly many instances of significant recovery in this population of sTBI. The combination of lack of reliable prognostic indicators and favourable outcomes supports the case for intensive acute management and rehabilitation as the default protocol in the cases of sTBI.
Positive therapeutic response to lithium in hypomania secondary to organic brain syndrome.
Rosenbaum, A H; Barry, M J
1975-10-01
A 57-year-old man with no personal or family history of manic-depressive disease developed symptoms of hypomania after a cerebrovascular accident and surgical trauma to the brain. The patient responded well to lithium carbonate treatment over a 2-year period. Although this therapy is contraindicated in cases of organic brain syndrome, the authors suggest that it should be considered in the management of hypomanic behavior following organic brain dysfunction.
Neuroendocrine models of social anxiety disorder
van Honk, Jack; Bos, Peter A.; Terburg, David; Heany, Sarah; Stein, Dan J.
2015-01-01
Social anxiety disorder (SAD) is a highly prevalent and disabling disorder with key behavioral traits of social fearfulness, social avoidance, and submissiveness. Here we argue that hormonal systems play a key role in mediating social anxiety, and so may be important in SAD. Hormonal alterations, often established early in development through the interaction between biological and psychological factors (eg, genetic predisposition x early trauma), predispose to socially fearful, avoidant, and submissive behavior. However, whereas gene variants and histories of trauma persist, hormonal systems can be remodeled over the course of life. Hormones play a key role during the periods of all sensitive developmental windows (ie, prenatal, neonatal, puberty, aging), and are capable of opening up new developmental windows in adulthood. Indeed, the developmental plasticity of our social brain, and thus of social behavior in adulthood, critically depends on steroid hormones such as testosterone and peptide hormones such as oxytocin. These steroid and peptide hormones in interaction with social experiences may have potential for reprogramming the socially anxious brain. Certainly, single administrations of oxytocin and testosterone in humans reduce socially fearful, avoidant, and submissive behavior. Such work may ultimately lead to new approaches to the treatment of SAD. PMID:26487809
Hypothermia is associated with poor outcome in pediatric trauma patients.
Sundberg, Jennifer; Estrada, Cristina; Jenkins, Cathy; Ray, Jacqueline; Abramo, Thomas
2011-11-01
The objective of the study was to determine if hypothermia in pediatric trauma patients is associated with increased mortality. We reviewed the charts of level 1 trauma patients aged 3 months to 17 years who presented between September 2006 and March 2008. We analyzed data for patients with temperatures recorded within 30 minutes of arrival to the pediatric emergency department. Logistic regression models were used to test for associations of hypothermia with death while adjusting for mode of transport, season of year, and presence of intracranial pathology as documented by an abnormal head computed tomographic scan. Of the 226 level 1 trauma patients presenting during the study period, 190 met inclusion criteria. Twenty-one patients (11%) died. The odds ratio (OR) of a hypothermic patient dying was 9.2 times that of a normothermic patient when adjusting for seasonal variation (95% confidence interval [CI], 3.2-26.2; P < 0.0001). The OR of a hypothermic patient dying was 8.7 times that of a normothermic patient when adjusting for mode of transport (ground vs air) (95% CI, 3.1-24.6; P < 0.0001). Although it did not reach statistical significance, there was a trend toward an association between hypothermia and the presence of traumatic brain injury as evidenced by an abnormal head computed tomographic scan (OR = 2.4; 95% CI, 0.9-6.0; P = .07). Hypothermia is a risk factor for increased mortality in pediatric trauma patients. This pilot study warrants a more detailed, multicenter analysis to assess the impact of hypothermia in the pediatric trauma patient. Copyright © 2011 Elsevier Inc. All rights reserved.
A mathematical model of endovascular heat transfer for human brain cooling
NASA Astrophysics Data System (ADS)
Salsac, Anne-Virginie; Lasheras, Juan Carlos; Yon, Steven; Magers, Mike; Dobak, John
2000-11-01
Selective cooling of the brain has been shown to exhibit protective effects in cerebral ischemia, trauma, and spinal injury/ischemia. A multi-compartment, unsteady thermal model of the response of the human brain to endovascular cooling is discussed and its results compared to recent experimental data conducted with sheep and other mammals. The model formulation is based on the extension of the bioheat equation, originally proposed by Pennes(1) and later modified by Wissler(2), Stolwijk(3) and Werner and Webb(4). The temporal response of the brain temperature and that of the various body compartments to the cooling of the blood flowing through the common carotid artery is calculated under various scenarios. The effect of the boundary conditions as well as the closure assumptions used in the model, i.e. perfusion rate, metabolism heat production, etc. on the cooling rate of the brain are systematically investigated. (1) Pennes H. H., “Analysis of tissue and arterial blood temperature in the resting forearm.” J. Appl. Physiol. 1: 93-122, 1948. (2) Wissler E. H., “Steady-state temperature distribution in man”, J. Appl. Physiol., 16: 764-740, 1961. (3) Stolwick J. A. J., “Mathematical model of thermoregulation” in “Physiological and behavioral temperature regulation”, edited by J. D. Hardy, A. P. Gagge and A. J. Stolwijk, Charles C. Thomas Publisher, Springfiels, Ill., 703-721, 1971. (4) Werner J., Webb P., “A six-cylinder model of human thermoregulation for general use on personal computers”, Ann. Physiol. Anthrop., 12(3): 123-134, 1993.
Taylor, Colman; Jan, Stephen; Curtis, Kate; Tzannes, Alex; Li, Qiang; Palmer, Cameron; Dickson, Cara; Myburgh, John
2012-11-01
Helicopter Emergency Medical Services (HEMS) are highly resource-intensive facilities that are well established as part of trauma systems in many high-income countries. We evaluated the cost-effectiveness of a physician-staffed HEMS intervention in combination with treatment at a major trauma centre versus ground ambulance or indirect transport (via a referral hospital) in New South Wales (NSW), Australia. Cost and effectiveness estimates were derived from a cohort of trauma patients arriving at St George Hospital in NSW, Australia during an 11-year period. Adjusted estimates of in-hospital mortality were derived using logistic regression and adjusted hospital costs were estimated through a general linear model incorporating a gamma distribution and log link. These estimates along with other assumptions were incorporated into a Markov model with an annual cycle length to estimate a cost per life saved and a cost per life-year saved at one year and over a patient's lifetime respectively in three patient groups (all patients; patients with serious injury [Injury Severity Score>12]; patients with traumatic brain injury [TBI]). Results showed HEMS to be more costly but more effective at reducing in-hospital mortality leading to a cost per life saved of $1,566,379, $533,781 and $519,787 in all patients, patients with serious injury and patients with TBI respectively. When modelled over a patient's lifetime, the improved mortality associated with HEMS led to a cost per life year saved of $96,524, $50,035 and $49,159 in the three patient groups respectively. Sensitivity analyses revealed a higher probability of HEMS being cost-effective in patients with serious injury and TBI. Our investigation confirms a HEMS intervention is associated with improved mortality in trauma patients, especially in patients with serious injury and TBI. The improved benefit of HEMS in patients with serious injury and TBI leads to improved estimated cost-effectiveness. Copyright © 2012 Elsevier Ltd. All rights reserved.
Clark, Ian A.; Niehaus, Katherine E.; Duff, Eugene P.; Di Simplicio, Martina C.; Clifford, Gari D.; Smith, Stephen M.; Mackay, Clare E.; Woolrich, Mark W.; Holmes, Emily A.
2014-01-01
After psychological trauma, why do some only some parts of the traumatic event return as intrusive memories while others do not? Intrusive memories are key to cognitive behavioural treatment for post-traumatic stress disorder, and an aetiological understanding is warranted. We present here analyses using multivariate pattern analysis (MVPA) and a machine learning classifier to investigate whether peri-traumatic brain activation was able to predict later intrusive memories (i.e. before they had happened). To provide a methodological basis for understanding the context of the current results, we first show how functional magnetic resonance imaging (fMRI) during an experimental analogue of trauma (a trauma film) via a prospective event-related design was able to capture an individual's later intrusive memories. Results showed widespread increases in brain activation at encoding when viewing a scene in the scanner that would later return as an intrusive memory in the real world. These fMRI results were replicated in a second study. While traditional mass univariate regression analysis highlighted an association between brain processing and symptomatology, this is not the same as prediction. Using MVPA and a machine learning classifier, it was possible to predict later intrusive memories across participants with 68% accuracy, and within a participant with 97% accuracy; i.e. the classifier could identify out of multiple scenes those that would later return as an intrusive memory. We also report here brain networks key in intrusive memory prediction. MVPA opens the possibility of decoding brain activity to reconstruct idiosyncratic cognitive events with relevance to understanding and predicting mental health symptoms. PMID:25151915
Vaughan, Jay; McCullough, Elaine; Burnell, Alan
2016-10-01
This article describes the development and application of a wrap-around, multidisciplinary, brain-based, developmental and attachment-focussed intervention for children who have experienced significant trauma in the context of their early life. It outlines the presentation of the children and families who are referred to the service and the model of treatment that they receive. In doing so, it identifies the core components underpinning Neuro-Physiological Psychotherapy (NPP) and links the application of the integrative model to research and practice in the field of neuroscience and attachment and to the use of therapeutic approaches that are beneficial to maltreated children and their adoptive parents. It highlights the need for a neuro-sequential approach that impacts all aspects of the child's life in the effort to redress the impact of developmental trauma with the aim of improving their overall functioning and their ability to develop healthy relationships into the future. © The Author(s) 2016.
Gatt, Justine M; Burton, Karen L O; Routledge, Kylie M; Grasby, Katrina L; Korgaonkar, Mayuresh S; Grieve, Stuart M; Schofield, Peter R; Harris, Anthony W F; Clark, C Richard; Williams, Leanne M
2018-06-20
Associations between well-being, resilience to trauma and the volume of grey-matter regions involved in affective processing (e.g., threat/reward circuits) are largely unexplored, as are the roles of shared genetic and environmental factors derived from multivariate twin modelling. This study presents, to our knowledge, the first exploration of well-being and volumes of grey-matter regions involved in affective processing using a region-of-interest, voxel-based approach in 263 healthy adult twins (60% monozygotic pairs, 61% females, mean age 39.69 yr). To examine patterns for resilience (i.e., positive adaptation following adversity), we evaluated associations between the same brain regions and well-being in a trauma-exposed subgroup. We found a correlated effect between increased well-being and reduced grey-matter volume of the pontine nuclei. This association was strongest for individuals with higher resilience to trauma. Multivariate twin modelling suggested that the common variance between the pons volume and well-being scores was due to environmental factors. We used a cross-sectional sample; results need to be replicated longitudinally and in a larger sample. Associations with altered grey matter of the pontine nuclei suggest that basic sensory processes, such as arousal, startle, memory consolidation and/or emotional conditioning, may have a role in well-being and resilience.
Günther, Mattias; Plantman, Stefan; Davidsson, Johan; Angéria, Maria; Mathiesen, Tiit; Risling, Mårten
2015-04-01
Traumatic brain injury is followed by secondary neuronal degeneration, largely dependent on an inflammatory response. This response is probably gender specific, since females are better protected than males in experimental models. The reasons are not fully known. We examined aspects of the inflammatory response following experimental TBI in male and female rats to explore possible gender differences at 24 h and 72 h after trauma, times of peak histological inflammation and neuronal degeneration. A penetrating brain injury model was used to produce penetrating focal TBI in 20 Sprague-Dawley rats, 5 males and 5 females for each time point. After 24 and 72 h the brains were removed and subjected to in situ hybridization and immunohistochemical analyses for COX-2, iNOS, osteopontin, glial fibrillary acidic protein, 3-nitrotyrosine, TUNEL and Fluoro-Jade. COX-2 mRNA and protein levels were increased in the perilesional area compared to the uninjured contralateral side and significantly higher in males at 24 h and 72 h (p < 0.05). iNOS mRNA was significantly increased in females at 24 h (p < 0.05) although protein was not. TUNEL was increased in male rats after 24 h (p < 0.05). Glial fibrillary acidic protein, osteopontin, 3-nitrotyrosine and Fluoro-Jade stained degenerating neurons were increased in the perilesional area, showing no difference between genders. COX-2 regulation differed between genders after TBI. The increased COX-2 expression in male rats correlated with increased apoptotic cell death detected by increased TUNEL staining at 24 h, but not with neuronal necrosis measured by Flouro-Jade. Astrogliosis and microgliosis did not differ, confirming a comparable level of trauma. The gender-specific trait of the secondary inflammatory response may be connected to prostaglandin regulation, which may partially explain gender variances in outcome after TBI.
Xenon Protects against Blast-Induced Traumatic Brain Injury in an In Vitro Model
Campos-Pires, Rita; Koziakova, Mariia; Yonis, Amina; Pau, Ashni; Macdonald, Warren; Harris, Katie; Edge, Christopher J.; Franks, Nicholas P.; Mahoney, Peter F.
2018-01-01
Abstract The aim of this study was to evaluate the neuroprotective efficacy of the inert gas xenon as a treatment for patients with blast-induced traumatic brain injury in an in vitro laboratory model. We developed a novel blast traumatic brain injury model using C57BL/6N mouse organotypic hippocampal brain-slice cultures exposed to a single shockwave, with the resulting injury quantified using propidium iodide fluorescence. A shock tube blast generator was used to simulate open field explosive blast shockwaves, modeled by the Friedlander waveform. Exposure to blast shockwave resulted in significant (p < 0.01) injury that increased with peak-overpressure and impulse of the shockwave, and which exhibited a secondary injury development up to 72 h after trauma. Blast-induced propidium iodide fluorescence overlapped with cleaved caspase-3 immunofluorescence, indicating that shock-wave–induced cell death involves apoptosis. Xenon (50% atm) applied 1 h after blast exposure reduced injury 24 h (p < 0.01), 48 h (p < 0.05), and 72 h (p < 0.001) later, compared with untreated control injury. Xenon-treated injured slices were not significantly different from uninjured sham slices at 24 h and 72 h. We demonstrate for the first time that xenon treatment after blast traumatic brain injury reduces initial injury and prevents subsequent injury development in vitro. Our findings support the idea that xenon may be a potential first-line treatment for those with blast-induced traumatic brain injury. PMID:29285980
NASA Astrophysics Data System (ADS)
Chico-Calero, Isabel; Shishkov, Milen; Welt, Jonathan; Blatter, Cedric; Vakoc, Benjamin J.
2016-03-01
While most people recover completely from mild traumatic brain injuries (mTBIs) and concussions, a subset develop lasting neurological disorders. Understanding the complex pathophysiology of these injuries is critical to developing improved prognostic and therapeutic approaches. Multiple studies have shown that the structure and perfusion of brain vessels are altered after mTBI. It is possible that these vascular injuries contribute to or trigger neurodegeneration. Intravital microscopy and mouse models of TBI offer a powerful platform to study the vascular component of mTBI. Because optical coherence tomography based angiography is based on perfusion contrast and is not significantly degraded by vessel leakage or blood brain barrier disruption, it is uniquely suited to studies of brain perfusion in the setting of trauma. However, existing TBI imaging models require surgical exposure of the brain at the time of injury which conflates TBI-related vascular changes with those caused by surgery. In this work, we describe a modified cranial window preparation based on a flexible, transparent polyurethane membrane. Impact injuries were delivered directly through this membrane, and imaging was performed immediately after injury without the need for additional surgical procedures. Using this model, we demonstrate that mTBI induces a transient cessation of flow in the capillaries and smaller vessels near the injury point. Reperfusion is observed in all animals within 3 hours of injury. This work describes new insight into the transient vascular changes induced by mTBI, and demonstrates more broadly the utility of the OCT/polyurethane window model platform in preclinical studies of mTBI.
Mild traumatic brain injury: a risk factor for neurodegeneration
2010-01-01
Recently, it has become clear that head trauma can lead to a progressive neurodegeneration known as chronic traumatic encephalopathy. Although the medical literature also implicates head trauma as a risk factor for Alzheimer's disease, these findings are predominantly based on clinical diagnostic criteria that lack specificity. The dementia that follows head injuries or repetitive mild trauma may be caused by chronic traumatic encephalopathy, alone or in conjunction with other neurodegenerations (for example, Alzheimer's disease). Prospective longitudinal studies of head-injured individuals, with neuropathological verification, will not only improve understanding of head trauma as a risk factor for dementia but will also enhance treatment and prevention of a variety of neurodegenerative diseases. PMID:20587081
The relationship between brain volumes and intelligence in bipolar disorder.
Vreeker, Annabel; Abramovic, Lucija; Boks, Marco P M; Verkooijen, Sanne; van Bergen, Annet H; Ophoff, Roel A; Kahn, René S; van Haren, Neeltje E M
2017-12-01
Bipolar disorder type-I (BD-I) patients show a lower Intelligence Quotient (IQ) and smaller brain volumes as compared with healthy controls. Considering that in healthy individuals lower IQ is related to smaller total brain volume, it is of interest to investigate whether IQ deficits in BD-I patients are related to smaller brain volumes and to what extent smaller brain volumes can explain differences between premorbid IQ estimates and IQ after a diagnosis of BD-I. Magnetic resonance imaging brain scans, IQ and premorbid IQ scores were obtained from 195 BDI patients and 160 controls. We studied the relationship of (global, cortical and subcortical) brain volumes with IQ and IQ change. Additionally, we investigated the relationship between childhood trauma, lithium- and antipsychotic use and IQ. Total brain volume and IQ were positively correlated in the entire sample. This correlation did not differ between patients and controls. Although brain volumes mediated the relationship between BD-I and IQ in part, the direct relationship between the diagnosis and IQ remained significant. Childhood trauma and use of lithium and antipsychotic medication did not affect the relationship between brain volumes and IQ. However, current lithium use was related to lower IQ in patients. Our data suggest a similar relationship between brain volume and IQ in BD-I patients and controls. Smaller brain volumes only partially explain IQ deficits in patients. Therefore, our findings indicate that in addition to brain volumes and lithium use other disease factors play a role in IQ deficits in BD-I patients. Copyright © 2017 Elsevier B.V. All rights reserved.
The importance of structural anisotropy in computational models of traumatic brain injury.
Carlsen, Rika W; Daphalapurkar, Nitin P
2015-01-01
Understanding the mechanisms of injury might prove useful in assisting the development of methods for the management and mitigation of traumatic brain injury (TBI). Computational head models can provide valuable insight into the multi-length-scale complexity associated with the primary nature of diffuse axonal injury. It involves understanding how the trauma to the head (at the centimeter length scale) translates to the white-matter tissue (at the millimeter length scale), and even further down to the axonal-length scale, where physical injury to axons (e.g., axon separation) may occur. However, to accurately represent the development of TBI, the biofidelity of these computational models is of utmost importance. There has been a focused effort to improve the biofidelity of computational models by including more sophisticated material definitions and implementing physiologically relevant measures of injury. This paper summarizes recent computational studies that have incorporated structural anisotropy in both the material definition of the white matter and the injury criterion as a means to improve the predictive capabilities of computational models for TBI. We discuss the role of structural anisotropy on both the mechanical response of the brain tissue and on the development of injury. We also outline future directions in the computational modeling of TBI.
Bilateral vertebral artery lesion after dislocating cervical spine trauma. A case report.
Wirbel, R; Pistorius, G; Braun, C; Eichler, A; Mutschler, W
1996-06-01
This case report illustrates the problems associated with diagnosis and management of vertebral artery injuries resulting from dislocating cervical spine trauma. Treatment involved the principles of anterior stabilization of dislocating cervical spine fracture as well as the diagnostic procedures and therapeutic modalities appropriate for vertebral artery lesions. Because vertebral artery injuries with cervical spine trauma are rarely symptomatic, they can easily be overlooked. Bilateral or dominant vertebral artery occlusion, however, may cause fatal ischemic damage to the brain stem and cerebellum. Cervical spine dislocation was stabilized immediately after admission using internal fixation by ventral plate and corticocancellous bone graft. Immediate angiography was performed when brain stem neurologic dysfunction manifested 36 hours after surgery. The patient was treated with anticoagulation, osmotherapy, and controlled hypertension. A fatal outcome resulted in this case of dominant left vertebral artery occlusion. Necropsy even revealed bilateral vertebral artery damage at the level of the osseous lesion. The possibility of the complication of a vertebral artery lesion should be kept in mind when examining patients with cervical spine trauma, especially in patients with fracture-dislocation. Immediate identification by vertebral angiography, magnetic resonance imaging, or thin-slice computed tomography scan is necessary for optimal management of this injury.
Andelic, Nada; Stevens, Lillian Flores; Sigurdardottir, Solrun; Arango-Lasprilla, Juan Carlos; Roe, Cecilie
2012-01-01
To investigate associations between disability and employment 1 year after traumatic brain injury (TBI) using the International Classification of Functioning, Disability and Health (ICF) as a conceptual model. A prospective study including 93 patients with moderate-to-severe TBI (aged 16-55 year). Disability components of the ICF model (impairments, activity limitations and participation restrictions) and personal factors (age, gender, pre-injury employment status) were used as independent variables. The outcome measure was employment at 1 year post-injury categorized into unemployed and employed groups. Personal factors, impairments (brain injury severity, overall trauma severity and number of impaired body functions) and activity limitations (motor and cognitive abilities) accounted for 57% of the variance in employment outcome. Multivariate analyses showed that the probabilities of being employed 1 year post-injury were 95% lower for patients who were unemployed pre-injury (OR = 0.05), 74% lower for those with more severe brain injury (OR = 0.26) and 82% lower for those with more cognitive limitations (OR = 0.18). Rehabilitation professionals should take into account the importance of the ICF model when planning vocational rehabilitation interventions for individuals with TBI and focus on targeting modifiable aspects related to employment outcome, such as the individual's cognitive ability.
38 CFR 71.20 - Eligible veterans and servicemembers.
Code of Federal Regulations, 2013 CFR
2013-07-01
... Armed Forces. (b) The individual has a serious injury, including traumatic brain injury, psychological... impairment or injury, including traumatic brain injury. (3) Psychological trauma or a mental disorder that..., naval, or air service on or after September 11, 2001. (c) Such serious injury renders the individual in...
38 CFR 71.20 - Eligible veterans and servicemembers.
Code of Federal Regulations, 2014 CFR
2014-07-01
... Armed Forces. (b) The individual has a serious injury, including traumatic brain injury, psychological... impairment or injury, including traumatic brain injury. (3) Psychological trauma or a mental disorder that..., naval, or air service on or after September 11, 2001. (c) Such serious injury renders the individual in...
38 CFR 71.20 - Eligible veterans and servicemembers.
Code of Federal Regulations, 2011 CFR
2011-07-01
... Armed Forces. (b) The individual has a serious injury, including traumatic brain injury, psychological... impairment or injury, including traumatic brain injury. (3) Psychological trauma or a mental disorder that..., naval, or air service on or after September 11, 2001. (c) Such serious injury renders the individual in...
38 CFR 71.20 - Eligible veterans and servicemembers.
Code of Federal Regulations, 2012 CFR
2012-07-01
... Armed Forces. (b) The individual has a serious injury, including traumatic brain injury, psychological... impairment or injury, including traumatic brain injury. (3) Psychological trauma or a mental disorder that..., naval, or air service on or after September 11, 2001. (c) Such serious injury renders the individual in...
Shulman, Abraham; Strashun, Arnold M
2009-01-01
It is hypothesized that in all traumatic brain injury (TBI) patients with a clinical history of closed or penetrating head injury, the initial head trauma is associated with a vibratory sensation and noise exposure, with resultant alteration in vascular supply to the structures and contents of the fluid compartments of brain and ear (i.e., the fluid dynamics vascular theory of brain-inner-ear function [FDVTBE]). The primary etiology-head trauma-results in an initial fluctuation, interference, or interaction in the normal fluid dynamics between brain and labyrinth of the inner ear, with a resultant clinical diversity of complaints varying in time of onset and severity. Normal function of the brain and ear is a reflection of a normal state of homeostasis between the fluid compartments in the brain of cerebrospinal fluid and perilymph-endolymph in the labyrinth of the ear. The normal homeostasis in the structures and contents between the two fluid compartment systems--intracerebral and intralabyrinthine--is controlled by mechanisms involved in the maintenance of normal pressures, water and electrolyte content, and neurotransmitter activities. The initial pathophysiology (a reflection of an alteration in the vascular supply to the brain-ear) is hypothesized to be an initial acute inflammatory response, persistence of which results in ischemia and an irreversible alteration in the involved neural substrates of brain-ear. Clinically, a chronic multisymptom complex becomes manifest. The multisymptom complex, individual for each TBI patient regardless of the diagnostic TBI category (i.e., mild, moderate, or severe), initially reflects processes of inflammation and ischemia which, in brain, result in brain volume loss identified as neurodegeneration and hydrocephalus ex vacuo or an alteration in cerebrospinal fluid production (i.e., pseudotumor cerebri) and, in ear, secondary endolymphatic hydrops with associated cochleovestibular complaints of hearing loss, tinnitus, vertigo, ear blockage, and hyperacusis. The FDVTBE integrates and translates a neurovascular hypothesis for Alzheimer's disease to TBI. This study presents an FDVTBE hypothesis of TBI to explain the clinical association of head trauma (TBI) and central nervous system neurodegeneration with multisensory complaints, highlighted by and focusing on cochleovestibular complaints. A clinical case report, previously published for demonstration of the cerebrovascular medical significance of a particular type of tinnitus, and evidence-based basic science and clinical medicine are cited to provide objective evidence in support and demonstration of the FDVTBE.
Helm, M; Hauke, J; Kohler, J; Lampl, L
2013-04-01
Prompt hemorrhage control and adequate fluid resuscitation are the key components of early trauma care. However, the optimal resuscitation strategy remains controversial. In this context the small volume resuscitation (SVR) concept with hypertonic-hyperoncotic solutions is a new strategy. This was a retrospective study in the Helicopter Emergency Medical Service over a 5-year period. Included were all major trauma victims if they were candidates for SVR (initially 4 ml HyperHaes/kg body weight, followed by conventional fluid resuscitation with crystalloids and colloids). Demographic data, type and cause of injury and injury severity score (ISS) were recorded and the amount of fluid volume and the hemodynamic profile were analyzed. Negative side-effects as well as sodium chloride serum levels on hospital admission were recorded. A total of 342 trauma victims (male 70.2%, mean age 39.0 ± 18.8 years, ISS 31.6 ± 16.9, ISS>16, 81.6%) underwent prehospital SVR. A blunt trauma mechanism was predominant (96.8%) and the leading cause of injury was motor vehicle accidents (61.5%) and motorcycle accidents (22.3%). Multiple trauma and polytrauma were noted in 87.4% of the cases. Predominant was traumatic brain injury (73.1%) as well as chest injury (73.1%) followed by limb injury (69.9%) and abdominal/pelvic trauma (45.0%). Within the whole study group in addition to 250 ml HyperHaes, mean volumes of 1214 ± 679 ml lactated Ringers and 1288 ± 954 ml hydroxethylstarch were infused during the prehospital treatment phase. There were no statistically significant differences in the amount of crystalloids and colloids infused regarding the subgroups multisystem trauma (ISS>16), severe traumatic brain injury (GCS<9) and entrapment trauma compared to the total study group. In patients with an initial systolic blood pressure (SBP) >80 mmHg significantly less colloids (1035 ± 659 ml vs. 1288 ± 954 ml, p<0.006) were infused, whereas in patients with an initial SBP ≤ 80 mmHg significantly more colloids were infused (1609 ± 1159 ml vs. 1288 ± 954 ml, p<0.002). There was a statistically significant increase in systolic as well as diastolic blood pressure at all times of blood pressure measurement during prehospital treatment after bolus infusion of HyperHaes within the whole study group. The same applies to the subgroups multisystem trauma, severe traumatic brain injury and entrapment trauma. Minor negative side-effects were observed in 4 cases (1.2%). The mean serum sodium chloride profile on hospital admission was 146.9 ± 5.0 mmol/l, the base excess (BE) was -5.7 ± 5.3 mmol/l) and the pH was 7.3 ± 0.1. The concept of small volume resuscitation provides early and effective hemodynamic control. Clinical side-effects associated with bolus infusion of hypertonic-hyperoncotic solutions are rare.
Yıldırım, Timur; Eylen, Alpaslan; Lule, Sevda; Erdener, Sefik Evren; Vural, Atay; Karatas, Hulya; Ozveren, Mehmet Faik; Dalkara, Turgay; Gursoy-Ozdemir, Yasemin
2015-01-01
Under pathological conditions such as brain trauma, subarachnoid hemorrhage and stroke, cortical spreading depression (CSD) or peri-infarct depolarizations contribute to brain damage in animal models of neurological disorders as well as in human neurological diseases. CSD causes transient megachannel opening on the neuronal membrane, which may compromise neuronal survival under pathological conditions. Poloxamer-188 (P-188) and citicoline are neuroprotectants with membrane sealing properties. The aim of this study is to investigate the effect of P-188 and citicoline on the neuronal megachannel opening induced by CSD in the mouse brain. We have monitored megachannel opening with propidium iodide, a membrane impermeable fluorescent dye and, demonstrate that P-188 and citicoline strikingly decreased CSD-induced neuronal PI influx in cortex and hippocampal dentate gyrus. Therefore, these agents may be providing neuroprotection by blocking megachannel opening, which may be related to their membrane sealing action and warrant further investigation for treatment of traumatic brain injury and ischemic stroke.
Krause, Anna Linda; Borchardt, Viola; Li, Meng; van Tol, Marie-José; Demenescu, Liliana Ramona; Strauss, Bernhard; Kirchmann, Helmut; Buchheim, Anna; Metzger, Coraline D; Nolte, Tobias; Walter, Martin
2016-01-01
Attachment patterns influence actions, thoughts and feeling through a person's "inner working model". Speech charged with attachment-dependent content was proposed to modulate the activation of cognitive-emotional schemata in listeners. We performed a 7 Tesla rest-task-rest functional magnetic resonance imaging (fMRI)-experiment, presenting auditory narratives prototypical of dismissing attachment representations to investigate their effect on 23 healthy males. We then examined effects of participants' attachment style and childhood trauma on brain state changes using seed-based functional connectivity (FC) analyses, and finally tested whether subjective differences in responsivity to narratives could be predicted by baseline network states. In comparison to a baseline state, we observed increased FC in a previously described "social aversion network" including dorsal anterior cingulated cortex (dACC) and left anterior middle temporal gyrus (aMTG) specifically after exposure to insecure-dismissing attachment narratives. Increased dACC-seeded FC within the social aversion network was positively related to the participants' avoidant attachment style and presence of a history of childhood trauma. Anxious attachment style on the other hand was positively correlated with FC between the dACC and a region outside of the "social aversion network", namely the dorsolateral prefrontal cortex, which suggests decreased network segregation as a function of anxious attachment. Finally, the extent of subjective experience of friendliness towards the dismissing narrative was predicted by low baseline FC-values between hippocampus and inferior parietal lobule (IPL). Taken together, our study demonstrates an activation of networks related to social aversion in terms of increased connectivity after listening to insecure-dismissing attachment narratives. A causal interrelation of brain state changes and subsequent changes in social reactivity was further supported by our observation of direct prediction of neuronal responses by individual attachment and trauma characteristics and reversely prediction of subjective experience by intrinsic functional connections. We consider these findings of activation of within-network and between-network connectivity modulated by inter-individual differences as substantial for the understanding of interpersonal processes, particularly in clinical settings.
Lagerstedt, Linnéa; Egea-Guerrero, Juan José; Bustamante, Alejandro; Montaner, Joan; Rodríguez-Rodríguez, Ana; El Rahal, Amir; Turck, Natacha; Quintana, Manuel; García-Armengol, Roser; Prica, Carmen Melinda; Andereggen, Elisabeth; Rinaldi, Lara; Sarrafzadeh, Asita; Schaller, Karl; Sanchez, Jean-Charles
2017-01-01
The majority of patients with mild traumatic brain injury (mTBI) will have normal Glasgow coma scale (GCS) of 15. Furthermore, only 5%–8% of them will be CT-positive for an mTBI. Having a useful biomarker would help clinicians evaluate a patient’s risk of developing intracranial lesions. The S100B protein is currently the most studied and promising biomarker for this purpose. Heart fatty-acid binding protein (H-FABP) has been highlighted in brain injury models and investigated as a biomarker for stroke and severe TBI, for example. Here, we evaluate the performances of S100B and H-FABP for differentiating between CT-positive and CT-negative patients. A total of 261 patients with a GCS score of 15 and at least one clinical symptom of mTBI were recruited at three different European sites. Blood samples from 172 of them were collected ≤ 6 h after trauma. Patients underwent a CT scan and were dichotomised into CT-positive and CT-negative groups for statistical analyses. H-FABP and S100B levels were measured using commercial kits, and their capacities to detect all CT-positive scans were evaluated, with sensitivity set to 100%. For patients recruited ≤ 6 h after trauma, the CT-positive group demonstrated significantly higher levels of both H-FABP (p = 0.004) and S100B (p = 0.003) than the CT-negative group. At 100% sensitivity, specificity reached 6% (95% CI 2.8–10.7) for S100B and 29% (95% CI 21.4–37.1) for H-FABP. Similar results were obtained when including all the patients recruited, i.e. hospital arrival within 24 h of trauma onset. H-FABP out-performed S100B and thus seems to be an interesting protein for detecting all CT-positive mTBI patients with a GCS score of 15 and at least one clinical symptom. PMID:28419114
Lagerstedt, Linnéa; Egea-Guerrero, Juan José; Bustamante, Alejandro; Montaner, Joan; Rodríguez-Rodríguez, Ana; El Rahal, Amir; Turck, Natacha; Quintana, Manuel; García-Armengol, Roser; Prica, Carmen Melinda; Andereggen, Elisabeth; Rinaldi, Lara; Sarrafzadeh, Asita; Schaller, Karl; Sanchez, Jean-Charles
2017-01-01
The majority of patients with mild traumatic brain injury (mTBI) will have normal Glasgow coma scale (GCS) of 15. Furthermore, only 5%-8% of them will be CT-positive for an mTBI. Having a useful biomarker would help clinicians evaluate a patient's risk of developing intracranial lesions. The S100B protein is currently the most studied and promising biomarker for this purpose. Heart fatty-acid binding protein (H-FABP) has been highlighted in brain injury models and investigated as a biomarker for stroke and severe TBI, for example. Here, we evaluate the performances of S100B and H-FABP for differentiating between CT-positive and CT-negative patients. A total of 261 patients with a GCS score of 15 and at least one clinical symptom of mTBI were recruited at three different European sites. Blood samples from 172 of them were collected ≤ 6 h after trauma. Patients underwent a CT scan and were dichotomised into CT-positive and CT-negative groups for statistical analyses. H-FABP and S100B levels were measured using commercial kits, and their capacities to detect all CT-positive scans were evaluated, with sensitivity set to 100%. For patients recruited ≤ 6 h after trauma, the CT-positive group demonstrated significantly higher levels of both H-FABP (p = 0.004) and S100B (p = 0.003) than the CT-negative group. At 100% sensitivity, specificity reached 6% (95% CI 2.8-10.7) for S100B and 29% (95% CI 21.4-37.1) for H-FABP. Similar results were obtained when including all the patients recruited, i.e. hospital arrival within 24 h of trauma onset. H-FABP out-performed S100B and thus seems to be an interesting protein for detecting all CT-positive mTBI patients with a GCS score of 15 and at least one clinical symptom.
Roettger, Richard H; Taylor, Spence M; Youkey, Jerry R; Blackhurst, Dawn W
2005-08-01
The contemporary model of trauma care where dedicated trauma/critical care surgeons exclusively manage trauma patients has become progressively unsustainable. Little objective data, however, is available documenting that a better model exists. From September 2002 through August 2003, the trauma model at a 735-bed level I trauma teaching hospital was changed from the contemporary model to a new one where selected general surgeons with Advanced Trauma Life Support (ATLS) certification covered in-house trauma and emergency surgery call on a rotational basis. As well, each pursued elective practices, admitting all inpatients (trauma, emergent, elective) to a single teaching service (formerly the trauma service). Critical care was managed by a separate group of intensivists. The purpose of this study was to objectively compare the two models. Quantitative, financial, and qualitative data were derived from August 2001 to January 2002 (trauma/critical care model) and compared to August 2003 to January 2004 (general surgery model). During the two periods (trauma/critical care vs general surgery), the mean Revised Trauma Score (7.1 vs 7.2; P = 0.029), the mean Injury Severity Score (ISS) (10.9 vs 10.8; P = 0.84), and the percentage of penetrating trauma (12.5% vs 13.2%; P = 0.79) were similar. Differences (trauma/critical care vs general surgery, % increase/P value) included average daily census (24 vs 54, 225%), cases/attending (262 vs 543, 207%), cases/resident (54 vs 262, 485%), charges/attending (353,811 dollars vs 471,725 dollars, 133%), collections/attending (106,143 dollars vs 165,103 dollars, 156%), number of trauma patients (643 vs 748, 116%), trauma mortality (7.3% vs 4.0%; P = 0.007), trauma mortality with ISS >15 (21.7% vs 12.0%; P = 0.035), trauma complications (33.1% vs 17%; P < 0.001), and ICU morbidity (66.8% vs 43.9%; P < .001). The new general surgery model produced superior financial results and better quantitative surgical experience while exceeding trauma and ICU quality outcomes compared to the former trauma/critical care model. These data objectively support a model such as ours--one that is financially sustainable and more professionally attractive.
Vasopressor use following traumatic injury - A single center retrospective study.
Hylands, Mathieu; Godbout, Marie-Pier; Mayer, Sandeep K; Fraser, William D; Vanasse, Alain; Leclair, Marc-André; Turgeon, Alexis F; Lauzier, François; Charbonney, Emmanuel; Trottier, Vincent; Razek, Tarek S; Roy, André; D'Aragon, Frédérick; Belley-Côté, Emilie; Day, Andrew G; Le Guillan, Soazig; Sabbagh, Robert; Lamontagne, François
2017-01-01
Vasopressors are not recommended by current trauma guidelines, but recent reports indicate that they are commonly used. We aimed to describe the early hemodynamic management of trauma patients outside densely populated urban centers. We conducted a single-center retrospective cohort study in a Canadian regional trauma center. All adult patients treated for traumatic injury in 2013 who died within 24 hours of admission or were transferred to the intensive care unit were included. A systolic blood pressure <90 mmHg, a mean arterial pressure <60 mmHg, the use of vasopressors or ≥2 L of intravenous fluids defined hemodynamic instability. Main outcome measures were use of intravenous fluids and vasopressors prior to surgical or endovascular management. Of 111 eligible patients, 63 met our criteria for hemodynamic instability. Of these, 60 (95%) had sustained blunt injury and 22 (35%) had concomitant severe traumatic brain injury. The subgroup of patients referred from a primary or secondary hospital (20 of 63, 32%) had significantly longer transport times (243 vs. 61 min, p<0.01). Vasopressors, used in 26 patients (41%), were independently associated with severe traumatic brain injury (odds ratio 10.2, 95% CI 2.7-38.5). In this cohort, most trauma patients had suffered multiple blunt injuries. Patients were likely to receive vasopressors during the early phase of trauma care, particularly if they exhibited signs of neurologic injury. While these results may be context-specific, determining the risk-benefit trade-offs of fluid resuscitation, vasopressors and permissive hypotension in specific patients subgroups constitutes a priority for trauma research going forwards.
Vasopressor use following traumatic injury – A single center retrospective study
Hylands, Mathieu; Godbout, Marie-Pier; Mayer, Sandeep K.; Fraser, William D.; Vanasse, Alain; Leclair, Marc-André; Turgeon, Alexis F.; Lauzier, François; Charbonney, Emmanuel; Trottier, Vincent; Razek, Tarek S.; Roy, André; D’Aragon, Frédérick; Belley-Côté, Emilie; Day, Andrew G.; Le Guillan, Soazig; Sabbagh, Robert
2017-01-01
Objectives Vasopressors are not recommended by current trauma guidelines, but recent reports indicate that they are commonly used. We aimed to describe the early hemodynamic management of trauma patients outside densely populated urban centers. Methods We conducted a single-center retrospective cohort study in a Canadian regional trauma center. All adult patients treated for traumatic injury in 2013 who died within 24 hours of admission or were transferred to the intensive care unit were included. A systolic blood pressure <90 mmHg, a mean arterial pressure <60 mmHg, the use of vasopressors or ≥2 L of intravenous fluids defined hemodynamic instability. Main outcome measures were use of intravenous fluids and vasopressors prior to surgical or endovascular management. Results Of 111 eligible patients, 63 met our criteria for hemodynamic instability. Of these, 60 (95%) had sustained blunt injury and 22 (35%) had concomitant severe traumatic brain injury. The subgroup of patients referred from a primary or secondary hospital (20 of 63, 32%) had significantly longer transport times (243 vs. 61 min, p<0.01). Vasopressors, used in 26 patients (41%), were independently associated with severe traumatic brain injury (odds ratio 10.2, 95% CI 2.7–38.5). Conclusions In this cohort, most trauma patients had suffered multiple blunt injuries. Patients were likely to receive vasopressors during the early phase of trauma care, particularly if they exhibited signs of neurologic injury. While these results may be context-specific, determining the risk-benefit trade-offs of fluid resuscitation, vasopressors and permissive hypotension in specific patients subgroups constitutes a priority for trauma research going forwards. PMID:28448605
Pregnancy and Birth-Related Brain Disorders.
ERIC Educational Resources Information Center
Fink, Leslie
1986-01-01
Although it once seemed simple to say that a single event such as birth trauma or asphyxia caused brain disorders like cerebral palsy, mental retardation, and epilepsy, a recent study showed that it is nearly impossible to pinpoint a single cause and its effects. Recommendations for further research are made. (BB)
The injury profile and acute treatment costs of major trauma in older people in New South Wales.
Curtis, Kate; Chan, Daniel Leonard; Lam, Mary Kit; Mitchell, Rebecca; King, Kate; Leonard, Liz; D'Amours, Scott; Black, Deborah
2014-12-01
To Describe injury profile and costs of older person trauma in New South Wales; quantify variations with peer group costs; and identify predictors of higher costs. Nine level 1 New South Wales trauma centres provided data on major traumas (aged ≥ 55 years) during 2008-2009 financial year. Trauma register and financial data of each institution were linked. Treatment costs were compared with peer group Australian Refined Diagnostic Related Groups costs, on which hospital funding is based. Variables examined through multivariate analyses. Six thousand two hundred and eighty-nine patients were admitted for trauma. Most common injury mechanism was falls (74.8%) then road trauma (14.9%). Median patient cost was $7044 (Q1-3: $3405-13 930) and total treatment costs $76 694 252. Treatment costs were $5 813 975 above peer group average. Intensive care unit admission, age, injury severity score, length of stay and traumatic brain injury were independent predictors of increased costs. Older person trauma attracts greater costs and length of stay. Cost increases with age and injury severity. Hospital financial information and trauma registry data provides accurate cost information that may inform future funding. © 2013 ACOTA.
2006-06-16
ischemic kidney model [121]. Photothrombic brain injury elicits the expression of HSP70 and HSP27 . HSP70 expression as early as one hour post-trauma...delineated the area of necrosis at 24 hours post-thrombic injury in ipsilateral cortex. HSP27 expression also was found to be upregulated and in fact...more globally expressed in the entire ipsilateral cerebral cortex, primarily in astrocytes [122]. 25 HSP25 and HSP27 Research demonstrates
2017-07-25
which would thereby preserve long - term platelet function. Dekker et al. (2014a) demonstrated that the addition of VPA to FFP resuscita- tion results in...pharmacologic resuscitation: Results of a long - term survival study in a swine polytrauma model. Journal of Trauma, 70, 636–645. Anglin, C. O., Spence...Alam, H. B. (2015b). Addition of low-dose valproic acid to saline resuscita- tion provides neuroprotection and improves long - term outcomes in a large
2011-01-01
6) While the rate of ventilator associated pneumonia ( VAP ) has been estimated at between 8% and 28% in non-trauma patients , intubated patients ...Recombinant Factor VIla (rFVIIa) is approved for use in the treatment and prophylaxis of bleeding in patients with Factor VIII and IX deficiencies...injured patients [3). In all of these trials, rFVIIa was administered only in the hospi- tal setting, after identification of either clinically relevant
Maren, Stephen; Holmes, Andrew
2016-01-01
Stress has a critical role in the development and expression of many psychiatric disorders, and is a defining feature of posttraumatic stress disorder (PTSD). Stress also limits the efficacy of behavioral therapies aimed at limiting pathological fear, such as exposure therapy. Here we examine emerging evidence that stress impairs recovery from trauma by impairing fear extinction, a form of learning thought to underlie the suppression of trauma-related fear memories. We describe the major structural and functional abnormalities in brain regions that are particularly vulnerable to stress, including the amygdala, prefrontal cortex, and hippocampus, which may underlie stress-induced impairments in extinction. We also discuss some of the stress-induced neurochemical and molecular alterations in these brain regions that are associated with extinction deficits, and the potential for targeting these changes to prevent or reverse impaired extinction. A better understanding of the neurobiological basis of stress effects on extinction promises to yield novel approaches to improving therapeutic outcomes for PTSD and other anxiety and trauma-related disorders. PMID:26105142
State of the Art: Novel Applications for Deep Brain Stimulation.
Roy, Holly A; Green, Alexander L; Aziz, Tipu Z
2018-02-01
Deep brain stimulation (DBS) is a rapidly developing field of neurosurgery with potential therapeutic applications that are relevant to conditions traditionally viewed as beyond the limits of neurosurgery. Our objective, in this review, is to highlight some of the emerging applications of DBS within three distinct but overlapping spheres, namely trauma, neuropsychiatry, and autonomic physiology. An extensive literature review was carried out in MEDLINE, to identify relevant studies and review articles describing applications of DBS in the areas of trauma, neuropsychiatry and autonomic neuroscience. A wide range of applications of DBS in these spheres was identified, some having only been tested in one or two cases, others much better studied. We have identified various avenues for DBS to be applied for patient benefit in cases relevant to trauma, neuropsychiatry and autonomic neuroscience. Further developments in DBS technology and clinical trial design will enable these novel applications to be effectively and rigorously assessed and utilized most effectively. © 2017 International Neuromodulation Society.
Perin, Cecilia; Meroni, Roberto; Rega, Vincenzo; Braghetto, Giacomo; Cerri, Cesare Giuseppe
2017-10-01
Introduction Tracheostomy weaning in patients who suffered a severe acquired brain injury is often a challenge and decannulation failures are not uncommon. Objective Our study objective is to describe the decannulation failure rate in patients undergoing rehabilitation following a severe acquired brain injury (sABI); to describe the factors associated with a successful tube weaning. Methods We conduct a retrospective analysis of charts, consecutively retrieved considering a 3-year window. Variables analyzed were: age, sex, body mass index (BMI), Glasgow Coma Scale (GCS), cause of hospitalization (stroke, trauma, cardiac arrest), date of the pathological event, gap between the index event and the first day of hospitalization, duration of Neurorehabilitation Ward hospitalization, comorbidities, chest morphological alteration, kind of tracheostomy tube used (overall dimension, cap, fenestration), SpO2, presentation and quantification of pulmonary secretion, maximal inspiratory pressure (MIP) and maximal expiratory pressure (MEP), respiratory frequency and pattern, cardiac frequency, presence of spontaneous cough, cough strength, and blood gas analysis. Results We analyzed 45 tracheostomised sABI patients following stroke, trauma, or cardiac arrest. The weaning success percentage was higher in Head Trauma patients and in patients presenting positive spontaneous cough. Failures seem to be associated with presence of secretions and anoxic brain damage. GCS seemed not related to the decannulation outcome. Conclusions Parameters that could be used as positive predictors of weaning are: mean expiratory pressure, presence of spontaneous cough, and cough strength. Provoked cough and GCS were not predictive of weaning success.
Mannitol dosing error during interfacility transfer for intracranial emergencies.
Elliott, Cameron A; MacKenzie, Mark; O'Kelly, Cian J
2015-11-01
Mannitol is commonly used to treat elevated intracranial pressure (ICP). The authors analyzed mannitol dosing errors at peripheral hospitals prior to or during transport to tertiary care facilities for intracranial emergencies. They also investigated the appropriateness of mannitol use based on the 2007 Brain Trauma Foundation guidelines for severe traumatic brain injury. The authors conducted a retrospective review of the Shock Trauma Air Rescue Society (STARS) electronic patient database of helicopter medical evacuations in Alberta, Canada, between 2004 and 2012, limited to patients receiving mannitol before transfer. They extracted data on mannitol administration and patient characteristics, including diagnosis, mechanism, Glasgow Coma Scale score, weight, age, and pupil status. A total of 120 patients with an intracranial emergency received a mannitol infusion initiated at a peripheral hospital (median Glasgow Coma Scale score 6; range 3-13). Overall, there was a 22% dosing error rate, which comprised an underdosing rate (<0.25 g/kg) of 8.3% (10 of 120 patients), an overdosing rate (>1.5 g/kg) of 7.5% (9 of 120), and a nonbolus administration rate (>1 hour) of 6.7% (8 of 120). Overall, 72% of patients had a clear indication to receive mannitol as defined by meeting at least one of the following criteria based on Brain Trauma Foundation guidelines: neurological deterioration (11%), severe traumatic brain injury (69%), or pupillary abnormality (25%). Mannitol administration at peripheral hospitals is prone to dosing error. Strategies such as a pretransport checklist may mitigate this risk.
Chronic traumatic encephalopathy: the dangers of getting "dinged"
2012-01-01
Chronic traumatic encephalopathy (CTE) is a form of neurodegeneration that results from repetitive brain trauma. Not surprisingly, CTE has been linked to participation in contact sports such as boxing, hockey and American football. In American football getting "dinged" equates to moments of dizziness, confusion, or grogginess that can follow a blow to the head. There are approximately 100,000 to 300,000 concussive episodes occurring in the game of American football alone each year. It is believed that repetitive brain trauma, with or possibly without symptomatic concussion, sets off a cascade of events that result in neurodegenerative changes highlighted by accumulations of hyperphosphorylated tau and neuronal TAR DNA-binding protein-43 (TDP-43). Symptoms of CTE may begin years or decades later and include a progressive decline of memory, as well as depression, poor impulse control, suicidal behavior, and, eventually, dementia similar to Alzheimer's disease. In some individuals, CTE is also associated with motor neuron disease similar to amyotrophic lateral sclerosis. Given the millions of athletes participating in contact sports that involve repetitive brain trauma, CTE represents an important public health issue. In this review, we discuss recent advances in understanding the etiology of CTE. It is now known that those instances of mild concussion or "dings" that we may have previously not noticed could very well be causing progressive neurodegenerative damage to a player's brain. In the future, focused and intensive study of the risk factors could potentially uncover methods to prevent and treat this disease. PMID:23984220
Günther, Mattias; Plantman, Stefan; Gahm, Caroline; Sondén, Anders; Risling, Mårten; Mathiesen, Tiit
2014-12-01
Experimental CNS trauma results in post-traumatic inflammation for which microglia and macrophages are vital. Experimental brain contusion entails iNOS synthesis and formation of free radicals, NO and peroxynitrite. Shock wave trauma can be used as a model of high-energy trauma in cell culture. It is known that shock wave trauma causes sub-lytic injury and inflammatory activation in endothelial cells. Mechanical disruption of red blood cells can induce iNOS synthesis in experimental systems. However, it is not known whether trauma can induce activation and iNOS synthesis in inflammatory cell lines with microglial or macrophage lineage. We studied the response and activation in two macrophage cell lines and the consequence for iNOS and NO formation after shock wave trauma. Two macrophage cell lines from rat (NR8383) and mouse (RAW264.7) were exposed to shock wave trauma by the Flyer Plate method. The cellular response was investigated by Affymetrix gene arrays. Cell survival and morphological activation was monitored for 24 h in a Cell-IQ live cell imaging system. iNOS induction and NO synthesis were analyzed by Western blot, in cell Western IR-immunofluorescence, and Griess nitrite assay. Morphological signs of activation were detected in both macrophage cell lines. The activation of RAW264.7 was statistically significant (p < 0.05), but activation of NR8383 did not pass the threshold of statistical significance alpha (p > 0.05). The growth rate of idle cells was unaffected and growth arrest was not seen. Trauma did not result in iNOS synthesis or NO induction. Gene array analyses showed high enrichment for inflammatory response, G-protein coupled signaling, detection of stimulus and chemotaxis. Shock wave trauma combined with low LPS stimulation instead led to high enrichment in apoptosis, IL-8 signaling, mitosis and DNA-related activities. LPS/IFN-ɣ stimulation caused iNOS and NO induction and morphological activation in both cell lines. Shock wave trauma by the Flyer Plate method caused an inflammatory response and morphological signs of activation in two macrophage cell lines, while iNOS induction appeared to require humoral signaling by LPS/IFN-ɣ. Our findings indicated that direct energy transfer by trauma can activate macrophages directly without humoral mediators, which comprises a novel activation mechanism of macrophages.
Pruneau, D; Chorny, I; Benkovitz, V; Artru, A; Roitblat, L; Shapira, Y
1999-11-01
Bradykinin is an endogenous nonapeptide which potently dilates the cerebral vasculature and markedly increases vascular permeability. These effects are mediated by B2 receptors located on the vascular endothelium. Previous experimental studies have shown that blockade of the kallikreinkinin system, which mediates the formation of bradykinin, afforded a reduction of the brain edema that developed following a cryogenic cortical lesion. In the present study, we investigated the effect of LF 16-0687MS, a novel nonpeptide B2 receptor antagonist, on cerebral edema and neurological severity score (NSS) after closed head injury to rats. LF 16-0687MS or its vehicle (NaCl 0.9%) was continuously infused at 10, 30, and 100 microg/kg/min over 23 h starting 1 h after a focal trauma to the left hemisphere was induced using a weight-drop device. The extent of edema formation was evaluated 24 h after trauma from left and right hemispheres samples by measurement of specific gravity and water content. In a separate study, a neurological severity score based on scoring of behavioural and motor functions was evaluated 1 h and over 1 week after trauma. LF 16-0687MS at 100 microg/kg/min markedly reduced the development of brain edema as indicated by a 68% increase in specific gravity (p<0.05) and a 64% decrease of water content (p<0.05) in the left hemisphere. In addition the recovery of neurological function was significantly improved by 100 microg/kg/min LF 16-0687MS from day 3 to day 7 after CHT. In a separate experiment, we also showed that LF 16-0687MS at 100 microg/kg/min given either 1 h before or 30 min after CHT did not affect mean arterial blood pressure. These results show that blockade of bradykinin B2 receptors is an effective approach to reduce cerebral edema and to improve neurological outcome after a focal contusion to the cranium.
Neuroprotective effects of MK-801 against traumatic brain injury in immature rats.
Sönmez, Ataç; Sayın, Oya; Gürgen, Seren Gülşen; Çalişir, Meryem
2015-06-15
Traumatic brain injury (TBI) is a major health problem in pediatric ages and also has major social, economic, and emotional outcomes, with diverse sequelae in many spheres of everyday life. We aimed to investigate the effect of MK-801, a competitive NMDA receptor antagonist, on hippocampal damage and behavioral deficits on 10-day-old rat pups subjected to contusion injury. The aims of the present study were to determine: (i) the short term effects of MK-801 on hippocampal BDNF, NGF and NMDA receptor immunoreactivity and neuron density in hippocampus (ii) long term effects of MK-801 on cognitive dysfunction following TBI in the immature rats. MK-801, was injected intraperitoneally at the doses of 1mg/kg of body weight immediately after induction of traumatic injury. Hippocampal damage was examined by cresyl violet staining, BDNF, NGF and NMDAR receptor immunohistochemistry on P10 day and behavioral alterations were evaluated using elevated plus maze and novel object recognition tests two months after the trauma. Histopathological and immunohistochemical evaluations showed that treatment with a single dose of 1mg/kg MK-801 (i.p.) significantly ameliorated the trauma induced hippocampal neuron loss and decreased BDNF, NGF and NMDAR expressions in CA1, CA3 and DG hippocampal brain regions. Additionally, treatment with MK-801 ameliorated anxiety and hippocampus dependent memory of animals subjected to trauma. These results show that acute treatment of MK-801 has a neuroprotective role against trauma induced hippocampal neuron loss and associated cognitive impairment in immature rats. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
A Placebo-Controlled Augmentation Trial of Prazosin for Combat Trauma PTSD
2013-08-01
sleep disturbance, and other hyperarousal symptoms typical of PTSD (11). Specific stimulation of CNS alpha-1 adreno- receptors disrupts REM sleep (36...result from excessive brain responsiveness to released norepinephrine disrupting rapid eye movement ( REM ) and other sleep stages (Mellman, Kumar, Kulick...in 2006, sought help for distressing combat trauma night- mares, sleep disruption, and daytime intrusive ruminations about previous combat events. He
Acromegaly resolution after traumatic brain injury: a case report.
Cob, Alejandro
2014-09-02
Anterior hypopituitarism is a common complication of head trauma, with a prevalence of 30% to 70% among long-term survivors. This is a much higher frequency than previously thought and suggests that most cases of post-traumatic hypopituitarism remain undiagnosed and untreated. Symptoms of hypopituitarism are very unspecific and very similar to those in traumatic brain injury patients in general, which makes hypopituitarism difficult to diagnose. The factors that predict the likelihood of developing hypopituitarism following traumatic brain injury remain poorly understood. The incidence of a specific hormone deficiency is variable, with growth hormone deficiency reported in 18% to 23% of cases. A 23-year-old Hispanic man with a 2-year history of hypertension and diabetes presented with severe closed-head trauma producing diffuse axonal injury, subarachnoid hemorrhage and a brain concussion. A computed tomography scan showed a pituitary macroadenoma. The patient has clinical features of acromegaly and gigantism without other pituitary hyperfunctional manifestations or mass effect syndrome. A short-term post-traumatic laboratory test showed high levels of insulin like growth factor 1 and growth hormone, which are compatible with a growth hormone-producing pituitary tumor. At the third month post-trauma, the patient's levels of insulin like growth factor 1 had decreased to low normal levels, with basal low levels of growth hormone. A glucose tolerance test completely suppressed the growth hormone, which confirmed resolution of acromegaly. An insulin tolerance test showed lack of stimulation of growth hormone and cortisol, demonstrating hypopituitarism of both axes. Even though hypopituitarism is a frequent complication of traumatic brain injury, there are no reports in the literature, to the best of my knowledge, of patients with hyperfunctional pituitary adenomas, such as growth hormone-producing adenoma, that resolved after head trauma. A clear protocol has not yet been established to identify which patients should be screened for hypopituitarism. Predictive factors that might determine the likelihood of developing post-traumatic hypopituitarism have not been clearly established, but there is no evidence of the presence of pituitary adenomas as a risk factor in otherwise healthy patients.
Comparison of injury epidemiology between the Wenchuan and Lushan earthquakes in Sichuan, China.
Hu, Yang; Zheng, Xi; Yuan, Yong; Pu, Qiang; Liu, Lunxu; Zhao, Yongfan
2014-12-01
We aimed to compare injury characteristics and the timing of admissions and surgeries in the Wenchuan earthquake in 2008 and the Lushan earthquake in 2013. We retrospectively compared the admission and operating times and injury profiles of patients admitted to our medical center during both earthquakes. We also explored the relationship between seismic intensity and injury type. The time from earthquake onset to the peak in patient admissions and surgeries differed between the 2 earthquakes. In the Wenchuan earthquake, injuries due to being struck by objects or being buried were more frequent than other types of injuries, and more patients suffered injuries of the extremities than thoracic injuries or brain trauma. In the Lushan earthquake, falls were the most common injury, and more patients suffered thoracic trauma or brain injuries. The types of injury seemed to vary with seismic intensity, whereas the anatomical location of the injury did not. Greater seismic intensity of an earthquake is associated with longer delay between the event and the peak in patient admissions and surgeries, higher frequencies of injuries due to being struck or buried, and lower frequencies of injuries due to falls and injuries to the chest and brain. These insights may prove useful for planning rescue interventions in trauma centers near the epicenter.
Orlando, Alessandro; Levy, A Stewart; Carrick, Matthew M; Tanner, Allen; Mains, Charles W; Bar-Or, David
2017-11-01
To outline differences in neurosurgical intervention (NI) rates between intracranial hemorrhage (ICH) types in mild traumatic brain injuries and help identify which ICH types are most likely to benefit from creation of predictive models for NI. A multicenter retrospective study of adult patients spanning 3 years at 4 U.S. trauma centers was performed. Patients were included if they presented with mild traumatic brain injury (Glasgow Coma Scale score 13-15) with head CT scan positive for ICH. Patients were excluded for skull fractures, "unspecified hemorrhage," or coagulopathy. Primary outcome was NI. Stepwise multivariable logistic regression models were built to analyze the independent association between ICH variables and outcome measures. The study comprised 1876 patients. NI rate was 6.7%. There was a significant difference in rate of NI by ICH type. Subdural hematomas had the highest rate of NI (15.5%) and accounted for 78% of all NIs. Isolated subarachnoid hemorrhages had the lowest, nonzero, NI rate (0.19%). Logistic regression models identified ICH type as the most influential independent variable when examining NI. A model predicting NI for isolated subarachnoid hemorrhages would require 26,928 patients, but a model predicting NI for isolated subdural hematomas would require only 328 patients. This study highlighted disparate NI rates among ICH types in patients with mild traumatic brain injury and identified mild, isolated subdural hematomas as most appropriate for construction of predictive NI models. Increased health care efficiency will be driven by accurate understanding of risk, which can come only from accurate predictive models. Copyright © 2017 Elsevier Inc. All rights reserved.
[Post-trauma cerebral thrombophlebitis revealed by psychiatric disorders].
Kaaniche, F; Chaari, A; Turki, O; Chelly, H; Bouaziz, M
2015-05-01
Head injuries are described in the literature as a rare but possible etiology of cerebral venous thrombosis although no pathophysiological link has been identified. Trauma-related venous thrombi occurring in the brain produce a broad spectrum of clinical presentations. A purely psychiatric term is exceptional, leading to misinterpretation and late diagnosis. Positive diagnosis has been greatly improved by advances in magnetic resonance imaging with venous phase angiography, currently the gold standard exploration. We report the case of a patient who presented with post-trauma cerebral venous thrombosis revealed by psychiatric disorders. Copyright © 2015 Elsevier Masson SAS. All rights reserved.
Mkrtchyan, Garik V; Üçal, Muammer; Müllebner, Andrea; Dumitrescu, Sergiu; Kames, Martina; Moldzio, Rudolf; Molcanyi, Marek; Schaefer, Samuel; Weidinger, Adelheid; Schaefer, Ute; Hescheler, Juergen; Duvigneau, Johanna Catharina; Redl, Heinz; Bunik, Victoria I; Kozlov, Andrey V
2018-05-16
Based on the fact that traumatic brain injury is associated with mitochondrial dysfunction we aimed at localization of mitochondrial defect and attempted to correct it by thiamine. Interventional controlled experimental animal study was used. Adult male Sprague-Dawley rats were subjected to lateral fluid percussion traumatic brain injury. Thiamine was administered 1 h prior to trauma; cortex was extracted for analysis 4 h and 3 d after trauma. Increased expression of inducible nitric oxide synthase (iNOS) and tumor necrosis factor receptor 1 (TNF-R1) by 4 h was accompanied by a decrease in mitochondrial respiration with glutamate but neither with pyruvate nor succinate. Assays of TCA cycle flux-limiting 2-oxoglutarate dehydrogenase complex (OGDHC) and functionally linked enzymes (glutamate dehydrogenase, glutamine synthetase, pyruvate dehydrogenase, malate dehydrogenase and malic enzyme) indicated that only OGDHC activity was decreased. Application of the OGDHC coenzyme precursor thiamine rescued the activity of OGDHC and restored mitochondrial respiration. These effects were not mediated by changes in the expression of the OGDHC sub-units (E1k and E3), suggesting post-translational mechanism of thiamine effects. By the third day after TBI, thiamine treatment also decreased expression of TNF-R1. Specific markers of unfolded protein response did not change in response to thiamine. Our data point to OGDHC as a major site of damage in mitochondria upon traumatic brain injury, which is associated with neuroinflammation and can be corrected by thiamine. Further studies are required to evaluate the pathological impact of these findings in clinical settings. Copyright © 2018. Published by Elsevier B.V.
Vrettos, T; Poimenidi, E; Athanasopoulos, P; Balasis, S; Karagiorgos, N; Siklis, T; Gatzounis, G; Fligkou, F
2016-01-01
Optimal hemodynamic resuscitation strategy of the trauma patient with uncontrolled hemorrhage and severe head injury in the pre-hospital setting remains a special challenge. Permissive hypotension prior to definite surgical haemostasis promotes coagulation, decreases blood loss and favors survival. However, hypotension is associated with poor outcome in severe head injury. The purpose of this experimental animal study was to assess the impact of permissive hypotension on survival, hemodynamic profile and brain oxygenation parameters before and/or after definite surgical haemostasis. Six-week-old pigs (n=12) underwent general anesthesia and brain injury was produced by the fluid percussion model. Animals were instrumented to measure hemodynamic parameters and cerebral blood flow. All animals (n=12) were subjected to laparotomy and a surgical knot was placed through the abdominal aorta wall. Uncontrolled hemorrhage was simulated by pulling out the intentionally left protruding free ends of the suture (goal MAP=30 mmHg). Animals were randomly divided into two groups; group A (n=6) was subjected to aggressive fluid resuscitation (goal SAP >80 mmHg) and group B (n=6) was left hypotensive (permissive hypotension). Animals who survived one hour of hypotensive shock underwent definite surgical haemostasis and were resuscitated for one hour. We measured survival, hemodynamic and brain oxygenation parameters at different time points before and after surgical haemostasis. All animals from Group A and 50% from Group B died before surgical haemostasis. In surviving animals (Group B, 50%, p=0.033), MAP, CO, rCBF, SjO2 and AVDO2 were restored to pre-procedural levels. Permissive hypotension by delaying fluid resuscitation up to definite surgical haemostasis improves survival, hemodynamics and allows restoration of cerebral oxygenation in severe head injury.
Traumatic Brain Injury in the United States: An Epidemiologic Overview
2009-01-01
discussed. Mt Sinai J Med 76:105–110, 2009. 2009 Mount Sinai School of Medicine Key Words: epidemiology, head injury, traumatic brain injury. A...traumatic brain injury in the civilian population of the United States. J Head Trauma Rehabil 2008; 23: 394–400. 3. Sosin DM, Sniezek JE, Thurman DJ...consciousness, a practical scale. Lancet 1974; 2: 81–84. 5. Kay T, Harrington DE, Adams R, et al. Definition of mild traumatic brain injury. J Head
Oxidative Burst of Circulating Neutrophils Following Traumatic Brain Injury in Human
Liao, Yiliu; Liu, Peng; Guo, Fangyuan; Zhang, Zhi-Yuan; Zhang, Zhiren
2013-01-01
Besides secondary injury at the lesional site, Traumatic brain injury (TBI) can cause a systemic inflammatory response, which may cause damage to initially unaffected organs and potentially further exacerbate the original injury. Here we investigated plasma levels of important inflammatory mediators, oxidative activity of circulating leukocytes, particularly focusing on neutrophils, from TBI subjects and control subjects with general trauma from 6 hours to 2 weeks following injury, comparing with values from uninjured subjects. We observed increased plasma level of inflammatory cytokines/molecules TNF-α, IL-6 and CRP, dramatically increased circulating leukocyte counts and elevated expression of TNF-α and iNOS in circulating leukocytes from TBI patients, which suggests a systemic inflammatory response following TBI. Our data further showed increased free radical production in leukocyte homogenates and elevated expression of key oxidative enzymes iNOS, COX-2 and NADPH oxidase (gp91phox) in circulating leukocytes, indicating an intense induction of oxidative burst following TBI, which is significantly greater than that in control subjects with general trauma. Furthermore, flow cytometry assay proved neutrophils as the largest population in circulation after TBI and showed significantly up-regulated oxidative activity and suppressed phagocytosis rate for circulating neutrophils following brain trauma. It suggests that the highly activated neutrophils might play an important role in the secondary damage, even outside the injured brain. Taken together, the potent systemic inflammatory response induced by TBI, especially the intensively increase oxidative activity of circulating leukocytes, mainly neutrophils, may lead to a systemic damage, dysfunction/damage of bystander tissues/organs and even further exacerbate secondary local damage. Controlling these pathophysiological processes may be a promising therapeutic strategy and will protect unaffected organs and the injured brain from the secondary damage. PMID:23894384
Aas, Monica; Haukvik, Unn K; Djurovic, Srdjan; Bergmann, Ørjan; Athanasiu, Lavinia; Tesli, Martin S; Hellvin, Tone; Steen, Nils Eiel; Agartz, Ingrid; Lorentzen, Steinar; Sundet, Kjetil; Andreassen, Ole A; Melle, Ingrid
2013-10-01
Brain derived neurotrophic factor (BDNF) is important for brain development and plasticity, and here we tested if the functional BDNF val66met variant modulates the association between high levels of childhood abuse, cognitive function, and brain abnormalities in psychoses. 249 patients with a broad DSM-IV schizophrenia spectrum disorder or bipolar disorder were consecutively recruited to the TOP research study (mean±age: 30.7±10.9; gender: 49% males). History of childhood trauma was obtained using the Childhood Trauma Questionnaire. Cognitive function was assessed through a standardized neuropsychological test battery. BDNF val66met was genotyped using standardized procedures. A sub-sample of n=106 Caucasians with a broad DSM-IV schizophrenia spectrum disorder or bipolar disorder (mean±age: 32.67±10.85; 49% males) had data on sMRI. Carriers of the Methionine (met) allele exposed to high level of childhood abuse demonstrated significantly poorer cognitive functioning compared to homozygotic Valine (val/val) carriers. Taking in consideration multiple testing, using a more conservative p value, this was still shown for physical abuse and emotional abuse, as well as a trend level for sexual abuse. Further, met carriers exposed to high level of childhood sexual abuse showed reduced right hippocampal volume (r(2)=0.43; p=0.008), and larger right and left lateral ventricles (r(2)=0.37; p=0.002, and r(2)=0.27; p=0.009, respectively). Our findings were independent of age, gender, diagnosis and intracranial volume. Our data demonstrate that in patients with psychoses, met carriers of the BDNF val66met with high level of childhood abuse have more cognitive and brain abnormalities than all other groups. © 2013.
Synergistic Mechanisms Between Traumatic Brain Injury and Migraine
2016-08-01
AWARD NUMBER: W81XWH-15-1-0209 TITLE: Synergistic Mechanisms Between Traumatic Brain Injury and Migraine PRINCIPAL INVESTIGATOR: Amynah Pradhan...SUBTITLE Synergistic Mechanisms Between Traumatic Brain Injury and Migraine 5a. CONTRACT NUMBER 5b. GRANT NUMBER W81XWH-15-1-0209 5c. PROGRAM ELEMENT...and can persist for months after the initial trauma. The most severe and long lasting posttraumatic headaches are usually classified as migraine ; and
Boĭko, S S; Bobkov, Iu G; Dobrokhotova, T A; Kniazeva, N A; Neznamov, G G
1987-01-01
Experimental and clinical data indicated bemetil ability to penetrate through the blood-brain barrier. Bemetil concentration in the rat brain tissue was found to be significantly higher than in the plasma. Its concentration in the cerebrospinal fluid of patients with craniocerebral trauma was lower than in the plasma; the latter however does not exclude the possibility of bemetil accumulation in the brain structures.
Chen, Yun; Huang, Wei; Constantini, Shlomi
2013-01-01
After exposure of the human body to blast, kinetic energy of the blast shock waves might be transferred into hydraulic energy in the cardiovascular system to cause a rapid physical movement or displacement of blood (a volumetric blood surge). The volumetric blood surge moves through blood vessels from the high-pressure body cavity to the low-pressure cranial cavity, causing damage to tiny cerebral blood vessels and the blood-brain barrier (BBB). Large-scale cerebrovascular insults and BBB damage that occur globally throughout the brain may be the main causes of non-impact, blast-induced brain injuries, including the spectrum of traumatic brain injury (TBI) and posttraumatic stress disorder (PTSD). The volumetric blood surge may be a major contributor not only to blast-induced brain injuries resulting from physical trauma, but may also be the trigger to psychiatric disorders resulting from emotional and psychological trauma. Clinical imaging technologies, which are able to detect tiny cerebrovascular insults, changes in blood flow, and cerebral edema, may help diagnose both TBI and PTSD in the victims exposed to blasts. Potentially, prompt medical treatment aiming at prevention of secondary neuronal damage may slow down or even block the cascade of events that lead to progressive neuronal damage and subsequent long-term neurological and psychiatric impairment.
Thomsen, Gretchen M.
2015-01-01
Abstract Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disease in which upper and lower motor neurons degenerate, leading to muscle atrophy, paralysis, and death within 3 to 5 years of onset. While a small percentage of ALS cases are genetically linked, the majority are sporadic with unknown origin. Currently, etiological links are associated with disease onset without mechanistic understanding. Of all the putative risk factors, however, head trauma has emerged as a consistent candidate for initiating the molecular cascades of ALS. Here, we test the hypothesis that traumatic brain injury (TBI) in the SOD1 G93A transgenic rat model of ALS leads to early disease onset and shortened lifespan. We demonstrate, however, that a one-time acute focal injury caused by controlled cortical impact does not affect disease onset or survival. Establishing the negligible involvement of a single acute focal brain injury in an ALS rat model increases the current understanding of the disease. Critically, untangling a single focal TBI from multiple mild injuries provides a rationale for scientists and physicians to increase focus on repeat injuries to hopefully pinpoint a contributing cause of ALS. PMID:26464984
Kislin, Mikhail; Sword, Jeremy; Fomitcheva, Ioulia V.; Croom, Deborah; Pryazhnikov, Evgeny; Lihavainen, Eero; Toptunov, Dmytro; Rauvala, Heikki; Ribeiro, Andre S.
2017-01-01
Mitochondria play a variety of functional roles in cortical neurons, from metabolic support and neuroprotection to the release of cytokines that trigger apoptosis. In dendrites, mitochondrial structure is closely linked to their function, and fragmentation (fission) of the normally elongated mitochondria indicates loss of their function under pathological conditions, such as stroke and brain trauma. Using in vivo two-photon microscopy in mouse brain, we quantified mitochondrial fragmentation in a full spectrum of cortical injuries, ranging from severe to mild. Severe global ischemic injury was induced by bilateral common carotid artery occlusion, whereas severe focal stroke injury was induced by Rose Bengal photosensitization. The moderate and mild traumatic injury was inflicted by focal laser lesion and by mild photo-damage, respectively. Dendritic and mitochondrial structural changes were tracked longitudinally using transgenic mice expressing fluorescent proteins localized either in cytosol or in mitochondrial matrix. In response to severe injury, mitochondrial fragmentation developed in parallel with dendritic damage signified by dendritic beading. Reconstruction from serial section electron microscopy confirmed mitochondrial fragmentation. Unlike dendritic beading, fragmentation spread beyond the injury core in focal stroke and focal laser lesion models. In moderate and mild injury, mitochondrial fragmentation was reversible with full recovery of structural integrity after 1–2 weeks. The transient fragmentation observed in the mild photo-damage model was associated with changes in dendritic spine density without any signs of dendritic damage. Our findings indicate that alterations in neuronal mitochondria structure are very sensitive to the tissue damage and can be reversible in ischemic and traumatic injuries. SIGNIFICANCE STATEMENT During ischemic stroke or brain trauma, mitochondria can either protect neurons by supplying ATP and adsorbing excessive Ca2+, or kill neurons by releasing proapoptotic factors. Mitochondrial function is tightly linked to their morphology: healthy mitochondria are thin and long; dysfunctional mitochondria are thick (swollen) and short (fragmented). To date, fragmentation of mitochondria was studied either in dissociated cultured neurons or in brain slices, but not in the intact living brain. Using real-time in vivo two-photon microscopy, we quantified mitochondrial fragmentation during acute pathological conditions that mimic severe, moderate, and mild brain injury. We demonstrated that alterations in neuronal mitochondria structural integrity can be reversible in traumatic and ischemic injuries, highlighting mitochondria as a potential target for therapeutic interventions. PMID:28077713
Stone, Melvin E; Safadjou, Saman; Farber, Benjamin; Velazco, Nerissa; Man, Jianliang; Reddy, Srinivas H; Todor, Roxanne; Teperman, Sheldon
2015-07-01
Mild traumatic brain injury (mTBI) constitutes 75% of more than 1.5 million traumatic brain injuries annually. There exists no consensus on point-of-care screening for mTBI. The Military Acute Concussion Evaluation (MACE) is a quick and easy test used by the US Army to screen for mTBI; however, its utility in civilian trauma is unclear. It has two parts: a history section and the Standardized Assessment of Concussion (SAC) score (0-30) previously validated in sports injury. As a performance improvement project, our institution sought to evaluate the MACE as a concussion screening tool that could be used by housestaff in a general civilian trauma population. From June 2013 to May 2014, patients 18 years to 65 years old with suspected concussion were given the MACE within 72 hours of admission to our urban Level I trauma center. Patients with a positive head computed tomography were excluded. Demographic data and MACE scores were recorded in prospect. Concussion was defined as loss of consciousness and/or posttraumatic amnesia; concussed patients were compared with those nonconcussed. Sensitivity and specificity for each respective MACE score were used to plot a receiver operating characteristic (ROC) curve. An ROC curve area of 0.8 was set as the benchmark for a good screening test to distinguish concussion from nonconcussion. There were 84 concussions and 30 nonconcussed patients. Both groups were similar; however, the concussion group had a lower mean MACE score than the nonconcussed patients. Data analysis demonstrated the sensitivity and specificity of a range of MACE scores used to generate an ROC curve area of only 0.65. The MACE showed a lower mean score for individuals with concussion, defined by loss of consciousness and/or posttraumatic amnesia. However, the ROC curve area of 0.65 highly suggests that MACE alone would be a poor screening test for mTBI in a general civilian trauma population. Diagnostic study, level II.
Cervical spine imaging for young children with inflicted trauma: Expanding the injury pattern.
Baerg, Joanne; Thirumoorthi, Arul; Vannix, Rosemary; Taha, Asma; Young, Amy; Zouros, Alexander
2017-05-01
The purpose of this study was to document the incidence and pattern of cervical spine (c-spine) injuries in children below 36months with inflicted trauma. An IRB approved, prospective cohort study was performed between July 2011 and January 2016. Inclusion criteria were: age below 36months, loss of consciousness after inflicted trauma, and one initial head computed tomography finding: a subdural, intraventricular, intraparenchymal, subarachnoid hemorrhage, diffuse axonal injury, hypoxic injury, or cerebral edema. A protocol of brain and neck magnetic resonance imaging and angiography was obtained within 48h. Variables were compared by t-test and Fisher-exact test. There were 53 children (median age: five months; range: 1-35months), 38 males (71.7%), of which seven died (13.2%). C-spine injury was identified in 8 (15.1%): ligamentous injury (2), vertebral artery shear injury (1), atlantooccipital dissociation (AOD) (1), cord injury with cord epidural hematoma (2), and isolated cord epidural hematoma (2). Retinal hemorrhages (p=0.02), shaking (p=0.04), lower Glasgow coma score (GCS) (p=0.01), brain infarcts (p=0.01), and hypoxic/ischemic injury (p=0.01) were associated with c-spine injury. One with AOD died. Six had significant disability. For small children with inflicted trauma, the c-spine injury incidence is 15.1%. The injury pattern includes retinal hemorrhages, shaking, lower GCS, and brain injury. Evaluation of shaken infants should include c-spine imaging. Level 2 A- This is a prospective cohort study with complete follow-up to hospital discharge or death. In all cases, inflicted trauma was confirmed. Owing to the nature of child abuse, the precise time of injury is not known. All children underwent a strict imaging protocol on arrival to hospital that was supervised on a prospective basis. Copyright © 2017 Elsevier Inc. All rights reserved.
Adams, Sasha D; Holcomb, John B
2015-12-01
The landscape of trauma is changing due to an aging population. Geriatric patients represent an increasing number and proportion of trauma admissions and deaths. This review explores recent literature on geriatric trauma, including triage criteria, assessment of frailty, fall-related injury, treatment of head injury complicated by coagulopathy, goals of care, and the need for ongoing education of all surgeons in the care of the elderly. Early identification of high-risk geriatric patients is imperative to initiate early resuscitative efforts. Geriatric patients are typically undertriaged because of their baseline frailty being underappreciated; however, centers that see more geriatric patients do better. Rapid reversal of anticoagulation is important in preventing progression of brain injury. Anticipation of difficult disposition necessitates early involvement of physical therapy for rehabilitation and case management for appropriate placement. Optimal care of geriatric trauma patients will be based on the well established tenets of trauma resuscitation and injury repair, but with distinct elements that address the physiological and anatomical challenges presented by geriatric patients.
Assessment of traumatic deaths in a level one trauma center in Ankara, Turkey.
Arslan, E D; Kaya, E; Sonmez, M; Kavalci, C; Solakoglu, A; Yilmaz, F; Durdu, T; Karakilic, E
2015-06-01
Trauma management shows significant progress in last decades. Determining the time and place of deaths indicate where to focus to improve our knowledge about trauma. We conducted this retrospective study from data of trauma victims who were brought to a major tertiary hospital which is a level one trauma center in Ankara, Turkey, and died even if during transport or in the hospital between 1 March 2010 and 1 March 2013. The patients' demographic characteristics, trauma mechanisms, time frames and causes of deaths determined by physicians were recorded. Traumas were grouped as "high energy trauma" (HET) and "low energy trauma" (LET). Falls from ground level were defined as LET. 209 traumatic deaths due to trauma or trauma-related conditions were found in the study period. 161 of 209 (78 %) patients suffered from HET. Motor vehicle collisions (MVC) (56 %) were the most common mechanism of trauma followed by burns (16 %), falls (11 %), gunshots (9 %) and stabs (6 %) in this group and traumatic brain injuries (TBI) (41 %) were the most common cause of death followed by circulatory collapse (22 %) and multi-organ failure (20 %). 36 % of deaths occurred before arrival at hospital, 25 % in the first 24 h of admission, 18 % between 2nd and 7th day and 21 % after first week. Trimodal distribution of traumatic deaths was not valid for all types of injuries and the most important factor to decrease traumatic deaths is still prevention. Also we have to keep on searching to improve our knowledge about trauma management.
Converging early responses to brain injury pave the road to epileptogenesis.
Neuberger, Eric J; Gupta, Akshay; Subramanian, Deepak; Korgaonkar, Akshata A; Santhakumar, Vijayalakshmi
2017-11-29
Epilepsy, characterized by recurrent seizures and abnormal electrical activity in the brain, is one of the most prevalent brain disorders. Over two million people in the United States have been diagnosed with epilepsy and 3% of the general population will be diagnosed with it at some point in their lives. While most developmental epilepsies occur due to genetic predisposition, a class of "acquired" epilepsies results from a variety of brain insults. A leading etiological factor for epilepsy that is currently on the rise is traumatic brain injury (TBI), which accounts for up to 20% of all symptomatic epilepsies. Remarkably, the presence of an identified early insult that constitutes a risk for development of epilepsy provides a therapeutic window in which the pathological processes associated with brain injury can be manipulated to limit the subsequent development of recurrent seizure activity and epilepsy. Recent studies have revealed diverse pathologies, including enhanced excitability, activated immune signaling, cell death, and enhanced neurogenesis within a week after injury, suggesting a period of heightened adaptive and maladaptive plasticity. An integrated understanding of these processes and their cellular and molecular underpinnings could lead to novel targets to arrest epileptogenesis after trauma. This review attempts to highlight and relate the diverse early changes after trauma and their role in development of epilepsy and suggests potential strategies to limit neurological complications in the injured brain. © 2017 Wiley Periodicals, Inc.
Haven, Terri J
2009-01-01
The past 2 decades have brought a significant surge in interest and research regarding the ways in which psychological trauma relates to the physical body. Researchers now understand a great deal about how the brain and the body process traumatic experiences, as well as the increased likelihood of an array of physical health consequences associated with both childhood and adult trauma and posttraumatic stress disorder. Experts are increasingly challenging mind-body dualism through solid theoretical and clinical bases for the central importance of listening to and communicating with trauma clients' bodies as part of reducing the suffering and long-lasting consequences of trauma. This article integrates this growing body of knowledge through a particular focus on trauma-induced dissociation and the implications of the physical and neurological processes and consequences of dissociation on clients' ability to participate in caring for their own bodies. The author utilizes an in-depth clinical example of expanding relational trauma psychotherapy to include a focus on working directly with trauma-related sensorimotor and physiological sensations and patterns.
Intellectual Performance and Reading Skills after Localized Head Injury in Childhood.
ERIC Educational Resources Information Center
Chadwick, Oliver; And Others
1981-01-01
Ninety-seven school-age children who had previously sustained a unilateral compound depressed fracture of the skull were studied using tests of intelligence and reading attainment. Intellectual impairment was significantly associated with overall severity of brain trauma. Neither the child's age at injury nor the brain hemisphere damaged had…
Assessment of mechanical properties of human head tissues for trauma modelling.
Lozano-Mínguez, Estívaliz; Palomar, Marta; Infante-García, Diego; Rupérez, María José; Giner, Eugenio
2018-05-01
Many discrepancies are found in the literature regarding the damage and constitutive models for head tissues as well as the values of the constants involved in the constitutive equations. Their proper definition is required for consistent numerical model performance when predicting human head behaviour, and hence skull fracture and brain damage. The objective of this research is to perform a critical review of constitutive models and damage indicators describing human head tissue response under impact loading. A 3D finite element human head model has been generated by using computed tomography images, which has been validated through the comparison to experimental data in the literature. The threshold values of the skull and the scalp that lead to fracture have been analysed. We conclude that (1) compact bone properties are critical in skull fracture, (2) the elastic constants of the cerebrospinal fluid affect the intracranial pressure distribution, and (3) the consideration of brain tissue as a nearly incompressible solid with a high (but not complete) water content offers pressure responses consistent with the experimental data. Copyright © 2018 John Wiley & Sons, Ltd.
Head Transplantation in Mouse Model.
Ren, Xiao-Ping; Ye, Yi-Jie; Li, Peng-Wei; Shen, Zi-Long; Han, Ke-Cheng; Song, Yang
2015-08-01
The mouse model of allo-head and body reconstruction (AHBR) has recently been established to further the clinical development of this strategy for patients who are suffering from mortal bodily trauma or disease, yet whose mind remains healthy. Animal model studies are indispensable for developing such novel surgical practices. The goal of this work was to establish head transplant mouse model, then the next step through the feasible biological model to investigate immune rejection and brain function in next step, thereby promoting the goal of translation of AHBR to the clinic in the future. Our approach involves retaining adequate blood perfusion in the transplanted head throughout the surgical procedure by establishing donor-to-recipient cross-circulation by cannulating and anastomosing the carotid artery on one side of the body and the jugular vein on the other side. Neurological function was preserved by this strategy as indicated by electroencephalogram and intact cranial nerve reflexes. The results of this study support the feasibility of this method for avoiding brain ischemia during transplantation, thereby allowing for the possibility of long-term studies of head transplantation. © 2015 John Wiley & Sons Ltd.
Song, Zhi; Zhao, Xiu; Gao, Yan; Liu, Martin; Hou, Mingxiao; Jin, Hongxu; Cui, Yan
2015-05-01
JAK/STAT signal pathway plays an important role in the inflammation process of acute lung injury (ALI). This study aimed to investigate the correlation between recombinant human brain natriuretic peptide (rhBNP) and the JAK/STAT signaling pathway and to explore the protective mechanism of rhBNP against trauma-induced ALI. The arterial partial pressure in oxygen, lung wet-dry weight ratios, protein content in bronchoalveolar lavage fluid, the histopathologic of the lung, as well as the protein expressions of STAT1, JAK2, and STAT3 were detected. Sprague-Dawley rats were randomly divided into five groups: a control group, a sham-operated group, an ALI group, an ALI + rhBNP group, and an ALI + AG490 group. At 4 hours, 12 hours, 1 day, 3 days, and 7 days after injury, injured lung specimens were harvested. rhBNP pretreatment significantly ameliorated hypoxemia and histopathologic changes and alleviated pulmonary edema in trauma-induced ALI rats. rhBNP pretreatment reduced the phosphorylated protein and total protein level of STAT1. Similarly to JAK-specific inhibitor AG490, rhBNP was shown to significantly inhibit the phosphorylation of JAK2 and STAT3 in rats with trauma-induced ALI. Our experimental findings indicated that rhBNP can protect rats against trauma-induced ALI and that its underlying mechanism may be related to the inhibition of JAK/STAT signaling pathway activation.
Xia, Yang; Kong, Liang; Yao, Yingjia; Jiao, Yanan; Song, Jie; Tao, Zhenyu; You, Zhong; Yang, Jingxian
2015-09-04
Neuroendoscopy is an innovative technique for neurosurgery that can nonetheless result in traumatic brain injury. The accompanying neuroinflammation may lead to secondary tissue damage, which is the major cause of delayed neuronal death after surgery. The present study investigated the capacity of osthole to prevent secondary brain injury and the underlying mechanism of action in a mouse model of stab wound injury. A mouse model of cortical stab wound injury was established by inserting a needle into the cerebral cortex for 20 min to mimic neuroendoscopy. Mice received an intraperitoneal injection of osthole 30 min after surgery and continued for 14 days. Neurological severity was evaluated 12 h and up to 21 days after the trauma. Brains were collected 3-21 days post-injury for histological analysis, immunocytochemistry, quantitative real-time PCR, and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and enzyme-linked immunosorbent assays. Neurological function improved in mice treated with osthole and was accompanied by reduced brain water content and accelerated wound closure relative to untreated mice. Osthole treatment reduced the number of macrophages/microglia and peripheral infiltrating of neutrophils and lowered the level of the proinflammatory cytokines interleukin-6 and tumor necrosis factor α in the lesioned cortex. Osthole-treated mice had fewer TUNEL+ apoptotic neurons surrounding the lesion than controls, indicating increased neuronal survival. Osthole reduced secondary brain damage by suppressing inflammation and apoptosis in a mouse model of stab wound injury. These results suggest a new strategy for promoting neuronal survival and function after neurosurgery to improve long-term patient outcome.
Stetler, R. Anne; Leak, Rehana K.; Gan, Yu; Li, Peiying; Hu, Xiaoming; Jing, Zheng; Chen, Jun; Zigmond, Michael J.; Gao, Yanqin
2014-01-01
Preconditioning is a phenomenon in which brief episodes of a sublethal insult induce robust protection against subsequent lethal injuries. Preconditioning has been observed in multiple organisms and can occur in the brain as well as other tissues. Extensive animal studies suggest that the brain can be preconditioned to resist acute injuries, such as ischemic stroke, neonatal hypoxia/ischemia, trauma, and agents that are used in models of neurodegenerative diseases, such as Parkinson’s disease and Alzheimer’s disease. Effective preconditioning stimuli are numerous and diverse, ranging from transient ischemia, hypoxia, hyperbaric oxygen, hypothermia and hyperthermia, to exposure to neurotoxins and pharmacological agents. The phenomenon of “cross-tolerance,” in which a sublethal stress protects against a different type of injury, suggests that different preconditioning stimuli may confer protection against a wide range of injuries. Research conducted over the past few decades indicates that brain preconditioning is complex, involving multiple effectors such as metabolic inhibition, activation of extra- and intracellular defense mechanisms, a shift in the neuronal excitatory/inhibitory balance, and reduction in inflammatory sequelae. An improved understanding of brain preconditioning should help us identify innovative therapeutic strategies that prevent or at least reduce neuronal damage in susceptible patients. In this review, we focus on the experimental evidence of preconditioning in the brain and systematically survey the models used to develop paradigms for neuroprotection, and then discuss the clinical potential of brain preconditioning. In a subsequent components of this two-part series, we will discuss the cellular and molecular events that are likely to underlie these phenomena. PMID:24389580
Moran, Richard; Smith, Joshua H; García, José J
2014-11-28
The mechanical properties of human brain tissue are the subject of interest because of their use in understanding brain trauma and in developing therapeutic treatments and procedures. To represent the behavior of the tissue, we have developed hyperelastic mechanical models whose parameters are fitted in accordance with experimental test results. However, most studies available in the literature have fitted parameters with data of a single type of loading, such as tension, compression, or shear. Recently, Jin et al. (Journal of Biomechanics 46:2795-2801, 2013) reported data from ex vivo tests of human brain tissue under tension, compression, and shear loading using four strain rates and four different brain regions. However, they do not report parameters of energy functions that can be readily used in finite element simulations. To represent the tissue behavior for the quasi-static loading conditions, we aimed to determine the best fit of the hyperelastic parameters of the hyperfoam, Ogden, and polynomial strain energy functions available in ABAQUS for the low strain rate data, while simultaneously considering all three loading modes. We used an optimization process conducted in MATLAB, calling iteratively three finite element models developed in ABAQUS that represent the three loadings. Results showed a relatively good fit to experimental data in all loading modes using two terms in the energy functions. Values for the shear modulus obtained in this analysis (897-1653Pa) are in the range of those presented in other studies. These energy-function parameters can be used in brain tissue simulations using finite element models. Copyright © 2014 Elsevier Ltd. All rights reserved.
Acute vitreoretinal trauma and inflammation after traumatic brain injury in mice.
Evans, Lucy P; Newell, Elizabeth A; Mahajan, MaryAnn; Tsang, Stephen H; Ferguson, Polly J; Mahoney, Jolonda; Hue, Christopher D; Vogel, Edward W; Morrison, Barclay; Arancio, Ottavio; Nichols, Russell; Bassuk, Alexander G; Mahajan, Vinit B
2018-03-01
Limited attention has been given to ocular injuries associated with traumatic brain injury (TBI). The retina is an extension of the central nervous system and evaluation of ocular damage may offer a less-invasive approach to gauge TBI severity and response to treatment. We aim to characterize acute changes in the mouse eye after exposure to two different models of TBI to assess the utility of eye damage as a surrogate to brain injury. A model of blast TBI (bTBI) using a shock tube was compared to a lateral fluid percussion injury model (LFPI) using fluid pressure applied directly to the brain. Whole eyes were collected from mice 3 days post LFPI and 24 days post bTBI and were evaluated histologically using a hematoxylin and eosin stain. bTBI mice showed evidence of vitreous detachment in the posterior chamber in addition to vitreous hemorrhage with inflammatory cells. Subretinal hemorrhage, photoreceptor degeneration, and decreased cellularity in the retinal ganglion cell layer was also seen in bTBI mice. In contrast, eyes of LFPI mice showed evidence of anterior uveitis and subcapsular cataracts. We demonstrated that variations in the type of TBI can result in drastically different phenotypic changes within the eye. As such, molecular and phenotypic changes in the eye following TBI may provide valuable information regarding the mechanism, severity, and ongoing pathophysiology of brain injury. Because vitreous samples are easily obtained, molecular changes within the eye could be utilized as biomarkers of TBI in human patients.
Vythilingam, Meena; Nelson, Eric E.; Scaramozza, Matthew; Waldeck, Tracy; Hazlett, Gary; Southwick, Steven M.; Pine, Daniel S.; Drevets, Wayne; Charney, Dennis S.; Ernst, Monique
2008-01-01
Enhanced brain reward function could contribute to resilience to trauma. Reward circuitry in active duty, resilient special forces (SF) soldiers was evaluated using fMRI during a monetary incentive delay task. Findings in this group of resilient individuals revealed unique patterns of activation during expectation of reward in the subgenual prefrontal cortex and nucleus accumbens area; regions pivotal to reward processes. PMID:19243926
Loder, Randall T; Feinberg, Judy R
2007-06-01
The purpose of this study was to examine the demographic and injury characteristics of children hospitalized with nonaccidental trauma as a causative factor using a large national database. Of the nearly 2.5 million cases in the database, 1794 (0.1%) were identified through diagnostic coding of abuse. Both sexes were equally represented, and two thirds had Medicaid as their primary payer. About one half of the children were younger than 1 year, but all ages were represented. The most common orthopaedic injuries were fractures of the femur or humerus, and most of those fractures occurred in children younger than 2 years. The most common nonorthopaedic injuries were contusions and brain injuries, with or without skull fracture, and 62 (3.5%) of the abused children died; almost all deaths were associated with brain trauma. Nearly one half of the abused hospitalized children between the ages of 3 and 20 years had a concomitant psychiatric or neurological condition. These data provide the orthopaedic surgeon with additional information to assist in identification of potential cases of nonaccidental trauma. In addition to presence of long bone fractures in infants and toddlers, older children with concomitant psychiatric or neurological conditions presenting with nonaccidental injuries should be assessed for possible abuse.
van den Heuvel, Leigh; Suliman, Sharain; Malan-Müller, Stefanie; Hemmings, Sian; Seedat, Soraya
2016-11-01
Alterations in brain-derived neurotrophic factor (BDNF) expression and release may play a role in the pathogenesis of post-traumatic stress disorder (PTSD). This study evaluated road traffic accident (RTA) survivors to determine whether PTSD and trauma-related factors were associated with plasma BDNF levels and BDNF Val66Met carrier status following RTA exposure. One hundred and twenty-three RTA survivors (mean age 33.2 years, SD = 10.6 years; 56.9% male) were assessed 10 (SD = 4.9) days after RTA exposure. Acute stress disorder (ASD), as assessed with the Acute Stress Disorder Scale, was present in 50 (42.0%) of the participants. Plasma BDNF levels were measured with enzyme-linked immunosorbent assay and BDNF Val66Met genotyping was performed. PTSD, as assessed with the Clinician-Administered PTSD Scale, was present in 10 (10.8%) participants at 6 months follow-up. Neither BDNF Val66Met genotype nor plasma BDNF was significantly associated with the presence or severity of ASD or PTSD. Plasma BDNF levels were, however, significantly correlated with the lifetime number of trauma exposures. In RTA survivors, plasma BDNF levels increased with increasing number of prior trauma exposures. Plasma BDNF may, therefore, be a marker of trauma load.
Oeur, R Anna; Karton, Clara; Post, Andrew; Rousseau, Philippe; Hoshizaki, T Blaine; Marshall, Shawn; Brien, Susan E; Smith, Aynsley; Cusimano, Michael D; Gilchrist, Michael D
2015-08-01
Concussions typically resolve within several days, but in a few cases the symptoms last for a month or longer and are termed persistent postconcussive symptoms (PPCS). These persisting symptoms may also be associated with more serious brain trauma similar to subdural hematoma (SDH). The objective of this study was to investigate the head dynamic and brain tissue responses of injury reconstructions resulting in concussion, PPCS, and SDH. Reconstruction cases were obtained from sports medicine clinics and hospitals. All subjects received a direct blow to the head resulting in symptoms. Those symptoms that resolved in 9 days or fewer were defined as concussions (n = 3). Those with symptoms lasting longer than 18 months were defined as PPCS (n = 3), and 3 patients presented with SDHs (n = 3). A Hybrid III headform was used in reconstruction to obtain linear and rotational accelerations of the head. These dynamic response data were then input into the University College Dublin Brain Trauma Model to calculate maximum principal strain and von Mises stress. A Kruskal-Wallis test followed by Tukey post hoc tests were used to compare head dynamic and brain tissue responses between injury groups. Statistical significance was set at p < 0.05. A significant difference was identified for peak resultant linear and rotational acceleration between injury groups. Post hoc analyses revealed the SDH group had higher linear and rotational acceleration responses (316 g and 23,181 rad/sec(2), respectively) than the concussion group (149 g and 8111 rad/sec(2), respectively; p < 0.05). No significant differences were found between groups for either brain tissue measures of maximum principal strain or von Mises stress. The reconstruction of accidents resulting in a concussion with transient symptoms (low severity) and SDHs revealed a positive relationship between an increase in head dynamic response and the risk for more serious brain injury. This type of relationship was not found for brain tissue stress and strain results derived by finite element analysis. Future research should be undertaken using a larger sample size to confirm these initial findings. Understanding the relationship between the head dynamic and brain tissue response and the nature of the injury provides important information for developing strategies for injury prevention.
Krajewska, Maryla; You, Zerong; Rong, Juan; Kress, Christina; Huang, Xianshu; Yang, Jinsheng; Kyoda, Tiffany; Leyva, Ricardo; Banares, Steven; Hu, Yue; Sze, Chia-Hung; Whalen, Michael J.; Salmena, Leonardo; Hakem, Razqallah; Head, Brian P.; Reed, John C.; Krajewski, Stan
2011-01-01
Background Acute brain injury is an important health problem. Given the critical position of caspase 8 at the crossroads of cell death pathways, we generated a new viable mouse line (Ncasp8 −/−), in which the gene encoding caspase 8 was selectively deleted in neurons by cre-lox system. Methodology/Principal Findings Caspase 8 deletion reduced rates of neuronal cell death in primary neuronal cultures and in whole brain organotypic coronal slice cultures prepared from 4 and 8 month old mice and cultivated up to 14 days in vitro. Treatments of cultures with recombinant murine TNFα (100 ng/ml) or TRAIL (250 ng/mL) plus cyclohexamide significantly protected neurons against cell death induced by these apoptosis-inducing ligands. A protective role of caspase 8 deletion in vivo was also demonstrated using a controlled cortical impact (CCI) model of traumatic brain injury (TBI) and seizure-induced brain injury caused by kainic acid (KA). Morphometric analyses were performed using digital imaging in conjunction with image analysis algorithms. By employing virtual images of hundreds of brain sections, we were able to perform quantitative morphometry of histological and immunohistochemical staining data in an unbiased manner. In the TBI model, homozygous deletion of caspase 8 resulted in reduced lesion volumes, improved post-injury motor performance, superior learning and memory retention, decreased apoptosis, diminished proteolytic processing of caspases and caspase substrates, and less neuronal degeneration, compared to wild type, homozygous cre, and caspase 8-floxed control mice. In the KA model, Ncasp8 −/− mice demonstrated superior survival, reduced seizure severity, less apoptosis, and reduced caspase 3 processing. Uninjured aged knockout mice showed improved learning and memory, implicating a possible role for caspase 8 in cognitive decline with aging. Conclusions Neuron-specific deletion of caspase 8 reduces brain damage and improves post-traumatic functional outcomes, suggesting an important role for this caspase in pathophysiology of acute brain trauma. PMID:21957448
2009-01-01
applications for recovering from disaster and trauma Defense and Veterans Brain Injury Center Develops and delivers advanced TBI-specifi c treatment...specifically aimed at developing cognitive and motor therapy tools using videogame technology, game-based PH outreach tools and support tools for children of...Defense Centers of Excellence for Psychological Health and Traumatic Brain Injury Annual Report 2009 Report Documentation Page Form ApprovedOMB No
La Fountaine, Michael F
2017-11-29
Concussion is defined as a complex pathophysiological process affecting the brain that is induced by the application or transmission of traumatic biomechanical forces to the head. The result of the impact is the onset of transient symptoms that may be experienced for approximately 2weeks in most individuals. However, in some individuals, symptoms may not resolve and persist for a protracted period and a chronic injury ensues. Concussion symptoms are generally characterized by their emergence through changes in affect, cognition, or multi-sensory processes including the visual and vestibular systems. An emerging consequence of concussion is the presence of cardiovascular autonomic nervous system dysfunction that is most apparent through hemodynamic perturbations and provocations. Further interrogation of data that are derived from continuous digital electrocardiograms and/or beat-to-beat blood pressure monitoring often reveal an imbalance of parasympathetic or sympathetic nervous system activity during a provocation after an injury. The disturbance is often greatest early after injury and a resolution of the dysfunction occurs in parallel with other symptoms. The possibility exists that the disturbance may remain if the concussion does not resolve. Unfortunately, there is little evidence in humans to support the etiology for the emergence of this post-injury dysfunction. As such, evidence from experimental models of traumatic brain injury and casual observations from human studies of concussion implicate a transient abnormality of the anatomical structures and functions of the cardiovascular autonomic nervous system. The purpose of this review article is to provide a mechanistic narrative of multi-disciplinary evidence to support the anatomical and physiological basis of cardiovascular autonomic nervous system dysfunction after concussion. The review article will identify the anatomical structures of the autonomic nervous system and propose a theoretical framework to demonstrate the potential effects of concussive head trauma on corresponding outcome measurements. Evidence from experimental models will be used to describe abnormal cellular functions and provide a hypothetical mechanistic basis for the respective responses of the anatomical structures to concussive head trauma. When available, example observations from the human concussion literature will be presented to demonstrate the effects of concussive head trauma that may be related to anomalous activity in the respective anatomical structures of the autonomic nervous system. Copyright © 2017 Elsevier B.V. All rights reserved.
Jeter, Whitney K; Brannon, Laura A
2014-01-01
To date, trauma research has focused on the impact of physical trauma on posttraumatic stress (PTS) symptoms. Sometimes psychological trauma is measured with instances of physical trauma; however, less is known about solely psychological trauma. The current study addresses this by examining psychological trauma and PTS symptoms using the chronic relational trauma (CRT) model. The CRT model examines physical and possible concurrent psychological childhood, peer, and intimate partner trauma; however, psychological trauma alone has yet to be tested. A total of 232 female undergraduates (M age = 18.32, SD = 1.60) completed a series of questionnaires. Structural equation modeling indicated that childhood, peer, and intimate partner psychological trauma predict current PTS symptoms. Contributions of these findings are discussed.
Fingelkurts, Andrew A; Fingelkurts, Alexander A
2017-09-01
In this report, we describe the case of a patient who sustained extremely severe traumatic brain damage with diffuse axonal injury in a traffic accident and whose recovery was monitored during 6 years. Specifically, we were interested in the recovery dynamics of 3-dimensional components of selfhood (a 3-dimensional construct model for the complex experiential selfhood has been recently proposed based on the empirical findings on the functional-topographical specialization of 3 operational modules of brain functional network responsible for the self-consciousness processing) derived from the electroencephalographic (EEG) signal. The analysis revealed progressive (though not monotonous) restoration of EEG functional connectivity of 3 modules of brain functional network responsible for the self-consciousness processing, which was also paralleled by the clinically significant functional recovery. We propose that restoration of normal integrity of the operational modules of the self-referential brain network may underlie the positive dynamics of 3 aspects of selfhood and provide a neurobiological mechanism for their recovery. The results are discussed in the context of recent experimental studies that support this inference. Studies of ongoing recovery after severe brain injury utilizing knowledge about each separate aspect of complex selfhood will likely help to develop more efficient and targeted rehabilitation programs for patients with brain trauma.
NASA Astrophysics Data System (ADS)
Semyachkina-Glushkovskaya, Oxana; Abdurashitov, Arkady; Dubrovsky, Alexander; Bragin, Denis; Bragina, Olga; Shushunova, Nataliya; Maslyakova, Galina; Navolokin, Nikita; Bucharskaya, Alla; Tuchin, Valery; Kurths, Juergen; Shirokov, Alexander
2017-12-01
The meningeal lymphatic vessels were discovered 2 years ago as the drainage system involved in the mechanisms underlying the clearance of waste products from the brain. The blood-brain barrier (BBB) is a gatekeeper that strongly controls the movement of different molecules from the blood into the brain. We know the scenarios during the opening of the BBB, but there is extremely limited information on how the brain clears the substances that cross the BBB. Here, using the model of sound-induced opening of the BBB, we clearly show how the brain clears dextran after it crosses the BBB via the meningeal lymphatic vessels. We first demonstrate successful application of optical coherence tomography (OCT) for imaging of the lymphatic vessels in the meninges after opening of the BBB, which might be a new useful strategy for noninvasive analysis of lymphatic drainage in daily clinical practice. Also, we give information about the depth and size of the meningeal lymphatic vessels in mice. These new fundamental data with the applied focus on the OCT shed light on the mechanisms of brain clearance and the role of lymphatic drainage in these processes that could serve as an informative platform for a development of therapy and diagnostics of diseases associated with injuries of the BBB such as stroke, brain trauma, glioma, depression, or Alzheimer disease.
Diagnostic Performance of Ultrafast Brain MRI for Evaluation of Abusive Head Trauma.
Kralik, S F; Yasrebi, M; Supakul, N; Lin, C; Netter, L G; Hicks, R A; Hibbard, R A; Ackerman, L L; Harris, M L; Ho, C Y
2017-04-01
MR imaging with sedation is commonly used to detect intracranial traumatic pathology in the pediatric population. Our purpose was to compare nonsedated ultrafast MR imaging, noncontrast head CT, and standard MR imaging for the detection of intracranial trauma in patients with potential abusive head trauma. A prospective study was performed in 24 pediatric patients who were evaluated for potential abusive head trauma. All patients received noncontrast head CT, ultrafast brain MR imaging without sedation, and standard MR imaging with general anesthesia or an immobilizer, sequentially. Two pediatric neuroradiologists independently reviewed each technique blinded to other modalities for intracranial trauma. We performed interreader agreement and consensus interpretation for standard MR imaging as the criterion standard. Diagnostic accuracy was calculated for ultrafast MR imaging, noncontrast head CT, and combined ultrafast MR imaging and noncontrast head CT. Interreader agreement was moderate for ultrafast MR imaging (κ = 0.42), substantial for noncontrast head CT (κ = 0.63), and nearly perfect for standard MR imaging (κ = 0.86). Forty-two percent of patients had discrepancies between ultrafast MR imaging and standard MR imaging, which included detection of subarachnoid hemorrhage and subdural hemorrhage. Sensitivity, specificity, and positive and negative predictive values were obtained for any traumatic pathology for each examination: ultrafast MR imaging (50%, 100%, 100%, 31%), noncontrast head CT (25%, 100%, 100%, 21%), and a combination of ultrafast MR imaging and noncontrast head CT (60%, 100%, 100%, 33%). Ultrafast MR imaging was more sensitive than noncontrast head CT for the detection of intraparenchymal hemorrhage ( P = .03), and the combination of ultrafast MR imaging and noncontrast head CT was more sensitive than noncontrast head CT alone for intracranial trauma ( P = .02). In abusive head trauma, ultrafast MR imaging, even combined with noncontrast head CT, demonstrated low sensitivity compared with standard MR imaging for intracranial traumatic pathology, which may limit its utility in this patient population. © 2017 by American Journal of Neuroradiology.
Analysis of the Revised Trauma Score (RTS) in 200 victims of different trauma mechanisms.
Alvarez, Bruno Durante; Razente, Danilo Mardegam; Lacerda, Daniel Augusto Mauad; Lother, Nicole Silveira; VON-Bahten, Luiz Carlos; Stahlschmidt, Carla Martinez Menini
2016-01-01
to analyze the epidemiological profile and mortality associated with the Revised Trauma Score (RTS) in trauma victims treated at a university hospital. we conducted a descriptive, cross-sectional study of trauma protocols (prospectively collected) from December 2013 to February 2014, including trauma victims admitted in the emergency room of the Cajuru University Hospital. We set up three groups: (G1) penetrating trauma to the abdomen and chest, (G2) blunt trauma to the abdomen and chest, and (G3) traumatic brain injury. The variables we analyzed were: gender, age, day of week, mechanism of injury, type of transportation, RTS, hospitalization time and mortality. we analyzed 200 patients, with a mean age of 36.42 ± 17.63 years, and 73.5% were male. The mean age was significantly lower in G1 than in the other groups (p <0.001). Most (40%) of the visits occurred on weekends and the most common pre-hospital transport service (58%) was the SIATE (Emergency Trauma Care Integrated Service). The hospital stay was significantly higher in G1 compared with the other groups (p <0.01). Regarding mortality, there were 12%, 1.35% and 3.95% of deaths in G1, G2 and G3, respectively. The median RTS among the deaths was 5.49, 7.84 and 1.16, respectively, for the three groups. the majority of patients were young men. RTS was effective in predicting mortality in traumatic brain injury, however failing to predict it in patients suffering from blunt and penetrating trauma. analisar o perfil epidemiológico e a mortalidade associada ao escore de trauma revisado (RTS) em vítimas de trauma atendidas em um hospital universitário. estudo transversal descritivo de protocolos de trauma (coletados prospectivamente) de dezembro de 2013 a fevereiro de 2014, incluindo vítimas de trauma admitidas na sala de emergência do Hospital Universitário Cajuru. Três grupos foram criados: (G1) trauma penetrante em abdome e tórax, (G2) trauma contuso em abdome e tórax, e (G3) trauma cranioencefálico. As variáveis analisadas foram: sexo, idade, dia da semana, mecanismo de trauma, tipo de transporte, RTS, tempo de internamento e mortalidade. analisou-se 200 pacientes, com média de idade de 36,42 ± 17,63 anos, sendo 73,5% do sexo masculino. A média de idade no G1 foi significativamente menor do que nos demais grupos (p <0,001). A maioria (40%) dos atendimentos ocorreu nos finais de semana e o serviço de transporte pré-hospitalar mais frequente (58%) foi o SIATE (Serviço Integrado de Atendimento ao Trauma em Emergência). O tempo de internamento foi significativamente maior no G1, em comparação aos demais grupos (p <0,01). Quanto à mortalidade, houve 12%, 1,35% e 3,95% de óbitos nos grupos G1, G2 e G3, respectivamente. A mediana do RTS entre os óbitos foi 5,49, 7,84 e 1,16, respectivamente, para os três grupos. a maioria dos pacientes eram homens jovens. O RTS mostrou-se efetivo na predição de mortalidade no trauma cranioencefálico, entretanto falhou ao analisar pacientes vítimas de trauma contuso e penetrante.
Ganon-Elazar, Eti; Akirav, Irit
2013-09-01
Considerable evidence suggests that cannabinoids modulate the behavioral and physiological response to stressful events. We have recently shown that activating the cannabinoid system using the CB1/CB2 receptor agonist WIN55,212-2 (WIN) in proximity to exposure to single-prolonged stress (SPS), a rat model of emotional trauma, prevented the stress-induced enhancement of acoustic startle response, the impairment in avoidance extinction and the enhanced negative feedback on the hypothalamic-pituitary-adrenal (HPA) axis (Ganon-Elazar and Akirav, 2012). Some of the effects were found to be mediated by CB1 receptors in the basolateral amygdala (BLA). Here we examined whether cannabinoid receptor activation in a putative brain circuit that includes the BLA, hippocampus and prefrontal cortex (PFC), could prevent the effects of traumatic stress on contextual fear extinction and alterations in glucocorticoid receptor (GR) protein levels. We found that: (i) SPS impaired contextual fear extinction tested one week after trauma exposure and that WIN prevented the stress-induced impairment of extinction when microinjected immediately after trauma exposure into the BLA or hippocampus (5 μg), but not when microinjected into the PFC, (ii) the ameliorating effects of WIN on contextual extinction were prevented by blocking GRs in the BLA and hippocampus, and (iii) SPS up regulated GRs in the BLA, PFC and hippocampus and systemic WIN administration (0.5 mg/kg) after trauma exposure normalized GR levels in the BLA and hippocampus, but not in the PFC. Cannabinoid receptor activation in the aftermath of trauma exposure may regulate the emotional response to the trauma and prevent stress-induced impairment of extinction and GR up regulation through the mediation of CB1 receptors in the BLA and hippocampus. Taken together, the findings suggest that the interaction between the cannabinoid and glucocorticoid systems is crucial in the modulation of emotional trauma. Copyright © 2013 Elsevier Ltd. All rights reserved.
Brain Management During Trauma
NASA Astrophysics Data System (ADS)
Shatsky, Stanley A.
1984-01-01
The Neurosurgeon faces a dilemma, that is, how to treat and reconstruct the injured skull and brain with limited knowledge as to how the injury occurred. In an attempt to understand such injuries, our group assembled a series of acceleration sleds to experimentally reproduce these injuries in primates and high frame rate flash x-ray cine system to radiographically study their time course.
2012-04-25
Jiang J, Bian X, Savic J. Cognitive deficits following blast injury- induced neurotrauma: possible involvement of nitric oxide. Brain Inj 2001;15: 593...612. [8] Cernak I, Wang Z, Jiang J, Bian X, Savic J. Ultrastructural and functional character- istics of blast injury-induced neurotrauma. J Trauma
Commentary on Blau (1936): Mental Changes following Head Trauma in Children
ERIC Educational Resources Information Center
Barkley, Russell A.
2010-01-01
The discussion of the Blau (1936) article continues the welcome tradition established in this journal in acquainting readers with historically important articles in the history of ADHD. That history began with efforts to understand the functions of the brain likely to be impaired from injury to various brain regions and especially the frontal…
Intracerebral hemorrhage (image)
Intracerebral hemorrhage may be caused by trauma (brain injury) or abnormalities of the blood vessels (aneurysm or angioma), but it is most commonly associated with high blood pressure (hypertensive intracerebral hemorrhage).
Morey, Rajendra A.; Dolcos, Florin; Petty, Christopher M.; Cooper, Debra A.; Hayes, Jasmeet Pannu; LaBar, Kevin S.; McCarthy, Gregory
2009-01-01
The relevance of emotional stimuli to threat and survival confers a privileged role in their processing. In PTSD, the ability of trauma-related information to divert attention is especially pronounced. Information unrelated to the trauma may also be highly distracting when it shares perceptual features with trauma material. Our goal was to study how trauma-related environmental cues modulate working memory networks in PTSD. We examined neural activity in participants performing a visual working memory task while distracted by task-irrelevant trauma and non-trauma material. Recent post-9/11 veterans were divided into a PTSD group (n = 22) and a trauma-exposed control group (n = 20) based on the Davidson trauma scale. Using fMRI, we measured hemodynamic change in response to emotional (trauma-related) and neutral distraction presented during the active maintenance period of a delayed-response working memory task. The goal was to examine differences in functional networks associated with working memory (dorsolateral prefrontal cortex and lateral parietal cortex) and emotion processing (amygdala, ventrolateral prefrontal cortex, and fusiform gyrus). The PTSD group showed markedly different neural activity compared to the trauma-exposed control group in response to task-irrelevant visual distractors. Enhanced activity in ventral emotion processing regions was associated with trauma distractors in the PTSD group, whereas activity in brain regions associated with working memory and attention regions was disrupted by distractor stimuli independent of trauma content. Neural evidence for the impact of distraction on working memory is consistent with PTSD symptoms of hypervigilance and general distractibility during goal-directed cognitive processing. PMID:19091328
Mathematical modeling of human brain physiological data
NASA Astrophysics Data System (ADS)
Böhm, Matthias; Faltermeier, Rupert; Brawanski, Alexander; Lang, Elmar W.
2013-12-01
Recently, a mathematical model of the basic physiological processes regulating the cerebral perfusion and oxygen supply was introduced [Jung , J. Math. Biol.JMBLAJ0303-681210.1007/s00285-005-0343-5 51, 491 (2005)]. Although this model correctly describes the interdependence of arterial blood pressure (ABP) and intracranial pressure (ICP), it fails badly when it comes to explaining certain abnormal correlations seen in about 80% of the recordings of ABP together with ICP and the partial oxygen pressure (TiPO2) of the neuronal tissue, taken at an intensive care unit during neuromonitoring of patients with a severe brain trauma. Such recordings occasionally show segments, where the mean arterial blood pressure is correlated with the partial oxygen pressure in tissue but anticorrelated with the intracranial pressure. The origin of such abnormal correlations has not been fully understood yet. Here, two extensions to the previous approach are proposed which can reproduce such abnormal correlations in simulations quantitatively. Furthermore, as the simulations are based on a mathematical model, additional insight into the physiological mechanisms from which such abnormal correlations originate can be gained.
Khalili, Hosseinali; Sadraei, Nazanin; Niakan, Amin; Ghaffarpasand, Fariborz; Sadraei, Amin
2016-10-01
To determine the role of intracranial pressure (ICP) monitoring in management of patients with severe traumatic brain injury (TBI) admitted to a large level I trauma center in Southern Iran. This was a cohort study performed during a 2-year period in a level I trauma center in Southern Iran including all adult patients (>16 years) with severe TBI (Glasgow Coma Scale [GCS] score, 3-8) who underwent ICP monitoring through ventriculostomy. The management was based on the recorded ICP values with threshold of 20 mm Hg. Decompressive craniectomy was performed in patients with intractable intracranial hypertension (persistent ICP ≥25 mm Hg). In unresponsive patients, barbiturate coma was induced. Patients were followed for 6 months and Glasgow Outcome Scale Extended was recorded. The determinants of favorable and unfavorable outcome were also determined. Overall, we included 248 patients with mean age of 34.6 ± 16.6 years, among whom there were 216 men (87.1%) and 32 women (12.9%). Eighty-five patients (34.2%) had favorable and 163 (65.8%) unfavorable outcomes. Those with favorable outcome had significantly lower age (P = 0.004), higher GCS score on admission (P < 0.001), lower Rotterdam score (P = 0.035), fewer episodes of intracranial hypertension (P < 0.001), and lower maximum recorded ICP (P = 0.041). These factors remained statistically significant after elimination of confounders by multivariate logistic regression model. Age, GCS score on admission, Rotterdam score, intracranial hypertension, and maximum recorded ICP are important determinants of outcome in patients with severe TBI. ICP monitoring assisted us in targeted therapy and management of patients with severe TBI. Copyright © 2016 Elsevier Inc. All rights reserved.
Roden-Foreman, Kenleigh; Solis, Jaicus; Jones, Alan; Bennett, Monica; Roden-Foreman, Jacob W; Rainey, Evan E; Foreman, Michael L; Warren, Ann Marie
2017-09-01
Psychological morbidities after injury [eg, posttraumatic stress disorder (PTSD) and depression] are increasingly recognized as a significant determinant of overall outcome. Traumatic brain injury (TBI) negatively impacts outcomes of patients with orthopaedic injury, but the association of concurrent TBI, orthopaedic injury, and symptoms of PTSD and depression has not been examined. This study's objective was to examine symptoms of PTSD and depression in patients with orthopaedic trauma with and without TBI. Longitudinal prospective cohort study. Urban Level I Trauma Center in the Southwest United States. Orthopaedic trauma patients older than 18 years admitted for ≥24 hours. Questionnaires examining demographics, injury-related variables, PTSD, and depression were administered during hospitalization and 3, 6, and 12 months later. Orthopaedic injury and TBI were determined based on ICD-9 codes. Generalized linear models determined whether PTSD and depression at follow-up were associated with TBI. Of the total sample (N = 214), 44 (21%) sustained a TBI. Those with TBI had higher rates of PTSD symptoms, 12 months postinjury (P = 0.04). The TBI group also had higher rates of depressive symptoms, 6 months postinjury (P = 0.038). Having a TBI in addition to orthopaedic injury was associated with significantly higher rates of PTSD at 12 months and depression at 6 months postinjury. This suggests that sustaining a TBI in addition to orthopaedic injury places patients at a higher risk for negative psychological outcomes. The findings of this study may help clinicians to identify patients who are in need for psychological screening and could potentially benefit from intervention. Prognostic Level III. See Instructions for Authors for a complete description of levels of evidence.
Sullivan, Karen A; Wade, Christina
2017-05-01
A controlled experiment of the effect of injury cause on expectations of outcome from mild traumatic brain injury (TBI) was conducted. Ninety-three participants were randomly assigned to one of four conditions. The participants read a vignette that described a mild TBI (with fixed injury parameters) from a different cause (sport, domestic assault, fall, or motor vehicle accident). The effect of the manipulation on expectations of persistent postconcussion symptoms and psychological trauma was assessed with standard measures and a novel "threat-to-life" measure. The Kruskal-Wallis H test for group differences revealed a significant but selective effect of group on symptom and trauma outcomes (ŋ 2 s ≥ .10; large effects). Post hoc pairwise tests showed that, in most cases, there was an expectation of a worse outcome following mild TBI from a domestic assault than from the other causes (small-to-medium effects). Expectations were selectively altered by an experimental manipulation of injury cause. Given that expectations of outcome are known to affect mild TBI prognosis, the findings suggest the need for greater attention to injury cause.
Association of head trauma with cervical spine injury, spinal cord injury, or both.
Iida, H; Tachibana, S; Kitahara, T; Horiike, S; Ohwada, T; Fujii, K
1999-03-01
Links between cervical spine and/or spinal cord injuries and head trauma have not been reported in detail. 188 patients with cervical spine and/or spinal cord injury were divided into two groups, i.e., with upper cervical and mid-lower cervical injury, and compared for head injury. Associated head trauma was investigated in 188 patients with cervical spine and/or spinal cord injuries; 35% had moderate or severe injuries. Brain damage was more frequently observed in patients with upper cervical injury than in those with mid to lower cervical injury. Those patients with upper cervical injury appeared to have an elevated risk of suffering skull base fractures, traumatic subarachnoid hemorrhage, and contusional hemotoma. Approximately one third of patients with cervical spine and/or spinal cord injuries had moderate or severe head injuries. Brain damage was more frequently associated with upper cervical injury. Those patients with upper cervical injury are at greater risk of suffering from skull base fractures and severe intracranial hematomas than those with mid to lower cervical injury.
Toward a Theory of Stuttering.
Mawson, Anthony R; Radford, Nola T; Jacob, Binu
2016-01-01
Stuttering affects about 1% of the general population and from 8 to 11% of children. The onset of persistent developmental stuttering (PDS) typically occurs between 2 and 4 years of age. The etiology of stuttering is unknown and a unifying hypothesis is lacking. Clues to the pathogenesis of stuttering include the following observations: PDS is associated with adverse perinatal outcomes and birth-associated trauma; stuttering can recur or develop in adulthood following traumatic events such as brain injury and stroke; PDS is associated with structural and functional abnormalities in the brain associated with speech and language; and stuttering resolves spontaneously in a high percentage of affected children. Evidence marshaled from the literature on stuttering and from related sources suggests the hypothesis that stuttering is a neuro-motor disorder resulting from perinatal or later-onset hypoxic-ischemic injury (HII), and that chronic stuttering and its behavioral correlates are manifestations of recurrent transient ischemic episodes affecting speech-motor pathways. The hypothesis could be tested by comparing children who stutter and nonstutterers (controls) in terms of the occurrence of perinatal trauma, based on birth records, and by determining rates of stuttering in children exposed to HII during the perinatal period. Subject to testing, the hypothesis suggests that interventions to increase brain perfusion directly could be effective both in the treatment of stuttering and its prevention at the time of birth or later trauma. © 2016 S. Karger AG, Basel.
Rothman, Sarah M; Griffioen, Kathleen J; Wan, Ruiqian; Mattson, Mark P
2012-01-01
Overweight sedentary individuals are at increased risk for cardiovascular disease, diabetes, and some neurological disorders. Beneficial effects of dietary energy restriction (DER) and exercise on brain structural plasticity and behaviors have been demonstrated in animal models of aging and acute (stroke and trauma) and chronic (Alzheimer's and Parkinson's diseases) neurological disorders. The findings described later, and evolutionary considerations, suggest brain-derived neurotrophic factor (BDNF) plays a critical role in the integration and optimization of behavioral and metabolic responses to environments with limited energy resources and intense competition. In particular, BDNF signaling mediates adaptive responses of the central, autonomic, and peripheral nervous systems from exercise and DER. In the hypothalamus, BDNF inhibits food intake and increases energy expenditure. By promoting synaptic plasticity and neurogenesis in the hippocampus, BDNF mediates exercise- and DER-induced improvements in cognitive function and neuroprotection. DER improves cardiovascular stress adaptation by a mechanism involving enhancement of brainstem cholinergic activity. Collectively, findings reviewed in this paper provide a rationale for targeting BDNF signaling for novel therapeutic interventions in a range of metabolic and neurological disorders. PMID:22548651
Morley, Wendy A; Seneff, Stephanie
2014-01-01
The number of sports-related concussions has been steadily rising in recent years. Diminished brain resilience syndrome is a term coined by the lead author to describe a particular physiological state of nutrient functional deficiency and disrupted homeostatic mechanisms leading to increased susceptibility to previously considered innocuous concussion. We discuss how modern day environmental toxicant exposure, along with major changes in our food supply and lifestyle practices, profoundly reduce the bioavailability of neuro-critical nutrients such that the normal processes of homeostatic balance and resilience are no longer functional. Their diminished capacity triggers physiological and biochemical 'work around' processes that result in undesirable downstream consequences. Exposure to certain environmental chemicals, particularly glyphosate, the active ingredient in the herbicide, Roundup(®), may disrupt the body's innate switching mechanism, which normally turns off the immune response to brain injury once danger has been removed. Deficiencies in serotonin, due to disruption of the shikimate pathway, may lead to impaired melatonin supply, which reduces the resiliency of the brain through reduced antioxidant capacity and alterations in the cerebrospinal fluid, reducing critical protective buffering mechanisms in impact trauma. Depletion of certain rare minerals, overuse of sunscreen and/or overprotection from sun exposure, as well as overindulgence in heavily processed, nutrient deficient foods, further compromise the brain's resilience. Modifications to lifestyle practices, if widely implemented, could significantly reduce this trend of neurological damage.
A time-course analysis of changes in cerebral metal levels following a controlled cortical impact.
Portbury, Stuart D; Hare, Dominic J; Sgambelloni, Charlotte; Finkelstein, David I; Adlard, Paul A
2016-02-01
Traumatic brain injury (TBI) is complicated by a sudden and dramatic change in brain metal levels, including iron (Fe), copper (Cu) and zinc (Zn). Specific 'metallo-pathological' features of TBI include increased non-heme bound Fe and the liberation of free Zn ions, both of which may contribute to the pathogenesis of TBI. To further characterise the metal dyshomeostasis that occurs following brain trauma, we performed a quantitative time-course survey of spatial Fe, Cu and Zn distribution in mice receiving a controlled cortical impact TBI. Images of brain metal levels produced using laser ablation-inductively coupled plasma-mass spectrometry (LA-ICP-MS) in the upper quadrant of the ipsilateral hemisphere were compared to the corresponding contralateral hemisphere, together with regional areas radiating toward the center of the brain from the site of lesion. Significant regional and time point specific elevations in Fe, Zn and Cu were detected immediately and up to 28 days after TBI. The magnitude and timeframe of many of these changes suggest that TBI results in a pronounced and sustained alteration in normal metal levels within the brain. Such alterations are likely to play a role in both the short- and long-term consequences of head trauma and suggest that pharmacological modulation to normalize these metal levels may be efficacious in improving functional outcome.
Qian, A; Zhang, M; Zhao, G
2015-02-01
NT-proBNP and BNP have been demonstrated to be prognostic markers in cardiac disease and sepsis. However, the prognostic value and the dynamic changes of BNP or NT-proBNP in trauma patients remain unclear. The present study was conducted to investigate the dynamic changes of NT-proBNP in patients with major trauma (injury severity score ≥16), determine whether NT-proBNP could be used as a simple index to predict mortality in major trauma patients. This prospective observational study included 60 patients with major trauma. Serum NT-proBNP levels were measured on the 1st, 3rd and 7th day after injury The NT-proBNP levels in survivors were compared with those in non-survivors. The efficacy of NT-proBNP to predict survival was analyzed using receiver operating characteristic curves. An analysis of correlations between NT-proBNP and various factors, including injury severity score, Glasgow coma score, acute physiology and chronic health evaluation II, central venous pressure, creatine kinase-MB, cardiac troponin I and procalcitonin (PCT) was performed. NT-proBNP levels in patients with traumatic brain injury were compared with those in patients without traumatic brain injury. A comparison of NT-proBNP levels between patients with and without sepsis was also performed at each time point. NT-proBNP levels in non-survivors were significantly higher than those in survivors at all the indicated time points. In the group of non-survivors, NT-proBNP levels on the 7th day were markedly higher than those on the 1st day. In contrast, NT-proBNP levels in survivors showed a reduction over time. The efficacy of NT-proBNP to predict survival was analyzed using ROC curves, and there was no difference in the area under the ROC between NT-proBNP and APACHE II/ISS at the three time points. A significant correlation was found between NT-proBNP and ISS on the 1st day, NT-proBNP and CK-MB, Tn-I and APACHE II on the 3rd day, NT-proBNP and PCT on the 7th day. There were no significant differences in NT-proBNP levels between patients with or without brain trauma at all the indicated time points. NT-proBNP levels in patients with sepsis were significantly higher than those in patients without sepsis at all the indicated time points. These findings suggest that dynamic detection of serum NT-proBNP might help to predict death in patients with major trauma. A high level of NT-proBNP at admission or maintained for several days after trauma indicates poor survival.
Aykaç, Aslı; Aydın, Banu; Cabadak, Hülya; Gören, M Zafer
2012-06-15
This study shows the possible contribution of muscarinic receptors in the pathophysiology of post-traumatic stress disorder. Sprague-Dawley rats of both sexes were exposed to dirty cat litter (trauma) for 10 min and the protocol was repeated 1 week later with a trauma reminder (clean litter). The rats also received intraperitoneal fluoxetine (2.5, 5 or 10 mg/kg/day), propranolol (10 mg/kg/day) or saline for 7 days between two exposure sessions. Functional behavioral experiments were performed using elevated plus maze, following exposure to trauma reminder. Western blot analyses for M(1), M(2), M(3), M(4) and M(5) receptor proteins were employed in the homogenates of the hippocampus, the frontal cortex and the amygdaloid complex. The anxiety indices increased from 0.63±0.02 to 0.89±0.04 in rats exposed to the trauma reminder. The freezing times were also recorded as 47±6 and 133±12 s, in control and test animals respectively. Fluoxetine or propranolol treatments restored the increases in the anxiety indices and the freezing times. Female rats had higher anxiety indices compared to males. Western blot data showed increases in M(2) and M(5) expression in the frontal cortex. Expression of M(1) receptors increased and M(4) subtype decreased in the hippocampus. In the amygdaloid complex of rats, we also detected a down-regulation of M(4) receptors. Fluoxetine and propranolol only corrected the changes occurred in the frontal cortex. These results may imply that muscarinic receptors are involved in this experimental model of post-traumatic stress disorder. Copyright © 2012 Elsevier B.V. All rights reserved.
NASA Astrophysics Data System (ADS)
Abookasis, David; Shochat, Ariel
2016-03-01
We present a comparative evaluation of five different neuroprotective drugs in the early phase following focal traumatic brain injury (TBI) in mouse intact head. The effectiveness of these drugs in terms of changes in brain tissue morphology and hemodynamic properties was experimentally evaluated through analysis of the optical absorption coefficient and spectral reduced scattering parameters in the range of 650-1000 nm. Anesthetized male mice (n=50 and n=10 control) were subjected to weight drop model mimics real life focal head trauma. Monitoring the effect of injury and neuroprotective drugs was obtained by using a diffuse reflectance spectroscopy system utilizing independent source-detector separation and location. Result indicates that administration of minocycline improve hemodynamic and reduced the level of tissue injury at an early phase post-injury while hypertonic saline treatment decrease brain water content. These findings highlight the heterogeneity between neuroprotective drugs and the ongoing controversy among researchers regarding which drug therapy is preferred for treatment of TBI. On the other hand, our results show the capability of optical spectroscopy technique to noninvasively study brain function following injury and drug therapy.
CRHR1 genotypes, neural circuits and the diathesis for anxiety and depression.
Rogers, J; Raveendran, M; Fawcett, G L; Fox, A S; Shelton, S E; Oler, J A; Cheverud, J; Muzny, D M; Gibbs, R A; Davidson, R J; Kalin, N H
2013-06-01
The corticotrophin-releasing hormone (CRH) system integrates the stress response and is associated with stress-related psychopathology. Previous reports have identified interactions between childhood trauma and sequence variation in the CRH receptor 1 gene (CRHR1) that increase risk for affective disorders. However, the underlying mechanisms that connect variation in CRHR1 to psychopathology are unknown. To explore potential mechanisms, we used a validated rhesus macaque model to investigate association between genetic variation in CRHR1, anxious temperament (AT) and brain metabolic activity. In young rhesus monkeys, AT is analogous to the childhood risk phenotype that predicts the development of human anxiety and depressive disorders. Regional brain metabolism was assessed with (18)F-labeled fluoro-2-deoxyglucose (FDG) positron emission tomography in 236 young, normally reared macaques that were also characterized for AT. We show that single nucleotide polymorphisms (SNPs) affecting exon 6 of CRHR1 influence both AT and metabolic activity in the anterior hippocampus and amygdala, components of the neural circuit underlying AT. We also find evidence for association between SNPs in CRHR1 and metabolism in the intraparietal sulcus and precuneus. These translational data suggest that genetic variation in CRHR1 affects the risk for affective disorders by influencing the function of the neural circuit underlying AT and that differences in gene expression or the protein sequence involving exon 6 may be important. These results suggest that variation in CRHR1 may influence brain function before any childhood adversity and may be a diathesis for the interaction between CRHR1 genotypes and childhood trauma reported to affect human psychopathology.
Brooks, Samantha J; Dalvie, Shareefa; Cuzen, Natalie L; Cardenas, Valerie; Fein, George; Stein, Dan J
2014-06-01
Previous neuroimaging studies link both alcohol use disorder (AUD) and early adversity to neurobiological differences in the adult brain. However, the association between AUD and childhood adversity and effects on the developing adolescent brain are less clear, due in part to the confound of psychiatric comorbidity. Here we examine early life adversity and its association with brain volume in a unique sample of 116 South African adolescents (aged 12-16) with AUD but without psychiatric comorbidity. Participants were 58 adolescents with DSM-IV alcohol dependence and with no other psychiatric comorbidities, and 58 age-, gender- and protocol-matched light/non-drinking controls (HC). Assessments included the Childhood Trauma Questionnaire (CTQ). MR images were acquired on a 3T Siemens Magnetom Allegra scanner. Volumes of global and regional structures were estimated using SPM8 Voxel Based Morphometry (VBM), with analysis of covariance (ANCOVA) and regression analyses. In whole brain ANCOVA analyses, a main effect of group when examining the AUD effect after covarying out CTQ was observed on brain volume in bilateral superior temporal gyrus. Subsequent regression analyses to examine how childhood trauma scores are linked to brain volumes in the total cohort revealed a negative correlation in the left hippocampus and right precentral gyrus. Furthermore, bilateral (but most significantly left) hippocampal volume was negatively associated with sub-scores on the CTQ in the total cohort. These findings support our view that some alterations found in brain volumes in studies of adolescent AUD may reflect the impact of confounding factors such as psychiatric comorbidity rather than the effects of alcohol per se. In particular, early life adversity may influence the developing adolescent brain in specific brain regions, such as the hippocampus.
Combes, Robert D
2013-11-01
Military research, testing, and surgical and resuscitation training, are aimed at mitigating the consequences of warfare and terrorism to armed forces and civilians. Traumatisation and tissue damage due to explosions, and acute loss of blood due to haemorrhage, remain crucial, potentially preventable, causes of battlefield casualties and mortalities. There is also the additional threat from inhalation of chemical and aerosolised biological weapons. The use of anaesthetised animal models, and their respective replacement alternatives, for military purposes -- particularly for blast injury, haemorrhaging and resuscitation training -- is critically reviewed. Scientific problems with the animal models include the use of crude, uncontrolled and non-standardised methods for traumatisation, an inability to model all key trauma mechanisms, and complex modulating effects of general anaesthesia on target organ physiology. Such effects depend on the anaesthetic and influence the cardiovascular system, respiration, breathing, cerebral haemodynamics, neuroprotection, and the integrity of the blood-brain barrier. Some anaesthetics also bind to the NMDA brain receptor with possible differential consequences in control and anaesthetised animals. There is also some evidence for gender-specific effects. Despite the fact that these issues are widely known, there is little published information on their potential, at best, to complicate data interpretation and, at worst, to invalidate animal models. There is also a paucity of detail on the anaesthesiology used in studies, and this can hinder correct data evaluation. Welfare issues relate mainly to the possibility of acute pain as a side-effect of traumatisation in recovered animals. Moreover, there is the increased potential for animals to suffer when anaesthesia is temporary, and the procedures invasive. These dilemmas can be addressed, however, as a diverse range of replacement approaches exist, including computer and mathematical dynamic modelling of the human body, cadavers, interactive human patient simulators for training, in vitro techniques involving organotypic cultures of target organs, and epidemiological and clinical studies. While the first four of these have long proven useful for developing protective measures and predicting the consequences of trauma, and although many phenomena and their sequelae arising from different forms of trauma in vivo can be induced and reproduced in vitro, non-animal approaches require further development, and their validation and use need to be coordinated and harmonised. Recommendations to these ends are proposed, and the scientific and welfare problems associated with animal models are addressed, with the future focus being on the use of batteries of complementary replacement methods deployed in integrated strategies, and on greater transparency and scientific cooperation. 2013 FRAME.
Bartanusz, Viktor; Corneille, Michael G; Sordo, Salvador; Gildea, Marianne; Michalek, Joel E; Nair, Prakash V; Stewart, Ronald M; Jezova, Daniela
2014-12-01
Acute trauma patients represent a specific subgroup of the critically ill population due to sudden and dramatic changes in homeostasis and consequently extreme demands on the activity of the hypothalamic-pituitary-adrenocortical (HPA) axis. Salivary cortisol is an accepted surrogate for serum free cortisol in the assessment of HPA axis function. The purpose of this study was (1) to establish the feasibility of salivary cortisol measurement in acute trauma patients in the neurosurgical-surgical intensive care unit (NSICU), and (2) to determine the diurnal pattern of salivary cortisol in the acute phase after injury. Saliva from 50 acute trauma patients was prospectively collected twice a day at 6AM and 4PM during the first week after injury in the NSICU. Mean PM cortisol concentrations were significantly higher in subjects versus controls (p<0.001). Subjects failed to develop the expected PM versus AM decrease in cortisol concentration seen in controls (p=0.005). Salivary cortisol did not vary significantly with baseline Glasgow Coma Scale (GCS), Injury Severity Score, sex, injury type, ethnicity, or age. When comparing mean AM and PM salivary cortisol by GCS severity category (GCS ⩽8 and GCS >8) the AM salivary cortisol was significantly higher in patients with GCS ⩽8 (p=0.002). The results show a loss of diurnal cortisol variation in acute trauma patient in the NSICU during the first week of hospitalization. Patients with severe brain injury had higher morning cortisol levels than those with mild/moderate brain injury. Copyright © 2014 Elsevier Ltd. All rights reserved.
Multicenter Retrospective Cohort Study of "Talk and Die" After Traumatic Brain Injury.
Shibahashi, Keita; Sugiyama, Kazuhiro; Okura, Yoshihiro; Hoda, Hidenori; Hamabe, Yuichi
2017-11-01
Patients who "talk and die" after traumatic brain injury (TBI) are potentially salvageable. The reported incidences and risk factors for the "talk and die" phenomenon are conflicting and do not take into account recent improvements in trauma care. The aim of this study was to determine the incidences of "talk and die" after TBI in a modern trauma care system, as well as associated risk factors. We identified patients who experienced TBI (abbreviated injury scale 3-5) between 2004 and 2015 who talked on admission (i.e., their verbal component on the Glasgow Coma Scale was ≥3 on admission) using a nationwide trauma registry (the Japan Trauma Data Bank). The end point was in-hospital mortality. We compared patients who talked and died with those who talked and survived. During the study period, 236,698 patients were registered in the database. Of the 24,833 patients who were eligible for analysis, 956 (4.0%) patients subsequently died in the hospital. The in-hospital mortality rate significantly decreased over the past 12 years. Older age; male sex; a higher injury severity score; a lower Glasgow Coma Scale score; comorbidities (congestive heart failure, chronic kidney disease, liver cirrhosis, and hematologic disorders); hypotension on arrival; subdural hemorrhage; contusion; and vault fracture were independently associated with higher in-hospital mortality. Even in modern trauma care systems, some patients still talk and die after TBI. We identified certain risk factors in patients with TBI that elicit the requirement for close observation, even if these patients talk after TBI. Copyright © 2017 Elsevier Inc. All rights reserved.
Concussion in Chronic Traumatic Encephalopathy
Stein, Thor D.; Alvarez, Victor E.; McKee, Ann C.
2015-01-01
Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease that occurs in association with repetitive mild traumatic brain injury. It is associated with a variety of clinical symptoms in multiple domains, and there is a distinct pattern of pathological changes. The abnormal tau pathology in CTE occurs uniquely in those regions of the brain that are likely most susceptible to stress concentration during trauma. CTE has been associated with a variety of types of repetitive head trauma, most frequently contact sports. In cases published to date, the mean length of exposure to repetitive head trauma was 15.4 years. The clinical symptoms of the disease began after a mean latency of 14.5 years with a mean age of death of 59.3 years. Most subjects had a reported history of concussions with a mean of 20.3. However, 16 % of published CTE subjects did not have a history of concussion suggesting that subconcussive hits are sufficient to lead to the development of CTE. Overall, the number of years of exposure, not the number of concussions, was significantly associated with worse tau pathology in CTE. This suggests that it is the chronic and repetitive nature of head trauma, irrespective of concussive symptoms, that is the most important driver of disease. CTE and exposure to repetitive head trauma is also associated with a variety of other neurodegenerations, including Alzheimer disease. In fact, amyloid β peptide deposition is altered and accelerated in CTE and is associated with worse disease. Here, we review the current exposure, clinical, and pathological associations of CTE. PMID:26260277
Trauma Imaging: A Literature Review.
Vela, Jason Heath; Wertz, Christopher Ira; Onstott, Kimberly L; Wertz, Joss R
2017-01-01
To inform radiologic technologists about which imaging modalities and examinations are best suited for evaluating specific anatomical structures in patients who have sustained a traumatic injury. Two scholarly research databases were searched to identify articles focused on trauma imaging of the head, cervical spine, thorax, abdomen, and pelvis. Articles focused on trauma diagnosis were excluded. Thirty-two articles were selected for analysis. Physical examination and plain-film radiographs typically are used to assess nasal bone fracures. Computed tomography (CT) can be used to assess zygomaticomaxillary complex, mandibular, and temporal bone fractures. Traumatic brain injuries are difficult to assess, and broad classifications are used. Depending on the severity of cervical spine trauma, plain-film radiographs or CT imaging is adequate, with magnetic resonance imaging used as a means for further evaluation. Trauma to the thorax typically is assessed with radiography and CT, and CT is recommended for assesment of abdominal and pelvic trauma. The literature was consistent regarding which examinations to perform to best evaluate suspected injuries to the chest, abdomen, and pelvis. The need for, and correct use of, imaging in evaluating trauma to the head and cervical spine is more controversial. Despite the need for additional research, emergency department care providers should be familiar with the structures most commonly injured during trauma and the role of medical imaging for diagnosis.
Lawrence, T; Bouamra, O; Woodford, M; Lecky, F; Hutchinson, P J
2016-01-01
Objectives To provide a comprehensive assessment of the management of traumatic brain injury (TBI) relating to epidemiology, complications and standardised mortality across specialist units. Design The Trauma Audit and Research Network collects data prospectively on patients suffering trauma across England and Wales. We analysed all data collected on patients with TBI between April 2014 and June 2015. Setting Data were collected on patients presenting to emergency departments across 187 hospitals including 26 with specialist neurosurgical services, incorporating factors previously identified in the Ps14 multivariate logistic regression (Ps14n) model multivariate TBI outcome prediction model. The frequency and timing of secondary transfer to neurosurgical centres was assessed. Results We identified 15 820 patients with TBI presenting to neurosurgical centres directly (6258), transferred from a district hospital to a neurosurgical centre (3682) and remaining in a district general hospital (5880). The commonest mechanisms of injury were falls in the elderly and road traffic collisions in the young, which were more likely to present in coma. In severe TBI (Glasgow Coma Score (GCS) ≤8), the median time from admission to imaging with CT scan is 0.5 hours. Median time to craniotomy from admission is 2.6 hours and median time to intracranial pressure monitoring is 3 hours. The most frequently documented complication of severe TBI is bronchopneumonia in 5% of patients. Risk-adjusted W scores derived from the Ps14n model indicate that no neurosurgical unit fell outside the 3 SD limits on a funnel plot. Conclusions We provide the first comprehensive report of the management of TBI in England and Wales, including data from all neurosurgical units. These data provide transparency and suggests equity of access to high-quality TBI management provided in England and Wales. PMID:27884843
Evaluation of the evidence for the trauma and fantasy models of dissociation.
Dalenberg, Constance J; Brand, Bethany L; Gleaves, David H; Dorahy, Martin J; Loewenstein, Richard J; Cardeña, Etzel; Frewen, Paul A; Carlson, Eve B; Spiegel, David
2012-05-01
The relationship between a reported history of trauma and dissociative symptoms has been explained in 2 conflicting ways. Pathological dissociation has been conceptualized as a response to antecedent traumatic stress and/or severe psychological adversity. Others have proposed that dissociation makes individuals prone to fantasy, thereby engendering confabulated memories of trauma. We examine data related to a series of 8 contrasting predictions based on the trauma model and the fantasy model of dissociation. In keeping with the trauma model, the relationship between trauma and dissociation was consistent and moderate in strength, and remained significant when objective measures of trauma were used. Dissociation was temporally related to trauma and trauma treatment, and was predictive of trauma history when fantasy proneness was controlled. Dissociation was not reliably associated with suggestibility, nor was there evidence for the fantasy model prediction of greater inaccuracy of recovered memory. Instead, dissociation was positively related to a history of trauma memory recovery and negatively related to the more general measures of narrative cohesion. Research also supports the trauma theory of dissociation as a regulatory response to fear or other extreme emotion with measurable biological correlates. We conclude, on the basis of evidence related to these 8 predictions, that there is strong empirical support for the hypothesis that trauma causes dissociation, and that dissociation remains related to trauma history when fantasy proneness is controlled. We find little support for the hypothesis that the dissociation-trauma relationship is due to fantasy proneness or confabulated memories of trauma. 2012 APA, all rights reserved
Designing a model for trauma system management using public health approach: the case of Iran.
Tarighi, Payam; Tabibi, Seyed Jamaledin; Motevalian, Seyed Abbas; Tofighi, Shahram; Maleki, Mohammad Reza; Delgoshaei, Bahram; Panahi, Farzad; Masoomi, Gholam Reza
2012-01-01
Trauma is a leading cause of death and disability around the world. Injuries are responsible for about six million deaths annually, of which ninety percent occur in developing countries. In Iran, injuries are the most common cause of death among age groups below fifty. Trauma system development is a systematic and comprehensive approach to injury prevention and treatment whose effectiveness has been proved. The present study aims at designing a trauma system management model as the first step toward trauma system establishment in Iran. In this qualitative research, a conceptual framework was developed based on the public health approach and three well-known trauma system models. We used Benchmarks, Indicators and Scoring (BIS) to analyze the current situation of Iran trauma care system. Then the trauma system management was designed using the policy development phase of public health approach The trauma system management model, validated by a panel of experts, describes lead agency, trauma system plan, policy-making councils, and data-based control according to the four main functions of management: leading, planning, organizing and controlling. This model may be implemented in two phases: the exclusive phase, focusing on resource integration and the inclusive phase, which concentrates on system development. The model could facilitate the development of trauma system in Iran through pilot studies as the assurance phase of public health approach. Furthermore, the model can provide a practical framework for trauma system management at the international level.
A viscoelastic analysis of the P56 mouse brain under large-deformation dynamic indentation.
MacManus, David B; Pierrat, Baptiste; Murphy, Jeremiah G; Gilchrist, Michael D
2017-01-15
The brain is a complex organ made up of many different functional and structural regions consisting of different types of cells such as neurons and glia, as well as complex anatomical geometries. It is hypothesized that the different regions of the brain exhibit significantly different mechanical properties which may be attributed to the diversity of cells within individual brain regions. The regional viscoelastic properties of P56 mouse brain tissue, up to 70μm displacement, are presented and discussed in the context of traumatic brain injury, particularly how the different regions of the brain respond to mechanical loads. Force-relaxation data obtained from micro-indentation measurements were fit to both linear and quasi-linear viscoelastic models to determine the time and frequency domain viscoelastic response of the pons, cortex, medulla oblongata, cerebellum, and thalamus. The damping ratio of each region was also determined. Each region was found to have a unique mechanical response to the applied displacement, with the pons and thalamus exhibiting the largest and smallest force-response, respectively. All brain regions appear to have an optimal frequency for the dissipation of energies which lies between 1 and 10Hz. We present the first mechanical characterization of the viscoelastic response for different regions of mouse brain. Force-relaxation tests are performed under large strain dynamic micro-indentation, and viscoelastic models are used subsequently, providing time-dependent mechanical properties of brain tissue under loading conditions comparable to what is experienced in TBI. The unique mechanical properties of different brain regions are highlighted, with substantial variations in the viscoelastic properties and damping ratio of each region. Cortex and pons were the stiffest regions, while the thalamus and medulla were most compliant. The cerebellum and thalamus had highest damping ratio values and those of the medulla were lowest. The reported material parameters can be implemented into finite element computer models of the mouse to investigate the effects of trauma on individual brain regions. Copyright © 2016 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved.
Improving survival rates after civilian gunshot wounds to the brain.
Joseph, Bellal; Aziz, Hassan; Pandit, Viraj; Kulvatunyou, Narong; O'Keeffe, Terence; Wynne, Julie; Tang, Andrew; Friese, Randall S; Rhee, Peter
2014-01-01
Gunshot wounds to the brain are the most lethal of all firearm injuries, with reported survival rates of 10% to 15%. The aim of this study was to determine outcomes in patients with gunshot wounds to the brain, presenting to our institution over time. We hypothesized that aggressive management can increase survival and the rate of organ donation in patients with gunshot wounds to the brain. We analyzed all patients with gunshot wounds to the brain presenting to our level 1 trauma center over a 5-year period. Aggressive management was defined as resuscitation with blood products, hyperosmolar therapy, and/or prothrombin complex concentrate (PCC). The primary outcome was survival and the secondary outcome was organ donation. There were 132 patients with gunshot wounds to the brain, and the survival rates increased incrementally every year, from 10% in 2008 to 46% in 2011, with the adoption of aggressive management. Among survivors, 40% (16 of 40) of the patients had bi-hemispheric injuries. Aggressive management with blood products (p = 0.02) and hyperosmolar therapy (p = 0.01) was independently associated with survival. Of the survivors, 20% had a Glasgow Coma Scale score ≥ 13 at hospital discharge. In patients who died (n = 92), 56% patients were eligible for organ donation, and they donated 60 organs. Aggressive management is associated with significant improvement in survival and organ procurement in patients with gunshot wounds to the brain. The bias of resource use can no longer be used to preclude trauma surgeons from abandoning aggressive attempts to save patients with gunshot wound to the brain. Published by Elsevier Inc.
Assessment of systemic administration of PEGylated IGF-1 in a mouse model of traumatic brain injury.
Sama, Diana M; Carlson, Shaun W; Joseph, Binoy; Saenger, Stefanie; Metzger, Friedrich; Saatman, Kathryn E
2018-06-06
Traumatic brain injury can result in lasting cognitive dysfunction due to degeneration of mature hippocampal neurons as well as the loss of immature neurons within the dentate gyrus. While endogenous neurogenesis affords a partial recovery of the immature neuron population, hippocampal neurogenesis may be enhanced through therapeutic intervention. Insulin-like growth factor-1 (IGF-1) has the potential to improve cognitive function and promote neurogenesis after TBI, but its short half-life in the systemic circulation makes it difficult to maintain a therapeutic concentration. IGF-1 modified with a polyethylene glycol moiety (PEG-IGF-1) exhibits improved stability and half-life while retaining its ability to enter the brain from the periphery, increasing its viability as a translational approach. The goal of this study was to evaluate the ability of systemic PEG-IGF-1 administration to attenuate acute neuronal loss and stimulate the recovery of hippocampal immature neurons in brain-injured mice. In a series of studies utilizing a well-established contusion brain injury model, PEG-IGF-1 was administered subcutaneously after injury. Serum levels of PEG were verified using ELISA and histological staining was used to investigate numbers of degenerating neurons and cortical contusion size at 24 h after injury. Immunofluorescent staining was used to evaluate numbers of immature neurons at 10 d after injury. Although subcutaneous injections of PEG-IGF-1 increased serum IGF-1 levels in a dose-dependent manner, no effects were observed on cortical contusion size, neurodegeneration within the dentate gyrus, or recovery of hippocampal immature neuron numbers. In contrast to its efficacy in rodent models of neurodegenerative diseases, PEG- IGF-1 was not effective in ameliorating early neuronal loss after contusion brain trauma.
The Epidemiology of Emergency Department Trauma Discharges in the United States.
DiMaggio, Charles J; Avraham, Jacob B; Lee, David C; Frangos, Spiros G; Wall, Stephen P
2017-10-01
Injury-related morbidity and mortality is an important emergency medicine and public health challenge in the United States. Here we describe the epidemiology of traumatic injury presenting to U.S. emergency departments (EDs), define changes in types and causes of injury among the elderly and the young, characterize the role of trauma centers and teaching hospitals in providing emergency trauma care, and estimate the overall economic burden of treating such injuries. We conducted a secondary retrospective, repeated cross-sectional study of the Nationwide Emergency Department Data Sample (NEDS), the largest all-payer ED survey database in the United States. Main outcomes and measures were survey-adjusted counts, proportions, means, and rates with associated standard errors (SEs) and 95% confidence intervals. We plotted annual age-stratified ED discharge rates for traumatic injury and present tables of proportions of common injuries and external causes. We modeled the association of Level I or II trauma center care with injury fatality using a multivariable survey-adjusted logistic regression analysis that controlled for age, sex, injury severity, comorbid diagnoses, and teaching hospital status. There were 181,194,431 (SE = 4,234) traumatic injury discharges from U.S. EDs between 2006 and 2012. There was a mean year-to-year decrease of 143 (95% CI = -184.3 to -68.5) visits per 100,000 U.S. population during the study period. The all-age, all-cause case-fatality rate for traumatic injuries across U.S. EDs during the study period was 0.17% (SE = 0.001%). The case-fatality rate for the most severely injured averaged 4.8% (SE = 0.001%), and severely injured patients were nearly four times as likely to be seen in Level I or II trauma centers (relative risk = 3.9 [95% CI = 3.7 to 4.1]). The unadjusted risk ratio, based on group counts, for the association of Level I or II trauma centers with mortality was risk ratio = 4.9 (95% CI = 4.5 to 5.3); however, after sex, age, injury severity, and comorbidities were accounted for, Level I or II trauma centers were not associated with an increased risk of fatality (odds ratio = 0.96 [95% CI = 0.79 to 1.18]). There were notable changes at the extremes of age in types and causes of ED discharges for traumatic injury between 2009 and 2012. Age-stratified rates of diagnoses of traumatic brain injury increased 29.5% (SE = 2.6%) for adults older than 85 and increased 44.9% (SE = 1.3%) for children younger than 18. Firearm-related injuries increased 31.7% (SE = 0.2%) in children 5 years and younger. The total inflation-adjusted cost of ED injury care in the United States between 2006 and 2012 was $99.75 billion (SE = $0.03 billion). Emergency departments are a sensitive barometer of the continuing impact of traumatic injury as an important cause of morbidity and mortality in the United States. Level I or II trauma centers remain a bulwark against the tide of severe trauma in the United States, but the types and causes of traumatic injury in the United States are changing in consequential ways, particularly at the extremes of age, with traumatic brain injuries and firearm-related trauma presenting increased challenges. © 2017 by the Society for Academic Emergency Medicine.
Zuckerman, Scott L; Prather, Colin T; Yengo-Kahn, Aaron M; Solomon, Gary S; Sills, Allen K; Bonfield, Christopher M
2016-04-01
OBJECTIVE Arachnoid cysts (ACs) are congenital lesions bordered by an arachnoid membrane. Researchers have postulated that individuals with an AC demonstrate a higher rate of structural brain injury after trauma. Given the potential neurological consequences of a structural brain injury requiring neurosurgical intervention, the authors sought to perform a systematic review of sport-related structural-brain injury associated with ACs with a corresponding quantitative analysis. METHODS Titles and abstracts were searched systematically across the following databases: PubMed, Embase, CINAHL, and PsycINFO. The review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement. Peer-reviewed case reports, case series, or observational studies that reported a structural brain injury due to a sport or recreational activity (hereafter referred to as sport-related) with an associated AC were included. Patients were excluded if they did not have an AC, suffered a concussion without structural brain injury, or sustained the injury during a non-sport-related activity (e.g., fall, motor vehicle collision). Descriptive statistical analysis and time to presentation data were summarized. Univariate logistic regression models to assess predictors of neurological deficit, open craniotomy, and cystoperitoneal shunt were completed. RESULTS After an initial search of 994 original articles, 52 studies were found that reported 65 cases of sport-related structural brain injury associated with an AC. The median age at presentation was 16 years (range 4-75 years). Headache was the most common presenting symptom (98%), followed by nausea and vomiting in 49%. Thirteen patients (21%) presented with a neurological deficit, most commonly hemiparesis. Open craniotomy was the most common form of treatment (49%). Bur holes and cyst fenestration were performed in 29 (45%) and 31 (48%) patients, respectively. Seven patients (11%) received a cystoperitoneal shunt. Four cases reported medical management only without any surgical intervention. No significant predictors were found for neurological deficit or open craniotomy. In the univariate model predicting the need for a cystoperitoneal shunt, the odds of receiving a shunt decreased as age increased (p = 0.004, OR 0.62 [95% CI 0.45-0.86]) and with male sex (p = 0.036, OR 0.15 [95% CI 0.03-0.88]). CONCLUSIONS This systematic review yielded 65 cases of sport-related structural brain injury associated with ACs. The majority of patients presented with chronic symptoms, and recovery was reported generally to be good. Although the review is subject to publication bias, the authors do not find at present that there is contraindication for patients with an AC to participate in sports, although parents and children should be counseled appropriately. Further studies are necessary to better evaluate AC characteristics that could pose a higher risk of adverse events after trauma.
Evaluation of SOCOM Wireless Monitor in Trauma Patients
2016-02-01
the need for craniotomy in the absence of neurologic change. J Trauma Acute Care Surg 2013 Apr;74(4):967-75. 35) Thorson CM, Van Haren RM, Ryan...Guarch GA, Hanna M, Allen CJ, Ray JJ, Schulman CI, Proctor KG, Sleeman D, Namias N: Need for percutaneous drainage after cholecystectomy is higher in...Repeat head CT after minimal brain injury predicts need for craniotomy in absence of neurologic change. a. Presented at 71rst Annual Meeting of
Neural and Behavioral Sequelae of Blast-Related Traumatic Brain Injury
2012-11-01
testing and advanced MRI techniques [task-activated functional MRI (fMRI) and diffusion tensor imaging ( DTI )] to gain a comprehensive understanding of... DTI fiber tracking) and neurobehavioral testing (computerized assessment and standard neuropsychological testing) on 60 chronic trauma patients: 15...data analysis. 15. SUBJECT TERMS Blast-related traumatic brain injury (TBI), fMRI, DTI , cognition 16. SECURITY CLASSIFICATION OF: 17. LIMITATION
ERIC Educational Resources Information Center
Max, Jeffrey E.; Schachar, Russell J.; Levin, Harvey S.; Ewing-Cobbs, Linda; Chapman, Sandra B.; Dennis, Maureen; Saunders, Ann; Landis, Julie
2005-01-01
Objective: To assess the phenomenology and predictive factors of attention-deficit/hyperactivity disorder (ADHD) after traumatic brain injury (TBI), also called secondary ADHD (SADHD). Method: Children without preinjury ADHD 5-14 years old with TBI from consecutive admissions (n = 143) to five trauma centers were observed prospectively from 6 to…
ERIC Educational Resources Information Center
Fraas, Michael R.
2015-01-01
Survivors of brain injury from trauma and stroke often lose their sense of identity and face a series of lifelong obstacles that challenge their ability to integrate back into their communities and live meaningful and productive lives. Their stories provide powerful accounts of these challenges, which can inform clinical decision-making. Arguably,…
ERIC Educational Resources Information Center
Kramer, Michaela M.; Davies, Susan C.
2016-01-01
Students who have sustained traumatic brain injuries (TBIs) may experience a number of consequences, all of which can impede the transition from high school to postsecondary educational settings. This study, which relied on interviews with students who had sustained TBIs and who had persistent problems related to their traumas, helped gain an…
Elzinga, B M; Bremner, J D
2002-06-01
A model for the posttraumatic stress disorder (PTSD) as a disorder of memory is presented drawing both on psychological and neurobiological data. Evidence on intrusive memories and deficits in declarative memory function in PTSD-patients is reviewed in relation to three brain areas that are involved in memory functioning and the stress response: the hippocampus, amygdala, and the prefrontal cortex. Neurobiological studies have shown that the noradrenergic stress-system is involved in enhanced encoding of emotional memories, sensitization, and fear conditioning, by way of its effects on the amygdala. Chronic stress also affects the hippocampus, a brain area involved in declarative memories, suggesting that hippocampal dysfunction may partly account for the deficits in declarative memory in PTSD-patients. Deficits in the medial prefrontal cortex, a structure that normally inhibits the amygdala, may further enhance the effects of the amygdala, thereby increasing the frequency and intensity of the traumatic memories. Thus, by way of its influence on these brain structures, exposure to severe stress may simultaneously result in strong emotional reactions and in difficulties to recall the emotional event. This model is also relevant for understanding the distinction between declarative and non-declarative memory-functions in processing trauma-related information in PTSD. Implications of our model are reviewed.
Elzinga, B.M.; Bremner, J.D.
2017-01-01
A model for the posttraumatic stress disorder (PTSD) as a disorder of memory is presented drawing both on psychological and neurobiological data. Evidence on intrusive memories and deficits in declarative memory function in PTSD-patients is reviewed in relation to three brain areas that are involved in memory functioning and the stress response: the hippocampus, amygdala, and the prefrontal cortex. Neurobiological studies have shown that the noradrenergic stress-system is involved in enhanced encoding of emotional memories, sensitization, and fear conditioning, by way of its effects on the amygdala. Chronic stress also affects the hippocampus, a brain area involved in declarative memories, suggesting that hippocampal dysfunction may partly account for the deficits in declarative memory in PTSD-patients. Deficits in the medial prefrontal cortex, a structure that normally inhibits the amygdala, may further enhance the effects of the amygdala, thereby increasing the frequency and intensity of the traumatic memories. Thus, by way of its influence on these brain structures, exposure to severe stress may simultaneously result in strong emotional reactions and in difficulties to recall the emotional event. This model is also relevant for understanding the distinction between declarative and non-declarative memory-functions in processing trauma-related information in PTSD. Implications of our model are reviewed. PMID:12113915
Gomez, David; Byrne, James P; Alali, Aziz S; Xiong, Wei; Hoeft, Chris; Neal, Melanie; Subacius, Harris; Nathens, Avery B
2017-12-01
The Glasgow Coma Scale (GCS) is the most widely used measure of traumatic brain injury (TBI) severity. Currently, the arrival GCS motor component (mGCS) score is used in risk-adjustment models for external benchmarking of mortality. However, there is evidence that the highest mGCS score in the first 24 hours after injury might be a better predictor of death. Our objective was to evaluate the impact of including the highest mGCS score on the performance of risk-adjustment models and subsequent external benchmarking results. Data were derived from the Trauma Quality Improvement Program analytic dataset (January 2014 through March 2015) and were limited to the severe TBI cohort (16 years or older, isolated head injury, GCS ≤8). Risk-adjustment models were created that varied in the mGCS covariates only (initial score, highest score, or both initial and highest mGCS scores). Model performance and fit, as well as external benchmarking results, were compared. There were 6,553 patients with severe TBI across 231 trauma centers included. Initial and highest mGCS scores were different in 47% of patients (n = 3,097). Model performance and fit improved when both initial and highest mGCS scores were included, as evidenced by improved C-statistic, Akaike Information Criterion, and adjusted R-squared values. Three-quarters of centers changed their adjusted odds ratio decile, 2.6% of centers changed outlier status, and 45% of centers exhibited a ≥0.5-SD change in the odds ratio of death after including highest mGCS score in the model. This study supports the concept that additional clinical information has the potential to not only improve the performance of current risk-adjustment models, but can also have a meaningful impact on external benchmarking strategies. Highest mGCS score is a good potential candidate for inclusion in additional models. Copyright © 2017 American College of Surgeons. Published by Elsevier Inc. All rights reserved.
Kassis, Hayah; Marnejon, Thomas; Gemmel, David; Cutrona, Anthony; Gottimukkula, Rajashree
2010-06-01
A 19-year-old male patient was diagnosed with S. sanguinis brain abscess of unknown etiopathology as a complication of subclinical endocarditis. While viridans streptococci are implicated in dental seeding to the heart, S. sanguinis brain abscesses are rare. Six previous cases of S. sanguinis brain abscess in the literature reported dental procedures and maxillofacial trauma. In our patient, there was no obvious source of infective endocarditis preceding the development of brain abscess. This demonstrates the importance of prompt diagnosis and initiation of antimicrobial therapy given the potential for long-term sequelae such as focal deficits and seizures.
Menut, R; Larrieu, N; Conil, J-M; Georges, B; Fourcade, O; Geeraerts, T
2013-10-01
Traumatic brain injuries are fairly sensitive to hypoxia. For patient with associated lung and brain traumas, different means used to improve oxygen blood level are poorly described. We report the use of ECMO in a refractory hypoxemia occurred to a multitrauma young patient with neurological lesions. Copyright © 2013 Société française d’anesthésie et de réanimation (Sfar). Published by Elsevier SAS. All rights reserved.
Simulation of blast-induced, early-time intracranial wave physics leading to traumatic brain injury.
DOE Office of Scientific and Technical Information (OSTI.GOV)
Taylor, Paul Allen; Ford, Corey C.
U.S. soldiers are surviving blast and impacts due to effective body armor, trauma evacuation and care. Blast injuries are the leading cause of traumatic brain injury (TBI) in military personnel returning from combat. Understanding of Primary Blast Injury may be needed to develop better means of blast mitigation strategies. The objective of this paper is to investigate the effects of blast direction and strength on the resulting mechanical stress and wave energy distributions generated in the brain.
Central diabetes insipidus in pediatric severe traumatic brain injury.
Alharfi, Ibrahim M; Stewart, Tanya Charyk; Foster, Jennifer; Morrison, Gavin C; Fraser, Douglas D
2013-02-01
To determine the occurrence rate of central diabetes insipidus in pediatric patients with severe traumatic brain injury and to describe the clinical, injury, biochemical, imaging, and intervention variables associated with mortality. Retrospective chart and imaging review. Children's Hospital, level 1 trauma center. Severely injured (Injury Severity Score ≥ 12) pediatric trauma patients (>1 month and <18 yr) with severe traumatic brain injury (presedation Glasgow Coma Scale ≤ 8 and head Maximum Abbreviated Injury Scale ≥ 4) that developed acute central diabetes insipidus between January 2000 and December 2011. Of 818 severely injured trauma patients, 180 had severe traumatic brain injury with an overall mortality rate of 27.2%. Thirty-two of the severe traumatic brain injury patients developed acute central diabetes insipidus that responded to desamino-8-D-arginine vasopressin and/or vasopressin infusion, providing an occurrence rate of 18%. At the time of central diabetes insipidus diagnosis, median urine output and serum sodium were 6.8 ml/kg/hr (interquartile range = 5-11) and 154 mmol/L (interquartile range = 149-159), respectively. The mortality rate of central diabetes insipidus patients was 87.5%, with 71.4% declared brain dead after central diabetes insipidus diagnosis. Early central diabetes insipidus onset, within the first 2 days of severe traumatic brain injury, was strongly associated with mortality (p < 0.001), as were a lower presedation Glasgow Coma Scale (p = 0.03), a lower motor Glasgow Coma Scale (p = 0.01), an occurrence of fixed pupils (p = 0.04), and a prolonged partial thromboplastin time (p = 0.04). Cerebral edema on the initial computed tomography, obtained in the first 24 hrs after injury, was the only imaging finding associated with death (p = 0.002). Survivors of central diabetes insipidus were more likely to have intracranial pressure monitoring (p = 0.03), have thiopental administered to induce coma (p = 0.04) and have received a decompressive craniectomy for elevated intracranial pressure (p = 0.04). The incidence of central diabetes insipidus in pediatric patients with severe traumatic brain injury is 18%. Mortality was associated with early central diabetes insipidus onset and cerebral edema on head computed tomography. Central diabetes insipidus nonsurvivors were less likely to have received intracranial pressure monitoring, thiopental coma and decompressive craniectomy.
Photon dynamics in tissue imaging
NASA Astrophysics Data System (ADS)
Chance, Britton; Haselgrove, John C.; Wang, NaiGuang; Maris, Michael B.; Sevick-Muraca, Eva M.
1991-11-01
The emerging need for a fast, safe economical approach to global and localized measures of desaturation of hemoglobin with oxygen (HbO2) in the human brain motivates further research on time-resolved spectroscopy in four areas of study. (1) To afford quantization of hemoglobin saturation through time-resolved spectroscopy in the time domain (TD) and in the frequency domain (FD). Evaluation of dual-wavelength TD and FD spectrometers for determining quantitatively hemoglobin desaturation and blood-volume changes by calculations that are insensitive to mutual interference is proposed. The diffusion equation, as it applies especially to TD studies, and the absorption ((mu) a) and scattering ((mu) s) coefficients provide their independent determination from the late and early respective portions of the kinetics of the emergent photons in response to a short input pulse (50-100 psec). (2) The identification of the photon-pathlength change due to the arterial pulse in the brain tissue by FD methods with Fourier transformation affords an opportunity to employ principles of pulse oximetry to vessels localized deep within the brain tissue. (3) Localization of desaturation of hemoglobin in portions of the brain can be achieved through dual-wavelength scanning of the input/output optical fibers across the head for an X-Y coordinate and varying the distance between input and output ((rho) ) or the time delay in data acquisition to afford an in-depth Z scan. Localizations of shed blood, which have an effective concentration of over 10 times that of capillary-bed blood, are identified by X, Y, Z scans using only a single wavelength. (4) Independent measurements of absorption ((mu) a) and scattering ((mu) s) coefficients, particularly by TD techniques, affords structural mapping of the brain, which can be used to diagnose brain tumor and neuronal degeneration. Two experimental systems are used to critically evaluate these studies; the first, a hemoglobin/lipid/yeast model in which intermittent oxygenation gives saturation/desaturation effects and addition of hemoglobin simulates increased blood volume. These models can be global or may contain localized ''black'' absorbers simulating brain bleeds or model-stroke volumes in which oxygenation/deoxygenation simulates normoxia/hypoxia. Secondly, animal brains are used to model the following changes in vivo: global or localized hypoxia, brain bleeding, and hematomas by epidural blood injection, and physiological changes by epilepsy. Neuronal degeneration causing scattering effects is modeled by injection, epidurally or into the animal model brain, highly scattering material such as polystyrene spheres. The proposal envisages a basic science study of photon migration in the brain with important applications to stroke, epilepsy, brain trauma, and neuronal degenerative disease.
Jin, Guang; DeMoya, Marc A; Duggan, Michael; Knightly, Thomas; Mejaddam, Ali Y; Hwabejire, John; Lu, Jennifer; Smith, William Michael; Kasotakis, Georgios; Velmahos, George C; Socrate, Simona; Alam, Hasan B
2012-07-01
Traumatic brain injury (TBI) and hemorrhagic shock (HS) are the leading causes of trauma-related mortality and morbidity. Combination of TBI and HS (TBI + HS) is highly lethal, and the optimal resuscitation strategy for this combined insult remains unclear. A critical limitation is the lack of suitable large animal models to test different treatment strategies. We have developed a clinically relevant large animal model of TBI + HS, which was used to evaluate the impact of different treatments on brain lesion size and associated edema. Yorkshire swine (42-50 kg) were instrumented to measure hemodynamic parameters and intracranial pressure. A computer-controlled cortical impact device was used to create a TBI through a 20-mm craniotomy: 15-mm cylindrical tip impactor at 4 m/s velocity, 100-ms dwell time, and 12-mm penetration depth. Volume-controlled hemorrhage was started (40% blood volume) concurrent with the TBI. After 2 h of shock, animals were randomized to one of three resuscitation groups (n = 5/group): (a) normal saline (NS); (b) 6% hetastarch, Hextend (Hex); and (c) fresh frozen plasma (FFP). Volumes of Hex and FFP matched the shed blood, whereas NS was three times the volume. After 6 h of postresuscitation monitoring, brains were sectioned into 5-mm slices and stained with TTC (2,3,5-triphenyltetrazolium chloride) to quantify the lesion size and brain swelling. Combination of 40% blood loss with cortical impact and a period of shock (2 h) resulted in a highly reproducible brain injury. Total fluid requirements were lower in the Hex and FFP groups. Lesion size and brain swelling in the FFP group (2,160 ± 202.63 mm and 22% ± 1.0%, respectively) were significantly smaller than those in the NS group (3,285 ± 130.8 mm3 and 37% ± 1.6%, respectively) (P < 0.05). Hex treatment decreased the swelling (29% ± 1.6%) without reducing the lesion size. Early administration of FFP reduces the size of brain lesion and associated swelling in a large animal model of TBI + HS. In contrast, artificial colloid (Hex) decreases swelling without reducing the actual size of the brain lesion.
Mete, Mesut; Aydemir, Isıl; Unsal, Ulkun Unlu; Collu, Fatih; Vatandas, Gokhan; Gurcu, Beyhan; Duransoy, Yusuf Kurtulus; Taneli, Fatma; Tugrul, Mehmet Ibrahim; Selcuki, Mehmet
2017-11-01
TBI has two distinct phases: primary and secondary injury. Many agents have been used to prevent secondary injury. Oleocanthal (OC) has anti-inflammatory and antioxidant properties similar nonsteroidal anti-inflammatory drug. We evaluated the neuroprotective effects of OC in a rat model of TBI. Twenty-six adult male, Wistar albino rats were used. The rats were divided into 4 groups. group 1, sham (n = 5). group 2, trauma (n = 5): Rats were treated with 10 mg/kg saline intraperitoneally (IP) twice a day. Groups 3 and 4, rats were treated with 10 (group 3, n = 8) or 30 (group 4, n = 8) mg/kg OC IP twice a day. For each group brain samples were collected 72 h after injury. Brain samples and blood were evaluated with histopathological and biochemical methods. Histopathological evaluation revealed a significant difference between group 2 and group 4. Biochemical findings demonstrated that, oxidative stress index was the highest in group 2 and was the lowest in the group 4. Results indicated that OC has a protective effect on neural cells after TBI. This effect is achieved by reducing oxidative stress and apoptosis.
Therapeutic Potential of Intravenous Immunoglobulin in Acute Brain Injury
Thom, Vivien; Arumugam, Thiruma V.; Magnus, Tim; Gelderblom, Mathias
2017-01-01
Acute ischemic and traumatic injury of the central nervous system (CNS) is known to induce a cascade of inflammatory events that lead to secondary tissue damage. In particular, the sterile inflammatory response in stroke has been intensively investigated in the last decade, and numerous experimental studies demonstrated the neuroprotective potential of a targeted modulation of the immune system. Among the investigated immunomodulatory agents, intravenous immunoglobulin (IVIg) stand out due to their beneficial therapeutic potential in experimental stroke as well as several other experimental models of acute brain injuries, which are characterized by a rapidly evolving sterile inflammatory response, e.g., trauma, subarachnoid hemorrhage. IVIg are therapeutic preparations of polyclonal immunoglobulin G, extracted from the plasma of thousands of donors. In clinical practice, IVIg are the treatment of choice for diverse autoimmune diseases and various mechanisms of action have been proposed. Only recently, several experimental studies implicated a therapeutic potential of IVIg even in models of acute CNS injury, and suggested that the immune system as well as neuronal cells can directly be targeted by IVIg. This review gives further insight into the role of secondary inflammation in acute brain injury with an emphasis on stroke and investigates the therapeutic potential of IVIg. PMID:28824617
Early fever after trauma: Does it matter?
Hinson, Holly E; Rowell, Susan; Morris, Cynthia; Lin, Amber L; Schreiber, Martin A
2018-01-01
Fever is strongly associated with poor outcome after traumatic brain injury (TBI). We hypothesized that early fever is a direct result of brain injury and thus would be more common in TBI than in patients without brain injury and associated with inflammation. We prospectively enrolled patients with major trauma with and without TBI from a busy Level I trauma center intensive care unit (ICU). Patients were assigned to one of four groups based on their presenting Head Abbreviated Injury Severity Scale scores: multiple injuries: head Abbreviated Injury Scale (AIS) score greater than 2, one other region greater than 2; isolated head: head AIS score greater than 2, all other regions less than 3; isolated body: one region greater than 2, excluding head/face; minor injury: no region with AIS greater than 2. Early fever was defined as at least one recorded temperature greater than 38.3°C in the first 48 hours after admission. Outcome measures included neurologic deterioration, length of stay in the ICU, hospital mortality, discharge Glasgow Outcome Scale-Extended, and plasma levels of seven key cytokines at admission and 24 hours (exploratory). Two hundred sixty-eight patients were enrolled, including subjects with multiple injuries (n = 59), isolated head (n = 97), isolated body (n = 100), and minor trauma (n = 12). The incidence of fever was similar in all groups irrespective of injury (11-24%). In all groups, there was a significant association between the presence of early fever and death in the hospital (6-18% vs. 0-3%), as well as longer median ICU stays (3-7 days vs. 2-3 days). Fever was significantly associated with elevated IL-6 at admission (50.7 pg/dL vs. 16.9 pg/dL, p = 0.0067) and at 24 hours (83.1 pg/dL vs. 17.1 pg/dL, p = 0.0025) in the isolated head injury group. Contrary to our hypothesis, early fever was not more common in patients with brain injury, though fever was associated with longer ICU stays and death in all groups. Additionally, fever was associated with elevated IL-6 levels in isolated head injury. Prognostic and Epidemiological study, level III.
Abbas, Kausar; Shenk, Trey E; Poole, Victoria N; Breedlove, Evan L; Leverenz, Larry J; Nauman, Eric A; Talavage, Thomas M; Robinson, Meghan E
2015-03-01
Long-term neurological damage as a result of head trauma while playing sports is a major concern for football athletes today. Repetitive concussions have been linked to many neurological disorders. Recently, it has been reported that repetitive subconcussive events can be a significant source of accrued damage. Since football athletes can experience hundreds of subconcussive hits during a single season, it is of utmost importance to understand their effect on brain health in the short and long term. In this study, resting-state functional magnetic resonance imaging (rs-fMRI) was used to study changes in the default mode network (DMN) after repetitive subconcussive mild traumatic brain injury. Twenty-two high school American football athletes, clinically asymptomatic, were scanned using the rs-fMRI for a single season. Baseline scans were acquired before the start of the season, and follow-up scans were obtained during and after the season to track the potential changes in the DMN as a result of experienced trauma. Ten noncollision-sport athletes were scanned over two sessions as controls. Overall, football athletes had significantly different functional connectivity measures than controls for most of the year. The presence of this deviation of football athletes from their healthy peers even before the start of the season suggests a neurological change that has accumulated over the years of playing the sport. Football athletes also demonstrate short-term changes relative to their own baseline at the start of the season. Football athletes exhibited hyperconnectivity in the DMN compared to controls for most of the sessions, which indicates that, despite the absence of symptoms typically associated with concussion, the repetitive trauma accrued produced long-term brain changes compared to their healthy peers.
Sundman, Mark H; Hall, Eric E; Chen, Nan-kuei
2014-01-01
Traumatic brain injuries (TBI) are induced by sudden acceleration-deceleration and/or rotational forces acting on the brain. Diffuse axonal injury (DAI) has been identified as one of the chief underlying causes of morbidity and mortality in head trauma incidents. DAIs refer to microscopic white matter (WM) injuries as a result of shearing forces that induce pathological and anatomical changes within the brain, which potentially contribute to significant impairments later in life. These microscopic injuries are often unidentifiable by the conventional computed tomography (CT) and magnetic resonance (MR) scans employed by emergency departments to initially assess head trauma patients and, as a result, TBIs are incredibly difficult to diagnose. The impairments associated with TBI may be caused by secondary mechanisms that are initiated at the moment of injury, but often have delayed clinical presentations that are difficult to assess due to the initial misdiagnosis. As a result, the true consequences of these head injuries may go unnoticed at the time of injury and for many years thereafter. The purpose of this review is to investigate these consequences of TBI and their potential link to neurodegenerative disease (ND). This review will summarize the current epidemiological findings, the pathological similarities, and new neuroimaging techniques that may help delineate the relationship between TBI and ND. Lastly, this review will discuss future directions and propose new methods to overcome the limitations that are currently impeding research progress. It is imperative that improved techniques are developed to adequately and retrospectively assess TBI history in patients that may have been previously undiagnosed in order to increase the validity and reliability across future epidemiological studies. The authors introduce a new surveillance tool (Retrospective Screening of Traumatic Brain Injury Questionnaire, RESTBI) to address this concern. PMID:25324979
Daskalakis, Nikolaos P; Cohen, Hagit; Cai, Guiqing; Buxbaum, Joseph D; Yehuda, Rachel
2014-09-16
Delineating the molecular basis of individual differences in the stress response is critical to understanding the pathophysiology and treatment of posttraumatic stress disorder (PTSD). In this study, 7 d after predator-scent-stress (PSS) exposure, male and female rats were classified into vulnerable (i.e., "PTSD-like") and resilient (i.e., minimally affected) phenotypes on the basis of their performance on a variety of behavioral measures. Genome-wide expression profiling in blood and two limbic brain regions (amygdala and hippocampus), followed by quantitative PCR validation, was performed in these two groups of animals, as well as in an unexposed control group. Differentially expressed genes were identified in blood and brain associated with PSS-exposure and with distinct behavioral profiles postexposure. There was a small but significant between-tissue overlap (4-21%) for the genes associated with exposure-related individual differences, indicating convergent gene expression in both sexes. To uncover convergent signaling pathways across tissue and sex, upstream activated/deactivated transcription factors were first predicted for each tissue and then the respective pathways were identified. Glucocorticoid receptor (GR) signaling was the only convergent pathway associated with individual differences when using the most stringent statistical threshold. Corticosterone treatment 1 h after PSS-exposure prevented anxiety and hyperarousal 7 d later in both sexes, confirming the GR involvement in the PSS behavioral response. In conclusion, genes and pathways associated with extreme differences in the traumatic stress behavioral response can be distinguished from those associated with trauma exposure. Blood-based biomarkers can predict aspects of brain signaling. GR signaling is a convergent signaling pathway, associated with trauma-related individual differences in both sexes.
Rau, Cheng-Shyuan; Liu, Hang-Tsung; Hsu, Shiun-Yuan; Cho, Tzu-Yu; Hsieh, Ching-Hua
2014-01-01
Objectives To provide an overview of the demographic characteristics of patients with positive blood alcohol concentration (BAC) and to investigate the performance of brain CT scans in these patients. Design Cross-sectional study. Setting Taiwan. Participants 2192 patients who had undergone a test for blood alcohol of 13 233 patients registered in the Trauma Registry System between 1 January 2009 and 31 December 2012. A BAC level of 50 mg/dL was defined as the cut-off value. Detailed information was retrieved from the patients with positive BAC (n=793) and was compared with information from those with a negative BAC (n=1399). Main outcome measures Glasgow Coma Scale (GCS) and Injury Severity Score (ISS) as well as the performance and findings of obtained brain CT scans. Results Patients with positive BAC had a higher rate of face injury, but a lower GCS score, a lower rate of head and neck injury, a lower ISS and New Injury Severity Score. Alcohol use was associated with a shorter length of hospital stay (8.6 vs 11.4 days, p=0.000) in patients with an ISS of <16. Of 496 patients with positive BAC who underwent brain CT, 164 (33.1%) showed positive findings on CT scan. In contrast, of 891 patients with negative BAC who underwent brain CT, 389 (43.7%) had positive findings on CT scan. The lower percentage of positive CT scan findings in patients with positive BAC was particularly evident in patients with an ISS <16 (18.0% vs 28.8%, p=0.001). Conclusions Patients who consumed alcohol tended to have a low GCS score and injuries that were less severe. However, given the significantly low percentage of positive findings, brain CT might be overused in these patients with less severe injuries. PMID:25361838
Mollica, Richard F; Lyoo, In Kyoon; Chernoff, Miriam C; Bui, Hoan X; Lavelle, James; Yoon, Sujung J; Kim, Jieun E; Renshaw, Perry F
2009-11-01
A pilot study of South Vietnamese ex-political detainees who had been incarcerated in Vietnamese reeducation camps and resettled in the United States disclosed significant mental health problems associated with torture and traumatic head injury (THI). To identify structural brain alterations associated with THI and to investigate whether these deficits are associated with posttraumatic stress disorder and depression. Cross-sectional neuroimaging study. Massachusetts General Hospital and McLean Hospital. A subsample of Vietnamese ex-political detainees (n = 42) and comparison subjects (n = 16) selected from a community study of 337 ex-political detainees and 82 comparison subjects. Scores on the Vietnamese versions of the Hopkins Symptom Checklist-25 (HSCL) and Harvard Trauma Questionnaire for depression and posttraumatic stress disorder, respectively; cerebral regional cortical thickness; and manual volumetric morphometry of the amygdala, hippocampus, and thalamus. Ex-political detainees exposed to THI (n = 16) showed a higher rate of depression (odds ratio, 10.2; 95% confidence interval, 1.2-90.0) than those without THI exposure (n = 26). Ex-political detainees with THI had thinner prefrontotemporal cortices than those without THI exposure (P < .001 by the statistical difference brain map) in the left dorsolateral prefrontal and bilateral superior temporal cortices, controlling for age, handedness, and number of trauma/torture events (left superior frontal cortex [SFC], P = .006; left middle frontal cortex, P = .01; left superior temporal cortex [STC], P = .007; right STC, P = .01). Trauma/torture events were associated with bilateral amygdala volume loss (left, P = .045; right, P = .003). Cortical thinning associated with THI in the left SFC and bilateral STC was related to HSCL depression scores in THI-exposed (vs non-THI-exposed) ex-political detainees (left SFC, P for interaction = .007; left STC, P for interaction = .03; right STC, P for interaction = .02). Structural deficits in prefrontotemporal brain regions are linked to THI exposures. These brain lesions are associated with the symptom severity of depression in Vietnamese ex-political detainees.
Wang, Shang-Yu; Liao, Chien-Hung; Fu, Chih-Yuan; Kang, Shih-Ching; Ouyang, Chun-Hsiang; Kuo, I-Ming; Lin, Jr-Rung; Hsu, Yu-Pao; Yeh, Chun-Nan; Chen, Shao-Wei
2014-04-28
We present a series of patients with blunt abdominal trauma who underwent damage control laparotomy (DCL) and introduce a nomogram that we created to predict survival among these patients. This was a retrospective study. From January 2002 to June 2012, 91 patients underwent DCL for hemorrhagic shock. We excluded patients with the following characteristics: a penetrating abdominal injury, age younger than 18 or older than 65 years, a severe or life-threatening brain injury (Abbreviated Injury Scale [AIS] ≥ 4), emergency department (ED) arrival more than 6 hours after injury, pregnancy, end-stage renal disease, or cirrhosis. In addition, we excluded patients who underwent DCL after ICU admission or later in the course of hospitalization. The overall mortality rate was 61.5%: 35 patients survived and 56 died. We identified independent survival predictors, which included a preoperative Glasgow Coma Scale (GCS) score < 8 and a base excess (BE) value < -13.9 mEq/L. We created a nomogram for outcome prediction that included four variables: preoperative GCS, initial BE, preoperative diastolic pressure, and preoperative cardiopulmonary cerebral resuscitation (CPCR). DCL is a life-saving procedure performed in critical patients, and devastating clinical outcomes can be expected under such dire circumstances as blunt abdominal trauma with exsanguination. The nomogram presented here may provide ED physicians and trauma surgeons with a tool for early stratification and risk evaluation in critical, exsanguinating patients.
A Policy Relevant US Trauma Care System Pragmatic Trial for PTSD and Comorbidity
2016-05-18
Posttraumatic Stress Disorder; Depression; Alcohol-Related Disorders; Suicidal Ideation; Substance-Related Disorders; Mild Cognitive Impairment; Quality of Life; Pain; Wounds and Injury; Brain Injuries; Chronic Disease
Presenting an evaluation model of the trauma registry software.
Asadi, Farkhondeh; Paydar, Somayeh
2018-04-01
Trauma is a major cause of 10% death in the worldwide and is considered as a global concern. This problem has made healthcare policy makers and managers to adopt a basic strategy in this context. Trauma registry has an important and basic role in decreasing the mortality and the disabilities due to injuries resulted from trauma. Today, different software are designed for trauma registry. Evaluation of this software improves management, increases efficiency and effectiveness of these systems. Therefore, the aim of this study is to present an evaluation model for trauma registry software. The present study is an applied research. In this study, general and specific criteria of trauma registry software were identified by reviewing literature including books, articles, scientific documents, valid websites and related software in this domain. According to general and specific criteria and related software, a model for evaluating trauma registry software was proposed. Based on the proposed model, a checklist designed and its validity and reliability evaluated. Mentioned model by using of the Delphi technique presented to 12 experts and specialists. To analyze the results, an agreed coefficient of %75 was determined in order to apply changes. Finally, when the model was approved by the experts and professionals, the final version of the evaluation model for the trauma registry software was presented. For evaluating of criteria of trauma registry software, two groups were presented: 1- General criteria, 2- Specific criteria. General criteria of trauma registry software were classified into four main categories including: 1- usability, 2- security, 3- maintainability, and 4-interoperability. Specific criteria were divided into four main categories including: 1- data submission and entry, 2- reporting, 3- quality control, 4- decision and research support. The presented model in this research has introduced important general and specific criteria of trauma registry software and sub criteria related to each main criteria separately. This model was validated by experts in this field. Therefore, this model can be used as a comprehensive model and a standard evaluation tool for measuring efficiency and effectiveness and performance improvement of trauma registry software. Copyright © 2018 Elsevier B.V. All rights reserved.
Tert-butylhydroquinone post-treatment attenuates neonatal hypoxic-ischemic brain damage in rats.
Zhang, Juan; Tucker, Lorelei Donovan; DongYan; Lu, Yujiao; Yang, Luodan; Wu, Chongyun; Li, Yong; Zhang, Quanguang
2018-06-01
Hypoxic-ischemic (HI) encephalopathy is a leading cause of dire mortality and morbidity in neonates. Unfortunately, no effective therapies have been developed as of yet. Oxidative stress plays a critical role in pathogenesis and progression of neonatal HI. Previously, as a Nrf2 activator, tert-butylhydroquinone (TBHQ) has been demonstrated to exert neuroprotection on brain trauma and ischemic stroke models, as well as oxidative stress-induced cytotoxicity in neurons. It is, however, still unknown whether TBHQ administration can protect against oxidative stress in neonatal HI brain injury. This study was undertaken to determine the neuroprotective effects and mechanisms of TBHQ post-treatment on neonatal HI brain damage. Using a neonatal HI rat model, we demonstrated that TBHQ markedly abated oxidative stress compared to the HI group, as evidenced by decreased oxidative stress indexes, enhanced Nrf2 nuclear accumulation and DNA binding activity, and up-regulated expression of Nrf2 downstream antioxidative genes. Administration of TBHQ likewise significantly suppressed reactive gliosis and release of inflammatory cytokines, and inhibited apoptosis and neuronal degeneration in the neonatal rat cerebral cortex. In addition, infarct size and neuronal damage were attenuated distinctly. These beneficial effects were accompanied by improved neurological reflex and motor coordination as well as amelioration of spatial learning and memory deficits. Overall, our results provide the first documentation of the beneficial effects of TBHQ in neonatal HI model, in part conferred by activation of Nrf2 mediated antioxidative signaling pathways. Copyright © 2018 Elsevier Ltd. All rights reserved.
Posttraumatic Stress Disorder: A Theoretical Model of the Hyperarousal Subtype
Weston, Charles Stewart E.
2014-01-01
Posttraumatic stress disorder (PTSD) is a frequent and distressing mental disorder, about which much remains to be learned. It is a heterogeneous disorder; the hyperarousal subtype (about 70% of occurrences and simply termed PTSD in this paper) is the topic of this article, but the dissociative subtype (about 30% of occurrences and likely involving quite different brain mechanisms) is outside its scope. A theoretical model is presented that integrates neuroscience data on diverse brain regions known to be involved in PTSD, and extensive psychiatric findings on the disorder. Specifically, the amygdala is a multifunctional brain region that is crucial to PTSD, and processes peritraumatic hyperarousal on grounded cognition principles to produce hyperarousal symptoms. Amygdala activity also modulates hippocampal function, which is supported by a large body of evidence, and likewise amygdala activity modulates several brainstem regions, visual cortex, rostral anterior cingulate cortex (rACC), and medial orbitofrontal cortex (mOFC), to produce diverse startle, visual, memory, numbing, anger, and recklessness symptoms. Additional brain regions process other aspects of peritraumatic responses to produce further symptoms. These contentions are supported by neuroimaging, neuropsychological, neuroanatomical, physiological, cognitive, and behavioral evidence. Collectively, the model offers an account of how responses at the time of trauma are transformed into an extensive array of the 20 PTSD symptoms that are specified in the Diagnostic and Statistical Manual of Mental Disorders, Fifth edition. It elucidates the neural mechanisms of a specific form of psychopathology, and accords with the Research Domain Criteria framework. PMID:24772094
A new multiple trauma model of the mouse.
Fitschen-Oestern, Stefanie; Lippross, Sebastian; Klueter, Tim; Weuster, Matthias; Varoga, Deike; Tohidnezhad, Mersedeh; Pufe, Thomas; Rose-John, Stefan; Andruszkow, Hagen; Hildebrand, Frank; Steubesand, Nadine; Seekamp, Andreas; Neunaber, Claudia
2017-11-21
Blunt trauma is the most frequent mechanism of injury in multiple trauma, commonly resulting from road traffic collisions or falls. Two of the most frequent injuries in patients with multiple trauma are chest trauma and extremity fracture. Several trauma mouse models combine chest trauma and head injury, but no trauma mouse model to date includes the combination of long bone fractures and chest trauma. Outcome is essentially determined by the combination of these injuries. In this study, we attempted to establish a reproducible novel multiple trauma model in mice that combines blunt trauma, major injuries and simple practicability. Ninety-six male C57BL/6 N mice (n = 8/group) were subjected to trauma for isolated femur fracture and a combination of femur fracture and chest injury. Serum samples of mice were obtained by heart puncture at defined time points of 0 h (hour), 6 h, 12 h, 24 h, 3 d (days), and 7 d. A tendency toward reduced weight and temperature was observed at 24 h after chest trauma and femur fracture. Blood analyses revealed a decrease in hemoglobin during the first 24 h after trauma. Some animals were killed by heart puncture immediately after chest contusion; these animals showed the most severe lung contusion and hemorrhage. The extent of structural lung injury varied in different mice but was evident in all animals. Representative H&E-stained (Haematoxylin and Eosin-stained) paraffin lung sections of mice with multiple trauma revealed hemorrhage and an inflammatory immune response. Plasma samples of mice with chest trauma and femur fracture showed an up-regulation of IL-1β (Interleukin-1β), IL-6, IL-10, IL-12p70 and TNF-α (Tumor necrosis factor- α) compared with the control group. Mice with femur fracture and chest trauma showed a significant up-regulation of IL-6 compared to group with isolated femur fracture. The multiple trauma mouse model comprising chest trauma and femur fracture enables many analogies to clinical cases of multiple trauma in humans and demonstrates associated characteristic clinical and pathophysiological changes. This model is easy to perform, is economical and can be used for further research examining specific immunological questions.
Raab, Phillip Andrew; Claypoole, Keith Harvey; Hayashi, Kentaro; Baker, Charlene
2012-10-01
Based on the concept of allostatic load, this study proposed and evaluated a model for the relationship between childhood trauma, chronic medical conditions, and intervening variables affecting this relationship in individuals with severe mental illness. Childhood trauma, adult trauma, major depressive disorder symptoms, posttraumatic stress disorder symptoms, health risk factors, and chronic medical conditions were retrospectively assessed using a cross-sectional survey design in a sample of 117 individuals with severe mental illness receiving public mental health services. Path analyses produced a good-fitting model, with significant pathways from childhood to adult trauma and from adult trauma to chronic medical conditions. Multisample path analyses revealed the equivalence of the model across sex. The results support a model for the relationship between childhood and adult trauma and chronic medical conditions, which highlights the pathophysiological toll of cumulative trauma experienced across the life span and the pressing need to prevent retraumatization in this population.
... thinning medicines such as Coumadin Trauma Uncontrolled (severe) high blood pressure STROKES Most strokes are caused when blood clots move to a blood vessel in the brain and block blood flow to that area. For such strokes (ischemic strokes), ...
Return to play guidelines cannot solve the football-related concussion problem.
Johnson, L Syd M
2012-04-01
High school football players are the single largest cohort of athletes playing tackle football, and account for the majority of sport-related concussions. Return to play guidelines (RTPs) have emerged as the preferred approach for addressing the problem of sport-related concussion in youth athletes. This article reviews evidence of the risks and effects of football-related concussion and subconcussive brain trauma, as well as the effectiveness of RTPs as a preventative measure. Literature review utilized PubMed and Google Scholar, using combinations of the search terms "football,"sports,"concussion,"Chronic Traumatic Encephalopathy,"athlete,"youth," and "pediatric." Literature review emphasized medical journals and primary neuroscientific research on sport-related concussion and concussion recovery, particularly in youth athletes. Sport-related concussion is a significant problem among student athletes. Student athletes are more vulnerable to concussion, and at risk of neurocognitive deficits lasting a year or more, with serious effects on academic and athletic performance. RTPs do little to address the problem of sport-related concussion or the chronic damage caused by subconcussive brain trauma. Emphasizing RTPs as the solution to the concussion problem in tackle football risks neglecting genuine reforms that would prevent concussions. More effective concussion prevention is needed. Eliminating tackling from school football for youth under 16 is recommended to reduce concussions. Additional modifications to football are recommended to enhance safety and reduce brain trauma at all levels of play. © 2012, American School Health Association.
Hliebova, O S; Tkachenko, O V
2008-01-01
Main data of the research were data obtained after a complex treatment of 120 persons with late consequences of closed craniocereberal trauma (CCRCT). The treatment included administration of one of nootropic agents (noophen, aminolon or entropil), magnesium sulfate, group B vitamins. All patients have passed a complex examination: specially developed questionnaire, anamnesis gathering, neurologic status, neuropsychological status with the use of multiple-aspect scales and questionnaires, examination of fundus of eye, rheoencephalography, echoencephalography, brain MRT. Results of a complex examination proved positive effect of the use of nootropic agents, in particular noophen, entropil and aminolon in complex treatment of late consequences of closed craniocereberal trauma. For optimisation of the use of nootropic agents in the treatment of late consequences of closed craniocereberal trauma it is recommended to consider features of influence of nootropic agents on certain clinical aspects of the disease.
Philip, Noah S; Tyrka, Audrey R; Albright, Sarah E; Sweet, Lawrence H; Almeida, Jorge; Price, Lawrence H; Carpenter, Linda L
2016-08-01
Early life stress (ELS) is an established risk factor for psychiatric illness and is associated with altered functional connectivity within- and between intrinsic neural networks. The widespread nature of these disruptions suggests that broad imaging measures of neural connectivity, such as global based connectivity (GBC), may be particularly appropriate for studies of this population. GBC is designed to identify brain regions having maximal functional connectedness with the rest of the brain, and alterations in GBC may reflect a restriction or broadening of network synchronization. We evaluated whether ELS severity predicted GBC in a sample (N = 46) with a spectrum of ELS exposure. Participants included healthy controls without ELS, those with at least moderate ELS but without psychiatric disorders, and a group of patients with ELS- related psychiatric disorders. The spatial distribution of GBC peaked in regions of the salience and default mode networks, and ELS severity predicted increased GBC of the left thalamus (corrected p < 0.005, r = 0.498). Thalamic connectivity was subsequently evaluated and revealed reduced connectivity with the salience network, particularly the dorsal anterior cingulate cortex (corrected p < 0.005), only in the patient group. These findings support a model of disrupted thalamic connectivity in ELS and trauma-related negative affect states, and underscore the importance of a transdiagnostic, dimensional neuroimaging approach to understanding the sequelae of trauma exposure. Published by Elsevier Ltd.
Tyagi, Ethika; Agrawal, Rahul; Zhuang, Yumei; Abad, Catalina; Waschek, James A.; Gomez-Pinilla, Fernando
2013-01-01
Mild traumatic brain injury (mTBI, cerebral concussion) is a risk factor for the development of psychiatric illness such as posttraumatic stress disorder (PTSD). We sought to evaluate how omega-3 fatty acids during brain maturation can influence challenges incurred during adulthood (transitioning to unhealthy diet and mTBI) and predispose the brain to a PTSD-like pathobiology. Rats exposed to diets enriched or deficient in omega-3 fatty acids (n-3) during their brain maturation period, were transitioned to a western diet (WD) when becoming adult and then subjected to mTBI. TBI resulted in an increase in anxiety-like behavior and its molecular counterpart NPY1R, a hallmark of PTSD, but these effects were more pronounced in the animals exposed to n-3 deficient diet and switched to WD. The n-3 deficiency followed by WD disrupted BDNF signaling and the activation of elements of BDNF signaling pathway (TrkB, CaMKII, Akt and CREB) in frontal cortex. TBI worsened these effects and more prominently in combination with the n-3 deficiency condition. Moreover, the n-3 deficiency primed the immune system to the challenges imposed by the WD and brain trauma as evidenced by results showing that the WD or mTBI affected brain IL1β levels and peripheral Th17 and Treg subsets only in animals previously conditioned to the n-3 deficient diet. These results provide novel evidence for the capacity of maladaptive dietary habits to lower the threshold for neurological disorders in response to challenges. PMID:23483949
Tyagi, Ethika; Agrawal, Rahul; Zhuang, Yumei; Abad, Catalina; Waschek, James A; Gomez-Pinilla, Fernando
2013-01-01
Mild traumatic brain injury (mTBI, cerebral concussion) is a risk factor for the development of psychiatric illness such as posttraumatic stress disorder (PTSD). We sought to evaluate how omega-3 fatty acids during brain maturation can influence challenges incurred during adulthood (transitioning to unhealthy diet and mTBI) and predispose the brain to a PTSD-like pathobiology. Rats exposed to diets enriched or deficient in omega-3 fatty acids (n-3) during their brain maturation period, were transitioned to a western diet (WD) when becoming adult and then subjected to mTBI. TBI resulted in an increase in anxiety-like behavior and its molecular counterpart NPY1R, a hallmark of PTSD, but these effects were more pronounced in the animals exposed to n-3 deficient diet and switched to WD. The n-3 deficiency followed by WD disrupted BDNF signaling and the activation of elements of BDNF signaling pathway (TrkB, CaMKII, Akt and CREB) in frontal cortex. TBI worsened these effects and more prominently in combination with the n-3 deficiency condition. Moreover, the n-3 deficiency primed the immune system to the challenges imposed by the WD and brain trauma as evidenced by results showing that the WD or mTBI affected brain IL1β levels and peripheral Th17 and Treg subsets only in animals previously conditioned to the n-3 deficient diet. These results provide novel evidence for the capacity of maladaptive dietary habits to lower the threshold for neurological disorders in response to challenges.
Hensler, Thorsten; Sauerland, Stefan; Bouillon, Bertil; Raum, Marcus; Rixen, Dieter; Helling, Hanns-J; Andermahr, Jonas; Neugebauer, Edmund A M
2002-05-01
Our knowledge about the bidirectional interactions between brain and whole organism after trauma is still limited. It was the purpose of this prospective clinical study to determine the influence of severe head trauma (SHT) as well as trauma in different anatomic injury regions on posttraumatic inflammatory mediator levels from patients with multiple injuries. Thirty-five healthy controls, 33 patients with an isolated SHT, 47 patients with multiple injuries without SHT, and 45 patients with both SHT and multiple injuries were studied. The posttraumatic plasma levels of soluble tumor necrosis factor receptors p55 and p75, interleukin (IL)-6, IL-10, and polymorphonuclear neutrophil (PMN) elastase were monitored using enzyme-linked immunosorbent assay technique. The influence of head injuries as well as thorax, abdomen, and extremity injuries on the mediator release from patients with multiple injuries was investigated by multivariate linear regression models. The soluble tumor necrosis factor receptor p55/p75 ratio was significantly elevated within 3 hours of trauma in all three injury groups and returned to reference ratios after 12 hours. The lowest increase was found in patients suffering from an isolated SHT. Lowest mediator levels in this patient population were also found for IL-6, IL-10, and PMN elastase during the first 36 hours after trauma. Additional injuries to the head, thorax, abdomen, and extremity modulated mediator levels to a different degree. No specific effect was found for SHT when compared with other injury groups. Thorax injuries caused the quickest rise in mediator levels, whereas abdominal injuries significantly increased PMN elastase levels 12 to 24 hours after trauma. Traumatic injuries cause the liberation of various mediators, without any specific association between anatomic injury pattern and the pattern of mediator release.
Prehospital helicopter transport and survival of patients with traumatic brain injury.
Bekelis, Kimon; Missios, Symeon; Mackenzie, Todd A
2015-03-01
To investigate the association of helicopter transport with survival of patients with traumatic brain injury (TBI), in comparison with ground emergency medical services (EMS). Helicopter utilization and its effect on the outcomes of TBI remain controversial. We performed a retrospective cohort study involving patients with TBI who were registered in the National Trauma Data Bank between 2009 and 2011. Regression techniques with propensity score matching were used to investigate the association of helicopter transport with survival of patients with TBI, in comparison with ground EMS. During the study period, there were 209,529 patients with TBI who were registered in the National Trauma Data Bank and met the inclusion criteria. Of these patients, 35,334 were transported via helicopters and 174,195 via ground EMS. For patients transported to level I trauma centers, 2797 deaths (12%) were recorded after helicopter transport and 8161 (7.8%) after ground EMS. Multivariable logistic regression analysis demonstrated an association of helicopter transport with increased survival [OR (odds ratio), 1.95; 95% confidence interval (CI), 1.81-2.10; absolute risk reduction (ARR), 6.37%]. This persisted after propensity score matching (OR, 1.88; 95% CI, 1.74-2.03; ARR, 5.93%). For patients transported to level II trauma centers, 1282 deaths (10.6%) were recorded after helicopter transport and 5097 (7.3%) after ground EMS. Multivariable logistic regression analysis demonstrated an association of helicopter transport with increased survival (OR, 1.81; 95% CI, 1.64-2.00; ARR 5.17%). This again persisted after propensity score matching (OR, 1.73; 95% CI, 1.55-1.94; ARR, 4.69). Helicopter transport of patients with TBI to level I and II trauma centers was associated with improved survival, in comparison with ground EMS.
Prehospital Helicopter Transport and Survival of Patients With Traumatic Brain Injury
Mackenzie, Todd A.
2015-01-01
Objective To investigate the association of helicopter transport with survival of patients with traumatic brain injury (TBI), in comparison with ground emergency medical services (EMS). Background Helicopter utilization and its effect on the outcomes of TBI remain controversial. Methods We performed a retrospective cohort study involving patients with TBI who were registered in the National Trauma Data Bank between 2009 and 2011. Regression techniques with propensity score matching were used to investigate the association of helicopter transport with survival of patients with TBI, in comparison with ground EMS. Results During the study period, there were 209,529 patients with TBI who were registered in the National Trauma Data Bank and met the inclusion criteria. Of these patients, 35,334 were transported via helicopters and 174,195 via ground EMS. For patients transported to level I trauma centers, 2797 deaths (12%) were recorded after helicopter transport and 8161 (7.8%) after ground EMS. Multivariable logistic regression analysis demonstrated an association of helicopter transport with increased survival [OR (odds ratio), 1.95; 95% confidence interval (CI), 1.81–2.10; absolute risk reduction (ARR), 6.37%]. This persisted after propensity score matching (OR, 1.88; 95% CI, 1.74–2.03; ARR, 5.93%). For patients transported to level II trauma centers, 1282 deaths (10.6%) were recorded after helicopter transport and 5097 (7.3%) after ground EMS. Multivariable logistic regression analysis demonstrated an association of helicopter transport with increased survival (OR, 1.81; 95% CI, 1.64–2.00; ARR 5.17%). This again persisted after propensity score matching (OR, 1.73; 95% CI, 1.55–1.94; ARR, 4.69). Conclusions Helicopter transport of patients with TBI to level I and II trauma centers was associated with improved survival, in comparison with ground EMS. PMID:24743624
Mickleborough, Marla J.S.; Daniels, Judith K.; Coupland, Nicholas J.; Kao, Raymond; Williamson, Peter C.; Lanius, Ulrich F.; Hegadoren, Kathy; Schore, Allan; Densmore, Maria; Stevens, Todd; Lanius, Ruth A.
2011-01-01
Background Imaging studies of pain processing in primary psychiatric disorders are just emerging. This study explored the neural correlates of stress-induced analgesia in individuals with posttraumatic stress disorder (PTSD). It combined functional magnetic resonance imaging (fMRI) and the traumatic script-driven imagery symptom provocation paradigm to examine the effects of trauma-related cues on pain perception in individuals with PTSD. Methods The study included 17 patients with PTSD and 26 healthy, trauma-exposed controls. Participants received warm (nonpainful) or hot (painful) thermal stimuli after listening to a neutral or a traumatic script while they were undergoing an fMRI scan at a 4.0 T field strength. Results Between-group analyses revealed that after exposure to the traumatic scripts, the blood oxygen level–dependent (BOLD) signal during pain perception was greater in the PTSD group than the control group in the head of the caudate. In the PTSD group, strong positive correlations resulted between BOLD signal and symptom severity in a number of brain regions previously implicated in stress-induced analgesia, such as the thalamus and the head of the caudate nucleus. Trait dissociation as measured by the Dissociative Experiences Scale correlated negatively with the right amygdala and the left putamen. Limitations This study included heterogeneous traumatic experiences, a different proportion of military trauma in the PTSD versus the control group and medicated patients with PTSD. Conclusion These data indicate that in patients with PTSD trauma recall will lead in a state-dependent manner to greater activation in brain regions implicated in stress-induced analgesia. Correlational analyses lend support to cortical hyperinhibition of the amygdala as a function of dissociation. PMID:20964954
Essential trauma care in Ghana: adaptation and implementation on the political tough road.
Quansah, Robert
2006-06-01
The main goal of the Essential Trauma Care (EsTC) project is to promote affordable and sustainable improvements in trauma care, on the ground in individual countries and their health care facilities. This has been occurring in several countries, including Ghana. The EsTC project has helped to solidify previously haphazard interactions between stakeholders from different sectors. It has allowed trauma care clinicians to interact more effectively with other groups, such as the Ministry of Health and the WHO country office. It has allowed the clinicians and other stakeholders to more effectively lobby government for increased attention to trauma care services. These interactions have led to a high-profile stakeholders meeting, the Road Safety and Essential Trauma Care Workshop, which has represented the highest level of attention to trauma care in the country thus far. This meeting has generated a set of policy recommendations, which has been presented to Parliament for study, and, it is hoped, adoption. To convert these recommendations to solid, sustainable action in improving care for the injured, we need to continue to engage in advocacy and to work with Parliament, the Ministry of Health, and other stakeholders, as well as to confront the deeper problems of Ghana's brain drain, civil strife, and poverty.
Age-related injury patterns in Spanish trauma ICU patients. Results from the RETRAUCI.
Llompart-Pou, Juan Antonio; Chico-Fernández, Mario; Sánchez-Casado, Marcelino; Alberdi-Odriozola, Fermín; Guerrero-López, Francisco; Mayor-García, María Dolores; González-Robledo, Javier; Ballesteros-Sanz, María Ángeles; Herrán-Monge, Rubén; León-López, Rafael; López-Amor, Lucía; Bueno-González, Ana
2016-09-01
Injury patterns may differ in trauma patients when age is considered. This information is relevant in the management of trauma patients and for planning preventive measures. We included in the study all patients admitted for traumatic disease in the participating ICUs from November 23 rd , 2012 to July 31 st , 2015 with complete records. Data on epidemiology, injury patterns, severity scores, acute management, resources utilisation and outcome were recorded and compared in the following groups of age: ≤55years (young adults), 56-65 years (adults), 66-75 years (elderly), >75years (very elderly). Quantitative data were reported as median (Interquartile Range (IQR) 25-75) and categorical data as number and percentage. Comparison between groups of age with quantitative variables was performed using the analysis of variance (ANOVA) test. Differences between groups with categorical variables were compared using the chi-square test. A value of p<0.05 was considered significant. We included 2700 patients (78.9% male). Median age was 46 (31-62) years. Blunt trauma was present in 93.7% of the patients. Median RTS was 7.55 (5.97-7.84). Median ISS was 20 (13-26). High-energy trauma secondary to motor-vehicle accident with rhabdomyolysis and drugs abuse showed an inverse linear association with ageing, whilst pedestrian falls with isolated brain injury, being run-over and pre-injury antiplatelets or anticoagulant treatment increased with age (in all cases p<0.001). Multiple injuries were more common in young adults (p<0.001). Acute kidney injury prevalence was higher in elderly and very elderly patients (p<0.001). ICU Mortality increased with age in spite of similar severity scores in all groups (p<0.001). The main cause of death in all groups was intracranial hypertension. Different injury patterns exist in relation with ageing in trauma ICU patients. Adult patients were more likely to present high-energy trauma with significant injuries in different areas whilst elderly patients were prone to low-energy falls, complicated by antiplatelets or anticoagulants use, resulting in severe brain injury and increased mortality. © 2016 Elsevier Ltd. All rights reserved.
A Comparison of Two Models of Risky Sexual Behavior During Late Adolescence.
Braje, Sopagna Eap; Eddy, J Mark; Hall, Gordon C N
2016-01-01
Two models of risky sexual behavior (RSB) were compared in a community sample of late adolescents (N = 223). For the traumagenic model, early negative sexual experiences were posited to lead to an association between negative affect with sexual relationships. For the cognitive escape model, depressive affect was posited to lead to engagement in RSB as a way to avoid negative emotions. The current study examined whether depression explained the relationship between sexual trauma and RSB, supporting the cognitive escape model, or whether it was sexual trauma that led specifically to RSB, supporting the traumagenic model. Physical trauma experiences were also examined to disentangle the effects of sexual trauma compared to other emotionally distressing events. The study examined whether the results would be moderated by participant sex. For males, support was found for the cognitive escape model but not the traumagenic model. Among males, physical trauma and depression predicted engagement in RSB but sexual trauma did not. For females, support was found for the traumagenic and cognitive escape model. Among females, depression and sexual trauma both uniquely predicted RSB. There was an additional suppressor effect of socioeconomic status in predicting RSB among females. Results suggest that the association of trauma type with RSB depends on participant sex. Implications of the current study for RSB prevention efforts are discussed.
Hou, Cailan; Liu, Jun; Wang, Kun; Li, Lingjiang; Liang, Meng; He, Zhong; Liu, Yong; Zhang, Yan; Li, Weihui; Jiang, Tianzi
2007-05-04
Functional neuroimaging studies have largely been performed in patients with longstanding chronic posttraumatic stress disorder (PTSD). Additionally, memory function of PTSD patients has been proved to be impaired. We sought to characterize the brain responses of patients with acute PTSD and implemented a trauma-related short-term memory recall paradigm. Individuals with acute severe PTSD (n=10) resulting from a mining accident and 7 men exposed to the mining accident without PTSD underwent functional magnetic resonance imaging (fMRI) while performing the symptom provocation and trauma-related short-term memory recall paradigms. During symptom provocation paradigm, PTSD subjects showed diminished responses in right anterior cingulate gyrus, left inferior frontal gyrus and bilateral middle frontal gyrus and enhanced left parahippocampal gyrus response compared with controls. During the short-term memory recall paradigm, PTSD group showed diminished responses in right inferior frontal gyrus, right middle frontal and left middle occipital gyrus in comparison with controls. PTSD group exhibited diminished right parahippocampal gyrus response during the memory recall task as compared to the symptom provocation task. Our findings suggest that neurophysiological alterations and memory performance deficit have developed in acute severe PTSD.
Schalinski, I; Moran, J K; Elbert, T; Reindl, V; Wienbruch, C
2017-08-15
Individuals with trauma-related disorders are complex and heterogeneous; part of this complexity derives from additional psychopathology like dissociation as well as environmental adversities such as traumatic stress, experienced throughout the lifespan. Understanding the neurophysiological abnormalities in Post-traumatic stress disorder (PTSD) requires a simultaneous consideration of these factors. Resting state magnetoencephalography (MEG) recordings were obtained from 41 women with PTSD and comorbid depressive symptoms, and 16 healthy women. Oscillatory brain activity was extracted for five frequency bands and 11 source locations, and analyzed in relation to shutdown dissociation and adversity-related measures. Dissociative symptoms were related to increased delta and lowered beta power. Adversity-related measures modulated theta and alpha oscillatory power (in particular childhood sexual abuse) and differed between patients and controls. Findings are based on women with comorbid depressive symptoms and therefore may not be applicable for men or groups with other clinical profiles. In respect to childhood adversities, we had no reliable source for the early infancy. Trauma-related abnormalities in neural organization vary with both exposure to adversities as well as their potential to evoke ongoing shutdown responses. Copyright © 2017 Elsevier B.V. All rights reserved.
Chronic Effects of Mild Neurotrauma: Putting the Cart Before the Horse?
Castellani, Rudy J.; Perry, George; Iverson, Grant L.
2015-01-01
Accumulation of phosphorylated tau (p-tau) is accepted by many as a long-term consequence of repetitive mild neurotrauma, based largely on brain findings in boxers (dementia pugilistica) and, more recently, former professional athletes, military service members, and others exposed to repetitive head trauma. The pathogenic construct is also largely accepted and suggests that repetitive head trauma (typically concussions or subconcussive forces) acts on brain parenchyma to produce a deleterious neuroinflammatory cascade, encompassing p-tau templating, trans-synaptic neurotoxicity, progressive neurodegenerative disease, and associated clinical features. Some caution before accepting these concepts and assumptions is warranted, however. The association between history of concussion and findings of p-tau at autopsy is unclear. Concussions and subconcussive head trauma exposure are poorly defined in available cases and the clinical features reported in CTE are not at present distinguishable from other disorders. Because control groups are limited, the idea that p-tau drives the disease process via protein templating or some other mechanism is preliminary. Much additional research in CTE is needed to determine if it has unique neuropathology and clinical features, the extent to which the neuropathologic alterations cause the clinical features, and whether it can be identified accurately in a living person. PMID:25933385
Yen, Ting-Lin; Chang, Chao-Chien; Chung, Chi-Li; Ko, Wen-Chin; Yang, Chih-Hao; Hsieh, Cheng-Ying
2018-04-06
Traumatic brain injury (TBI) is one of the leading causes of mortality worldwide and leads to persistent cognitive, sensory, motor dysfunction, and emotional disorders. TBI-caused primary injury results in structural damage to brain tissues. Following the primary injury, secondary injuries which are accompanied by neuroinflammation, microglial activation, and additional cell death subsequently occur. Platonin, a cyanine photosensitizing dye, has been used to treat trauma, ulcers, and some types of acute inflammation. In the present study, the neuroprotective effects of platonin against TBI were explored in a controlled cortical impact (CCI) injury model in mice. Treatment with platonin (200 µg/kg) significantly reduced the neurological severity score, general locomotor activity, and anxiety-related behavior, and improved the rotarod performance of CCI-injured mice. In addition, platonin reduced lesion volumes, the expression of cleaved caspase-3, and microglial activation in TBI-insulted brains. Platonin also suppressed messenger (m)RNA levels of caspase-3, caspase-1, cyclooxygenase-2, tumor necrosis factor-α, interleukin-6, and interleukin-1β. On the other hand, free radical production after TBI was obviously attenuated in platonin-treated mice. Treatment with platonin exhibited prominent neuroprotective properties against TBI in a CCI mouse model through its anti-inflammatory, anti-apoptotic, and anti-free radical capabilities. This evidence collectively indicates that platonin may be a potential therapeutic medicine for use with TBIs.
Quality of life of victims of traumatic brain injury six months after the trauma.
Vieira, Rita de Cássia Almeida; Hora, Edilene Curvelo; de Oliveira, Daniel Vieira de; Ribeiro, Maria do Carmo de Oliveira; de Sousa, Regina Márcia Cardoso
2013-01-01
to describe the quality of life of victims of traumatic brain injury six months after the event and to show the relationship between the results observed and the clinical, sociodemographic and return to productivity data. data were analyzed from 47 victims assisted in a trauma reference hospital in the municipality of Aracaju and monitored in an outpatient neurosurgery clinic. The data were obtained through analysis of the patient records and structured interviews, with the application of the World Health Organization Quality of Life, brief version, questionnaire. the victims presented positive perceptions of their quality of life, and the physical domain presented the highest mean value (68.4±22.9). Among the sociodemographic characteristics, a statistically significant correlation was found between marital status and the psychological domain. However, the return to productivity was related to all the domains. the return to productivity was an important factor for the quality of life of the victims of traumatic brain injury and should direct the public policies in promoting the health of these victims.
Pseudofracture: an acute peripheral tissue trauma model.
Darwiche, Sophie S; Kobbe, Philipp; Pfeifer, Roman; Kohut, Lauryn; Pape, Hans-Christoph; Billiar, Timothy
2011-04-18
Following trauma there is an early hyper-reactive inflammatory response that can lead to multiple organ dysfunction and high mortality in trauma patients; this response is often accompanied by a delayed immunosuppression that adds the clinical complications of infection and can also increase mortality. Many studies have begun to assess these changes in the reactivity of the immune system following trauma. Immunologic studies are greatly supported through the wide variety of transgenic and knockout mice available for in vivo modeling; these strains aid in detailed investigations to assess the molecular pathways involved in the immunologic responses. The challenge in experimental murine trauma modeling is long term investigation, as fracture fixation techniques in mice, can be complex and not easily reproducible. This pseudofracture model, an easily reproduced trauma model, overcomes these difficulties by immunologically mimicking an extremity fracture environment, while allowing freedom of movement in the animals and long term survival without the continual, prolonged use of anaesthesia. The intent is to recreate the features of long bone fracture; injured muscle and soft tissue are exposed to damaged bone and bone marrow without breaking the native bone. The pseudofracture model consists of two parts: a bilateral muscle crush injury to the hindlimbs, followed by injection of a bone solution into these injured muscles. The bone solution is prepared by harvesting the long bones from both hindlimbs of an age- and weight-matched syngeneic donor. These bones are then crushed and resuspended in phosphate buffered saline to create the bone solution. Bilateral femur fracture is a commonly used and well-established model of extremity trauma, and was the comparative model during the development of the pseudofracture model. Among the variety of available fracture models, we chose to use a closed method of fracture with soft tissue injury as our comparison to the pseudofracture, as we wanted a sterile yet proportionally severe peripheral tissue trauma model. Hemorrhagic shock is a common finding in the setting of severe trauma, and the global hypoperfusion adds a very relevant element to a trauma model. The pseudofracture model can be easily combined with a hemorrhagic shock model for a multiple trauma model of high severity.
Compact and mobile high resolution PET brain imager
Majewski, Stanislaw [Yorktown, VA; Proffitt, James [Newport News, VA
2011-02-08
A brain imager includes a compact ring-like static PET imager mounted in a helmet-like structure. When attached to a patient's head, the helmet-like brain imager maintains the relative head-to-imager geometry fixed through the whole imaging procedure. The brain imaging helmet contains radiation sensors and minimal front-end electronics. A flexible mechanical suspension/harness system supports the weight of the helmet thereby allowing for patient to have limited movements of the head during imaging scans. The compact ring-like PET imager enables very high resolution imaging of neurological brain functions, cancer, and effects of trauma using a rather simple mobile scanner with limited space needs for use and storage.
Nanowired Drug Delivery Across the Blood-Brain Barrier in Central Nervous System Injury and Repair.
Sharma, Aruna; Menon, Preeti; Muresanu, Dafin F; Ozkizilcik, Asya; Tian, Z Ryan; Lafuente, José V; Sharma, Hari S
2016-01-01
The blood-brain barrier (BBB) is a physiological regulator of transport of essential items from blood to brain for the maintenance of homeostasis of the central nervous system (CNS) within narrow limits. The BBB is also responsible for export of harmful or metabolic products from brain to blood to keep the CNS fluid microenvironment healthy. However, noxious insults to the brain caused by trauma, ischemia or environmental/chemical toxins alter the BBB function to small as well as large molecules e.g., proteins. When proteins enter the CNS fluid microenvironment, development of brain edema occurs due to altered osmotic balance between blood and brain. On the other hand, almost all neurodegenerative diseases and traumatic insults to the CNS and subsequent BBB dysfunction lead to edema formation and cell injury. To treat these brain disorders suitable drug therapy reaching their brain targets is needed. However, due to edema formation or only a focal disruption of the BBB e.g., around brain tumors, many drugs are unable to reach their CNS targets in sufficient quantity. This results in poor therapeutic outcome. Thus, new technology such as nanodelivery is needed for drugs to reach their CNS targets and be effective. In this review, use of nanowires as a possible novel tool to enhance drug delivery into the CNS in various disease models is discussed based on our investigations. These data show that nanowired delivery of drugs may have superior neuroprotective ability to treat several CNS diseases effectively indicating their role in future therapeutic strategies.
Incidence of pulmonary fat embolism at autopsy: an undiagnosed epidemic.
Eriksson, Evert Austin; Pellegrini, Daniela C; Vanderkolk, Wayne E; Minshall, Christian T; Fakhry, Samir M; Cohle, Stephen D
2011-08-01
To determine the incidence, time course, and severity of pulmonary fat embolism (PFE) and cerebral fat embolism (CFE) in trauma and nontrauma patients at the time of autopsy. Prospectively, consecutive patients presenting for autopsy were evaluated for evidence pulmonary and brain fat embolism. The lung sections were obtained from the upper and lower lobe of the patients' lungs on the right and left and brain tissue. This tissue was prepared with osmium tetroxide for histologic evaluation. The number of fat droplets per high power field was counted for all sections. The autopsy reports and medical records were used to determine cause of death, time to death, injuries, if cardiopulmonary resuscitation (CPR) was attempted, sex, height, weight, and age. Fifty decedents were evaluated for PFE and CFE. The average age was 45.8 years ± 17.4 years, average body mass index was 30.1 kg/cm² ± 7.0 kg/cm², and 68% of the patients were men. The cause of death was determined to be trauma in 68% (34/50) of decedents, with 88% (30/34) blunt and 12% (4/34) penetrating. CPR was performed on 30% (15/50), and PFE was present in 76% (38/50) of all patients. Subjects with PFE had no difference with respect to sex, trauma, mechanism of injury, CPR, external contusions, fractures, head, spine, chest, abdominal, pelvic, and extremity injuries. However, subjects without PFE had significantly increased weight (109 ± 29 kg vs. 86 ± 18 kg; p = 0.023) but no difference in height or body mass index. PFE was present in 82% (28/34) of trauma patents and 63% (10/16) nontrauma patients. Eighty-eight percent of nontrauma patients and 86% of trauma patients who received CPR had PFE. Trauma patients with PFE showed no significant difference in any group. Eighty-eight percent of trauma patients died within 1 hour of injury, and 80% (24/30) of them had PFE at the time of autopsy. CFE was present only in one patient with a severe head and cervical spine injury. PFE is common in trauma patients. CPR is associated with a high incidence of PFE regardless of cause of death. PFE occurs acutely within the "golden hour" and should be considered in traumatically injured patients. Further studies are needed to evaluate the pathogenesis of PFE.
Cerebrospinal fluid leak (image)
... brain and spinal cord by acting like a liquid cushion. The fluid allows the organs to be buoyant protecting them from blows or other trauma. Inside the skull the cerebrospinal fluid is contained by the dura which covers ...
... sound different from the way it normally sounds. Causes Some of these disorders develop gradually, but anyone can develop a speech and language impairment suddenly, usually in a trauma. APHASIA Alzheimer disease Brain tumor (more common in aphasia than ...
Concussion: Doug Flutie: "Be on the Safe Side."
... of this page please turn JavaScript on. Feature: Concussion Doug Flutie: "Be on the Safe Side." Past ... for NBC Sports. Flutie is often asked about concussions and brain trauma associated with sports like football, ...
Chen, Ligang; Sun, Xiaochuan; Jiang, Yong; Kuai, Li
2015-06-10
Traumatic brain injury (TBI) is a commonly encountered emergency and severe neurosurgical injury. Previous studies have shown that the presence of the apolipoprotein E (APOE) ε4 allele has adverse outcomes across the spectrum of TBI severity. Our objective was to evaluate the effects of APOE alleles on trauma induced early apoptosis via modification of delayed rectifier K(+) current (Ik(DR)) in neuronal/glial co-cultures model. An ex vivo neuronal/glial co-cultures model carrying individual APOE alleles (ε2, ε3, ε4) of mechanical injury was developed. Flow cytometry and patch clamp recording were performed to analyze the correlations among APOE genotypes, early apoptosis and Ik(DR). We found that APOEε4 increased early apoptosis at 24h (p<0.05) compared to the ones transfected with APOEε3 and APOEε2. Noticeably, APOEε4 significantly reduced the amplitude of the Ik(DR) at 24h compared to the APOEε3 and APOEε2 (p<0.05) which exacerbate Ca(2+) influx. This indicates a possible effect of APOEε4 on early apoptosis via inhibiting Ik(DR) following injury which may adversely affect the outcome of TBI. Copyright © 2015 Elsevier Inc. All rights reserved.
Epidemiology of severe trauma in Spain. Registry of trauma in the ICU (RETRAUCI). Pilot phase.
Chico-Fernández, M; Llompart-Pou, J A; Guerrero-López, F; Sánchez-Casado, M; García-Sáez, I; Mayor-García, M D; Egea-Guerrero, J; Fernández-Ortega, J F; Bueno-González, A; González-Robledo, J; Servià-Goixart, L; Roldán-Ramírez, J; Ballesteros-Sanz, M Á; Tejerina-Alvarez, E; García-Fuentes, C; Alberdi-Odriozola, F
2016-01-01
To describe the characteristics and management of severe trauma disease in Spanish Intensive Care Units (ICUs). Registry of trauma in the ICU (RETRAUCI). Pilot phase. A prospective, multicenter registry. Thirteen Spanish ICUs. Patients with trauma disease admitted to the ICU. None. Epidemiology, out-of-hospital attention, registry of injuries, resources utilization, complications and outcome were evaluated. Patients, n=2242. Mean age 47.1±19.02 years. Males 79%. Blunt trauma 93.9%. Injury Severity Score 22.2±12.1, Revised Trauma Score 6.7±1.6. Non-intentional in 84.4% of the cases. The most common causes of trauma were traffic accidents followed by pedestrian and high-energy falls. Up to 12.4% were taking antiplatelet medication or anticoagulants. Almost 28% had a suspected or confirmed toxic influence in trauma. Up to 31.5% required an out-of-hospital artificial airway. The time from trauma to ICU admission was 4.7±5.3hours. At ICU admission, 68.5% were hemodynamically stable. Brain and chest injuries predominated. A large number of complications were documented. Mechanical ventilation was used in 69.5% of the patients (mean 8.2±9.9 days), of which 24.9% finally required a tracheostomy. The median duration of stay in the ICU and in hospital was 5 (range 3-13) and 9 (5-19) days, respectively. The ICU mortality rate was 12.3%, while the in-hospital mortality rate was 16.0%. The pilot phase of the RETRAUCI offers a first impression of the epidemiology and management of trauma disease in Spanish ICUs. Copyright © 2015 Elsevier España, S.L.U. y SEMICYUC. All rights reserved.
Genomic responses in rat cerebral cortex after traumatic brain injury
von Gertten, Christina; Morales, Amilcar Flores; Holmin, Staffan; Mathiesen, Tiit; Nordqvist, Ann-Christin Sandberg
2005-01-01
Background Traumatic brain injury (TBI) initiates a complex sequence of destructive and neuroprotective cellular responses. The initial mechanical injury is followed by an extended time period of secondary brain damage. Due to the complicated pathological picture a better understanding of the molecular events occurring during this secondary phase of injury is needed. This study was aimed at analysing gene expression patterns following cerebral cortical contusion in rat using high throughput microarray technology with the goal of identifying genes involved in an early and in a more delayed phase of trauma, as genomic responses behind secondary mechanisms likely are time-dependent. Results Among the upregulated genes 1 day post injury, were transcription factors and genes involved in metabolism, e.g. STAT-3, C/EBP-δ and cytochrome p450. At 4 days post injury we observed increased gene expression of inflammatory factors, proteases and their inhibitors, like cathepsins, α-2-macroglobulin and C1q. Notably, genes with biological function clustered to immune response were significantly upregulated 4 days after injury, which was not found following 1 day. Osteopontin and one of its receptors, CD-44, were both upregulated showing a local mRNA- and immunoreactivity pattern in and around the injury site. Fewer genes had decreased expression both 1 and 4 days post injury and included genes implicated in transport, metabolism, signalling, and extra cellular matrix formation, e.g. vitronectin, neuroserpin and angiotensinogen. Conclusion The different patterns of gene expression, with little overlap in genes, 1 and 4 days post injury showed time dependence in genomic responses to trauma. An early induction of factors involved in transcription could lead to the later inflammatory response with strongly upregulated CD-44 and osteopontin expression. An increased knowledge of genes regulating the pathological mechanisms in trauma will help to find future treatment targets. Since trauma is a risk factor for development of neurodegenerative disease, this knowledge may also reduce late negative effects. PMID:16318630
James, Ella L; Lau-Zhu, Alex; Clark, Ian A; Visser, Renée M; Hagenaars, Muriel A; Holmes, Emily A
2016-07-01
A better understanding of psychological trauma is fundamental to clinical psychology. Following traumatic event(s), a clinically significant number of people develop symptoms, including those of Acute Stress Disorder and/or Post Traumatic Stress Disorder. The trauma film paradigm offers an experimental psychopathology model to study both exposure and reactions to psychological trauma, including the hallmark symptom of intrusive memories. We reviewed 74 articles that have used this paradigm since the earliest review (Holmes & Bourne, 2008) until July 2014. Highlighting the different stages of trauma processing, i.e. pre-, peri- and post-trauma, the studies are divided according to manipulations before, during and after film viewing, for experimental as well as correlational designs. While the majority of studies focussed on the frequency of intrusive memories, other reactions to trauma were also modelled. We discuss the strengths and weaknesses of the trauma film paradigm as an experimental psychopathology model of trauma, consider ethical issues, and suggest future directions. By understanding the basic mechanisms underlying trauma symptom development, we can begin to translate findings from the laboratory to the clinic, test innovative science-driven interventions, and in the future reduce the debilitating effects of psychopathology following stressful and/or traumatic events. Copyright © 2016 The Authors. Published by Elsevier Ltd.. All rights reserved.
Yousefsani, Seyed Abdolmajid; Shamloo, Amir; Farahmand, Farzam
2018-04-01
A transverse-plane hyperelastic micromechanical model of brain white matter tissue was developed using the embedded element technique (EET). The model consisted of a histology-informed probabilistic distribution of axonal fibers embedded within an extracellular matrix, both described using the generalized Ogden hyperelastic material model. A correcting method, based on the strain energy density function, was formulated to resolve the stiffness redundancy problem of the EET in large deformation regime. The model was then used to predict the homogenized tissue behavior and the associated localized responses of the axonal fibers under quasi-static, transverse, large deformations. Results indicated that with a sufficiently large representative volume element (RVE) and fine mesh, the statistically randomized microstructure implemented in the RVE exhibits directional independency in transverse plane, and the model predictions for the overall and local tissue responses, characterized by the normalized strain energy density and Cauchy and von Mises stresses, are independent from the modeling parameters. Comparison of the responses of the probabilistic model with that of a simple uniform RVE revealed that only the first one is capable of representing the localized behavior of the tissue constituents. The validity test of the model predictions for the corona radiata against experimental data from the literature indicated a very close agreement. In comparison with the conventional direct meshing method, the model provided almost the same results after correcting the stiffness redundancy, however, with much less computational cost and facilitated geometrical modeling, meshing, and boundary conditions imposing. It was concluded that the EET can be used effectively for detailed probabilistic micromechanical modeling of the white matter in order to provide more accurate predictions for the axonal responses, which are of great importance when simulating the brain trauma or tumor growth. Copyright © 2018 Elsevier Ltd. All rights reserved.
Characterization of blunt chest trauma in a long-term porcine model of severe multiple trauma
Horst, K.; Simon, T. P.; Pfeifer, R.; Teuben, M.; Almahmoud, K.; Zhi, Q.; Santos, S. Aguiar; Wembers, C. Castelar; Leonhardt, S.; Heussen, N.; Störmann, P.; Auner, B.; Relja, B.; Marzi, I.; Haug, A. T.; van Griensven, M.; Kalbitz, M.; Huber-Lang, M.; Tolba, R.; Reiss, L. K.; Uhlig, S.; Marx, G.; Pape, H. C.; Hildebrand, F.
2016-01-01
Chest trauma has a significant relevance on outcome after severe trauma. Clinically, impaired lung function typically occurs within 72 hours after trauma. However, the underlying pathophysiological mechanisms are still not fully elucidated. Therefore, we aimed to establish an experimental long-term model to investigate physiological, morphologic and inflammatory changes, after severe trauma. Male pigs (sus scrofa) sustained severe trauma (including unilateral chest trauma, femur fracture, liver laceration and hemorrhagic shock). Additionally, non-injured animals served as sham controls. Chest trauma resulted in severe lung damage on both CT and histological analyses. Furthermore, severe inflammation with a systemic increase of IL-6 (p = 0.0305) and a local increase of IL-8 in BAL (p = 0.0009) was observed. The pO2/FiO2 ratio in trauma animals decreased over the observation period (p < 0.0001) but not in the sham group (p = 0.2967). Electrical Impedance Tomography (EIT) revealed differences between the traumatized and healthy lung (p < 0.0001). In conclusion, a clinically relevant, long-term model of blunt chest trauma with concomitant injuries has been developed. This reproducible model allows to examine local and systemic consequences of trauma and is valid for investigation of potential diagnostic or therapeutic options. In this context, EIT might represent a radiation-free method for bedside diagnostics. PMID:28000769
Neuroprotective properties of citicoline: facts, doubts and unresolved issues.
Grieb, Pawel
2014-03-01
Citicoline is the generic name of the pharmaceutical substance that chemically is cytidine-5'-diphosphocholine (CDP-choline), which is identical to the natural intracellular precursor of phospholipid phosphatidylcholine. Following injection or ingestion, citicoline is believed to undergo quick hydrolysis and dephosphorylation to yield cytidine and choline, which then enter the brain separately and are used to resynthesize CDP-choline inside brain cells. Neuroprotective activity of citicoline has been repeatedly shown in preclinical models of brain ischaemia and trauma, but two recent, large, pivotal clinical trials have revealed no benefits in ischaemic stroke and traumatic brain injury. However, the substance seems to be beneficial in some slowly advancing neurodegenerative disorders such as glaucoma and mild vascular cognitive impairment. This paper critically discusses issues related to the clinical pharmacology of citicoline, including its pharmacokinetics/biotransformation and pharmacodynamics/mode of action. It is concluded that at present, there is no adequate description of the mechanism(s) of the pharmacological actions of this substance. The possibility should be considered and tested that, in spite of apparently fast catabolism, the intact citicoline molecule or the phosphorylated intermediate products of its hydrolysis, cytidine monophosphate and phosphocholine, are pharmacologically active.
2011-01-01
prognosis. Keywords: cortical spreading depression; electroencephalography; craniotomy ; signal processing; acute brain injury Introduction Cortical...Mannheim, Germany). Inclusion criteria were the clinical decision for craniotomy for lesion evacuation and/or decompression and age ~ 18 years...externalized through a burr hole in the skull (if the bone flap was replaced) and tu nne lied beneath the scalp to exit 2-3 em from the craniotomy
Goldstein, Lee E; McKee, Ann C; Stanton, Patric K
2014-01-01
The association of military blast exposure and brain injury was first appreciated in World War I as commotio cerebri, and later as shell shock. Similar injuries sustained in modern military conflicts are now classified as mild traumatic brain injury (TBI). Recent research has yielded new insights into the mechanisms by which blast exposure leads to acute brain injury and chronic sequelae, including postconcussive syndrome, post-traumatic stress disorder, post-traumatic headache, and chronic traumatic encephalopathy, a tau protein neurodegenerative disease. Impediments to delivery of effective medical care for individuals affected by blast-related TBI include: poor insight into the heterogeneity of neurological insults induced by blast exposure; limited understanding of the mechanisms by which blast exposure injures the brain and triggers sequelae; failure to appreciate interactive injuries that affect frontal lobe function, pituitary regulation, and neurovegetative homeostasis; unknown influence of genetic risk factors, prior trauma, and comorbidities; absence of validated diagnostic criteria and clinical nosology that differentiate clinical endophenotypes; and lack of empirical evidence to guide medical management and therapeutic intervention. While clinicopathological analysis can provide evidence of correlative association, experimental use of animal models remains the primary tool for establishing causal mechanisms of disease. However, the TBI field is confronted by a welter of animal models with varying clinical relevance, thereby impeding scientific coherence and hindering translational progress. Animal models of blast TBI will be far more translationally useful if experimental emphasis focuses on accurate reproduction of clinically relevant endpoints (output) rather than scaled replication of idealized blast shockwaves (input). The utility of an animal model is dependent on the degree to which the model recapitulates pathophysiological mechanisms, neuropathological features, and neurological sequelae observed in the corresponding human disorder. Understanding the purpose of an animal model and the criteria by which experimental results derived from the model are validated are critical components for useful animal modeling. Animal models that reliably demonstrate clinically relevant endpoints will expedite development of new treatments, diagnostics, preventive measures, and rehabilitative strategies for individuals affected by blast TBI and its aftermath.
2014-01-01
The association of military blast exposure and brain injury was first appreciated in World War I as commotio cerebri, and later as shell shock. Similar injuries sustained in modern military conflicts are now classified as mild traumatic brain injury (TBI). Recent research has yielded new insights into the mechanisms by which blast exposure leads to acute brain injury and chronic sequelae, including postconcussive syndrome, post-traumatic stress disorder, post-traumatic headache, and chronic traumatic encephalopathy, a tau protein neurodegenerative disease. Impediments to delivery of effective medical care for individuals affected by blast-related TBI include: poor insight into the heterogeneity of neurological insults induced by blast exposure; limited understanding of the mechanisms by which blast exposure injures the brain and triggers sequelae; failure to appreciate interactive injuries that affect frontal lobe function, pituitary regulation, and neurovegetative homeostasis; unknown influence of genetic risk factors, prior trauma, and comorbidities; absence of validated diagnostic criteria and clinical nosology that differentiate clinical endophenotypes; and lack of empirical evidence to guide medical management and therapeutic intervention. While clinicopathological analysis can provide evidence of correlative association, experimental use of animal models remains the primary tool for establishing causal mechanisms of disease. However, the TBI field is confronted by a welter of animal models with varying clinical relevance, thereby impeding scientific coherence and hindering translational progress. Animal models of blast TBI will be far more translationally useful if experimental emphasis focuses on accurate reproduction of clinically relevant endpoints (output) rather than scaled replication of idealized blast shockwaves (input). The utility of an animal model is dependent on the degree to which the model recapitulates pathophysiological mechanisms, neuropathological features, and neurological sequelae observed in the corresponding human disorder. Understanding the purpose of an animal model and the criteria by which experimental results derived from the model are validated are critical components for useful animal modeling. Animal models that reliably demonstrate clinically relevant endpoints will expedite development of new treatments, diagnostics, preventive measures, and rehabilitative strategies for individuals affected by blast TBI and its aftermath. PMID:25478023
Relational trauma in the context of intimate partner violence.
Lannert, Brittany K; Garcia, Antonia M; Smagur, Kathryn E; Yalch, Matthew M; Levendosky, Alytia A; Bogat, G Anne; Lonstein, Joseph S
2014-12-01
The relational model of trauma (Scheeringa & Zeanah, 2001) proposes that infants' trauma symptoms may be influenced by their mothers' trauma symptoms and disruptions in caregiving behavior, although the mechanisms by which this occurs are less well understood. In this research, we examined the direct and indirect effects of a traumatic event (maternal intimate partner violence [IPV]), maternal trauma symptoms, and impaired (harsh and neglectful) parenting on infant trauma symptoms in a sample of mother-infant dyads (N=182) using structural equation modeling. Mothers completed questionnaires on IPV experienced during pregnancy and the child's first year of life, their past-month trauma symptoms, their child's past-month trauma symptoms, and their parenting behaviors. Results indicated that the effects of prenatal IPV on infant trauma symptoms were partially mediated by maternal trauma symptoms, and the relationship between maternal and infant trauma symptoms was fully mediated by neglectful parenting. Postnatal IPV did not affect maternal or infant trauma symptoms. Findings support the application of the relational model to IPV-exposed mother-infant dyads, with regard to IPV experienced during pregnancy, and help identify potential foci of intervention for professionals working with mothers and children. Copyright © 2014 Elsevier Ltd. All rights reserved.
Impact of playing American professional football on long-term brain function.
Amen, Daniel G; Newberg, Andrew; Thatcher, Robert; Jin, Yi; Wu, Joseph; Keator, David; Willeumier, Kristen
2011-01-01
The authors recruited 100 active and former National Football League players, representing 27 teams and all positions. Players underwent a clinical history, brain SPECT imaging, qEEG, and multiple neuropsychological measures, including MicroCog. Relative to a healthy-comparison group, players showed global decreased perfusion, especially in the prefrontal, temporal, parietal, and occipital lobes, and cerebellar regions. Quantitative EEG findings were consistent, showing elevated slow waves in the frontal and temporal regions. Significant decreases from normal values were found in most neuropsychological tests. This is the first large-scale brain-imaging study to demonstrate significant differences consistent with a chronic brain trauma pattern in professional football players.
miR-98 and let-7g* protect the blood–brain barrier under neuroinflammatory conditions
Rom, Slava; Dykstra, Holly; Zuluaga-Ramirez, Viviana; Reichenbach, Nancy L; Persidsky, Yuri
2015-01-01
Pathologic conditions in the central nervous system, regardless of the underlying injury mechanism, show a certain level of blood–brain barrier (BBB) impairment. Endothelial dysfunction is the earliest event in the initiation of vascular damage caused by inflammation due to stroke, atherosclerosis, trauma, or brain infections. Recently, microRNAs (miRNAs) have emerged as a class of gene expression regulators. The relationship between neuroinflammation and miRNA expression in brain endothelium remains unexplored. Previously, we showed the BBB-protective and anti-inflammatory effects of glycogen synthase kinase (GSK) 3β inhibition in brain endothelium in in vitro and in vivo models of neuroinflammation. Using microarray screening, we identified miRNAs induced in primary human brain microvascular endothelial cells after exposure to the pro-inflammatory cytokine, tumor necrosis factor-α, with/out GSK3β inhibition. Among the highly modified miRNAs, let-7 and miR-98 were predicted to target the inflammatory molecules, CCL2 and CCL5. Overexpression of let-7 and miR-98 in vitro and in vivo resulted in reduced leukocyte adhesion to and migration across endothelium, diminished expression of pro-inflammatory cytokines, and increased BBB tightness, attenuating barrier ‘leakiness' in neuroinflammation conditions. For the first time, we showed that miRNAs could be used as a therapeutic tool to prevent the BBB dysfunction in neuroinflammation. PMID:26126865
miR-98 and let-7g* protect the blood-brain barrier under neuroinflammatory conditions.
Rom, Slava; Dykstra, Holly; Zuluaga-Ramirez, Viviana; Reichenbach, Nancy L; Persidsky, Yuri
2015-12-01
Pathologic conditions in the central nervous system, regardless of the underlying injury mechanism, show a certain level of blood-brain barrier (BBB) impairment. Endothelial dysfunction is the earliest event in the initiation of vascular damage caused by inflammation due to stroke, atherosclerosis, trauma, or brain infections. Recently, microRNAs (miRNAs) have emerged as a class of gene expression regulators. The relationship between neuroinflammation and miRNA expression in brain endothelium remains unexplored. Previously, we showed the BBB-protective and anti-inflammatory effects of glycogen synthase kinase (GSK) 3β inhibition in brain endothelium in in vitro and in vivo models of neuroinflammation. Using microarray screening, we identified miRNAs induced in primary human brain microvascular endothelial cells after exposure to the pro-inflammatory cytokine, tumor necrosis factor-α, with/out GSK3β inhibition. Among the highly modified miRNAs, let-7 and miR-98 were predicted to target the inflammatory molecules, CCL2 and CCL5. Overexpression of let-7 and miR-98 in vitro and in vivo resulted in reduced leukocyte adhesion to and migration across endothelium, diminished expression of pro-inflammatory cytokines, and increased BBB tightness, attenuating barrier 'leakiness' in neuroinflammation conditions. For the first time, we showed that miRNAs could be used as a therapeutic tool to prevent the BBB dysfunction in neuroinflammation.
The Neurobiology of Attachment to Nurturing and Abusive Caregivers
Sullivan, Regina M.
2013-01-01
Decades of research have shown that childhood experiences interact with our genetics to change the structure and function of the brain. Within the range of normal experiences, this system enables the brain to be modified during development to adapt to various environments and cultures. Experiences with and attachment to the caregiver appear particularly important, and recent research suggests this may be due, in part, to the attachment circuitry within the brain. Children have brain circuitry to ensure attachment to their caregivers. Attachment depends on the offspring learning about the caregiver in a process that begins prenatally and continues through most of early life. This attachment serves two basic functions. First, attachment ensures the infant remain in the proximity of the caregiver to procure resources for survival and protection. Second, attachment “quality programs” the brain. This programming impacts immediate behaviors, as well as behaviors that emerge later in development. Animal research has uncovered segments of the attachment circuitry within the brain and has highlighted rapid, robust learning to support this attachment. A child attaches to the caregiver regardless of the quality of care received, even if the caregiver is abusive and neglectful. While a neural system that ensures attachment regardless of the quality of care has immediate benefits, this attachment comes with a high cost. Traumatic experiences interact with genetics to change the structure and function of the brain, compromising emotional and cognitive development and initiating a pathway to pathology. Neurobiological research on animals suggests that trauma during attachment is processed differently by the brain, with maternal presence dramatically attenuating the fear center of the brain (amygdala). Thus, the immaturity of the brain combined with the unique processing of trauma may underlie the enduring effects of abuse, which remain largely hidden in early life but emerge as mental health issues in periadolescence. PMID:24049190
Multidimensional Model of Trauma and Correlated Antisocial Personality Disorder
ERIC Educational Resources Information Center
Martens, Willem H. J.
2005-01-01
Many studies have revealed an important relationship between psychosocial trauma and antisocial personality disorder. A multidimensional model is presented which describes the psychopathological route from trauma to antisocial development. A case report is also included that can illustrate the etiological process from trauma to severe antisocial…
Takayama, Wataru; Endo, Akira; Koguchi, Hazuki; Sugimoto, Momoko; Murata, Kiyoshi; Otomo, Yasuhiro
2018-05-02
Recent studies have implicated the differences in the ABO blood system as a potential risk for various diseases, including hemostatic disorders and hemorrhage. In this study, we evaluated the impact of the difference in the ABO blood type on mortality in patients with severe trauma. A retrospective observational study was conducted in two tertiary emergency critical care medical centers in Japan. Patients with trauma with an Injury Severity Score (ISS) > 15 were included. The association between the different blood types (type O versus other blood types) and the outcomes of all-cause mortality, cause-specific mortalities (exsanguination, traumatic brain injury, and others), ventilator-free days (VFD), and total transfusion volume were evaluated using univariate and multivariate competing-risk regression models. Moreover, the impact of blood type O on the outcomes was assessed using regression coefficients in the multivariate analysis adjusted for age, ISS, and the Revised Trauma Score (RTS). A total of 901 patients were included in this study. The study population was divided based on the ABO blood type: type O, 284 (32%); type A, 285 (32%); type B, 209 (23%); and type AB, 123 (13%). Blood type O was associated with high mortality (28% in patients with blood type O versus 11% in patients with other blood types; p < 0.001). Moreover, this association was observed in a multivariate model (adjusted odds ratio = 2.86, 95% confidence interval 1.84-4.46; p < 0.001). The impact of blood type O on all-cause in-hospital mortality was comparable to 12 increases in the ISS, 1.5 decreases in the RTS, and 26 increases in age. Furthermore, blood type O was significantly associated with higher cause-specific mortalities and shorter VFD compared with the other blood types; however, a significant difference was not observed in the transfusion volume between the two groups. Blood type O was significantly associated with high mortality in severe trauma patients and might have a great impact on outcomes. Further studies elucidating the mechanism underlying this association are warranted to develop the appropriate intervention.
77 FR 75639 - Center for Scientific Review; Notice of Closed Meeting
Federal Register 2010, 2011, 2012, 2013, 2014
2012-12-21
... personal privacy. Name of Committee: Center for Scientific Review Special Emphasis Panel; Brain Trauma....306, Comparative Medicine; 93.333, Clinical Research, 93.306, 93.333, 93.337, 93.393-93.396, 93.837-93...
[Neurophysiologic mechanisms of combat post-extreme state of health].
Tsygan, V N
2014-10-01
The effects of ecological and occupational stress (EOS) on brain neurodynamics of Soviet and Afghanistan servicemen have been studied. The investigations have been made in Afghanistan. Neurophysiological characteristics of traumatic stress and consequences of combat trauma were studied in patients wounded in Afghanistan, in the acute phase as well as since 0.5-3 years after leaving the battlefield. The combined effect of combat situation, hot climate, highlands and desert forms EOS. It does not cause an adaptation process in servicemen. EOS is characterized by changes in bioelectrical indices of brain in interhemispheric relations both as a whole and in isolated rhythm components of EEG, by activating the stress limiting system. It exhibits pathopsychological and autonomic components which remain significant during 3 years after leaving the combat conditions. The formation of a general adaptation syndrome is prevented in explosion trauma under the influence of EOS.
The choroid plexus: function, pathology and therapeutic potential of its transplantation.
Emerich, Dwaine F; Vasconcellos, Alfred V; Elliott, Robert B; Skinner, Stephen J M; Borlongan, Cesario V
2004-08-01
The choroid plexus (CP) produces cerebrospinal fluid (CSF) and forms the blood-CSF barrier. However, the CP may have additional functions in the CNS beyond these traditional roles. Preclinical and clinical studies in ageing and neurodegeneration demonstrate anatomical and physiological changes in CP, suggesting roles in normal and pathological conditions and potentially endogenous repair processes following trauma. One of the broadest functions of the CP is establishing and maintaining the extracellular milieu throughout the brain and spinal cord, in part by secreting numerous growth factors into the CSF. The endogenous secretion of growth factors raises the possibility that transplantable CP might enable delivery of these molecules to the brain, while avoiding the conventional molecular and genetic alterations associated with modifying cells to secrete selected products. This review describes some of the anatomical and functional changes of CP in ageing and neurodegeneration, and recent demonstrations of the therapeutic potential of transplanted CP for neural trauma.
Heim, C; Bosisio, F; Roth, A; Bloch, J; Borens, O; Daniel, R T; Denys, A; Oddo, M; Pasquier, M; Schmidt, S; Schoettker, P; Zingg, T; Wasserfallen, J B
2014-01-01
Switzerland, the country with the highest health expenditure per capita, is lacking data on trauma care and system planning. Recently, 12 trauma centres were designated to be reassessed through a future national trauma registry by 2015. Lausanne University Hospital launched the first Swiss trauma registry in 2008, which contains the largest database on trauma activity nationwide. Prospective analysis of data from consecutively admitted shock room patients from 1 January 2008 to 31 December 2012. Shock room admission is based on physiology and mechanism of injury, assessed by prehospital physicians. Management follows a surgeon-led multidisciplinary approach. Injuries are coded by Association for the Advancement of Automotive Medicine (AAAM) certified coders. Over the 5 years, 1,599 trauma patients were admitted, predominantly males with a median age of 41.4 years and median injury severity score (ISS) of 13. Rate of ISS >15 was 42%. Principal mechanisms of injury were road traffic (40.4%) and falls (34.4%), with 91.5% blunt trauma. Principal patterns were brain (64.4%), chest (59.8%) and extremity/pelvic girdle (52.9%) injuries. Severe (abbreviated injury scale [AIS] score ≥ 3) orthopaedic injuries, defined as extremity and spine injuries together, accounted for 67.1%. Overall, 29.1% underwent immediate intervention, mainly by orthopaedics (27.3%), neurosurgeons (26.3 %) and visceral surgeons (13.9%); 43.8% underwent a surgical intervention within the first 24 hours and 59.1% during their hospitalisation. In-hospital mortality for patients with ISS >15 was 26.2%. This is the first 5-year report on trauma in Switzerland. Trauma workload was similar to other European countries. Despite high levels of healthcare, mortality exceeds published rates by >50%. Regardless of the importance of a multidisciplinary approach, trauma remains a surgical disease and needs dedicated surgical resources.
European trauma guideline compliance assessment: the ETRAUSS study.
Hamada, Sophie Rym; Gauss, Tobias; Pann, Jakob; Dünser, Martin; Leone, Marc; Duranteau, Jacques
2015-12-08
Haemorrhagic shock is the leading cause of preventable death in trauma patients. The 2013 European trauma guidelines emphasise a comprehensive, multidisciplinary, protocol-based approach to trauma care. The aim of the present Europe-wide survey was to compare 2015 practice with the 2013 guidelines. A group of members of the Trauma and Emergency Medicine section of the European Society of Intensive Care Medicine developed a 50-item questionnaire based upon the core recommendations of the 2013 guidelines, employing a multistep approach. The questionnaire covered five fields: care structure and organisation, haemodynamic resuscitation targets, fluid management, transfusion and coagulopathy, and haemorrhage control. The sampling used a two-step approach comprising initial purposive sampling of eminent trauma care providers in each European country, followed by snowball sampling of a maximum number of trauma care providers. A total of 296 responses were collected, 243 (81 %) from European countries. Those from outside the European Union were excluded from the analysis. Approximately three-fourths (74 %) of responders were working in a designated trauma centre. Blunt trauma predominated, accounting for more than 90 % of trauma cases. Considerable heterogeneity was observed in all five core aspects of trauma care, along with frequent deviations from the 2013 guidelines. Only 92 (38 %) of responders claimed to comply with the recommended systolic blood pressure target, and only 81 (33 %) responded that they complied with the target pressure in patients with traumatic brain injury. Crystalloid use was predominant (n = 209; 86 %), and vasopressor use was frequent (n = 171, 76 %) but remained controversial. Only 160 respondents (66 %) declared that they used tranexamic acid always or often. This is the first European trauma survey, to our knowledge. Heterogeneity is significant across centres with regard to the clinical protocols for trauma patients and as to locally available resources. Deviations from guidelines are frequent, differ from region to region and are dependent upon specialty training. Further efforts are required to provide consensus guidelines and to improve their implementation across European countries.
Noninvasive Intracranial Volume and Pressure Measurements Using Ultrasound
NASA Technical Reports Server (NTRS)
Hargens, A. R.
1998-01-01
Prevention of secondary brain injuries following head can be accomplished most easily when intracranial pressure (ICP) is monitored. However, current measurement techniques are invasive and thus not practical in the combat environment. The Pulsed Phase Lock Loop (PPLL) devise, which was developed and patented, uses a unique, noninvasive ultrasonic phase comparison method to measure slight changes in cranial volume which occur with changes in ICP. Year one studies involved instrument improvements and measurement of altered intracranial distance with altered ICP in fresh cadavera. Our software was improved to facilitate future studies of normal subjects and trauma patients. Our bench studies proved that PPLL output correlated highly with changes in path length across a model cranium. Cadaveric studies demonstrated excellent compact, noninvasive devise for monitoring changes in intracranial distance may aid in the early detection of elevated ICP, decreasing risk of secondary brain injury and infection, and returning head-injured patients to duty.
Schuurman, Nadine; Bell, Nathaniel; Hameed, Morad S; Simons, Richard
2008-07-01
Timely access to definitive trauma care has been shown to improve survival rates after severe injury. Unfortunately, despite development of sophisticated trauma systems, prompt, definitive trauma care remains unavailable to over 50 million North Americans, particularly in rural areas. Measures to quantify social and geographic isolation may provide important insights for the development of health policy aimed at reducing the burden of injury and improving access to trauma care in presently under serviced populations. Indices of social deprivation based on census data, and spatial analyses of access to trauma centers based on street network files were combined into a single index, the Population Isolation Vulnerability Amplifier (PIVA) to characterize vulnerability to trauma in socioeconomically and geographically diverse rural and urban communities across British Columbia. Regions with a sufficient core population that are more than one hour travel time from existing services were ranked based on their level of socioeconomic vulnerability. Ten regions throughout the province were identified as most in need of trauma services based on population, isolation and vulnerability. Likewise, 10 communities were classified as some of the least isolated areas and were simultaneously classified as least vulnerable populations in province. The model was verified using trauma services utilization data from the British Columbia Trauma Registry. These data indicate that including vulnerability in the model provided superior results to running the model based only on population and road travel time. Using the PIVA model we have shown that across Census Urban Areas there are wide variations in population dependence on and distances to accredited tertiary/district trauma centers throughout British Columbia. Many of the factors that influence access to definitive trauma care can be combined into a single quantifiable model that researchers in the health sector can use to predict where to place new services. The model can also be used to locate optimal locations for any basket of health services.
Recovery of speed of information processing in closed-head-injury patients.
Zwaagstra, R; Schmidt, I; Vanier, M
1996-06-01
After severe traumatic brain injury, patients almost invariably demonstrate a slowing of reaction time, reflecting a slowing of central information processing. Methodological problems associated with the traditional method for the analysis of longitudinal data (MANOVA) severely complicate studies on cognitive recovery. It is argued that multilevel models are often better suited for the analysis of improvement over time in clinical settings. Multilevel models take into account individual differences in both overall performance level and recovery. These models enable individual predictions for the recovery of speed of information processing. Recovery is modelled in a group of closed-head-injury patients (N = 24). Recovery was predicted by age and severity of injury, as indicated by coma duration. Over a period up to 44 months post trauma, reaction times were found to decrease faster for patients with longer coma duration.
Michinaga, Shotaro; Nagase, Marina; Matsuyama, Emi; Yamanaka, Daisuke; Seno, Naoki; Fuka, Mayu; Yamamoto, Yui; Koyama, Yutaka
2014-01-01
Brain edema is a potentially fatal pathological condition that often occurs in stroke and head trauma. Following brain insults, endothelins (ETs) are increased and promote several pathophysiological responses. This study examined the effects of ETB antagonists on brain edema formation and disruption of the blood-brain barrier in a mouse cold injury model (Five- to six-week-old male ddY mice). Cold injury increased the water content of the injured cerebrum, and promoted extravasation of both Evans blue and endogenous albumin. In the injury area, expression of prepro-ET-1 mRNA and ET-1 peptide increased. Intracerebroventricular (ICV) administration of BQ788 (ETB antagonist), IRL-2500 (ETB antagonist), or FR139317 (ETA antagonist) prior to cold injury significantly attenuated the increase in brain water content. Bolus administration of BQ788, IRL-2500, or FR139317 also inhibited the cold injury-induced extravasation of Evans blue and albumin. Repeated administration of BQ788 and IRL-2500 beginning at 24 h after cold injury attenuated both the increase in brain water content and extravasation of markers. In contrast, FR139317 had no effect on edema formation when administrated after cold injury. Cold injury stimulated induction of glial fibrillary acidic protein-positive reactive astrocytes in the injured cerebrum. Induction of reactive astrocytes after cold injury was attenuated by ICV administration of BQ788 or IRL-2500. These results suggest that ETB receptor antagonists may be an effective approach to ameliorate brain edema formation following brain insults. PMID:25000290
Shimada, Ryo; Abe, Keiichi; Furutani, Rui; Kibayashi, Kazuhiko
2014-03-01
An association has been suggested between trauma and neurological degenerative diseases. Magnetic resonance imaging has revealed that traumatic brain injury (TBI) can cause primary lesions in the midbrain including the substantia nigra (SN). Dopamine transporter (DAT) is mainly expressed in the SN, ventral tegmental area (VTA), and retrorubral field (RRF) of the ventral midbrain. Previous western blot studies have examined DAT levels in the rat frontal cortex and striatum after a controlled cortical impact (CCI); however, no study has comprehensively examined DAT expression in the midbrain following TBI in an animal model. We used immunohistochemistry and in situ hybridization to examine the time-dependent changes in the expression of DAT in the midbrain during the first 14 days after TBI in a mouse CCI model. The expression of DAT protein in the RRF on the side ipsilateral to the site of injury decreased in 14 days after injury. Dopamine transporter mRNA expression in the RRF on the ipsilateral side decreased in 1, 7, and 14 days and increased in 4 days after injury. These findings indicated that TBI induced changes in DAT expression in the RRF. Because the DAT pumps dopamine (DA) out of the synapse back into the cytosol and maintains DA homeostasis, the decreased expression of DAT after TBI may result in decreased DA neurotransmission in the brain.
[Characteristics of traumatic death of people in high mountains].
Mechukaev, A A; Mechukaev, A M
2006-01-01
Lethal accidents with tourists who died of trauma in high mountains of Kabardino-Balkaria were retrospectively studied for the period from 1978 to 2003. The victims were 163 males and 17 females aged 14-72 years. Among causes of death most prevalent was a step-by-step blunt mechanical trauma as a result of falling from a great height. In such conditions the body obtains great kinetic energy causing a severe, often lethal, craniocerebral injury with destruction of the brain, blunt injury of the chest, thoracic and other organs.
Sharma, Hari Shanker; Muresanu, Dafin F; Lafuente, José V; Nozari, Ala; Patnaik, Ranjana; Skaper, Stephen D; Sharma, Aruna
2016-01-01
The blood-brain barrier (BBB) plays a pivotal role in the maintenance of central nervous system function in health and disease. Thus, in almost all neurodegenerative, traumatic or metabolic insults BBB breakdown occurs, allowing entry of serum proteins into the brain fluid microenvironment with subsequent edema formation and cellular injury. Accordingly, pharmacological restoration of BBB function will lead to neurorepair. However, brain injury which occurs following blast, bullet wounds, or knife injury appears to initiate different sets of pathophysiological responses. Moreover, other local factors at the time of injury such as cold or elevated ambient temperatures could also impact the final outcome. Obviously, drug therapy applied to different kinds of brain trauma occurring at either cold or hot environments may respond differently. This is largely due to the fact that internal defense mechanisms of the brain, gene expression, release of neurochemicals and binding of drugs to specific receptors are affected by external ambient temperature changes. These factors may also affect BBB function and development of edema formation after brain injury. In this review, the effects of seasonal exposure to heat and cold on traumatic brain injury using different models i.e., concussive brain injury and cerebral cortical lesion, on BBB dysfunction in relation to drug therapy are discussed. Our observations clearly suggest that closed head injury and open brain injury are two different entities and the external hot or cold environments affect both of them remarkably. Thus, effective pharmacological therapeutic strategies should be designed with these views in mind, as military personnel often experience blunt or penetrating head injuries in either cold or hot environments.
Efficacy of beta-blockade after isolated blunt head injury: does race matter?
Bukur, Marko; Mohseni, Shahin; Mosheni, Shahin; Ley, Eric; Salim, Ali; Margulies, Daniel; Talving, Peep; Demetriades, Demetrios; Inaba, Kenji
2012-04-01
Several retrospective clinical studies and recent prospective animal models demonstrate improved outcomes with beta-blocker administration after isolated blunt head injury. However, no investigations to date have examined the influence of race on the potential therapeutic effectiveness of these medications. Our hypothesis was that mortality benefits associated with beta-blocker exposure after isolated blunt head injury varies based on ethnicity. The trauma registry and the surgical intensive care unit (ICU) databases of an academic Level I trauma center were used to identify all patients sustaining blunt head injury requiring ICU admission from July 1998 to December 2009. Patients sustaining major associated extracranial injuries (Abbreviated Injury Scale [AIS] score ≥ 3 in any body region) were excluded. Patient demographics, injury profile, Injury Severity Score, and beta-blocker exposure were abstracted. The primary outcome evaluated was in-hospital mortality stratified by ethnicity. During the 11-year study period, 3,750 patients were admitted to the Los Angeles County + University of Southern California Medical Center trauma ICU because of blunt trauma. Of these, 65% (n = 2,446) had an "isolated" head injury. When stratified by race, most patients were Hispanics (60%), followed by Whites (21%), Asians (11%), and African Americans (8%). After adjusting for confounding variables with multivariate regression, only those of Asian and Hispanic descent demonstrated significantly improved outcomes associated with beta-blocker administration. Our results indicate that beta-blockade after traumatic brain injury may not benefit all races equally. Further prospective research is necessary to assess this discrepancy in treatment benefit and explore other possible therapeutic interventions.
Age, Ethnicity, and Socioeconomic Factors Impacting Infant and Toddler Fall-Related Trauma.
Shimony-Kanat, Sarit; Benbenishty, Julie
2016-10-04
To characterize trauma-related falls in infants and toddlers aged 0 to 3 years over a 4-year period and develop a risk stratification model of causes of fall injuries. Data on falls of 0 to 3 year olds from 2009 to 2012 were identified from a Jerusalem tertiary hospital trauma registry (N = 422) and the National Trauma Registry of Israel (N = 4,131). Almost half of falls occurred during the first year of life, and 57% of the children were Jewish. The majority of the children lived in low socioeconomic environments, both in the Jewish (59.2%) and Arab (97.6%) samples. Most (74%) of the falls resulted in head injury. A classification and regression tree analysis indicated that falls from furniture were the leading cause of injury in 0 to 12 month olds (estimated probability of 37.9%), whereas slipping is the leading cause in 13 to 36 month olds (estimated probability of 38.4%). Age and ethnicity emerged as the leading predictors of the nature of a fall; Injury Severity Score and the child's sex were secondary. Compared with the national data, Jerusalem children had a higher incidence of falls from buildings (9.3%; 2.4%), a higher moderate-severe Injury Severity Score (>16), a higher incidence of traumatic brain injury, and a longer hospital length of stay (P < 0.001). The leading determinants of fall injuries in children below the age of 3 years are age, ethnicity, and low socioeconomic status. Future outreach community interventions should target these risk groups and be tailored to their defining characteristics.
Ramsey, N F; Aarnoutse, E J; Vansteensel, M J
2014-01-01
Recent scientific achievements bring the concept of neural prosthetics for reinstating lost motor function closer to medical application. Current research involves severely paralyzed people under the age of 65, but implications for seniors with stroke or trauma-induced impairments are clearly on the horizon. Demographic changes will lead to a shortage of personnel to care for an increasing population of senior citizens, threatening maintenance of an acceptable level of care and urging ways for people to live longer at their home independent from personal assistance. This is particularly challenging when people suffer from disabilities such as partial paralysis after stroke or trauma, where daily personal assistance is required. For some of these people, neural prosthetics can reinstate some lost motor function and/or lost communication, thereby increasing independence and possibly quality of life. In this viewpoint article, we present the state of the art in decoding brain activity in the service of brain-computer interfacing. Although some noninvasive applications produce good results, we focus on brain implants that benefit from better quality brain signals. Fully implantable neural prostheses for home use are not available yet, but clinical trials are being prepared. More sophisticated systems are expected to follow in the years to come, with capabilities of interest for less severe paralysis. Eventually the combination of smart robotics and brain implants is expected to enable people to interact well enough with their environment to live an independent life in spite of motor disabilities. © 2014 S. Karger AG, Basel.
Dakouré, Patrick W H; Diallo, Malick; Traoré, André-Charles V; Gandéma, Salifou; Barro, Sie Drissa; Traoré, Ibrahim Alain; Zaré, Cyprien
2015-12-01
Falls from trees related traumas are rarely reported in literature. They are public health problems in developing countries where their frequency is still important. The aim of the study is to describe falls from trees related trauma patterns and to present preventative measures. An annual ongoing prospective study was held in our trauma emergency department (ED) about all the patients who sustained an injury after a recent fall from tree. A questionnaire related to the patient and to the trauma was established. The data were encoded and analysed by a statistical software. One hundred six patients who sustained a fall from tree trauma, out of a total of 139, were studied. Most patients were under 15 years old (76.4 %); they were injured in fruits season (33 %) after a fall from a fruit tree (mango trees, Shea trees, Néré, etc.) and were received late (86 %). Injuries were polymorphic from traumatic brain injuries (51.8 %) and spine injuries (13.2 %) to thoraco-abdominal (21.6 %) and limbs injuries (46.2 %). Three housewives were pregnant at the time of the trauma with secondary abortions. Patients were managed medically (33.9 %), surgically (19.8 %) or by casting (34.9 %) with good outcome in 59 cases. Twelve patients refused medical care and two died. Education programs must focus on picking fruits and leaves in order to make them safe and prevent injuries related to these traditional or professional activities.
Walsh, Mark; Thomas, Scott G.; Howard, Janet C.; Evans, Edward; Guyer, Kirk; Medvecz, Andrew; Swearingen, Andrew; Navari, Rudolph M.; Ploplis, Victoria; Castellino, Francis J.
2011-01-01
Abstract: 25–35% of all seriously injured multiple trauma patients are coagulopathic upon arrival to the emergency department, and therefore early diagnosis and intervention on this subset of patients is important. In addition to standard plasma based tests of coagulation, the thromboelastogram (TEG®) has resurfaced as an ideal test in the trauma population to help guide the clinician in the administration of blood components in a goal directed fashion. We describe how thromboelastographic analysis is used to assist in the management of trauma patients with coagulopathies presenting to the emergency department, in surgery, and in the postoperative period. Indications for the utilization of the TEG® and platelet mapping as point of care testing that can guide blood component therapy in a goal directed fashion in the trauma population are presented with emphasis on the more common reasons such as massive transfusion protocol, the management of traumatic brain injury with bleeding, the diagnosis and management of trauma in patients on platelet antagonists, the utilization of recombinant FVIIa, and the management of coagulopathy in terminal trauma patients in preparation for organ donation. The TEG® allows for judicious and protocol assisted utilization of blood components in a setting that has recently gained acceptance. In our program, the inclusion of the perfusionist with expertise in performing and interpreting TEG® analysis allows the multidisciplinary trauma team to more effectively manage blood products and resuscitation in this population. PMID:22164456
WIEBE, DOUGLAS J.; HOLENA, DANIEL N.; DELGADO, M. KIT; McWILLIAMS, NATHAN; ALTENBURG, JULIET; CARR, BRENDAN G.
2018-01-01
Trauma centers need objective feedback on performance to inform quality improvement efforts. The Trauma Quality Improvement Program recently published recommended methodology for case mix adjustment and benchmarking performance. We tested the feasibility of applying this methodology to develop risk-adjusted mortality models for a statewide trauma system. We performed a retrospective cohort study of patients ≥16 years old at Pennsylvania trauma centers from 2011 to 2013 (n = 100,278). Our main outcome measure was observed-to-expected mortality ratios (overall and within blunt, penetrating, multisystem, isolated head, and geriatric subgroups). Patient demographic variables, physiology, mechanism of injury, transfer status, injury severity, and pre-existing conditions were included as predictor variables. The statistical model had excellent discrimination (area under the curve = 0.94). Funnel plots of observed-to-expected identified five centers with lower than expected mortality and two centers with higher than expected mortality. No centers were outliers for management of penetrating trauma, but five centers had lower and three had higher than expected mortality for blunt trauma. It is feasible to use Trauma Quality Improvement Program methodology to develop risk-adjusted models for statewide trauma systems. Even with smaller numbers of trauma centers that are available in national datasets, it is possible to identify high and low outliers in performance. PMID:28541852
Wiebe, Douglas J; Holena, Daniel N; Delgado, M Kit; McWilliams, Nathan; Altenburg, Juliet; Carr, Brendan G
2017-05-01
Trauma centers need objective feedback on performance to inform quality improvement efforts. The Trauma Quality Improvement Program recently published recommended methodology for case mix adjustment and benchmarking performance. We tested the feasibility of applying this methodology to develop risk-adjusted mortality models for a statewide trauma system. We performed a retrospective cohort study of patients ≥16 years old at Pennsylvania trauma centers from 2011 to 2013 (n = 100,278). Our main outcome measure was observed-to-expected mortality ratios (overall and within blunt, penetrating, multisystem, isolated head, and geriatric subgroups). Patient demographic variables, physiology, mechanism of injury, transfer status, injury severity, and pre-existing conditions were included as predictor variables. The statistical model had excellent discrimination (area under the curve = 0.94). Funnel plots of observed-to-expected identified five centers with lower than expected mortality and two centers with higher than expected mortality. No centers were outliers for management of penetrating trauma, but five centers had lower and three had higher than expected mortality for blunt trauma. It is feasible to use Trauma Quality Improvement Program methodology to develop risk-adjusted models for statewide trauma systems. Even with smaller numbers of trauma centers that are available in national datasets, it is possible to identify high and low outliers in performance.
Skinner, S J M; Geaney, M S; Lin, H; Muzina, M; Anal, A K; Elliott, R B; Tan, P L J
2009-12-01
In neurodegenerative disease and in acute brain injury, there is often local up-regulation of neurotrophin production close to the site of the lesion. Treatment by direct injection of neurotrophins and growth factors close to these lesion sites has repeatedly been demonstrated to improve recovery. It has therefore been proposed that transplanting viable neurotrophin-producing cells close to the trauma lesion, or site of degenerative disease, might provide a novel means for continuous delivery of these molecules directly to the site of injury or to a degenerative region. The aim of this paper is to summarize recent published information and present new experimental data that indicate that long-lasting therapeutic implants of choroid plexus (CP) neuroepithelium may be used to treat brain disease. CP produces and secretes numerous biologically active neurotrophic factors (NT). New gene microarray and proteomics data presented here indicate that many other anti-oxidant, anti-toxin and neuronal support proteins are also produced and secreted by CP cells. In the healthy brain, these circulate in the cerebrospinal fluid through the brain and spinal cord, maintaining neuronal networks and associated cells. Recent publications describe how transplanted CP cells and tissue, either free or in an immunoprotected encapsulated form, can effectively deliver therapeutic molecules when placed near the lesion or site of degenerative disease in animal models. Using simple techniques, CP neuroepithelial cell clusters in suspension culture were very durable, remaining viable for 6 months or more in vitro. The cell culture conditions had little effect on the wide range and activity of genes expressed and proteins secreted. Recently, completed experiments show that implanting CP within alginate-poly-ornithine capsules effectively protected these xenogeneic cells from the host immune system and allowed their survival for 6 months or more in the brains of rats, causing no adverse effects. Previously reported evidence demonstrated that CP cells support the survival and differentiation of neuronal cells in vitro and effectively treat acute brain injury and disease in rodents and non-human primates in vivo. The accumulated preclinical data together with the long-term survival of implanted encapsulated cells in vivo provide a sound base for the investigation of these treatments for chronic inherited and established neurodegenerative conditions.
NASA Astrophysics Data System (ADS)
Skinner, S. J. M.; Geaney, M. S.; Lin, H.; Muzina, M.; Anal, A. K.; Elliott, R. B.; Tan, P. L. J.
2009-12-01
In neurodegenerative disease and in acute brain injury, there is often local up-regulation of neurotrophin production close to the site of the lesion. Treatment by direct injection of neurotrophins and growth factors close to these lesion sites has repeatedly been demonstrated to improve recovery. It has therefore been proposed that transplanting viable neurotrophin-producing cells close to the trauma lesion, or site of degenerative disease, might provide a novel means for continuous delivery of these molecules directly to the site of injury or to a degenerative region. The aim of this paper is to summarize recent published information and present new experimental data that indicate that long-lasting therapeutic implants of choroid plexus (CP) neuroepithelium may be used to treat brain disease. CP produces and secretes numerous biologically active neurotrophic factors (NT). New gene microarray and proteomics data presented here indicate that many other anti-oxidant, anti-toxin and neuronal support proteins are also produced and secreted by CP cells. In the healthy brain, these circulate in the cerebrospinal fluid through the brain and spinal cord, maintaining neuronal networks and associated cells. Recent publications describe how transplanted CP cells and tissue, either free or in an immunoprotected encapsulated form, can effectively deliver therapeutic molecules when placed near the lesion or site of degenerative disease in animal models. Using simple techniques, CP neuroepithelial cell clusters in suspension culture were very durable, remaining viable for 6 months or more in vitro. The cell culture conditions had little effect on the wide range and activity of genes expressed and proteins secreted. Recently, completed experiments show that implanting CP within alginate-poly-ornithine capsules effectively protected these xenogeneic cells from the host immune system and allowed their survival for 6 months or more in the brains of rats, causing no adverse effects. Previously reported evidence demonstrated that CP cells support the survival and differentiation of neuronal cells in vitro and effectively treat acute brain injury and disease in rodents and non-human primates in vivo. The accumulated preclinical data together with the long-term survival of implanted encapsulated cells in vivo provide a sound base for the investigation of these treatments for chronic inherited and established neurodegenerative conditions.
Accuracy of physician-estimated probability of brain injury in children with minor head trauma.
Daymont, Carrie; Klassen, Terry P; Osmond, Martin H
2015-07-01
To evaluate the accuracy of physician estimates of the probability of intracranial injury in children with minor head trauma. This is a subanalysis of a large prospective multicentre cohort study performed from July 2001 to November 2005. During data collection for the derivation of a clinical prediction rule for children with minor head trauma, physicians indicated their estimate of the probability of brain injury visible on computed tomography (P-Injury) and the probability of injury requiring intervention (P-Intervention) by choosing one of the following options: 0%, 1%, 2%, 3%, 4%, 5%, 10%, 20%, 30%, 40%, 50%, 75%, 90%, and 100%. We compared observed frequencies to expected frequencies of injury using Pearson's χ2-test in analyses stratified by the level of each type of predicted probability and by year of age. In 3771 eligible subjects, the mean predicted risk was 4.6% (P-Injury) and 1.4% (P-Intervention). The observed frequency of injury was 4.1% (any injury) and 0.6% (intervention). For all levels of P-Injury from 1% to 40%, the observed frequency of injury was consistent with the expected frequency. The observed frequencies for the 50%, 75%, and 90% levels were lower than expected (p<0.05). For estimates of P-Intervention, the observed frequency was consistently higher than the expected frequency. Physicians underestimated risk for infants (mean P-Intervention 6.2%, actual risk 12.3%, p<0.001). Physician estimates of probability of any brain injury in children were collectively accurate for children with low and moderate degrees of predicted risk. Risk was underestimated in infants.
Long Term Consequences: Effects on Normal Development Profile after Concussion
Daneshvar, Daniel H.; Riley, David O.; Nowinski, Christopher J.; McKee, Ann C.; Stern, Robert A.; Cantu, Robert C.
2011-01-01
Each year in the United States, approximately 1.7 million people are diagnosed with a traumatic brain injury (TBI); an estimated 75% of these injuries are classified as mild TBIs (mTBI) or concussions. The symptoms of such injuries include a variety of somatic, cognitive, and behavioral deficits. While these symptoms typically resolve in a matter of weeks, both children and adults may suffer from Post-Concussion Syndrome (PCS) for months or longer. Suffering from PCS-related symptoms for an extended time may delay an individual’s return to work, adversely affect one’s quality of life, and result in additional social and economic costs. Though a consensus has not been reached on the cause of long-term PCS, it is likely that biological, physiological, psychological, and social elements all play a role in symptom persistence. Additionally, persistent PCS may adversely affect one’s developmental trajectory. The enduring effects of head trauma are not limited to PCS-related effects, however. A progressive tauopathy, chronic traumatic encephalopathy (CTE) is believed to stem from repeated brain trauma. While CTE was originally associated with boxing, it has recently been found in other cases of repetitive head injury including former football and hockey players, and professional wrestlers. In addition to this observed pathology, repetitive brain trauma is also associated with Alzheimer’s-like dementia, Parkinsonism, and motor neuron disease including Amyotrophic Lateral Sclerosis (ALS). With these significant long-term effects of head injuries, there is a clear need to develop effective diagnoses, treatments, and education plans to reduce future burden and incidence. PMID:22050943
Janiri, Delfina; Sani, Gabriele; Rossi, Pietro De; Piras, Fabrizio; Iorio, Mariangela; Banaj, Nerisa; Giuseppin, Giulia; Spinazzola, Edoardo; Maggiora, Matteo; Ambrosi, Elisa; Simonetti, Alessio; Spalletta, Gianfranco
2017-08-01
Volumetric studies on deep gray matter structures in bipolar disorder (BP) have reported contrasting results. Childhood trauma, a relevant environmental stressor for BP, could account for the variability of the results, modulating differences in the amygdala and hippocampus in patients with BP compared with healthy controls (HC). Our study aimed to test this hypothesis. We assessed 105 outpatients, diagnosed with bipolar disorder type I (BP-I) or bipolar disorder type II (BP-II) according to DSM-IV-TR criteria, and 113 HC subjects. History of childhood trauma was obtained using the Childhood Trauma Questionnaire (CTQ). High-resolution magnetic resonance imaging was performed on all subjects and volumes of the amygdala, hippocampus, nucleus accumbens, caudate, pallidum, putamen, and thalamus were measured using FreeSurfer. Patients with BP showed a global reduction of deep gray matter volumes compared to HCs. However, childhood trauma modulated the impact of the diagnosis specifically on the amygdala and hippocampus. Childhood trauma was associated with bilateral decreased volumes in HCs and increased volumes in patients with BP. The results suggest that childhood trauma may have a different effect in health and disease on volumes of gray matter in the amygdala and hippocampus, which are brain areas specifically involved in response to stress and emotion processing. © 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
Cellular Therapies in Trauma and Critical Care Medicine: Forging New Frontiers
Pati, Shibani; Pilia, Marcello; Grimsley, Juanita M.; Karanikas, Alexia T.; Oyeniyi, Blessing; Holcomb, John B.; Cap, Andrew P.; Rasmussen, Todd E.
2015-01-01
ABSTRACT Trauma is a leading cause of death in both military and civilian populations worldwide. Although medical advances have improved the overall morbidity and mortality often associated with trauma, additional research and innovative advancements in therapeutic interventions are needed to optimize patient outcomes. Cell-based therapies present a novel opportunity to improve trauma and critical care at both the acute and chronic phases that often follow injury. Although this field is still in its infancy, animal and human studies suggest that stem cells may hold great promise for the treatment of brain and spinal cord injuries, organ injuries, and extremity injuries such as those caused by orthopedic trauma, burns, and critical limb ischemia. However, barriers in the translation of cell therapies that include regulatory obstacles, challenges in manufacturing and clinical trial design, and a lack of funding are critical areas in need of development. In 2015, the Department of Defense Combat Casualty Care Research Program held a joint military–civilian meeting as part of its effort to inform the research community about this field and allow for effective planning and programmatic decisions regarding research and development. The objective of this article is to provide a “state of the science” review regarding cellular therapies in trauma and critical care, and to provide a foundation from which the potential of this emerging field can be harnessed to mitigate outcomes in critically ill trauma patients. PMID:26428845
Cellular Therapies in Trauma and Critical Care Medicine: Forging New Frontiers.
Pati, Shibani; Pilia, Marcello; Grimsley, Juanita M; Karanikas, Alexia T; Oyeniyi, Blessing; Holcomb, John B; Cap, Andrew P; Rasmussen, Todd E
2015-12-01
Trauma is a leading cause of death in both military and civilian populations worldwide. Although medical advances have improved the overall morbidity and mortality often associated with trauma, additional research and innovative advancements in therapeutic interventions are needed to optimize patient outcomes. Cell-based therapies present a novel opportunity to improve trauma and critical care at both the acute and chronic phases that often follow injury. Although this field is still in its infancy, animal and human studies suggest that stem cells may hold great promise for the treatment of brain and spinal cord injuries, organ injuries, and extremity injuries such as those caused by orthopedic trauma, burns, and critical limb ischemia. However, barriers in the translation of cell therapies that include regulatory obstacles, challenges in manufacturing and clinical trial design, and a lack of funding are critical areas in need of development. In 2015, the Department of Defense Combat Casualty Care Research Program held a joint military-civilian meeting as part of its effort to inform the research community about this field and allow for effective planning and programmatic decisions regarding research and development. The objective of this article is to provide a "state of the science" review regarding cellular therapies in trauma and critical care, and to provide a foundation from which the potential of this emerging field can be harnessed to mitigate outcomes in critically ill trauma patients.
Blanco, Igor; Zirak, Peyman; Dragojević, Tanja; Castellvi, Clara; Durduran, Turgut; Justicia, Carles
2017-10-01
Neural activity is an important biomarker for the presence of neurodegenerative diseases, cerebrovascular alterations, and brain trauma; furthermore, it is a surrogate marker for treatment effects. These pathologies may occur and evolve in a long time-period, thus, noninvasive, transcutaneous techniques are necessary to allow a longitudinal follow-up. In the present work, we have customized noninvasive, transcutaneous, diffuse correlation spectroscopy (DCS) to localize changes in cerebral blood flow (CBF) induced by neural activity. We were able to detect changes in CBF in the somatosensory cortex by using a model of electrical forepaw stimulation in rats. The suitability of DCS measurements for longitudinal monitoring was demonstrated by performing multiple sessions with the same animals at different ages (from 6 to 18 months). In addition, functional DCS has been cross-validated by comparison with functional magnetic resonance imaging (fMRI) in the same animals in a subset of the time-points. The overall results obtained with transcutaneous DCS demonstrates that it can be utilized in longitudinal studies safely and reproducibly to locate changes in CBF induced by neural activity in the small animal brain.
Medical Management of the Severe Traumatic Brain Injury Patient.
Marehbian, Jonathan; Muehlschlegel, Susanne; Edlow, Brian L; Hinson, Holly E; Hwang, David Y
2017-12-01
Severe traumatic brain injury (sTBI) is a major contributor to long-term disability and a leading cause of death worldwide. Medical management of the sTBI patient, beginning with prehospital triage, is aimed at preventing secondary brain injury. This review discusses prehospital and emergency department management of sTBI, as well as aspects of TBI management in the intensive care unit where advances have been made in the past decade. Areas of emphasis include intracranial pressure management, neuromonitoring, management of paroxysmal sympathetic hyperactivity, neuroprotective strategies, prognostication, and communication with families about goals of care. Where appropriate, differences between the third and fourth editions of the Brain Trauma Foundation guidelines for the management of severe traumatic brain injury are highlighted.
Kraft, Reuben H.; Mckee, Phillip Justin; Dagro, Amy M.; Grafton, Scott T.
2012-01-01
This article presents the integration of brain injury biomechanics and graph theoretical analysis of neuronal connections, or connectomics, to form a neurocomputational model that captures spatiotemporal characteristics of trauma. We relate localized mechanical brain damage predicted from biofidelic finite element simulations of the human head subjected to impact with degradation in the structural connectome for a single individual. The finite element model incorporates various length scales into the full head simulations by including anisotropic constitutive laws informed by diffusion tensor imaging. Coupling between the finite element analysis and network-based tools is established through experimentally-based cellular injury thresholds for white matter regions. Once edges are degraded, graph theoretical measures are computed on the “damaged” network. For a frontal impact, the simulations predict that the temporal and occipital regions undergo the most axonal strain and strain rate at short times (less than 24 hrs), which leads to cellular death initiation, which results in damage that shows dependence on angle of impact and underlying microstructure of brain tissue. The monotonic cellular death relationships predict a spatiotemporal change of structural damage. Interestingly, at 96 hrs post-impact, computations predict no network nodes were completely disconnected from the network, despite significant damage to network edges. At early times () network measures of global and local efficiency were degraded little; however, as time increased to 96 hrs the network properties were significantly reduced. In the future, this computational framework could help inform functional networks from physics-based structural brain biomechanics to obtain not only a biomechanics-based understanding of injury, but also neurophysiological insight. PMID:22915997
Pimental, Patricia A; O'Hara, John B; Jandak, Jessica L
2018-01-01
By virtue of their extensive knowledge base and specialized training in brain-behavior relationships, neuropsychologists are especially poised to execute a unique broad-based approach to overall cognitive wellness and should be viewed as primary care providers of cognitive health. This article will describe a novel comprehensive cognitive wellness service delivery model including cognitive health, anti-aging, lifelong wellness, and longevity-oriented practices. These practice areas include brain-based cognitive wellness, emotional and spiritually centric exploration, and related multimodality health interventions. As experts in mind-body connections, neuropsychologists can provide a variety of evidence-based treatment options, empowering patients with a sense of value and purpose. Multiple areas of clinical therapy skill-based learning, tailor-made to fit individual needs, will be discussed including: brain stimulating activities, restorative techniques, automatic negative thoughts and maladaptive thinking reduction, inflammation and pain management techniques, nutrition and culinary focused cognitive wellness, spirituality based practices and mindfulness, movement and exercise, alternative/complimentary therapies, relationship restoration/social engagement, and trauma healing/meaning. Cognitive health rests upon the foundation of counteracting mind-body connection disruptions from multiple etiologies including inflammation, chronic stress, metabolic issues, cardiac conditions, autoimmune disease, neurological disorders, infectious diseases, and allergy spectrum disorders. Superimposed on these issues are lifestyle patterns and negative health behaviors that develop as ill-fated compensatory mechanisms used to cope with life stressors and aging. The brain and body are electrical systems that can "short circuit." The therapy practices inherent in the proposed cognitive wellness service delivery model can provide preventative insulation and circuit breaking against the shock of illness.
Endocannabinoids and traumatic brain injury.
Shohami, Esther; Cohen-Yeshurun, Ayelet; Magid, Lital; Algali, Merav; Mechoulam, Raphael
2011-08-01
Traumatic brain injury (TBI) represents the leading cause of death in young individuals. It triggers the accumulation of harmful mediators, leading to secondary damage, yet protective mechanisms are also set in motion. The endocannabinoid (eCB) system consists of ligands, such as anandamide and 2-arachidonoyl-glycerol (2-AG), receptors (e.g. CB1, CB2), transporters and enzymes, which are responsible for the 'on-demand' synthesis and degradation of these lipid mediators. There is a large body of evidence showing that eCB are markedly increased in response to pathogenic events. This fact, as well as numerous studies on experimental models of brain toxicity, neuroinflammation and trauma supports the notion that the eCB are part of the brain's compensatory or repair mechanisms. These are mediated via CB receptors signalling pathways that are linked to neuronal survival and repair. The levels of 2-AG, the most highly abundant eCB, are significantly elevated after TBI and when administered to TBI mice, 2-AG decreases brain oedema, inflammation and infarct volume and improves clinical recovery. The role of CB1 in mediating these effects was demonstrated using selective antagonists or CB1 knockout mice. CB2 were shown in other models of brain insults to reduce white blood cell rolling and adhesion, to reduce infarct size and to improve motor function. This review is focused on the role the eCB system plays as a self-neuroprotective mechanism and its potential as a basis for the development of novel therapeutic modality for the treatment of CNS pathologies with special emphasis on TBI. © 2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society.
Endocannabinoids and traumatic brain injury
Shohami, Esther; Cohen-Yeshurun, Ayelet; Magid, Lital; Algali, Merav; Mechoulam, Raphael
2011-01-01
Traumatic brain injury (TBI) represents the leading cause of death in young individuals. It triggers the accumulation of harmful mediators, leading to secondary damage, yet protective mechanisms are also set in motion. The endocannabinoid (eCB) system consists of ligands, such as anandamide and 2-arachidonoyl-glycerol (2-AG), receptors (e.g. CB1, CB2), transporters and enzymes, which are responsible for the ‘on-demand’ synthesis and degradation of these lipid mediators. There is a large body of evidence showing that eCB are markedly increased in response to pathogenic events. This fact, as well as numerous studies on experimental models of brain toxicity, neuroinflammation and trauma supports the notion that the eCB are part of the brain's compensatory or repair mechanisms. These are mediated via CB receptors signalling pathways that are linked to neuronal survival and repair. The levels of 2-AG, the most highly abundant eCB, are significantly elevated after TBI and when administered to TBI mice, 2-AG decreases brain oedema, inflammation and infarct volume and improves clinical recovery. The role of CB1 in mediating these effects was demonstrated using selective antagonists or CB1 knockout mice. CB2 were shown in other models of brain insults to reduce white blood cell rolling and adhesion, to reduce infarct size and to improve motor function. This review is focused on the role the eCB system plays as a self-neuroprotective mechanism and its potential as a basis for the development of novel therapeutic modality for the treatment of CNS pathologies with special emphasis on TBI. LINKED ARTICLES This article is part of a themed issue on Cannabinoids in Biology and Medicine. To view the other articles in this issue visit http://dx.doi.org/10.1111/bph.2011.163.issue-7 PMID:21418185
A Mouse Model of Blast-Induced mild Traumatic Brain Injury
Rubovitch, Vardit; Ten-Bosch, Meital; Zohar, Ofer; Harrison, Catherine R.; Tempel-Brami, Catherine; Stein, Elliot; Hoffer, Barry J.; Balaban, Carey D.; Schreiber, Shaul; Chiu, Wen-Ta; Pick, Chaim G.
2011-01-01
Improvised explosive devices (IEDs) are one of the main causes for casualties among civilians and military personnel in the present war against terror. Mild traumatic brain injury from IEDs induces various degrees of cognitive, emotional and behavioral disturbances but knowledge of the exact brain pathophysiology following exposure to blast is poorly understood. The study was aimed at establishing a murine model for a mild BI-TBI that isolates low-level blast pressure effects to the brain without systemic injuries. An open-field explosives detonation was used to replicate, as closely as possible, low-level blast trauma in the battlefield or at a terror-attack site. No alterations in basic neurological assessment or brain gross pathology were found acutely in the blast-exposed mice. At 7 days post blast, cognitive and behavioral tests revealed significantly decreased performance at both 4 and 7 meters distance from the blast (5.5 and 2.5 PSI, respectively). At 30 days post-blast, clear differences were found in animals at both distances in the object recognition test, and in the 7 m group in the Y maze test. Using MRI, T1 weighted images showed an increased BBB permeability one month post-blast. DTI analysis showed an increase in fractional anisotropy (FA) and a decrease in radial diffusivity. These changes correlated with sites of up-regulation of manganese superoxide dismutase 2 in neurons and CXC-motif chemokine receptor 3 around blood vessels in fiber tracts. These results may represent brain axonal and myelin abnormalities. Cellular and biochemical studies are underway in order to further correlate the blast-induced cognitive and behavioral changes and to identify possible underlying mechanisms that may help develop treatment- and neuroprotective modalities. PMID:21946269
Potts, Matthew B; Rola, Radoslaw; Claus, Catherine P; Ferriero, Donna M; Fike, John R; Noble-Haeusslein, Linda J
2009-06-01
Traumatic brain injury (TBI) is a leading cause of disability among young children and is associated with long-term cognitive deficits. These clinical findings have prompted an investigation of the hippocampus in an experimental model of trauma to the developing brain at postnatal day (p21). Previous studies using this model have revealed a progressive loss of neurons in the hippocampus as brain-injured animals mature to young adulthood. Here we determined whether this hippocampal vulnerability is likewise reflected in altered neurogenesis and whether the antioxidant glutathione peroxidase (GPx) modulates neurogenesis during maturation of the injured immature brain. Male transgenic mice that overexpress GPx and wild-type littermates were subjected to controlled cortical impact or sham surgery on p21. At 2 weeks postinjury, the numbers of proliferating cells and immature neurons within the subgranular zone were measured by using Ki-67 and doublecortin, respectively. Bromodeoxyuridine (BrdU) was used to label dividing cells beginning 2 weeks postinjury. Survival (BrdU(+)) and neuronal differentiation (BrdU(+)/NeuN(+)) were then measured 4 weeks later via confocal microscopy. Two-way ANOVA revealed no significant interaction between genotype and injury. Subsequent analysis of the individual effects of injury and genotype, however, showed a significant reduction in subgranular zone proliferation (Ki-67) at 2 weeks postinjury (P = 0.0003) and precursor cell survival (BrdU(+)) at 6 weeks postinjury (P = 0.016) and a trend toward reduced neuronal differentiation (BrdU(+)/NeuN(+)) at 6 weeks postinjury (P = 0.087). Overall, these data demonstrate that traumatic injury to the injured immature brain impairs neurogenesis during maturation and suggest that GPx cannot rescue this reduced neurogenesis. (c) 2009 Wiley-Liss, Inc.
Work-related mild-moderate traumatic brain injury and the construction industry.
Liu, Margaret; Wei, Wenli; Fergenbaum, Jennifer; Comper, Paul; Colantonio, Angela
2011-01-01
Consequences of traumatic brain injury underscore the need to study high-risk groups. Few studies have investigated work-related traumatic brain injuries (WrTBIs) in the construction industry. To examine WrTBIs in Ontario for the construction industry compared to other industries. A retrospective study of individuals who sustained a WrTBI and had a clinical assessment as an outpatient at a hospital-based referral centre. Data were collected for a number of factors including demographic, injury and occupation and were analyzed according to the Person-Environment-Occupation (PEO) model. 435 individuals who sustained a WrTBI. There were 19.1% in the construction industry, 80.9% in other industries. Compared to other industries, individuals in the construction industry were more likely to be male, to not have attained post-secondary education, and experience multiple traumas. WrTBIs in the construction industry were commonly due to elevated work. The construction occupations involved included skilled workers and general labourers, and compared to other industries, WrTBIs occurred most often for those employed for a short duration in the construction industry. Construction industry workers experience serious WrTBIs that are amenable to prevention. Use of the PEO model increased our understanding of WrTBIs in the construction industry.
Perception by Operators of Approach and Withdrawal of Moving Sound Sources
1999-01-01
repeated presentations of signals of the same azimuth value (Figs. 10-11) showed rather great variation in estimations of this subject. In anamnesis of...brain trauma, and in Subj. KL there was an stroke in anamnesis
Operation Brain Trauma Therapy
2013-10-01
Atorvastatin . Both are FDA approved and are, thus, low hanging fruit candidates. Sierra et al69 compared 9 statins with regard to their BBB penetration...et al. Simvastatin and atorvastatin improve behavioral outcome, reduce hippocampal degeneration, and improve cerebral blood flow after experimental
75 FR 38599 - Qualification of Drivers; Exemption Applications; Epilepsy and Seizure Disorders
Federal Register 2010, 2011, 2012, 2013, 2014
2010-07-02
... head-trauma. He did not experience a seizure; however, he was treated for migraine headaches. Mr... diagnosed with a seizure disorder after brain surgery in 1976. He experienced his last seizure in 1995, and...
Esnault, Pierre; Cardinale, Mickaël; Boret, Henry; D'Aranda, Erwan; Montcriol, Ambroise; Bordes, Julien; Prunet, Bertrand; Joubert, Christophe; Dagain, Arnaud; Goutorbe, Philippe; Kaiser, Eric; Meaudre, Eric
2017-07-01
OBJECTIVE Blunt cerebrovascular injuries (BCVIs) affect approximately 1% of patients with blunt trauma. An antithrombotic or anticoagulation therapy is recommended to prevent the occurrence or recurrence of neurovascular events. This treatment has to be carefully considered after severe traumatic brain injury (TBI), due to the risk of intracranial hemorrhage expansion. Thus, the physician in charge of the patient is confronted with a hemorrhagic and ischemic risk. The main objective of this study was to determine the incidence of BCVI after severe TBI. METHODS The authors conducted a prospective, observational, single-center study including all patients with severe TBI admitted in the trauma center. Diagnosis of BCVI was performed using a 64-channel multidetector CT. Characteristics of the patients, CT scan results, and outcomes were collected. A multivariate logistic regression model was developed to determine the risk factors of BCVI. Patients in whom BCVI was diagnosed were treated with systemic anticoagulation. RESULTS In total, 228 patients with severe TBI who were treated over a period of 7 years were included. The incidence of BCVI was 9.2%. The main risk factors were as follows: motorcycle crash (OR 8.2, 95% CI 1.9-34.8), fracture involving the carotid canal (OR 11.7, 95% CI 1.7-80.9), cervical spine injury (OR 13.5, 95% CI 3.1-59.4), thoracic trauma (OR 7.3, 95% CI 1.1-51.2), and hepatic lesion (OR 13.3, 95% CI 2.1-84.5). Among survivors, 82% of patients with BCVI received systemic anticoagulation therapy, beginning at a median of Day 1.5. The overall stroke rate was 19%. One patient had an intracranial hemorrhagic complication. CONCLUSIONS Blunt cerebrovascular injuries are frequent after severe TBI (incidence 9.2%). The main risk factors are high-velocity lesions and injuries near cervical arteries.
Measuring US Army medical evacuation: Metrics for performance improvement.
Galvagno, Samuel M; Mabry, Robert L; Maddry, Joseph; Kharod, Chetan U; Walrath, Benjamin D; Powell, Elizabeth; Shackelford, Stacy
2018-01-01
The US Army medical evacuation (MEDEVAC) community has maintained a reputation for high levels of success in transporting casualties from the point of injury to definitive care. This work served as a demonstration project to advance a model of quality assurance surveillance and medical direction for prehospital MEDEVAC providers within the Joint Trauma System. A retrospective interrupted time series analysis using prospectively collected data was performed as a process improvement project. Records were reviewed during two distinct periods: 2009 and 2014 to 2015. MEDEVAC records were matched to outcomes data available in the Department of Defense Trauma Registry. Abstracted deidentified data were reviewed for specific outcomes, procedures, and processes of care. Descriptive statistics were applied as appropriate. A total of 1,008 patients were included in this study. Nine quality assurance metrics were assessed. These metrics were: airway management, management of hypoxemia, compliance with a blood transfusion protocol, interventions for hypotensive patients, quality of battlefield analgesia, temperature measurement and interventions, proportion of traumatic brain injury (TBI) patients with hypoxemia and/or hypotension, proportion of traumatic brain injury patients with an appropriate assessment, and proportion of missing data. Overall survival in the subset of patients with outcomes data available in the Department of Defense Trauma Registry was 97.5%. The data analyzed for this study suggest overall high compliance with established tactical combat casualty care guidelines. In the present study, nearly 7% of patients had at least one documented oxygen saturation of less than 90%, and 13% of these patients had no documentation of any intervention for hypoxemia, indicating a need for training focus on airway management for hypoxemia. Advances in battlefield analgesia continued to evolve over the period when data for this study was collected. Given the inherent high-risk, high-acuity nature of prehospital advanced life support and emphasis on the use of nonphysician practitioners in an out-of-hospital setting, the need for ongoing medical oversight and quality improvement assessment is crucial. Care management, level IV.
Alexandru, Vlad Ciurea; Aurelia, Mihaela Sandu; Mihai, Popescu; Stefan, Mircea Iencean; Bogdan, Davidescu
2008-01-01
Cranial traumas have different particularities in infants, toddlers, preschool child, school child and teenagers. The assessment of these cases must be individualized according to age. It is completely different in children that in adults. Trauma scales, very useful in grading the severity and predicting outcome in traumatic brain injury, used in adults must be adapted in children. Children have age-related specificity and anatomic particularities, for each of this period of development. Neurotrauma scales, specific for infants and children, such as Pediatric Coma Scale, Children’s Coma Score, Trauma Infant Neurological Score, Glasgow Coma Scale, Liege Scale are reviewed, as well as neurotrauma outcome scales, like Glasgow Outcome Scale, modified Rankin score, KOSCHI score and Barthel Index. The authors present these scales in an exhaustive manner for thoroughgoing pediatric neurotrauma standards. PMID:20108520
Du, Xue; Li, Yu; Ran, Qian; Kim, Pilyoung; Ganzel, Barbara L; Liang, GuangSheng; Hao, Lei; Zhang, Qinglin; Meng, Huaqing; Qiu, Jiang
2016-03-01
Little is known about the effects of developmental trauma on the neural basis of cognitive control among adults who do not have posttraumatic stress disorder. To examine this question, we used functional magnetic resonance imaging to compare the effect of subliminal priming with earthquake-related images on attentional control during a Stroop task in survivors of the 2008 Wenchuan earthquake in China (survivor group, survivors were adolescents at the time of the earthquake) and in matched controls (control group). We found that the survivor group showed greater activation in the left ventral anterior cingulate cortex (vACC) and the bilateral parahippocampal gyrus during the congruent versus incongruent condition, as compared to the control group. Depressive symptoms were positively correlated with left vACC activation during the congruent condition. Moreover, psychophysiological interaction results showed that the survivor group had stronger functional connectivity between the left parahippocampal gyrus and the left vACC than the control group under the congruent-incongruent condition. These results suggested that trauma-related information was linked to abnormal activity in brain networks associated with cognitive control (e.g., vACC-parahippocampal gyrus). This may be a potential biomarker for depression following developmental trauma, and it may also provide a mechanism linking trauma reminders with depression.
Prediction of Chronic Subdural Hematoma in Minor Head Trauma Patients
Han, Sang-Beom; Song, Shi-Hun; Youm, Jin-Young; Koh, Hyeon-Song; Kim, Seon-Hwan; Kwon, Hyon-Jo
2014-01-01
Objective Chronic subdural hematoma (CSDH) is relatively common in neurosurgical field. However not all patients develop CSDH after minor head trauma. In this study, we evaluate the risk factors of post-traumatic CSDH. Methods Two-hundred and seventy-seven patients were enrolled and analyzed in this study from January 2012 to December 2013. Of those, 20 participants had minor head trauma developed CSDH afterward. We also included 257 patients with minor head trauma who did not develop CSDH during the same follow-up period as the control group. We investigated the risk factors related to the development of CSDH after minor head trauma. Results Old age (p=0.014), preexisting diabetes mellitus (p=0.010), hypertension (p=0.026), history of cerebral infarction (p=0.035), antiplatelet agents (p=0.000), acute subdural hematoma in the convexity (p=0.000), encephalomalacia (p=0.029), and long distance between skull and brain parenchyma (p=0.000) were significantly correlated with the development of CSDH after trauma. Multivariate analysis revealed that only the maximum distance between the skull and the cerebral parenchyma was the independent risk factor for the occurrence of CSDH (hazard ratio 2.55, p=0.000). Conclusion We should consider the possibility of developing CSDH in the post-traumatic patients with the identified risk factors. PMID:27169043
Non-accidental Trauma Injury Patterns and Outcomes: A Single Institutional Experience.
Ward, Austin; Iocono, Joseph A; Brown, Samuel; Ashley, Phillip; Draus, John M
2015-09-01
Non-accidental trauma (NAT) victims account for a significant percentage of our pediatric trauma population. We sought to better understand the injury patterns and outcomes of NAT victims who were treated at our level I pediatric trauma center. Trauma registry data were used to identify NAT victims between January 2008 and December 2012. Demographic data, injury severity, hospital course, and outcomes were evaluated. One hundred and eighty-eight cases of suspected NAT were identified. Children were mostly male and white. The median age was 1.1 years; the median Injury Severity Score was 9. Traumatic brain injuries, lower extremity fractures, and skull fractures were the most common injuries. Twenty-seven per cent required medical procedures; most were performed by orthopedic surgery. Twenty-four per cent required admission to the pediatric intensive care unit. The median length of stay was two days. The mortality rate was 9.6 per cent. We generated a hot spot map of our catchment area and identified areas of our state where NAT occurs at increased rates. NAT victims sustain significant morbidity and mortality. Due to the severity of injuries, pediatric trauma surgeons should be involved in the evaluation and management of these children. Much work is needed to prevent the death and disability incurred by victims of child abuse.
Pérez-Bárcena, Jon; Llompart-Pou, Juan A; Homar, Javier; Abadal, Josep M; Raurich, Joan M; Frontera, Guillem; Brell, Marta; Ibáñez, Javier; Ibáñez, Jordi
2008-01-01
Introduction Experimental research has demonstrated that the level of neuroprotection conferred by the various barbiturates is not equal. Until now no controlled studies have been conducted to compare their effectiveness, even though the Brain Trauma Foundation Guidelines recommend that such studies be undertaken. The objectives of the present study were to assess the effectiveness of pentobarbital and thiopental in terms of controlling refractory intracranial hypertension in patients with severe traumatic brain injury, and to evaluate the adverse effects of treatment. Methods This was a prospective, randomized, cohort study comparing two treatments: pentobarbital and thiopental. Patients who had suffered a severe traumatic brain injury (Glasgow Coma Scale score after resuscitation ≤ 8 points or neurological deterioration during the first week after trauma) and with refractory intracranial hypertension (intracranial pressure > 20 mmHg) first-tier measures, in accordance with the Brain Trauma Foundation Guidelines. Results A total of 44 patients (22 in each group) were included over a 5-year period. There were no statistically significant differences in ' baseline characteristics, except for admission computed cranial tomography characteristics, using the Traumatic Coma Data Bank classification. Uncontrollable intracranial pressure occurred in 11 patients (50%) in the thiopental treatment group and in 18 patients (82%) in the pentobarbital group (P = 0.03). Under logistic regression analysis – undertaken in an effort to adjust for the cranial tomography characteristics, which were unfavourable for pentobarbital – thiopental was more effective than pentobarbital in terms of controlling intracranial pressure (odds ratio = 5.1, 95% confidence interval 1.2 to 21.9; P = 0.027). There were no significant differences between the two groups with respect to the incidence of arterial hypotension or infection. Conclusions Thiopental appeared to be more effective than pentobarbital in controlling intracranial hypertension refractory to first-tier measures. These findings should be interpreted with caution because of the imbalance in cranial tomography characteristics and the different dosages employed in the two arms of the study. The incidence of adverse effects was similar in both groups. Trial Registration (Trial registration: US Clinical Trials registry NCT00622570.) PMID:18759980
Neuroendocrine abnormalities in patients with traumatic brain injury
NASA Technical Reports Server (NTRS)
Yuan, X. Q.; Wade, C. E.
1991-01-01
This article provides an overview of hypothalamic and pituitary alterations in brain trauma, including the incidence of hypothalamic-pituitary damage, injury mechanisms, features of the hypothalamic-pituitary defects, and major hypothalamic-pituitary disturbances in brain trauma. While hypothalamic-pituitary lesions have been commonly described at postmortem examination, only a limited number of clinical cases of traumatic hypothalamic-pituitary dysfunction have been reported, probably because head injury of sufficient severity to cause hypothalamic and pituitary damage usually leads to early death. With the improvement in rescue measures, an increasing number of severely head-injured patients with hypothalamic-pituitary dysfunction will survive to be seen by clinicians. Patterns of endocrine abnormalities following brain trauma vary depending on whether the injury site is in the hypothalamus, the anterior or posterior pituitary, or the upper or lower portion of the pituitary stalk. Injury predominantly to the hypothalamus can produce dissociated ACTH-cortisol levels with no response to insulin-induced hypoglycemia and a limited or failed metopirone test, hypothyroxinemia with a preserved thyroid-stimulating hormone response to thyrotropin-releasing hormone, low gonadotropin levels with a normal response to gonadotropin-releasing hormone, a variable growth hormone (GH) level with a paradoxical rise in GH after glucose loading, hyperprolactinemia, the syndrome of inappropriate ADH secretion (SIADH), temporary or permanent diabetes insipidus (DI), disturbed glucose metabolism, and loss of body temperature control. Severe damage to the lower pituitary stalk or anterior lobe can cause low basal levels of all anterior pituitary hormones and eliminate responses to their releasing factors. Only a few cases showed typical features of hypothalamic or pituitary dysfunction. Most severe injuries are sufficient to damage both structures and produce a mixed endocrine picture. Increased intracranial pressure, which releases vasopressin by altering normal hypothalamic anatomy, may represent a unique type of stress to neuroendocrine systems and may contribute to adrenal secretion by a mechanism that requires intact brainstem function. Endocrine function should be monitored in brain-injured patients with basilar skull fractures and protracted posttraumatic amnesia, and patients with SIADH or DI should be closely monitored for other endocrine abnormalities.
Liu, Hai; Kang, Jianyi; Chen, Jing; Li, Guanhua; Li, Xiaoxia; Wang, Jianmin
2012-01-01
This study was conducted to characterize the intracranial pressure response to non-penetrating ballistic impact using a "scalp-skull-brain" pig physical head model and live pigs. Forty-eight ballistic tests targeting the physical head model and anesthetized pigs protected by aramid plates were conducted with standard 9 mm bullets at low (279-297 m/s), moderate (350-372 m/s), and high (409-436 m/s) velocities. Intracranial pressure responses were recorded with pressure sensors embedded in similar brain locations in the physical head model and the anesthetized pigs. Three parameters of intracranial pressure were determined from the measured data: intracranial maximum pressure (Pmax), intracranial maximum pressure impulse (PImax), and the duration of the first positive phase (PPD). The intracranial pressure waves exhibited blast-like characteristics for both the physical model and l live pigs. Of all three parameters, Pmax is most sensitive to impact velocity, with means of 126 kPa (219 kPa), 178 kPa (474 kPa), and 241 kPa (751 kPa) for the physical model (live pigs) for low, moderate, and high impact velocities, respectively. The mean PPD becomes increasingly short as the impact velocity increases, whereas PImax shows the opposite trend. Although the pressure parameters of the physical model were much lower than those of the live pigs, good correlations between the physical model and the live pigs for the three pressure parameters, especially Pmax, were found using linear regression. This investigation suggests that Pmax is a preferred parameter for predicting the severity of the brain injury resulting from behind armor blunt trauma (BABT). PMID:23055817
Gabaeff, Steven C.
2011-01-01
Child abuse experts use diagnostic findings of subdural hematoma and retinal hemorrhages as near-pathognomonic findings to diagnose shaken baby syndrome. This article reviews the origin of this link and casts serious doubt on the specificity of the pathophysiologic connection. The forces required to cause brain injury were derived from an experiment of high velocity impacts on monkeys, that generated forces far above those which might occur with a shaking mechanism. These forces, if present, would invariably cause neck trauma, which is conspicuously absent in most babies allegedly injured by shaking. Subdural hematoma may also be the result of common birth trauma, complicated by prenatal vitamin D deficiency, which also contributes to the appearance of long bone fractures commonly associated with child abuse. Retinal hemorrhage is a non-specific finding that occurs with many causes of increased intracranial pressure, including infection and hypoxic brain injury. The evidence challenging these connections should prompt emergency physicians and others who care for children to consider a broad differential diagnosis before settling on occult shaking as the de-facto cause. While childhood non-accidental trauma is certainly a serious problem, the wide exposure of this information may have the potential to exonerate some innocent care-givers who have been convicted, or may be accused, of child abuse. PMID:21691518
Bar-Kochba, Eyal; Scimone, Mark T.; Estrada, Jonathan B.; Franck, Christian
2016-01-01
In the United States over 1.7 million cases of traumatic brain injury are reported yearly, but predictive correlation of cellular injury to impact tissue strain is still lacking, particularly for neuronal injury resulting from compression. Given the prevalence of compressive deformations in most blunt head trauma, this information is critically important for the development of future mitigation and diagnosis strategies. Using a 3D in vitro neuronal compression model, we investigated the role of impact strain and strain rate on neuronal lifetime, viability, and pathomorphology. We find that strain magnitude and rate have profound, yet distinctively different effects on the injury pathology. While strain magnitude affects the time of neuronal death, strain rate influences the pathomorphology and extent of population injury. Cellular injury is not initiated through localized deformation of the cytoskeleton but rather driven by excess strain on the entire cell. Furthermore we find that, mechanoporation, one of the key pathological trigger mechanisms in stretch and shear neuronal injuries, was not observed under compression. PMID:27480807
Halaweish, Ihab; Nikolian, Vahagn; Georgoff, Patrick; Li, Yongqing; Alam, Hasan B
2014-01-01
Traumatic injuries and their sequela represent a major source of mortality in the United States and globally. Initial treatment for shock, traumatic brain injury, and polytrauma is limited to resuscitation fluids to replace lost volume. To date, there are no treatments with inherent pro-survival properties. Our lab has investigated the use of histone deacetylase inhibitors (HDACIs) as pharmacological agents to improve survival. This class of drugs acts through posttranslational protein modifications and is a direct regulator of chromatin structure and function, as well as the function of numerous cytoplasmic proteins. In models of hemorrhagic shock and polytrauma, administration of HDACIs offers a significant survival advantage, even in the absence of fluid resuscitation. Positive results have also been shown in two-hit models of hemorrhage and sepsis and in hemorrhagic shock combined with traumatic brain injury. Accumulating data generated by our group and others continue to support the use of HDACIs for creation of a pro-survival phenotype. With further research and clinical trials, HDACIs have the potential to be an integral tool in treatment of trauma, especially in the pre-hospital phase. PMID:25565645
Singer, Wibke; Zuccotti, Annalisa; Jaumann, Mirko; Lee, Sze Chim; Panford-Walsh, Rama; Xiong, Hao; Zimmermann, Ulrike; Franz, Christoph; Geisler, Hyun-Soon; Köpschall, Iris; Rohbock, Karin; Varakina, Ksenya; Verpoorten, Sandrine; Reinbothe, Thomas; Schimmang, Thomas; Rüttiger, Lukas; Knipper, Marlies
2013-02-01
Increasing evidence shows that hearing loss is a risk factor for tinnitus and hyperacusis. Although both often coincide, a causal relationship between tinnitus and hyperacusis has not been shown. Currently, tinnitus and hyperacusis are assumed to be caused by elevated responsiveness in subcortical circuits. We examined both the impact of different degrees of cochlear damage and the influence of stress priming on tinnitus induction. We used (1) a behavioral animal model for tinnitus designed to minimize stress, (2) ribbon synapses in inner hair cells (IHCs) as a measure for deafferentation, (3) the integrity of auditory brainstem responses (ABR) to detect differences in stimulus-evoked neuronal activity, (4) the expression of the activity-regulated cytoskeletal protein, Arc, to identify long-lasting changes in network activity within the basolateral amygdala (BLA), hippocampal CA1, and auditory cortex (AC), and (5) stress priming to investigate the influence of corticosteroid on trauma-induced brain responses. We observed that IHC ribbon loss (deafferentation) leads to tinnitus when ABR functions remain reduced and Arc is not mobilized in the hippocampal CA1 and AC. If, however, ABR waves are functionally restored and Arc is mobilized, tinnitus does not occur. Both central response patterns were found to be independent of a profound threshold loss and could be shifted by the corticosterone level at the time of trauma. We, therefore, discuss the findings in the context of a history of stress that can trigger either an adaptive or nonadaptive brain response following injury.
Ahmadian, Amir; Baa J, Ali A; Garcia, Michael; Carey, Carolyn; Rodriguez, Luis; Storrs, Bruce; Tuite, Gerald F
2012-09-01
The authors present a case of extreme brain herniation encountered during decompressive craniectomy in a 21-month-old boy who suffered a trauma event that necessitated temporary scalp closure in which a sterile silicone sheet was placed. Although the clinical situation is usually expected to lead to brain death or severe disability, the patient's 3-year follow-up examination revealed a highly functional child with a good quality of life. The authors discuss the feasibility and advantages of temporary scalp expansion as a treatment option when extreme brain herniation is encountered during craniotomy.
Asensi, V; Alvarez, M; Carton, J A; Lago, M; Maradona, J A; Asensi, J M; Arribas, J M
2002-08-01
Eikenella corrodens is a facultatively anaerobic gram-negative rod that colonizes the oral cavity and very rarely produces central nervous system (CNS) infections. Frontal lobe abscesses are occasionally associated with a dental source of infection. We report a case of an adult man with overzealous dental cleaning habits who developed a right frontal brain abscess caused by E. corrodens. He underwent neurosurgical drainage of the pus and was successfully treated with imipenem 4 g/i.v./day for 4 weeks with no complications. Repeated periodontal trauma could explain the Eikenella brain abscess in this case.